Compounds that inhibit HMG-CoA reductases. They have been shown to directly lower cholesterol synthesis.
Enzymes that catalyze the reversible reduction of alpha-carboxyl group of 3-hydroxy-3-methylglutaryl-coenzyme A to yield MEVALONIC ACID.
Specific hydroxymethylglutaryl CoA reductases that utilize the cofactor NAD. This class of enzymes performs a catabolic role in microorganisms such as Pseudomonas mevalonii where it oxidatively acetylates MEVALONIC ACID to form 3-HYDROXY-3-METHYLGLUTARYL-COENZYME A and NADH.
A fungal metabolite isolated from cultures of Aspergillus terreus. The compound is a potent anticholesteremic agent. It inhibits 3-hydroxy-3-methylglutaryl coenzyme A reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES), which is the rate-limiting enzyme in cholesterol biosynthesis. It also stimulates the production of low-density lipoprotein receptors in the liver.
An enzyme that catalyzes the synthesis of hydroxymethylglutaryl-CoA from acetyl-CoA and acetoacetyl-CoA. This is a key enzyme in steroid biosynthesis. This enzyme was formerly listed as EC 4.1.3.5.
The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils.
A voluntary organization concerned with the prevention and treatment of heart and vascular diseases.
Persons living in the United States of Mexican (MEXICAN AMERICANS), Puerto Rican, Cuban, Central or South American, or other Spanish culture or origin. The concept does not include Brazilian Americans or Portuguese Americans.
Peptidoglycan immunoadjuvant originally isolated from bacterial cell wall fragments; also acts as pyrogen and may cause arthritis; stimulates both humoral and cellular immunity.
A derivative of LOVASTATIN and potent competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES), which is the rate-limiting enzyme in cholesterol biosynthesis. It may also interfere with steroid hormone production. Due to the induction of hepatic LDL RECEPTORS, it increases breakdown of LDL CHOLESTEROL.
Substances that lower the levels of certain LIPIDS in the BLOOD. They are used to treat HYPERLIPIDEMIAS.
Substances used to lower plasma CHOLESTEROL levels.
Cholesterol which is contained in or bound to low density lipoproteins (LDL), including CHOLESTEROL ESTERS and free cholesterol.
Distensibility measure of a chamber such as the lungs (LUNG COMPLIANCE) or bladder. Compliance is expressed as a change in volume per unit change in pressure.
Solid dosage forms, of varying weight, size, and shape, which may be molded or compressed, and which contain a medicinal substance in pure or diluted form. (Dorland, 28th ed)
Voluntary cooperation of the patient in following a prescribed regimen.
An imbalance between myocardial functional requirements and the capacity of the CORONARY VESSELS to supply sufficient blood flow. It is a form of MYOCARDIAL ISCHEMIA (insufficient blood supply to the heart muscle) caused by a decreased capacity of the coronary vessels.
Liver disease in which the normal microcirculation, the gross vascular anatomy, and the hepatic architecture have been variably destroyed and altered with fibrous septa surrounding regenerated or regenerating parenchymal nodules.
Steroid acids and salts. The primary bile acids are derived from cholesterol in the liver and usually conjugated with glycine or taurine. The secondary bile acids are further modified by bacteria in the intestine. They play an important role in the digestion and absorption of fat. They have also been used pharmacologically, especially in the treatment of gallstones.
Impairment of bile flow due to injury to the HEPATOCYTES; BILE CANALICULI; or the intrahepatic bile ducts (BILE DUCTS, INTRAHEPATIC).
The first alpha-globulins to appear in mammalian sera during FETAL DEVELOPMENT and the dominant serum proteins in early embryonic life.
Pathological processes of the LIVER.
Tumors or cancer of the LIVER.
Detailed account or statement or formal record of data resulting from empirical inquiry.
Databases containing information about PROTEINS such as AMINO ACID SEQUENCE; PROTEIN CONFORMATION; and other properties.
A loose confederation of computer communication networks around the world. The networks that make up the Internet are connected through several backbone networks. The Internet grew out of the US Government ARPAnet project and was designed to facilitate information exchange.
The portion of an interactive computer program that issues messages to and receives commands from a user.
Sequential operating programs and data which instruct the functioning of a digital computer.
Linear POLYPEPTIDES that are synthesized on RIBOSOMES and may be further modified, crosslinked, cleaved, or assembled into complex proteins with several subunits. The specific sequence of AMINO ACIDS determines the shape the polypeptide will take, during PROTEIN FOLDING, and the function of the protein.
Inflammation of the optic nerve. Commonly associated conditions include autoimmune disorders such as MULTIPLE SCLEROSIS, infections, and granulomatous diseases. Clinical features include retro-orbital pain that is aggravated by eye movement, loss of color vision, and contrast sensitivity that may progress to severe visual loss, an afferent pupillary defect (Marcus-Gunn pupil), and in some instances optic disc hyperemia and swelling. Inflammation may occur in the portion of the nerve within the globe (neuropapillitis or anterior optic neuritis) or the portion behind the globe (retrobulbar neuritis or posterior optic neuritis).
Clarity or sharpness of OCULAR VISION or the ability of the eye to see fine details. Visual acuity depends on the functions of RETINA, neuronal transmission, and the interpretative ability of the brain. Normal visual acuity is expressed as 20/20 indicating that one can see at 20 feet what should normally be seen at that distance. Visual acuity can also be influenced by brightness, color, and contrast.
Damage or trauma inflicted to the eye by external means. The concept includes both surface injuries and intraocular injuries.
Bleeding in the anterior chamber of the eye.
The 2nd cranial nerve which conveys visual information from the RETINA to the brain. The nerve carries the axons of the RETINAL GANGLION CELLS which sort at the OPTIC CHIASM and continue via the OPTIC TRACTS to the brain. The largest projection is to the lateral geniculate nuclei; other targets include the SUPERIOR COLLICULI and the SUPRACHIASMATIC NUCLEI. Though known as the second cranial nerve, it is considered part of the CENTRAL NERVOUS SYSTEM.
An autoimmune disorder mainly affecting young adults and characterized by destruction of myelin in the central nervous system. Pathologic findings include multiple sharply demarcated areas of demyelination throughout the white matter of the central nervous system. Clinical manifestations include visual loss, extra-ocular movement disorders, paresthesias, loss of sensation, weakness, dysarthria, spasticity, ataxia, and bladder dysfunction. The usual pattern is one of recurrent attacks followed by partial recovery (see MULTIPLE SCLEROSIS, RELAPSING-REMITTING), but acute fulminating and chronic progressive forms (see MULTIPLE SCLEROSIS, CHRONIC PROGRESSIVE) also occur. (Adams et al., Principles of Neurology, 6th ed, p903)
A plasma protein that circulates in increased amounts during inflammation and after tissue damage.
A hepatocyte nuclear factor that is closely related to HEPATOCYTE NUCLEAR FACTOR 1-ALPHA but is only weakly expressed in the LIVER. Mutations in hepatocyte nuclear factor 1-beta are associated with renal CYSTS and MATURITY-ONSET DIABETES MELLITUS type 5.
A subfamily of nuclear receptors that regulate GENETIC TRANSCRIPTION of a diverse group of GENES involved in the synthesis of BLOOD COAGULATION FACTORS; and in GLUCOSE; CHOLESTEROL; and FATTY ACIDS metabolism.
Hepatocyte nuclear factor 1-alpha is a transcription factor found in the LIVER; PANCREAS; and KIDNEY that regulates HOMEOSTASIS of GLUCOSE.
A transcription factor that regulates the expression of a large set of hepatic proteins including SERUM ALBUMIN; beta-fibrinogen; and ALPHA 1-ANTITRYPSIN. It is composed of hetero- or homo-dimers of HEPATOCYTE NUCLEAR FACTOR 1-ALPHA and HEPATOCYTE NUCLEAR FACTOR 1-BETA.
A onecut transcription factor that regulates expression of GENES involved in EMBRYONIC DEVELOPMENT of the PANCREAS and LIVER.
A forkhead transcription factor that regulates expression of metabolic GENES and is involved in EMBRYONIC DEVELOPMENT. Mutations in HNF-3beta have been associated with CONGENITAL HYPERINSULINISM.
Software used to locate data or information stored in machine-readable form locally or at a distance such as an INTERNET site.
Databases devoted to knowledge about specific genes and gene products.
The complete genetic complement contained in the DNA of a set of CHROMOSOMES in a HUMAN. The length of the human genome is about 3 billion base pairs.
Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the ANTIGEN (or a very similar shape) that induced their synthesis in cells of the lymphoid series (especially PLASMA CELLS).
Cell surface molecules on cells of the immune system that specifically bind surface molecules or messenger molecules and trigger changes in the behavior of cells. Although these receptors were first identified in the immune system, many have important functions elsewhere.
A category of nucleic acid sequences that function as units of heredity and which code for the basic instructions for the development, reproduction, and maintenance of organisms.

Distinct and combined vascular effects of ACE blockade and HMG-CoA reductase inhibition in hypertensive subjects. (1/4319)

Hypercholesterolemia and hypertension are frequently associated with elevated sympathetic activity. Both are independent cardiovascular risk factors and both affect endothelium-mediated vasodilation. To identify the effects of cholesterol-lowering and antihypertensive treatments on vascular reactivity and vasodilative capacity, we studied 30 hypercholesterolemic hypertensive subjects. They received placebo for 4 weeks, either enalapril or simvastatin for 14 weeks, and, finally, both medications for an additional 14 weeks. Postischemic forearm blood flow (MFBF) and minimal vascular resistance (mFVR) were used as indices of vasodilative capacity and structural vascular damage, respectively. Total (resting-stress-recovery phases) cardiovascular (blood pressure [BP] and heart rate [HR]) and regional hemodynamic (FBF and FVR) reactivity to stressful stimuli were calculated as area-under-the-curve (auc) (valuextime). Compared with baseline levels, simvastatin reduced total (TOT-C) and LDL cholesterol (LDL-C) (1.27 mmol/L, P<0.001 and 1.33 mmol/L, P<0.001, respectively). Enalapril also reduced TOT-C and LDL-C (0.6 mmol/L, P<0.001 and 0.58 mmol/L, P<0.05, respectively). MFBF was increased substantially by both treatments (P<0.001). Enalapril had a greater effect (-1.7 arbitrary units (AU), P<0.001) than simvastatin (-0.6 AU, P<0.05) on mFVR. During stress, FBF increased more with enalapril (4.4 FBFxminutes, P<0.001) than with simvastatin (1.8 FBFxminutes, P<0.01). Conversely, FVR stress response was reduced more with enalapril (9.1 FVRxminutes, P<0.001) than with simvastatin (2.9 FVRxminutes, P<0.01). During combination treatment, a significant (0.001>P<0.05) additive effect on hypercholesterolemia, structural vascular damage, BP, and FVR was shown. The findings suggest that angiotensin-converting enzyme (ACE) inhibition induces a larger reduction than HMG-CoA reductase blockade in vascular reactivity and structural damage in hypercholesterolemic hypertensive subjects.  (+info)

Involvement of tyrosine phosphorylation in HMG-CoA reductase inhibitor-induced cell death in L6 myoblasts. (2/4319)

Our previous studies have shown that the HMG-CoA reductase (HCR) inhibitor (HCRI), simvastatin, causes myopathy in rabbits and kills L6 myoblasts. The present study was designed to elucidate the molecular mechanism of HCRI-induced cell death. We have demonstrated that simvastatin induces the tyrosine phosphorylation of several cellular proteins within 10 min. These phosphorylations were followed by apoptosis, as evidenced by the occurrence of internucleosomal DNA fragmentation and by morphological changes detected with Nomarski optics. Simvastatin-induced cell death was prevented by tyrosine kinase inhibitors. The MTT assay revealed that the addition of mevalonic acid into the culture medium partially inhibited simvastatin-induced cell death. Thus, these results suggested that protein tyrosine phosphorylation might play an important role in the intracellular signal transduction pathway mediating the HCRI-induced death of myoblasts.  (+info)

Insulin and TSH promote growth in size of PC Cl3 rat thyroid cells, possibly via a pathway different from DNA synthesis: comparison with FRTL-5 cells. (3/4319)

In the rat thyroid cell lines PC Cl3, FRTL- 5 and WRT, proliferation is mainly regulated by insulin or IGF, and TSH. However, the mechanism regulating cell mass doubling prior to division is still unknown. Our laboratory has shown that in dog thyroid cells insulin promotes growth in size while TSH in the presence of insulin triggers DNA replication. In the absence of insulin, TSH has no effect on cell growth. In this report we investigated insulin action on both cell mass and DNA synthesis and its modulation by TSH and insulin in PC Cl3 and FRTL-5 cells. In PC Cl3 cells, insulin activated not only DNA synthesis but also protein synthesis and accumulation. Although TSH potentiated the stimulation of DNA synthesis induced by insulin, enhancement of protein synthesis by both agents was additive. All TSH effects were reproduced by forskolin. Similar effects were also obtained in FRTL-5 cells. This suggests that insulin and TSH, via cAMP, modulate both growth in size and DNA replication in these cell lines. Lovastatin, which blocks 3-hydroxy-3-methylglutaryl coenzyme A reductase, decreased the induction of DNA synthesis, but not of protein synthesis induced by insulin or TSH in PC Cl3 cells. In FRTL-5 cells, lovastatin reduced protein and DNA synthesis stimulated by insulin but not TSH-induced protein synthesis. Taking these data together, we propose that insulin and/or TSH both modulate cell mass doubling and DNA synthesis in these cell lines, presumably via different pathways, and that there are at least two pathways which regulate growth in size in FRTL-5 thyroid cells: one triggered by insulin, which is lovastatin sensitive, and the other activated by TSH, which is not sensitive to lovastatin.  (+info)

In vitro effects of simvastatin on tubulointerstitial cells in a human model of cyclosporin nephrotoxicity. (4/4319)

To investigate the possibility that 3-hydroxy-3-methylglutaryl CoA (HMGCoA) reductase inhibitors ameliorate renal disease via direct effects on the tubulointerstitium, primary cultures of human proximal tubule cells (PTC) and renal cortical fibroblasts (CF) were exposed for 24 h to simvastatin (0.1-10 micromol/l) under basal conditions and in the presence of 1,000 ng/ml of cyclosporin (CsA), which we have previously shown to promote in vitro interstitial matrix accumulation at least partially via activation of local cytokine networks. Simvastatin, in micromolar concentrations, engendered cholesterol-independent inhibition of CF and PTC thymidine incorporation and cholesterol-dependent suppression of PTC apical Na+/H+ exchange (NHE) (ethylisopropylamiloride-sensitive apical 22Na+ uptake). Similarly, CF secretion of insulin-like growth factor-I (IGF-I) and IGF binding protein-3 were depressed, whereas CF collagen synthesis ([3H]proline incorporation) and PTC secretion of the fibrogenic cytokines, transforming growth factor-beta1, and platelet-derived growth factor were unaffected. A lower concentration (0.1 micromol/l) of simvastatin did not affect any of the above parameters under basal conditions but completely prevented CsA-stimulated CF collagen synthesis (control, 6.6 +/- 0.6; CsA, 8.3 +/- 0.6; CsA+simvastatin, 6.2 +/- 0.5%; P < 0.05) and IGF-I secretion (89.5 +/- 16.6, 204.7 +/- 57.0, and 94.6 +/- 22.3 ng. mg protein-1. day-1, respectively; P < 0.05). The results suggest that simvastatin exerts direct cholesterol-dependent and -independent effects on the human kidney tubulointerstitium. HMGCoA reductase inhibitors may ameliorate interstitial fibrosis complicating CsA therapy via direct actions on human renal cortical fibroblasts.  (+info)

Effects of gamma-tocotrienol on ApoB synthesis, degradation, and secretion in HepG2 cells. (5/4319)

gamma-Tocotrienol (gamma-T3), a naturally occurring analog of tocopherol (vitamin E), has been shown to have a hypocholesterolemic effect in animals and humans. Unlike tocopherol, it has also been shown to reduce plasma apoB levels in hypercholesterolemic subjects. The aim of this study was to define the mechanism of action of gamma-T3 on hepatic modulation of apoB production using cultured HepG2 cells as the model system. HepG2 cells preincubated with gamma-T3 were initially shown to inhibit the rate of incorporation of [14C]acetate into cholesterol in a concentration- and time-dependent manner, with a maximum 86+/-3% inhibition at 50 micromol/L observed within 6 hours. gamma-T3, on the other hand, had no significant effect on the uptake of [14C]glycerol into pools of cellular triacylglycerol and phospholipid relative to untreated control. The rate of apoB synthesis and secretion was then studied by an [35S]methionine pulse-labeling experiment and quantified by immunoprecipitating apoB on chasing up to 3 hours. An average reduction of 24+/-3% in labeled apoB in the media was apparent with gamma-T3 despite a 60+/-2% increase in apoB synthesis. Fractionation of secreted apoB revealed a relatively denser lipoprotein particle, suggesting a less stable particle. Using a digitonin-permeabilized HepG2 cell system, the effects of gamma-T3 on apoB translocation and degradation in the endoplasmic reticulum were further investigated. The generation of a specific N-terminal 70-kDa proteolytic fragment proved to be a sensitive measure of the rate of apoB translocation and degradation. The abundance of this fragment increased significantly in gamma-T3-treated cells relative to untreated control cells (50+/-21%) after 2 hours of chase. In addition, the presence of gamma-T3 resulted in an average decrease of 64+/-8% in intact apoB. Taken together, the data suggest that gamma-T3 stimulates apoB degradation possibly as the result of decreased apoB translocation into the endoplasmic reticulum lumen. It is speculated that the lack of cholesterol availability reduces the number of secreted apoB-containing lipoprotein particles by limiting translocation of apoB into the endoplasmic reticulum lumen.  (+info)

Role of cholesterol ester mass in regulation of secretion of ApoB100 lipoprotein particles by hamster hepatocytes and effects of statins on that relationship. (6/4319)

Our understanding of the factors that regulate the secretion of apoB100 lipoproteins remains incomplete with considerable debate as to the role, if any, for cholesterol ester in this process. This study examines this issue in primary cultures of hamster hepatocytes, a species in which both cholesterol and apoB100 metabolism are very similar to man. Addition of oleate to medium increased the mass of triglyceride and cholesterol ester within the hepatocyte and also increased the secretion of triglycerides, cholesterol ester, and apoB100 into the medium. Next, the responses of hamster hepatocytes to addition of either an HMG-CoA reductase inhibitor (lovastatin) or an acyl-CoA cholesterol acyltransferase inhibitor (58-035) to the medium, with or without added oleate, were determined. Effects of either agent were only evident in the oleate-supplemented medium in which cholesterol ester mass had been increased above basal. If oleate was not added to the medium, neither agent reduced apoB100 secretion; equally important, over the 24-hour incubation, neither agent, at the concentration used, produced any detectable change in intracellular cholesterol ester mass. However, in contrast to the estimates of mass, which were unchanged, under the same conditions radioisotopic estimates of cholesterol ester synthesis were markedly reduced. Any conclusion as to the relation of cholesterol ester mass to apoB100 secretion would therefore depend on which of the 2 methods was used. Overall, the data indicate a close correlation between the mass of cholesterol ester within the hepatocyte and apoB100 secretion from it and they go far to explain previous apparently contradictory data as to this relation. More importantly, though, taken with other available data, they indicate that the primary response of the liver to increased delivery of lipid is increased secretion rather than decreased uptake. These results point, therefore, to a hierarchy of hepatic responses to increased flux of fatty acids and increased synthesis of cholesterol that in turn suggests a more dynamic model of cholesterol homeostasis in the liver than has been appreciated in the past.  (+info)

A randomized placebo-controlled trial of fluvastatin for prevention of restenosis after successful coronary balloon angioplasty; final results of the fluvastatin angiographic restenosis (FLARE) trial. (7/4319)

BACKGROUND: The 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors competitively inhibit biosynthesis of mevalonate, a precursor of non-sterol compounds involved in cell proliferation. Experimental evidence suggests that fluvastatin may, independent of any lipid lowering action, exert a greater direct inhibitory effect on proliferating vascular myocytes than other statins. The FLARE (Fluvastatin Angioplasty Restenosis) Trial was conceived to evaluate the ability of fluvastatin 40 mg twice daily to reduce restenosis after successful coronary balloon angioplasty (PTCA). METHODS: Patients were randomized to either placebo or fluvastatin 40 mg twice daily beginning 2-4 weeks prior to planned PTCA and continuing after a successful PTCA (without the use of a stent), to follow-up angiography at 26+/-2 weeks. Clinical follow-up was completed at 40 weeks. The primary end-point was angiographic restenosis, measured by quantitative coronary angiography at a core laboratory, as the loss in minimal luminal diameter during follow-up. Clinical end-points were death, myocardial infarction, coronary artery bypass graft surgery or re-intervention, up to 40 weeks after PTCA. RESULTS: Of 1054 patients randomized, 526 were allocated to fluvastatin and 528 to placebo. Among these, 409 in the fluvastatin group and 427 in the placebo group were included in the intention-to-treat analysis, having undergone a successful PTCA after a minimum of 2 weeks of pre-treatment. At the time of PTCA, fluvastatin had reduced LDL cholesterol by 37% and this was maintained at 33% at 26 weeks. There was no difference in the primary end-point between the treatment groups (fluvastatin 0.23+/-0.49 mm vs placebo 0.23+/-0.52 mm, P=0.95) or in the angiographic restenosis rate (fluvastatin 28%, placebo 31%, chi-square P=0.42), or in the incidence of the composite clinical end-point at 40 weeks (22.4% vs 23.3%; logrank P=0.74). However, a significantly lower incidence of total death and myocardial infarction was observed in six patients (1.4%) in the fluvastatin group and 17 (4.0%) in the placebo group (log rank P=0.025). CONCLUSION: Treatment with fluvastatin 80 mg daily did not affect the process of restenosis and is therefore not indicated for this purpose. However, the observed reduction in mortality and myocardial infarction 40 weeks after PTCA in the fluvastatin treated group has not been previously reported with statin therapy. Accordingly, a priori investigation of this finding is indicated and a new clinical trial with this intention is already underway.  (+info)

Effect of inhibition of cholesterol synthetic pathway on the activation of Ras and MAP kinase in mesangial cells. (8/4319)

Intermediary metabolites of cholesterol synthetic pathway are involved in cell proliferation. Lovastatin, an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, blocks mevalonate synthesis, and has been shown to inhibit mesangial cell proliferation associated with diverse glomerular diseases. Since inhibition of farnesylation and plasma membrane anchorage of the Ras proteins is one suggested mechanism by which lovastatin prevents cellular proliferation, we investigated the effect of lovastatin and key mevalonate metabolites on the activation of mitogen-activated protein kinase (MAP kinase) and Ras in murine glomerular mesangial cells. The preincubation of mesangial cells with lovastatin inhibited the activation of MAP kinase stimulated by either FBS, PDGF, or EGF. Mevalonic acid and farnesyl-pyrophosphate, but not cholesterol or LDL, significantly prevented lovastatin-induced inhibition of agonist-stimulated MAP kinase. Lovastatin inhibited agonist-induced activation of Ras, and mevalonic acid and farnesylpyrophosphate antagonized this effect. Parallel to the MAP kinase and Ras data, lovastatin suppressed cell growth stimulated by serum, and mevalonic acid and farnesylpyrophosphate prevented lovastatin-mediated inhibition of cellular growth. These results suggest that lovastatin, by inhibiting the synthesis of farnesol, a key isoprenoid metabolite of mevalonate, modulates Ras-mediated cell signaling events associated with mesangial cell proliferation.  (+info)

The first observational study in humans investigating the effect of pretreatment with statins on stroke outcome reported a borderline trend toward better outcome at hospital discharge.5 The unadjusted OR for early discharge to home was 1.41 (95% CI: 0.91 to 2.17) when patients on statin treatment were compared with referent stroke patients not on statins. However, this study did not distinguish between hemorrhagic and ischemic stroke, and only 8.3% of patients were taking statins.. In an observational study of 436 patients admitted to the National Institutes of Health Suburban Hospital Stroke Program between July 2000 and December 2002,6 22% of patients were taking a statin when they were admitted. In that study, 51% of patients taking statins had a good outcome compared with 38% of patients not taking statins (P=0.03). After adjustment for confounding factors, statin pretreatment was associated with a 2.9 odds (95% CI: 1.2 to 6.7, P=0.02) of a good outcome at the time of hospital ...
TY - JOUR. T1 - Statin administration did not influence the progression of lung injury or associated organ failures in a cohort of patients with acute lung injury. AU - Kor, Daryl J.. AU - Iscimen, Remzi. AU - Yilmaz, Murat. AU - Brown, Michael J.. AU - Brown, Daniel R.. AU - Gajic, Ognjen. PY - 2009/6/1. Y1 - 2009/6/1. N2 - Purpose: Preclinical studies suggest that HMG-CoA reductase inhibitors (statins) may attenuate organ dysfunction. We evaluated whether statins are associated with attenuation of lung injury and prevention of associated organ failure in patients with ALI/ARDS. Methods: From a database of patients with ALI/ARDS, we determined the presence and timing of statin administration. Main outcome measures were the development and progression of pulmonary and nonpulmonary organ failures as assessed by changes in PaO2/FiO 2 ratio and Sequential Organ Failure Assessment score (SOFA) between days 1 and 7 after the onset of ALI/ARDS. Secondary outcomes included ventilator free days, ICU and ...
Among Medicare beneficiaries with CHD, use of nonstatin lipid-lowering therapy has declined between 2008 and 2011 primarily due to a marked reduction in the use of ezetimibe, even though national cholesterol guidelines and treatment targets remained unchanged during the study period. This decrease in nonstatin lipid-lowering therapy occurred both among patients taking statins and not taking statins, but was more pronounced among statin users. Time trends in use of nonstatin lipid-lowering medications other than ezetimibe were less pronounced and heterogeneous. In any given calendar quarter, ,60% of Medicare beneficiaries with CHD filled a statin. Statin use was low at the beginning of the observation period and increased only modestly over time despite good evidence for efficacy to at least age 75 years and likely beyond and guideline recommendations in favor of statin use in these high-risk individuals.. As others have reported based on data from IMS Health (Danbury, Connecticut) and pharmacy ...
Statins do not decrease all-cause mortality in the vast majority of people. Long-term studies have never been able to demonstrate that women of any age or with any degree of heart disease live longer by taking statins. The same long-term studies show that men over the age of 65 live no longer by taking statins. Men under 65 who have never had heart disease - and were talking actual heart disease here, not just an elevated cholesterol level - gain no longevity benefit from taking statins. The only small group of people who have been shown to benefit from statins are men under 65 who have had a heart attack. But unfortunately that benefit is small. Multiple studies have shown that taking statins does reduce both the incidence and severity of heart attacks. But these same studies dont show any increase in longevity for those taking statins (other than the small benefit for men under 65 who have had heart attacks). Why. Statins simply trade one risk for another. Take them and you reduce the risk of ...
The report, by Symphony Health Solutions, estimated a 5% increase in the total number of patients prescribed statins, even though many media reports have predicted a doubling in statin use. About 36 million Americans are taking prescription cholesterol-lowering drugs, mostly statins, according to the market research firm. The study was based on a survey last week of 150 primary care physicians and cardiologists in the United States, as well as 100 cardiologists in Europe.. Other findings include almost universal awareness of the guidelines among U.S. physicians, as well as very high awareness in Europe, and positive reactions from physicians, who have indicated they are already treating patients in accordance with them. But despite the small increase in statin prescriptions thats expected, physicians in the United States and Europe expect an increase of 55% to 60% in PCSK9 inhibitors, biotech drugs for treating cholesterol that are still in clinical trials, but have been found highly effective. ...
In this study including 41,102 women from a large screening-based cohort, we found no evidence of an overall effect of statin use on absolute dense volume. Statin users had a significantly lower percent dense volume, but this difference was mainly attributable to a larger non-dense volume in statin users. While a large number of studies have investigated the effect of statin use on breast cancer risk and prognosis [6-14], only few studies have examined the association with mammographic density. Our results are in line with a longitudinal study showing no effect of statins on change in area-based mammographic density [28]. No differential effects were observed by statin class or treatment duration [13, 29] but interaction analyses revealed potential effect modification by HRT with a larger absolute dense volume among statin users who also reported HRT use.. Mammographic density can be expressed in both absolute and relative terms. The preferred MD measure for breast cancer risk prediction is ...
Background The goal of this study was to investigate the association between previous exposure to statins and the risk of non-Hodgkin lymphoma (NHL). study populace was composed of MC1568 1715 NHL patients and 16942 control subjects. The analysis revealed that previous statin administration was associated with a reduced risk of subsequent NHL with an adjusted OR of 0.52 (95% CI, 0.43C0.62). Additionally, there was a dose-response relationship between statin administration and the risk of NHL. The adjusted ORs were 0.63 (95% CI, 0.46C0.86), 0.58 (95% CI, 0.42C0.79), 0.51 (95% CI, 0.38C0.67), and 0.36 (95% CI, 0.24C0.53) for the subjects with statin administrations of fewer than 28, 28 to 90, 91 to 365, and more than 365 cDDDs, respectively, relative to the subjects without any statin MC1568 administration. Conclusions The results of this study suggest that previous statin administration is usually associated with a lower risk of subsequent NHL. As statins are widely used medications, the ...
Half of patients taking statins had a sub-optimal response to the treatment, a study has found, leading to calls for statin regimens to be tailored to individual patients.. Patients who didnt achieve NICE-recommended reductions in LDL-C were more likely than those who did to suffer cardiovascular events, the researchers found.. They found that 51% of patients on statins had a sub-optimal response to therapy after two years on treatment, meaning that they hadnt achieved a greater than 40% reduction in LDL-C levels.. When figures were adjusted for age, sub-optimal responders were 22% more likely to experience a CVD-related event, such as coronary artery disease, stroke or TIA, or peripheral vascular disease, than optimal responders.. Sub-optimal responders were also 25% more likely to die of CVD-related causes.. The study was carried out by primary care researchers at the University of Nottingham and looked at just over 165,400 primary care records for patients who were started on a statin ...
November 04, 2013 Two recent studies have examined how statins-a class of prescription drugs taken by millions of patients worldwide to lower or control cholesterol levels-might affect patients dental health.. Researchers at the University of North Carolina School of Dentistry have potentially linked statins to increased calcification of the tooths pulp chamber. The study was published in the September issue of the Journal of Endodontics.. The study evaluated patients taking statin medication versus patients not taking statin medication. Of 90 patient records reviewed, all were at least 60 years of age and half were on statins. The other half was not taking any medications.. The results revealed that the patients taking statins showed a significant reduction in the pulp chamber height, meaning an increased calcification of the pulp chamber, when compared to the control group, said Dr. Mary Pettiette, associate professor in the Department of Endodontics. Based on this limited data, systemic ...
Is lowering cholesterol with avocado, coconut oil, and other healthy fats more effective than taking statins? Read more to learn about lowering cholesterol.
Up to 3 million people are taking statins needlessly, doctors warn today in a comprehensive study that suggests they are ineffective in many cases and...
The effect of statin treatment on circulating coenzyme Q10 (CoQ10) has been studied in numerous randomized controlled trails (RCTs). However, whether statin treatment decreases circulating CoQ10 is still controversial. PubMed, EMBASE, and the Cochrane Library were searched to identify RCTs to investigate the effect of statin treatment on circulating CoQ10. We calculated the pooled standard mean difference (SMD) using a fixed effect model or random effect model to assess the effect of statin treatment on circulating CoQ10. The methodological quality of the studies was determined according to the Cochrane Handbook. Publication bias was evaluated by a funnel plot, the Egger regression test, and the Begg-Mazumdar correlation test. Twelve RCTs with a total of 1776 participants were evaluated. Compared with placebo, statin treatment resulted in a reduction of circulating CoQ10 (SMD, − 2.12; 95% CI, − 3.40 to − 0.84; p = 0.001), which was not associated with the duration of statin treatment (Exp, 1.00;
Background: Statins reduce mortality and morbidity in patients at risk or with documented coronary artery disease and thus are widely prescribed. Report from randomized trials (RCT) suggested that statins might be protective or even increase the incidence of diabetes mellitus (DM). The increase in DM may be related to the use of lipophilic statins.. Aim: To evaluate the use of statins and incident diabetes mellitus in randomized clinical trials (RCT) and pre-specify an analysis including lipophilic statins only.. Methods: An electronic search of the literature using MEDLINE with the following keywords: statins, diabetes mellitus, HMG CoA reductase inhibitors, incident diabetes. The selection criteria for the meta-analysis were:. ...
TY - JOUR. T1 - A HMG-CoA reductase inhibitor improved regression of atherosclerosis in the rabbit aorta without affecting serum lipid levels. T2 - Possible relevance of up-regulation of endothelial NO synthase mRNA. AU - Kano, Hatsuyo. AU - Hayashi, Toshio. AU - Sumi, Daigo. AU - Esaki, Teiji. AU - Asai, Yukako. AU - Thakur, Navin Kumar. AU - Jayachandran, Muthuvel. AU - Iguchi, Akihisa. PY - 1999/6/7. Y1 - 1999/6/7. N2 - We determined the role of Fluvastatin: HMG-CoA reductase inhibitor on the regression of atherosclerosis following removal of dietary cholesterol. Male rabbits fed a 0.5% cholesterol diet for 12 weeks were divided into three groups: A1, hypercholesterolemic; A2, fed a regular diet for an 12 additional weeks; and A3, fed a regular diet with fluvastatin (2 mg/kg/day). Fluvastatin treatment (A3) did not affect serum lipid levels compared with A2. However, it decreased the atherosclerotic area in the aortic arch and decreased total and esterified cholesterol concentrations in the ...
PubMed journal article HMG CoA reductase inhibitors (statins) for kidney transplant recipient were found in PRIME PubMed. Download Prime PubMed App to iPhone or iPad.
Press releases and media reports about statin drugs often dramatically overstate their effectiveness, while understating their risk.I just read a fantastic article by Dr. Malcolm Kendrick about how deceptive and misleading media reporting on statin drug trials can be.But thats not what the study showed at all. In fact, the following would be a more accurate report on the results of this study, couched in the context of what we know from other statin drug trials:Out of 100 high-risk people taking a statin for five years, 98.2 will not benefit at all-but they will be exposed to significant side effects and complications, including muscle damage and diabetes. The 1.8 people that do benefit will live an average of 6 months (and a maximum of one year) longer than those that didnt take the statin. These results only apply to the people at highest risk for a future heart attack: middle-aged men whove already had a heart attack (aka
TY - JOUR. T1 - Autoantibodies to oxidized ldl in hyperlotdemic patients treated with hmg-coa reductase inhibitors. AU - Bui, M. N.. AU - Caulfield, M. T.. AU - Katz, P.. AU - Cannon, R. O.. AU - Rackley, C. E.. PY - 1996/1/1. Y1 - 1996/1/1. N2 - Recent studies demonstrated that HMG-CoA reductase inhibitors slowed the progression and reduced the number of coronary events. Plaque stabilization has been proposed as an early beneficial mechanism. Nonisotopic ELISA technique was used to measure ox-LDL autoantibodies titers in 11 patients with hyperlipidemia LDL , IgG and IgM autoantibodies titers were measured at baseline and at 4 months after treatment with HMG-CoA reductase inhibitors. Baseline 4 months 12 months ofpauents 11 11 6 LDL(mg/dl) 173 ±37 138 ±28 128 ±15 Autoantibodies to ox-LDL,OD) IgG 0.138±0.076 0.154 + 0.087 0.180 + 0.071 IgM 0024 ±0.019 0.053± 0.044 p-valuc, 0.05 vs. baseline by paired Student t-test OD: optical density Six of the 11 patients had a 12-month follow-up with a ...
Dr. Eric Horwitz, clinical director of radiation oncology at the Fox Chase Cancer Center in Philadelphia, says he agrees with Dr. Zelefskys call for a tightly monitored clinical trial.. There has been great success in running these large tests, and Im sure it can be done, he says.. As it is, many men diagnosed with prostate cancer are already taking statins, and there is no reason for them to stop, says Dr. Horwitz.. This report is reassuring because of the overlap, he says.. Two recent reports have linked statin use with a lower risk of developing prostate cancer. One study, from the University of Alabama, Birmingham, found a decline in prostate cancer death rates that was most notable among Caucasian men who used statins.. Another study, from Duke University Medical Center, found lower blood levels of prostate-specific antigen, a potential marker of the cancer, among men taking statins.. A study on statin use in prostate cancer prevention or treatment should center on men at higher risk ...
In this study, we evaluated the influence of statin pretreatment and cholesterol levels on the incidence of ICH in patients receiving IAT with urokinase for acute ischemic stroke. The main finding is an independent association between statin pretreatment and the frequency of any ICH. However, statin pretreatment did not significantly influence the clinical outcome. Triglyceride and cholesterol levels on admission were not associated with bleeding. The fact that both hypertension and previous use of antiplatelets were independently associated with previous statin use might be partially explained by the fact that patients with cardiovascular risk factors are more likely to have cholesterol levels measured and are generally treated earlier and more aggressively.. Our findings are in contrast to previous reports. Bang et al analyzed 104 patients receiving intravenous or IAT with tissue-type plasminogen activator (tPA), including mechanical recanalization.10 In their study, lower LDL cholesterol ...
We examined the association among discharge statin use, statin intensity, clinical outcomes, and patient-centered outcomes in a real-world population of older ischemic stroke patients who were not taking statins at the time of admission. We found that (1) discharge statin therapy was associated with a lower adjusted risk of MACE and lower risk of all-cause mortality during the 2-year period after hospitalization; (2) discharge statins significantly improved an outcome prioritized by patients, home time, with 28 additional days at home over 2 years after adjustment; (3) the observed benefits of discharge statin use were consistent across clinically relevant subgroups; (4) nearly one third of ischemic stroke patients who received statins at discharge were treated with high-intensity statins; and (5) compared with low/moderate-intensity statins, high-intensity statin use did not improve clinical outcomes or days spent at home in the 2 years after discharge.. This analysis addresses a key knowledge ...
Our systematic review demonstrates that, among patients with coronary artery disease, the provision of more intensive statin monotherapy (compared with less intensive statin therapy) reduces LDL cholesterol levels by a further 0.72 mmol/L. This additional reduction in LDL cholesterol resulted in 17% fewer myocardial infarctions (absolute reduction 1.4%) and 18% fewer strokes (absolute reduction 0.5%) among patients randomized to more intensive statin regimens rather than less intensive regimens. These benefits of more intensive statin monotherapy were at the expense of small absolute increases in the frequency of drug discontinuation (about 2.5%), elevated aminotrasferase levels (about 1%) and myopathy (about 0.5%) when compared with less-intensive statin therapy (only the aminotransferase elevations were statistically significant). There was no difference in noncardiovascular mortality. All-cause mortality was not reduced among patients with chronic coronary artery disease, but it was reduced ...
While 2017 has certainly been a rollercoaster of a year for lipid research, it has also provided important insights for the management of residual cardiovascular risk. The FOURIER (Further Cardiovascular Outcomes Research With PCSK9 Inhibition in Subjects With Elevated Risk) trial was the first to lead the attack, demonstrating incremental benefit with a lower is better approach targeting low-density lipoprotein cholesterol (LDL-C) with the PCSK9 inhibitor evolocumab in patients with stable atherosclerotic cardiovascular disease (ASCVD) on intensive statin therapy 1. The landmark trial, CANTOS (Canakinumab Anti-inflammatory Thrombosis Outcomes Study), followed up in providing proof-of-concept for the relevance of targeting residual inflammatory risk with canakinumab, a monoclonal antibody to interleukin-1? in patients with a previous myocardial infarction and elevated levels of C-reactive protein, well-treated with statin therapy 2. Finally, COMPASS (Cardiovascular Outcomes for People Using ...
Kim J, Lee HS, Nam CM, Heo JH. Effects of Statin Intensity and Adherence on the Long-Term Prognosis After Acute Ischemic Stroke. Stroke. 2017. Statin medications and cholesterol management remain topics of debate over ten years after the publishing of the SPARCL (Stroke Prevention by Aggressive Reduction in Cholesterol Levels) trial. With many questions remaining, the authors investigated the effects of statin intensity and adherence on the long-term prognoses after acute ischemic strokes in Korea.. In this paper, Kim et al. present a retrospective cohort study based on nationwide Korean population-based health insurance data. They used diagnosis codes to identify patients with ischemic stroke and then collected prescription records (type, dosage, duration, and date) of statins. In order to determine adherence, they calculated the proportion of days covered (PDC) by any statin prescription for a period of 1 year after acute ischemic stroke. Poor adherence was PDC , 40%, intermediate adherence ...
The most common type of medicine to treat hypercholesterolemia are statin drugs. They are called statins because their names all end in -statin. They are also called HMG-CoA Reductase Inhibitors. This is because they work by inhibiting the enzyme HMG-CoA Reductase. Inhibiting an enzyme means to make it work less well. The HMG-CoA Reductase enzyme causes the body to make more cholesterol. If it is inhibited, the body makes less cholesterol. So statin drugs lower the amount of LDL (bad) cholesterol in the blood which stops atherosclerosis from getting worse. Statin drugs can even help make atherosclerosis better. However, statins are not as good at increasing the HDL (good) cholesterol. Low HDL is hard to treat with medicines, but goes up with more exercise! There are two big problems with taking statins: Liver problems and Rhabdomyolysis. Rhabdomyolysis means a disease where muscle cells are damaged and die. Statins can cause damage to muscle cells. This can cause weakness and muscle pain. ...
For patients taking statins for prevention of cardiovascular disease (CVD), extended care with nurse-led cardiovascular risk-factor counseling improves statin adherence and reduces anxiety, with improvements seen in low-density lipoprotein cholesterol for primary prevention patients.
Objective-Pleiotropic atheroprotective effects of HMG-CoA reductase inhibitors may be mediated on the level of vascular gene transcription. The aim of this study was to characterize the effects of statins on the activation of transcription factors known to regulate inflammation and cell proliferation/differentiation. Methods and Results-Simvastatin, atorvastatin, and lovastatin (0.1 to 10 mumol/L) inhibited the binding of nuclear proteins to both the nuclear factor-kappa B (NF-kappaB) and activator protein-1 (AP-1) DNA consensus oligonucleotides in human endothelial and vascular smooth muscle cells as assessed by electrophoretic mobility shift assay (EMSA). The inhibitory effects of statins on NF-kappaB or AP-1-dependent transcriptional activity were examined by transient transfection studies. HMG-CoA reductase inhibitors upregulated IkappaB-alpha protein levels in endothelial cells and decreased c-Jun mRNA expression in smooth muscle cells as analyzed by Western and Northern blotting, ...
But after identifying that statins had this effect due to the same mechanism which led to them reducing cholesterol, the researchers said the drugs still did more good than harm and patients should continue to take them as directed. ...
These large pharmaceutical companies (big pharma) want you to be taking statins most likely so that they can make more money (cash flow) with other drugs which the consumer of statins will need to offset the side effects associated with taking statins. Why is it that big pharmas are not introducing and advertising for products with policosanol? Why? Because policosanol is not a cash flow generator for big pharma because side effects will not materialize as they do with statins. Big pharma knows that policosanol is better for lowering cholesterol levels but big pharma wants to corner the market for the manner in which cholesterol levels are lowered, no matter what the financial and health costs are for the consumers. Big pharma has doctors right where they want them - telling doctors to push statins instead of the healthy policosanol alternative for lowering cholesterol levels; dont worry, the doctors are paid for the prescriptions they write for statins, given them a financial incentive to ...
New Targets of HMG-CoA Reductase Inhibitors (Statins) in the Central Nervous System. Statins are potent inhibitors of the hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase a key enzyme of the cellular cholesterol synthesis. They can induce comparatively large reductions in plasma cholesterol levels and are well proven drugs for the treatment of hypercholesterolaemia. Although the pharmacology of statins is well established for the peripheral system, data about their effects in the central nervous system (CNS) are still lacking. Clinical and epidemiological findings indicate prevention of stroke and possibly a beneficial effect on the progression of Alzheimers Disease (AD). Hence, statins are considered a promising drug in the CNS. Abnormal processing of amyloid precursor protein (APP) in the AD brain results in deposits of neurotoxic ß-amyloid (Aß) that represents one pathological hallmark of this disease. Statins lower the amyloidogenic processing of APP in vitro and in vivo. This effect ...
New research has shown that statins, one of the most commonly prescribed cardiovascular drugs worldwide, may reduce the positive effects of exercise in overweight individuals. Statins are primarily prescribed to lower elevated LDL cholesterol levels, but may be recommended for patients as a preventative health measure if they are deemed to be at risk of metabolic syndrome, or obese. Statin drugs are already associated with a range of debilitating side effects including moderate or serious liver dysfunction, acute renal failure, moderate or serious myopathy (muscle disease), and cataracts.. It seems ironic that they may also hinder the ability of exercise to improve fitness levels and health in the people that need it most - thereby worsening the very conditions they are supposed to treat. While this study was conducted on a small population of sedentary overweight and obese adults, clinically significant differences in cardiorespiratory fitness were reported in patients taking statin drugs ...
A review of previous research conducted at the University of Waterloo in Canada -- reported this past April -- concluded: Despite several reports of statin-associated cognitive impairment, this adverse effect remains a rare occurrence among the totality of the literature. If statin-associated cognitive impairment is suspected, a trial discontinuation can reveal a temporal relationship. Switching from lipophilic to hydrophilic statins may resolve cognitive impairment. The vascular benefits and putative cognitive benefits outweigh the risk of cognitive impairment associated with statin use; therefore, the current evidence does not support changing practice with respect to statin use, given this adverse effect. http://www.ncbi.nlm.nih.gov/pubmed/22474137 ...
Using EHRs and letters mailed to at-risk patients, physicians doubled the proportion of patients who received new lipid-lowering drug prescriptions. However, study results failed to show an improvement in levels of low density lipoprotein (LDL) cholesterol at nine months and only modest improvements at 18 months.
BY FRED G. ARNOLD, NMD. It is a common belief by many medical professionals that statin drugs lower the Incidence of cardiovascular disease by lowering LDL cholesterol. However, a recent study in the Journal of Clinical Nutrition shows that LDL cholesterol levels do not lower heart disease risk and do not lower the incidence of you dying from a heart attack. LDL cholesterol levels are considered the bad cholesterol and is why many doctors prescribe statin drugs to lower it. In this recent study the researchers evaluated 1,469 women between the ages of 72-78 and the relationship between their LDL levels and their chances of dying from cardiovascular disease for a 10 year period. During this time, 134 women died from cardiovascular disease that had nothing to do with high LDL levels. The women with the highest levels of LDL cholesterol were no more at risk than those with the lowest levels! They discovered that Baseline serum total and LDL cholesterol were not associated with atherosclerotic ...
BMJ 2013. 346 reported a study by Dr Aleesa carter and group from Ontario, Canada. They looked into the Canadian Institute of Health Information database, and the Discharge Abstract database, and also the Ontario Diabetes Database from Aug 1997 - March 2012, over 14 years. From the first two databases, they identified patients above age 66 yrs who were started on statins either for primary prevention or secondary prevention. From the third database, they identified those who were not diabetic before but over the followup period, developed diabetes ...
The correct answer is: D. Continue rosuvastatin 40 mg. Add ezetimibe 10 mg PO daily.. The patient has clinical ASCVD and is taking a high-intensity statin for secondary prevention. The patient states he is taking the high intensity statin therapy and following maximum lifestyle modifications.. The 2017 focused update to the ACC ECDP on non-statin therapies for LDL-C lowering in the management of ASCVD included thresholds to guide decision making when considering the addition of non-statin medications. For a patient with clinical ASCVD, the thresholds for considering the addition of non-statin therapy are when the patient achieves ,50% LDL-C reduction from baseline, the LDL-C is ,70 mg/dL, or if the non-HDL-C is ,100 mg/dL on maximally tolerated statin therapy. Mr. Smith achieved a 40% LDL-C reduction from baseline, his current LDL-C is 84 mg/dL, and his non-HDL-C is 112 mg/dL.. The clinician and patient should discuss potential additional ASCVD risk reduction from additional LDL-C lowering, risk ...
This distinction is important because individuals in the secondary prevention category are at generally high risk of further problems, and stand to benefit most from statin therapy. On the other hand, individuals in the primary prevention category are at generally low risk of cardiovascular disease issues (such as heart attack and stroke), and may therefore not benefit much from a strategy or treatment intended to prevent cardiovascular disease. This primary prevention category is particularly important when one considers that the vast majority of people taking statins are in this category, and if the pharmaceutical industry and some of its hired hands in the scientific and medical community have their way, increasing numbers of people will be taking statins in the future ...
Table 3: Emergent Biomarkers of Residual Cardiovascular Risk in Patients with Low HDL-c and/or High Triglycerides and Average LDL-c Concentrations: Focus on HDL Subpopulations, Oxidized LDL, Adiponectin, and Uric Acid
Cancer micrometastasis relies on the ability of malignancy cells to secrete angiogenic modulators to interact with the vascular endothelium and to overcome the resistance offered by the endothelial-barrier. numerous cancers investigations validating the use of statins for prostate malignancy therapy have been highly encouraging (Papadopoulos et al. MLN9708 2011 A recent clinical study has reported 45% reduction in the biochemical recurrence of prostate malignancy after radical prostatectomy in patients taking statins (Hamilton et al. 2010 Statins have been reported to be safe for humans even at doses 10-50 times higher than that is prescribed for cardiovascular disease (Holstein et al. 2006 Gauthaman et al. 2009 Previous studies from our group has exhibited the anti-cancer efficacy of simvastatin a highly lipophilic statin on androgen-responsive LNCaP cells and androgen-insensitive PC3 prostate malignancy cell lines and tumor xenografts (Kochuparambil et al. 2011 Simvastatin also induced ...
Every additional dollar spent on statin therapy for diabetes patients without cardiovascular disease has produced health gains valued between $7 and $31.
MONDAY, Jan. 6, 2020 (American Heart Association News) -- About 40 million adults in the U.S. take a statin to lower their cholesterol and reduce the risk for heart disease. They might also be getting an added anti-cancer benefit, a growing body of evidence suggests.. Scientists first began investigating a connection between statins and cancer while looking at the drugs potential long-term side effects. Early animal studies that showed statins could spur cancer growth in rodents initially raised concerns.. But results in people from observational studies and randomized controlled trials investigating the effect of statins on heart disease have quelled fears. These studies didnt show higher cancer rates. In fact, they have suggested people taking statins are less likely to be diagnosed with prostate cancer and are living longer after a breast, colorectal, kidney or lung cancer diagnosis than people not on statins.. Many researchers continue to study the relationship between statins and cancer. ...
MONDAY, Jan. 6, 2020 (American Heart Association News) -- About 40 million adults in the U.S. take a statin to lower their cholesterol and reduce the risk for heart disease. They might also be getting an added anti-cancer benefit, a growing body of evidence suggests.. Scientists first began investigating a connection between statins and cancer while looking at the drugs potential long-term side effects. Early animal studies that showed statins could spur cancer growth in rodents initially raised concerns.. But results in people from observational studies and randomized controlled trials investigating the effect of statins on heart disease have quelled fears. These studies didnt show higher cancer rates. In fact, they have suggested people taking statins are less likely to be diagnosed with prostate cancer and are living longer after a breast, colorectal, kidney or lung cancer diagnosis than people not on statins.. Many researchers continue to study the relationship between statins and cancer. ...
Statins may not only benefit patients diagnosed with heart disease. The results of a new study, recently reported in the American Heart Journal, suggested that the benefit of statin use extends to patients who have recently undergone surgery or angioplasty to treat their disease. To determine whether statins work in surgery or angioplasty patients, the researchers looked at the impact of cholesterol-lowering therapies in all 11,958 patients over age 65 who had coronary bypass surgery or angioplasty between 1995 and 1997. The investigators found that, during 3 years of follow-up, 1288 patients died, 810 had new heart attacks, and 1528 had a second operation to open the coronary blood vessels. The results of the study showed a 34% decreased risk of death and a 23% lower risk of heart attack in patients taking statins following surgery or angioplasty. Statins, however, were not connected with a reduction in the need for repeat surgery or angioplasty. The issue of cholesterol-lowering drugs in the ...
Thank you all for being part of PBNSG and supporting our hope for improved health through nutritional education. Many years ago when I was first diagnosed with high cholesterol, my cholesterol level was 347and my doctor suggested I improve my diet with skim milk, egg whites, fish, olive oil and more fiber. He also prescribed Zocor as my first cholesterol lowering drug.. After a few months, I woke up one day and could barely walk. This turned out to be one of the many side effects of taking statins. He had me go to a MS doctor who told me to stop taking Zocor and within a few days I was able to walk without pain. Even with taking statins and the change in diet, my cholesterol level was still over 280. I then was prescribed Lipitor. Six months later, I experienced the same side effect. I was still eating the diet he recommended and my number did not change. He then prescribed Pravastatin which was the weakest statin at that time. I was taking 80 mg a day and still my cholesterol level was between ...
Remyelination of lesions in the central nervous system contributes to neural repair following clinical relapses in multiple sclerosis. Remyelination is initiated by recruitment and differentiation of oligodendrocyte progenitor cells (OPCs) into myelinating oligodendrocytes. Simvastatin, a blood-brain barrier-permeable statin in multiple sclerosis clinical trials, has been shown to impact the in vitro processes that have been implicated in remyelination. Animals were fed a cuprizone-supplemented diet for 6 weeks to induce localized demyelination in the corpus callosum; subsequent return to normal diet for 3 weeks stimulated remyelination. Simvastatin was injected intraperitoneally during the period of coincident demyelination and OPC maturation (weeks 4 to 6), throughout the entire period of OPC responses (weeks 4 to 9), or during the remyelination-only phase (weeks 7 to 9). Simvastatin treatment (weeks 4 to 6) caused a decrease in myelin load and both Olig2(strong) and Nkx2.2(strong) OPC ...
Relative safety profiles of high dose statin regimens Carlos Escobar, Rocio Echarri, Vivencio BarriosDepartment of Cardiology, Hospital Ramón y Cajal, Madrid, SpainAbstract: Recent clinical trials recommend achieving a low-density lipoprotein cholesterol level of <100 mg/dl in high-risk and <70 mg/dl in very high risk patients. To attain these goals, however, many patients will need statins at high doses. The most frequent side effects related to the use of statins, myopathy, rhabdomyolysis, and increased levels of transaminases, are unusual. Although low and moderate doses show a favourable profile, there is concern about the tolerability of higher doses. During recent years, numerous trials to analyze the efficacy and tolerability of high doses of statins have been published. This paper updates the published data on the safety of statins at high doses.Keywords: statins, high doses, tolerability, liver, muscle
OBJECTIVES: The purpose of this study was to evaluate the effects of statin therapy on myocardial function as measured with echocardiography with tissue Doppler imaging (TDI) and strain imaging (SI) independent of its lipid-lowering effect. BACKGROUND: Statin use is known to improve outcomes in the primary and secondary prevention of ischemic heart disease, but their use is also associated with myopathy, muscle weakness and in rare cases, rhabdomyolysis. We sought to evaluate whether TDI and SI is able to identify changes in myocardial function associated with statin use. METHODS: Myocardial function was evaluated in 28 patients via echocardiography with TDI and SI. We identified 12 patients (5 females) without overt cardiovascular disease (including hypertension, smoking, and diabetes) that were on statin therapy and compared their echocardiographic findings with 16 (12 females) age, sex, and cholesterol-profile-matched controls. Tissue Doppler imaging parameters of diastolic (E()/A() and ...
In contrast to the current belief that cholesterol reduction with statins decreases atherosclerosis, we present a perspective that statins may be causative in coronary artery calcification and can function as mitochondrial toxins that impair muscle function in the heart and blood vessels through the depletion of coenzyme Q10 and heme A, and thereby ATP generation. Statins inhibit the synthesis of vitamin K2, the cofactor for matrix Gla-protein activation, which in turn protects arteries from calcification. Statins inhibit the biosynthesis of selenium containing proteins, one of which is glutathione peroxidase serving to suppress peroxidative stress. An impairment of selenoprotein biosynthesis may be a factor in congestive heart failure, reminiscent of the dilated cardiomyopathies seen with selenium deficiency. Thus, the epidemic of heart failure and atherosclerosis that plagues the modern world may paradoxically be aggravated by the pervasive use of statin drugs. We propose that current statin ...
This study will recruit individuals who have had muscle symptoms while using a statin. During the first part of the study, volunteers will be given a statin medication to see if their muscle symptoms return. Those who experience muscle symptoms on this statin rechallenge will be invited to continue in the second part of the trial, in which participants will be randomly assigned to receive either CoQ10 or a placebo (sugar pill) to take with statin medication. We hypothesize that those who receive CoQ10 will experience an improvement in their muscle symptoms compared to those who receive placebo, and, secondarily, that those who receive CoQ10 will be more likely to continue taking the statin medication ...
Hypothesis: Study subjects receiving fenofibrate 54mg will maintain similar triglyceride levels as patients on 160mg of fenofibrate.. The primary objective of this randomized trial is to measure the impact of converting patients on statin therapy from fenofibrate 160mg to 54mg per day compared to patients who continue fenofibrate 160mg per day for triglycerides. Secondary objectives include evaluating effect of the dosage change on low-density lipoprotein (LDL), HDL, alanine aminotransferase (ALT), aspartate aminotransferase (AST), and serum creatinine (SCr), and the potential cost savings associated with prescribing 54mg instead of 160mg. Electronic medical records will be used to identify subjects and gather data on demographics, comorbid conditions, and concomitant lipid lowering therapy. Subjects will be recruited for enrollment via telephone by the principal investigator (PI), co-principal investigators (Co-PIs), or provider referral after eligibility screening and approval from their ...
TY - JOUR. T1 - Assessment of omega-3 carboxylic acids in statin-treated patients with high levels of triglycerides and low levels of high-density lipoprotein cholesterol. T2 - Rationale and design of the STRENGTH trial. AU - Nicholls, Stephen J.. AU - Lincoff, A. Michael. AU - Bash, Dianna. AU - Ballantyne, Christie M.. AU - Barter, Philip J.. AU - Davidson, Michael H.. AU - Kastelein, John J.P.. AU - Koenig, Wolfgang. AU - McGuire, Darren K. AU - Mozaffarian, Dariush. AU - Pedersen, Terje R.. AU - Ridker, Paul M.. AU - Ray, Kausik. AU - Karlson, Björn W.. AU - Lundström, Torbjörn. AU - Wolski, Kathy. AU - Nissen, Steven E.. N1 - Publisher Copyright: © 2018 Wiley Periodicals, Inc.. PY - 2018/10. Y1 - 2018/10. N2 - It is uncertain whether omega-3 fatty acids are beneficial in statin-treated patients. Epanova is a mix of omega-3 free fatty acids, not requiring co-ingestion with food, which can lower triglycerides by up to 31%. STRENGTH will examine whether Epanova 4 g daily reduces the rate ...
Recent evidence suggests that 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) re-ductase inhibitors (statins) may stimulate osteoblast activity. However, it is unclear whether a possible increase in bone mineral density is clinically meaningful or associated with fewer fractures. Wang and colleagues conducted a case-control study to determine whether the risk of hip fracture is decreased in elderly patients taking statins.. Data on patients were drawn from the New Jersey Medicaid Program, the New Jersey Pharmacy Assistance for the Aged and Disabled Program and New Jersey Medicare. Patients younger than 65 years and those who had recently been hospitalized were excluded. All patients with a diagnosis of hip fracture were included and were matched (by age and sex) with four randomly selected control patients who had not had a hip fracture (1,222 cases and 4,888 controls). Patients who had filled any statin prescription in the previous six months were classified as having been exposed to a statin, ...
TY - JOUR. T1 - Benefit of early statin therapy in patients with acute myocardial infarction who have extremely low low-density lipoprotein cholesterol. AU - Lee, Ki Hong. AU - Jeong, Myung Ho. AU - Kim, Ha Mi. AU - Ahn, Youngkeun. AU - Kim, Jong Hyun. AU - Chae, Shung Chull. AU - Kim, Young Jo. AU - Hur, Seung Ho. AU - Seong, In Whan. AU - Hong, Taek Jong. AU - Choi, Dong Hoon. AU - Cho, Myeong Chan. AU - Kim, Chong Jin. AU - Seung, Ki Bae. AU - Chung, Wook Sung. AU - Jang, Yang Soo. AU - Rha, Seung Woon. AU - Bae, Jang Ho. AU - Cho, Jeong Gwan. AU - Park, Seung Jung. N1 - Copyright: Copyright 2013 Elsevier B.V., All rights reserved.. PY - 2011/10/11. Y1 - 2011/10/11. N2 - Objectives: We investigated whether statin therapy could be beneficial in patients with acute myocardial infarction (AMI) who have baseline low-density lipoprotein cholesterol (LDL-C) levels below 70 mg/dl. Background: Intensive lipid-lowering therapy with a target LDL-C value ,70 mg/dl is recommended in patients with very ...
Nearly two out of five people with diabetes who could benefit from statin therapy were not prescribed one, according to a research letter published Sept. 12 in the Journal of the American College of Cardiology. The analysis, which uses data from ACCs PINNACLE Registry, also showed wide variation in statin use across cardiology practices.. Yashashwi Pokharel, MD, MSCR, and colleagues examined practice-level variations in statin therapy among 40-75 year old patients with diabetes and no overt cardiovascular disease between May 2008 and October 2013 - before the present guidelines were issued. A total of 215,193 patients from 204 cardiology practices were included in the study.. The researchers found that 38 percent of patients with diabetes were not taking a statin. Compared with patients not receiving statins, those on statins had a higher prevalence of cardiovascular risk factors, were more likely to receive non-statin cholesterol-lowering therapy (28 vs. 13 percent) and had lower mean LDL ...
Patients with diabetes and ischemic heart disease (IHD) are at high risk for adverse cardiac outcomes. Clinical practice guidelines recommend multiple cardioprotective medications to reduce recurrent events. We evaluated the association between cardioprotective medication adherence and mortality among patients with diabetes and IHD. In a retrospective cohort study of 3,998 patients with diabetes and IHD, we evaluated use of ACE inhibitors or angiotensin receptor blockers, β-blockers, and statin medications. Receipt of cardioprotective medications was based on filled prescriptions. Medication adherence was calculated as the proportion of days covered (PDC) for filled prescriptions. The primary outcome of interest was all-cause mortality. The majority of patients (92.8%) received at least 1 cardioprotective medication. Patients receiving any medications had lower unadjusted mortality rates compared to patients not receiving any medications (7.9% vs. 11.5%; p = 0.03). In multivariable analysis, receipt of
At a time when new guidelines have been issued for an increase in the use of statin drugs, patients may remain unaware of alternatives such as turmeric that can replace these medications and aid in the treatment of cardiovascular disease. Research behind the new guidelines suggests that they should be prescribed not only for elevated cholesterol, but also to prevent heart attack and stroke in those at risk. This could result in more than a 50% increase in use in certain populations. The new guidelines purport that statins should be used for many more patients, but there are more natural, highly effective and affordable treatments available. The research and medical community is looking more closely at turmeric for a low-cost, low side-effect, but potently effective treatment for many different disorders including cardiovascular disease.. While statin drugs are generally considered safe they can sometimes cost up to $500 for a one-month supply. Turmeric on the other hand is much more affordable. ...
Background: A previous study has shown that variations in threshold and intensity (lipid goal attainment) of statins for primary prevention contribute to regional differences in overall consumption of statins in Norway. Our objective was to explore how differences in prevalences of use, dosing characteristics, choice of statin and continuity of therapy in individual patients adds new information to previous results. Methods: Data were retrieved from The Norwegian Prescription Database. We included individuals from counties with high, average, and low statin consumption, who had at least one statin prescription dispensed during 2004 (N = 40 143). 1-year prevalence, prescribed daily dose (PDD), statin of choice, and continuity of therapy assessed by mean number of tablets per day. Results: The high-consumption county had higher prevalence of statin use in all age groups. Atorvastatin and simvastatin were dispensed in 79-87% of all statin users, and the proportion was significantly higher in the ...
Statins are widely used and well tolerated cholesterol-lowering drugs, and when used for therapy purposes reduce morbidity and mortality from coronary heart disease. Simvastatin is one of nine known statins, specific inhibitors of hepatic enzyme 3-hydroxy-3-methylglutaryl-coenzyme A reductase, the rate-limiting step of cholesterol biosynthesis, and is believed to reduce plasma cholesterol levels by decreasing the activity of this enzyme. Statin drugs represent the major improvement in the treatment of hypercholesterolemia that constitutes the main origin of atherosclerosis, leading to coronary heart disease. Although statins are generally safe, minor and severe adverse reactions are well known complications of statin use. Adverse events associated with simvastatin therapy are uncommon, but potentially serious. In this review some details about statins including their adverse effects in humans and animals, the effects of simvastatin on various intracellular and mitochondrial processes, and ...
The authors are certainly correct that the risk of statin-induced rhabdomyolysis is associated with coadministration of such drugs as cyclosporin, antifungal agents, calcium-channel blockers, and amiodarone. However, there is a much broader array of medications that is likely to inhibit the metabolism or otherwise raise blood levels of statins to increase the risk of rhabdomyolysis. Atorvastatin, lovastatin, and simvastatin are primarily metabolized by the enzyme cytochrome P450 3A4 (CYP3A4). Coadministration of any of the many inhibitors on CYP3A4 (including cyclosporin, etc .) will raise blood levels of these specific statins. In addition, fluvastatin is metabolized by CYP2C9, and inhibitors of that enzymes function will raise fluvastatin levels as well. Pravastatins metabolism is primarily through phase II, or conjugative, metabolism, which is more difficult to inhibit to a clinically significant degree, so it is much less susceptible to these metabolic drug interactions. Rosuvastatin ...
1 Ridker PM, Danielson E, Fonseca FA, Genest J, Gotto AM Jr, Kastelein JJ, et al. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein. N Engl J Med. 2008;359:2195-207. 2 Ridker PM, Cannon CP, Morrow D, Rifai N, Rose LM, McCabe CH, et al.; Pravastatin or Atorvastatin Evaluation and Infection Therapy-Thrombolysis in Myocardial Infarction 22 (PROVE IT-TIMI 22) Investigators. C-reactive protein levels and outcomes after statin therapy. N Engl J Med. 2005;352:20-8. 3 Chatzizisis YS, Koskinas KC, Misirli G, Vaklavas C, Hatzitolios A, Giannoglou GD. Risk factors and drug interactions predisposing to statin-induced myopathy: implications for risk assessment, prevention and treatment. Drug Saf. 2010;33:171-87. 4 Armitage J. The safety of statins in clinical practice. Lancet. 2007;370:1781-90. 5 Stroes ES, Thompson PD, Corsini A, Vladutiu GD, Raal FJ, Ray KK, et al. Statin-associated muscle symptoms: impact on statin therapy. European Atherosclerosis Society consensus ...
TY - JOUR. T1 - Role of serum cholesterol and statin use in the risk of prostate cancer detection and tumor aggressiveness. AU - Morote, Juan. AU - Celma, Anna. AU - Planas, Jacques. AU - Placer, José. AU - de Torres, Inés. AU - Olivan, Mireia. AU - Carles, Juan. AU - Reventós, Jaume. AU - Doll, Andreas. PY - 2014/8/6. Y1 - 2014/8/6. N2 - The aim of this study was to analyze the relationship between statin use along with serum cholesterol levels and prostate cancer (PCa) detection and aggressiveness. Statin users of three years or more and serum cholesterol levels (SC) were assessed in 2408 men scheduled for prostate biopsy. SC was classified as normal (NSC: ,200 mg/dL) or high (HSC: ,200 mg/dL). High-grade PCa (HGPCa) was considered if the Gleason score was greater than 7. Statin users comprised 30.9% of those studied. The PCa detection rate was 31.2% of men on statins and 37% of non-statin users (p , 0.006). The PCa detection rate was 26.3% in men with NSC and 40.6% in those with HSC (p , ...
This study tested the hypothesis that simvastatin treatment can improve cardiovascular and autonomic functions and membrane lipoperoxidation, with an improved effect when applied to physically qualified ovariectomized rats. the other organizations. Tachycardic and bradycardic reactions were enhanced in both simvastatin-treated organizations. The vagal effect was improved in the qualified+simvastatin group and the sympathetic effect was decreased in the sedentary+simvastatin group. Hepatic lipoperoxidation was reduced in sedentary+simvastatin (21%) and qualified+simvastatin organizations (57%) compared to the sedentary group. Correlation analysis involving all animals shown that cardiac lipoperoxidation was negatively related to the vagal effect (r = -0.7) and positively correlated to the sympathetic effect (r = 0.7). In conclusion, improvement in cardiovascular and autonomic functions associated with a reduction of lipoperoxidation with simvastatin treatment was improved in qualified ...
Most days I eat beans cooked with lots of vegetables, and staggering amounts of raw fresh fruit, tomatoes, and romaine lettuce. Its delicious, simple, and easy. There isnt anything difficult about it. Its less complicated than the way I used to eat, faster, easier, and cheaper - especially since I used to eat out every day, instead of cooking - and it eliminated a lot of my cholesterol problems. With this diet, plus statin medications, I saw at least the same amount of cholesterol improvement in three months that my father and my uncle each saw after ten years of statin medications only. (I think I actually saw a slightly better improvement when it comes to LDL cholesterol, and a significantly better improvement when it comes to triglycerides.) Ive also lost around 30 or 40 pounds, and am still losing weight (which is good because I was technically obese and am not so any longer ...
Traumatic compartment syndrome is a well-known condition and usually easily recognized for its high level of suspicion. Otherwise, the Chronic Form is insidious and difficult to diagnose if the patient is not an athlete and there is no temporal correlation with excessive physical stress.. Our case is unusual because it is not very easy to place it in a specific category; the onset was acute but the predisposing factors more typical of chronic forms are easily recognizable. Moreover, the patient was not an athlete and he was at rest during the onset.. The revascularization origin, before being suspected, was excluded by echo-colo-doppler; the biopsy indicated an autoimmunogenic, parasitic or allergic myopathy.. Actually this aspect is still obscure; nevertheless, it was not confirmed by any variation in white blood cells or the presence of self-antibodies and consequently this hypothesis was rejected.. The other hypothesis derived from two specific factors: the diagnosis of type-II Diabetes ...
Q: I just read that taking statins can cause diabetes, which can seriously increase my risk for heart disease. I thought statins were supposed to reduce my risk. Whats the story? - Bernardo S., Boca Raton, Florida A: Youre referring to the six-year follow-up to the Metabolic Syndrome in Men study that was recently
TY - JOUR. T1 - Familial hypercholesterolemia patients treated with statins at no increased risk for intracranial vascular lesions despite increased cholesterol burden and extracranial atherosclerosis. AU - Soljanlahti, Sami. AU - Autti, Taina. AU - Lauerma, Kirsi. AU - Raininko, Raili. AU - Keto, Pekka. AU - Turtola, Hannu. AU - Vuorio, Alpo. AU - Vuorio, Alpo F. PY - 2005. Y1 - 2005. U2 - 10.1161/01.STR.0000169920.64180.fa. DO - 10.1161/01.STR.0000169920.64180.fa. M3 - Article. VL - 36. SP - 1572. EP - 1574. JO - Stroke. JF - Stroke. SN - 0039-2499. IS - 7. ER - ...
In Dr. Sethis view, the AIM-HIGH study was truly trying to aim high, as it was seeking additional cardiovascular benefits in a group of patients that already were very well treated with respect to their LDL-C levels. All patients had been on statin for a longer period of time, but had elevated triglycerides and low HDL-C levels. This, he says, is a very tough patient population to achieve any additional cardiovascular benefit from. We know for a fact that there is a residual cardiovascular risk in patients on statin therapy, but currently we just dont know how to treat them, if not with HDL increasing drugs such as niacin. Although no benefits were observed in this study it doesnt mean that niacin would not be beneficial in other dyslipidemic phenotypes. For this reason, it would be of extreme interest to explore the effect of the niacin treatment in specific subgroups of the study population ...
Atorvastatin cholesterol-lowering drug. Box containing tablets of the cholesterol-lowering drug atorvastatin on an ECG (electrocardiogram) readout. Statins are used to lower the levels of low-density lipoprotein (LDL) cholesterol (bad cholesterol) in the bloodstream. High levels of LDL cholesterol (hypercholesterolaemia) are a major cause of heart disease and strokes. Statins work by blocking the effects of the enzyme HMG-CoA reductase, which normally causes the body to produce LDL cholesterol from foods. - Stock Image C026/3783
Transparency and raw data is needed to show us who really benefits from taking statins, and what side effects they can have. Its been almost 35 years since scientists Michael S. Brown and Joseph L. Goldstein won the Nobel Prize for discovering...
Compared to women in the study who were given placebo, women on the statin therapy nearly cut in half their risk for cardiovascular disease, a risk reduction similar to those found among men in the study. The findings appear in the February 22, 2009 on line edition of the journal Circulation.. The JUPITER findings were also compared to a meta-analysis of five peer- reviewed, randomized, placebo-controlled statin trials. Put in context with this material, the women on statin therapy from the meta-analysis had a one third reduced risk of CVD compared to those taking a placebo.. For this research, 6801 female participants in the JUPITER study, who did not have cardiovascular disease, were greater than age 60 with acceptable levels of LDL cholesterol but elevated hsCRP, were randomized to receive rosuvastatin or placebo. Among the group receiving rosuvastatin, the researchers found cardiovascular events such as heart attack, stroke, unstable angina, and revascularization were reduced by 46 percent ...
The increased HMGco A reductase therapy in the field of cardiovascular disease can be well explained by potent LDL and total cholesterol lowering ability. About 5 to 7.78 percentage of Indian population receiving daily statin therapy. Since statins are less suspected for its long term events, the improved understanding of long term effects of commonly used statins are necessary to reduce the accumulation of drug induced complications in hospitals. Long term effects of statins include neuropsychiatry adverse effects like cognitive impairment, dementia and short term memory loss. Diabetics, risk of carcinoma, interstial lung disease, and myopathy were few among vast data. In CAD and CKD patients, long-term statin therapy reduced the rates ADR and death rates and also statins can decrease the intra-hepatic vascular resistance in a cirrhotic liver and improves the flow mediated vasodilatation of liver vasculature. In the treatment of neurological diseases like multiple sclerosis, stroke and ...
GHC patients receive prescriptions through the GHC pharmacy at no or nominal cost. The GHC pharmacy database was established in January 1977. Its data files contain information on drug, dosage, quantity dispensed, prescription date, and instructions. Use of statin medications (simvastatin, lovastatin, pravastatin, and atorvastatin) and other lipid-lowering agents (LLAs), including niacin,cholestyramine, colestipol, gemfibrozil, and clofibrate, was defined as at least three filled prescriptions for statins or LLAs of 15 tablets or more. Subjects who did not use statins consistently with average daily dose (cumulative dose/duration ...
FDA had changed the cholesterol medication guidelines. According to FDA, statins are good to lower the cholesterol. Many patients in the United States may get prescriptions to buy statins to lower their bad cholesterol. They will not have to necessarily be suffering from a previous heart attack or stroke. Known as PCSK9 inhibitors, the drugs decrease the LDL or low density lipoproteins. Read the Latest NES Classic News. This is of course the bad cholesterol as opposed to the good cholesterol which is HDL or high density lipoproteins. Statins do their stuff by putting an end to the livers ability to make LDL. As of now, the drugs will be available to reduce cholesterol levels as cholesterol medication instead of just for the high risk category.. If you happen to be above 75 and suffering from a variety of debilitating diseases of civilization then you definitely deserve to be taking statins for your condition. The list of diseases includes diabetes and coronary thrombosis. However, even if you ...
Study subjects. Subjects were recruited from internal clinical trial databases and from advertisements in local newspapers and postings at each study site (Columbia University Medical Center and the University of Pennsylvania). Eligible subjects included nonsmoking or social smoking (fewer than 5 cigarettes over 3 months) men and women between 18 and 75 years of age with a BMI between 18.5 and 40 kg/m2. All subjects had an LDL-C level of 100 mg/dl or higher and 190 mg/dl or lower (subjects with 0-1 coronary heart disease [CHD] risk factor) or 160 mg/dl or lower (subjects with ≥2 CHD risk factors) at screening for statin-naive subjects, or following a 2- to 3-week washout period for subjects taking statins at screening. The initial upper limit for BMI (35 kg/m2) and lower limit for LDL (≥120 mg/dl) were modified to aid in recruitment. A requirement for subjects to have an LDL cholesterol level of 70 mg/dl or higher after 2 weeks on ATV treatment was removed to increase enrollment numbers. ...
Lowering of low-density lipoprotein cholesterol is well achieved by 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins). Statins inhibit the conversion of HMG-CoA to mevalonate, a precursor for cholesterol and coenzyme Q10 (CoQ10). In HepG2 cells, simvastatin decreased mitochondrial CoQ10 levels, and at higher concentrations was associated with a moderately higher degree of cell death, increased DNA oxidative damage and a reduction in ATP synthesis. Supplementation of CoQ10, reduced cell death and DNA oxidative stress, and increased ATP synthesis. It is suggested that CoQ10 deficiency plays an important role in statin-induced hepatopathy, and that CoQ10 supplementation protects HepG2 cells from this complication. © 2007 Elsevier Inc. All rights reserved ...
TY - JOUR. T1 - Under-prescription of statins in patients with non-alcoholic fatty liver disease. AU - Averna, Maurizio. AU - Polimeni, Licia. AU - Violi, Francesco. AU - Pastori, Daniele. AU - Baratta, Francesco. AU - Del Ben, Maria. AU - Loffredo, Lorenzo. AU - Angelico, Francesco. PY - 2017. Y1 - 2017. N2 - Background and Aim Non-alcoholic fatty liver disease (NAFLD) is a common disease associated with high cardiovascular risk. Management of dyslipidaemia plays a pivotal role in the prevention of CV events and statins have proved to be safe in these patients. However, in everyday clinical practice statin prescription is sometimes limited because of the concern of physicians about side-effects. The aim of the study was to investigate if the presence of NAFLD affects the prescription of lipid-lowering treatment in a large series of patients with cardio-metabolic disorders. Methods and Results Cardiovascular risk and LDL-C targets were defined according to ESC/EAS Guidelines in 605 consecutive ...
Our study is the first to show national trends in statin use following the AHA/ACC 2013 guideline. We find nearly flat trends in statin use for secondary prevention, despite the introduction of a generic statin over the last decade (eg, generic atorvastatin in 2011). Unfortunately, gaps in recommended ASCVD services are not unique to statins for secondary prevention or other recommended clinical services.24,25 For example, less than 35% of patients who reported having an acute myocardial infarction received cardiac rehabilitation.26,27. We find a gender disparity in statin use for secondary prevention, consistent with prior research,28,29 finding that women have approximately 35% lower odds of statin use after accounting for other demographic and health factors. Though the prevalence of ASCVD is higher in men, ASCVD mortality is actually higher among women and there is no evidence that statins are less effective for secondary prevention or not tolerated as well by women as men.29⇓⇓-32 People ...
Title:Glycation and HMG-CoA Reductase Inhibitors: Implication in Diabetes and Associated Complications. VOLUME: 15 ISSUE: 3. Author(s):Rabia Nabi, Sahir Sultan Alvi, Mohd. Saeed, Saheem Ahmad and Mohammad Salman Khan*. Affiliation:Clinical Biochemistry & Natural Product Research Lab, Department of Biosciences, Integral University, Lucknow, 226026, U.P, Clinical Biochemistry & Natural Product Research Lab, Department of Biosciences, Integral University, Lucknow, 226026, U.P, Department of Clinical Lab. Sciences, College of Applied Medical Sciences, University of Hail, Hail, Laboratory of Glycation Biology and Metabolic Disorders, Department of Biosciences, Integral University Lucknow, 226026, U.P, Clinical Biochemistry & Natural Product Research Lab, Department of Biosciences, Integral University, Lucknow, 226026, U.P. Keywords:Glycation, Advanced Glycation end products (AGEs), HMG-R inhibitors, diabetic complications, Cardiovascular disease (CVD), Receptor for AGEs ...
CAN catalyzed one-pot synthesis of Imidazole derivatives in PEG-400 as HMG-CoA reductase inhibitor for benefit in atherosclerosis, Zong-Sheng Guo, Xin-Chun Yang
Tim its an unfortunate misunderstanding that many people have that statins can damage your liver. I have been in practice for over 23 years and treated many hundreds if not thousands of patients with statins during that time. Not one has ever developed liver damage. As with many myths there is a grain of truth to this one which has been exaggerated and misunderstood.. Statins like many other drugs ( and foods) are metabolized through the liver. A small minority of individuals may see a slight elevation of their enzyme levels as a result of taking statins but this can also be seen with many other medications that people frequently take and in fact the most common reason by far for elevated liver enzymes is diet. Too many carbs and calories often cause a condition known as fatty liver or NASH and this is far far more common than statin related liver enzyme elevations. Most physicians check statin users enzyme levels several times a year when they check the cholesterol levels. Minor elevations ...
We assessed baseline differences between the exposure and control groups using χ2 tests for categorical variables and t tests for continuous variables. Crude incidence rates of stroke or TIA (primary outcome) and crude all cause mortality (secondary outcome) were calculated in patients with resolved atrial fibrillation, atrial fibrillation, and no atrial fibrillation. We calculated crude and adjusted incidence rate ratios comparing the incidence of stroke or TIA and mortality in patients with resolved atrial fibrillation versus those with and without atrial fibrillation.. Poisson regression was used to calculate adjusted incidence rate ratios, adjusting for the baseline covariates age, sex, Townsend deprivation fifth, body mass index (BMI), smoking status (current smoker), alcohol consumption (non-drinker, drinker, excessive drinker), Charlson comorbidity index category, current statin prescription, and current anticoagulant prescription. A sensitivity analysis was carried out in which we ...
In an in vitro study, we compared the cytochrome P450 (CYP)-dependent metabolism and drug interactions of the acid and lactone forms of the 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase inhibitor atorvastatin. Metabolism of atorvastatin acid and lactone by human liver microsomes resulted in para-hydroxy andortho-hydroxy metabolites. Both substrates were metabolized mainly by CYP3A4 and CYP3A5. Atorvastatin lactone had a significantly higher affinity to CYP3A4 than the acid (Km: para-hydroxy atorvastatin, 25.6 ± 5.0 μM; para-hydroxy atorvastatin lactone, 1.4 ± 0.2 μM;ortho-hydroxy atorvastatin, 29.7 ± 9.4 μM; andortho-hydroxy atorvastatin lactone, 3.9 ± 0.2 μM). Compared with atorvastatin acid, CYP-dependent metabolism of atorvastatin lactone to its para-hydroxy metabolite was 83-fold higher [formation CLint(Vmax/Km): lactone 2949 ± 3511 versus acid 35.5 ± 48.1 μl · min−1 · mg−1] and to itsortho-hydroxy metabolite was 20-fold higher (CLint: lactone 923 ± 965 versus acid 45.8 ± ...
These results support the current guidelines established by the National Institute of Healths National Cholesterol Education Program. These guidelines recommend statin therapy for people who have diabetes even if they have average or below-average LDL (or bad) cholesterol levels. Another study, published in the European Heart Journal in October, showed that statin drugs are just as beneficial in people who have diabetes and a condition called acute coronary syndrome (ACS) as they are in people who have ACS but do not have diabetes. (People are identified as having ACS if they have previously had either a heart attack or an episode of severe angina.) The study, which analyzed a subgroup of people within a larger trial of statin therapy, followed 978 people with ACS and diabetes and 3,184 people with ACS and without diabetes for about two years. Half of the study subjects received intensive statin therapy and the other half received standard statin therapy. At the end of the study, researchers ...
Ever since Anitschkows pioneering experiments on the role of cholesterol in the causation of atherosclerotic plaques in rabbits (2), this intriguing molecule has been at the heart of debate and controversy (3). Initially, the total cholesterol level was used as a measure of risk, then a distinction between α- and β-lipoproteins emerged. As the role of specific lipoproteins became clear, attention focused on the cholesterol content of low-density lipoprotein (LDL), which constitutes the major cholesterol-carrying lipoprotein in serum. The National Cholesterol Education Programs Adult Treatment Program (ATP), first published in 1988, recommended using the LDL cholesterol level as the marker for initiating treatment as well as for gauging therapeutic target goals (4). The well orchestrated campaign that followed these guidelines familiarized the medical community with LDL cholesterol. Since then numerous clinical studies have confirmed the value of nutritional and pharmacologic treatment of ...
Learn more about Statin Drugs at Sky Ridge Medical Center Chaparral, Comfrey, and Coltsfoot -Possible Harmful Interaction .....
Learn more about Statin Drugs at Reston Hospital Center Chaparral, Comfrey, and Coltsfoot -Possible Harmful Interaction ...
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Learn more about Statin Drugs at Grand Strand Medical Center Chaparral, Comfrey, and Coltsfoot -Possible Harmful Interaction ...
In this paper, researchers investigated associations of genetic inhibition of CETP on detailed lipoproteins using variants associated with CETP (rs247617) and HMGCR (rs12916) expression in 62,400 Europeans and detailed lipoprotein profiling. Results found that CETP inhibition does not affect size-specific
... human organic anion transporting polypeptide and identification of rat and human hydroxymethylglutaryl-CoA reductase inhibitor ...
... hydroxymethylglutaryl-coa reductase inhibitors MeSH D27.505.519.389.375 - integrase inhibitors MeSH D27.505.519.389.375.400 - ... hydroxymethylglutaryl-coa reductase inhibitors MeSH D27.505.519.186.071.601 - lipotropic agents MeSH D27.505.519.186.144 - ... hydroxymethylglutaryl-coa reductase inhibitors MeSH D27.505.954.230.601 - lipotropic agents MeSH D27.505.954.248 - ... enzyme inhibitors MeSH D27.505.519.389.099 - aromatase inhibitors MeSH D27.505.519.389.200 - carbonic anhydrase inhibitors MeSH ...
Hydroxymethylglutaryl-coenzyme A reductase inhibitors (HMG-CoA inhibitors or statins) Statins may sometimes cause myalgia and ...
... pravastatin inhibits the function of hydroxymethylglutaryl-CoA (HMG-CoA) reductase. As a reversible competitive inhibitor, ... Tobert JA (July 2003). "Lovastatin and beyond: the history of the HMG-CoA reductase inhibitors". Nature Reviews. Drug Discovery ... Like all statins, pravastatin works by inhibiting HMG-CoA reductase, an enzyme found in liver that plays a role in producing ... pravastatin sterically hinders the action of HMG-CoA reductase by occupying the active site of the enzyme. Taking place ...
The discovery of HMG-CoA (3-hydroxy-3-methylglutaryl-CoA) reductase inhibitors, called statins, was a breakthrough in the ... Moghadasian, Mohammed H. (May 1999). "Clinical pharmacology of 3-hydroxy-methylglutaryl coenzyme A reductase inhibitors". Life ... Tobert, Jonathan A. (July 2003). "Lovastatin and beyond: The history of the HMG-CoA reductase inhibitors". Nature Reviews Drug ... Endo, Akira (November 1, 1992). "The Discovery and development of HMG-CoA reductase inhibitors". Journal of Lipid Research. 33 ...
... and mononuclear leukocyte hydroxymethylglutaryl-coenzyme A reductase (HMG-CoA reductase), the rate-controlling enzyme in the ... In October 2002, a new cholesterol absorption inhibitor, ezetimibe, received US Food and Drug Administration (FDA) approval for ... recent data indicate that secondary effects of unknown regulators other than sitosterol can lead to reduced HMG-CoA reductase ...
"On the Inhibitor Effects of Bergamot Juice Flavonoids Binding to the 3-Hydroxy-3-methylglutaryl-CoA Reductase (HMGR) Enzyme". J ... Isolation of 3-Hydroxymethylglutaryl Flavonoid Glycosides". Journal of Natural Products. 72 (7): 1352-1354. doi:10.1021/ ...
Statins act by inhibiting the enzyme hydroxymethylglutaryl CoA reductase (HMG-CoA-reductase) in the liver. In response, the ... Lomitapide, an inhibitor of the microsomal triglyceride transfer protein, was approved by the US FDA in December 2012 as an ... Synthesis of cholesterol by the liver is suppressed in the HMG-CoA reductase pathway. In FH, LDL receptor function is reduced ... Initially, they found increased activity of HMG-CoA reductase, but studies showed that this did not explain the very abnormal ...
SEARCH RESULTS for: Hydroxymethylglutaryl-CoA Reductase Inhibitors [Drug Class] (644 results) * Share : JavaScript needed for ...
The Natural Products as Hydroxymethylglutaryl-Coa Reductase Inhibitors. (E-pub Ahead of Print). Author(s): Hayrettin Ozan ... "The Natural Products as Hydroxymethylglutaryl-Coa Reductase Inhibitors", Letters in Drug Design & Discovery (2019) 16: 1. https ... directly obtained from fungi-like molds and mushrooms and they are potent inhibitors of hydroxymethylglutaryl-CoA reductase, ... directly obtained from fungi-like molds and mushrooms and they are potent inhibitors of hydroxymethylglutaryl-CoA reductase, ...
Compounds that inhibit HMG-CoA reductases. They have been shown to directly lower cholesterol synthesis. ... Inhibitors, Hydroxymethylglutaryl-CoA Reductase; Reductase Inhibitors, HMG-CoA; Reductase Inhibitors, Hydroxymethylglutaryl-CoA ... HMG-CoA Reductase Inhibitors; Inhibitors, HMG-CoA Reductase; Inhibitors, Hydroxymethylglutaryl-CoA; Inhibitors, ... HMG CoA Reductase Inhibitors; HMG-CoA Statins; Hydroxymethylglutaryl CoA Reductase Inhibitors; Hydroxymethylglutaryl-CoA ...
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Simvastatin, the methylated form of lovastatin, is an oral antilipemic agent which inhibits HMG-CoA reductase. simvastatin is ...
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Hydroxymethylglutaryl-CoA Reductase Inhibitors. LinkOut - more resources. Full Text Sources. *Wiley. Medical. *Cholesterol ...
Hydroxymethylglutaryl-CoA Reductase Inhibitors/administration & dosage*. *Hydroxymethylglutaryl-CoA Reductase Inhibitors/ ...
Hydroxymethylglutaryl-CoA Reductase Inhibitors. Anticholesteremic Agents. Hypolipidemic Agents. Antimetabolites. Molecular ...
Hydroxymethylglutaryl-CoA Reductase Inhibitors. Enzyme Inhibitors. To Top. *For Patients and Families ... strong CYP3A4 inhibitors (e.g., itraconazole, ketoconazole, posaconazole, voriconazole, human immunodeficiency virus [HIV] ... protease inhibitors, boceprevir, telaprevir, erythromycin, clarithromycin, telithromycin, nefazodone, or cobicistat-containing ...
Hydroxymethylglutaryl-CoA Reductase Inhibitors. Enzyme Inhibitors. To Top. *For Patients and Families ...
Subjects with a clinically indicated need for statin (HMG-CoA reductase inhibitor) therapy other than atorvastatin or other ... taking any drugs known to be associated with an increased risk of myositis in combination with HMG-CoA reductase inhibitors. ...
Hydroxymethylglutaryl-CoA Reductase Inhibitors. Anticholesteremic Agents. Hypolipidemic Agents. Antimetabolites. Molecular ... Patients hypersensitive to HMG-CoA reductase inhibitors or ezetimibe.. *Patient who is unable to give informed consent (the ... Medications that are potent inhibitors of CYP3A4, including cyclosporine, systemic itraconazole or ketoconazole, erythromycin ... or clarithromycin, nefazodone, verapamil and human immunodeficiency virus (HIV) protease inhibitors.. *Lipid-lowering agents ...
"Hydroxymethylglutaryl-CoA Reductase Inhibitors"; "Metformin"; "Acarbose"; and "Gemfibrozil" and free-text terms: "fatty liver ... α-Glucosidase inhibitors.. The α-glucosidase inhibitors may be particularly useful in patients with liver disease because they ... All of the ACE inhibitors have been implicated in hepatic injury including fulminant hepatic failure (123-126). The reactions ... Miglitol, another α-glucosidase inhibitor, has not been associated with hepatotoxicity.. TZDs.. TZDs may be especially useful ...
Hydroxymethylglutaryl-CoA Reductase Inhibitors. *Micronutrients. *Organic Chemicals. *Pharmacologic Actions. *Physiological ...
Hydroxymethylglutaryl-CoA Reductase Inhibitors / therapeutic use* * Magnetic Resonance Imaging * Male * Middle Aged ... reductase inhibitors exert pleiotropic immunomodulatory effects, with potential therapeutic implications in multiple sclerosis ...
Hydroxymethylglutaryl-CoA Reductase Inhibitors / therapeutic use * Male * Middle Aged * Polymorphism, Single Nucleotide ...
acceptor) inhibitor that inhibits HMG-CoA reductases. Hydroxymethylglutaryl-CoA reductase inhibitors have been shown to lower ... EC 1.1.1.34/EC 1.1.1.88 (hydroxymethylglutaryl-CoA reductase) inhibitor Any EC 1.1.1.* (oxidoreductase acting on donor CH-OH ...
acceptor) inhibitor that inhibits HMG-CoA reductases. Hydroxymethylglutaryl-CoA reductase inhibitors have been shown to lower ... EC 1.1.1.34/EC 1.1.1.88 (hydroxymethylglutaryl-CoA reductase) inhibitor Any EC 1.1.1.* (oxidoreductase acting on donor CH-OH ... 3-hydroxy-3-methylglutaric acid (CHEBI:16831) has role EC 1.1.1.34/EC 1.1.1.88 (hydroxymethylglutaryl-CoA reductase) inhibitor ... It has been found to accumulate in urine of patients suffering from HMG-CoA lyase (3-hydroxy-3-methylglutaryl-CoA lyase, EC 4.1 ...
Hydroxymethylglutaryl-CoA Reductase Inhibitors. *MalaCards. *Medline Plus. Pharma. 2369. Hypolipidemic Agents. *MalaCards ... Contains 2 copies of a cytoplasmic motif that is referred to as the immunoreceptor tyrosine-based inhibitor motif (ITIM). This ... Contains 2 copies of a cytoplasmic motif that is referred to as the immunoreceptor tyrosine-based inhibitor motif (ITIM). This ...
Hydroxymethylglutaryl-CoA Reductase Inhibitors / therapeutic use*. Incidence. Male. Middle Aged. Preoperative Care. ... preoperative angiotensin-converting enzyme inhibitor therapy (OR, 1.26; 95% CI, 1.07 to 1.49), ejection fraction less than 0.30 ...
Hydroxymethylglutaryl-CoA Reductase Inhibitors / chemistry, pharmacology, therapeutic use*. Hypercholesterolemia / ... 0/Anticholesteremic Agents; 0/Cholesterol, LDL; 0/Hydroxymethylglutaryl-CoA Reductase Inhibitors From MEDLINE®/PubMed®, a ... The introduction of more potent HMG-CoA reductase inhibitors, or the use of higher doses of older statins, should allow more ... The 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) are considered the drugs of choice for ...
0 (Antibodies, Monoclonal); 0 (Cholesterol, LDL); 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors); 0 (Hypolipidemic Agents ... Inibidores de Hidroximetilglutaril-CoA Redutases/farmacologia. Hiperlipoproteinemia Tipo III. Pr -Prote na Convertase 9/ ...
Hydroxymethylglutaryl-CoA Reductase Inhibitors); EC 1.1.1.- (HMGCR protein, human); EC 1.1.1.- (Hydroxymethylglutaryl CoA ... Hidroximetilglutaril-CoA Redutases/gen tica. Hipercolesterolemia/gen tica. [Mh] Termos MeSH secund rio:. Anticolesterolemiantes ... both alone and in combination with variants in the 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) gene. Design, Setting, and ... Inibidores de Hidroximetilglutaril-CoA Redutases/uso terap utico. Hipercolesterolemia/sangue. Hipercolesterolemia/tratamento ...
Lovastatin is an inhibitor of hydroxymethyl glutaryl (HMG)-CoA reductase, the rate-limiting enzyme in cholesterol synthesis. ... Assay for HMG-CoA Reductase Activity.. The HMG-CoA reductase assays in MDA-MB-157 cells were performed as described (27). ... and pravastatin to inhibit HMG-CoA reductase we prepared cell extracts from MDA-MB-157 cells and assayed for HMG-CoA reductase ... inhibit the HMG-CoA reductase enzyme, lovastatin pro-drug inhibits the proteasome but does not inhibit HMG-CoA reductase. In ...
ClinicalTrials.gov: Hydroxymethylglutaryl-CoA Reductase Inhibitors (National Institutes of Health) Journal Articles References ...
ClinicalTrials.gov: Hydroxymethylglutaryl-CoA Reductase Inhibitors (National Institutes of Health) * ClinicalTrials.gov: ... PCSK9 inhibitors, which block a protein called PCSK9. This helps your liver remove and clear LDL cholesterol from your blood. ... Cholesterol absorption inhibitors, which decrease the amount of cholesterol absorbed from food and lower triglycerides. ...
Hydroxymethylglutaryl-CoA Reductase Inhibitors Antibody Responses to Fusobacterium nucleatum Proteins in Prediagnostic Blood ...
Hydroxymethylglutaryl-CoA Reductase Inhibitors · Imidazoles · Inflammation · Lipids · Macrophages · Mice · Mice, Transgenic · ... Hydroxymethylglutaryl-CoA Reductase Inhibitors · Lipids · Lipoproteins · Macrophages · Mice · Mice, Transgenic · Monocytes · ... Hydroxymethylglutaryl-CoA Reductase Inhibitors; Lipids; Lipoproteins; Pyrimidines; rosuvastatin, 287714-41-4; Sulfonamides ... Hydroxymethylglutaryl coenzyme A reductase inhibitor · Lipid · Lipoprotein · Pyrimidine derivative · Sulfonamide · Animal cell ...
  • In fact, the original statins are natural products directly obtained from fungi-like molds and mushrooms and they are potent inhibitors of hydroxymethylglutaryl-CoA reductase, the key enzyme in the biosynthesis of cholesterol. (eurekaselect.com)
  • This review focuses on the first identification of natural statins, their synthetic and semi-synthetic analogues, and the validation of hydroxymethylglutaryl-CoA reductase as a target in the treatment of hypercholesterolemia. (eurekaselect.com)
  • In recent years, small-scale clinical trials have indicated that statins or 3-hydroxy-3-methylglutaryl coenzyme A (HMGCoA) reductase inhibitors exert pleiotropic immunomodulatory effects, with potential therapeutic implications in multiple sclerosis (MS). (nih.gov)
  • The 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) are considered the drugs of choice for lowering LDL-C in patients with hypercholesterolaemia. (biomedsearch.com)
  • The introduction of more potent HMG-CoA reductase inhibitors, or the use of higher doses of older statins, should allow more patients to achieve LDL-C target levels. (biomedsearch.com)
  • Hydroxymethylglutaryl-CoA reductase inhibitors (statins) are potent cholesterol-lowering drugs. (ahajournals.org)
  • 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors (statins) are the most commonly used drugs in the treatment of hypercholesterolemia, which potently reduce plasma cholesterol levels. (plos.org)
  • Recently, 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMG-CoAR) inhibitors (statins) have been proposed as a potential class of chemoprevention agents due to their immunomodulatory and anti-inflammatory effects [ 3 , 4 ]. (jcancer.org)
  • The exposures were treatment at discharge with statins, angiotensin-converting enzyme inhibitors/angiotensin receptor blockers, beta-blockers, and dual antiplatelet therapy. (diva-portal.org)
  • The hazard ratios (95% confidence intervals) for major adverse cardiac events were 0.77 (0.68-0.87), 0.82 (0.73-0.93), and 0.86 (0.74-1.01) in patients on statins, angiotensin-converting enzyme inhibitors/angiotensin receptor blockers, and beta-blockers, respectively. (diva-portal.org)
  • CONCLUSIONS: The results indicate long-term beneficial effects of treatment with statins and angiotensin-converting enzyme inhibitors/angiotensin receptor blockers on outcome in patients with MINOCA, a trend toward a positive effect of beta-blocker treatment, and a neutral effect of dual antiplatelet therapy. (diva-portal.org)
  • Hydroxy--methylglutaryl coenzyme a hmg-coa reductase inhibitors statins are more effec-tive than afterload-reducing medications, the. (nrha.org)
  • Hydroxymethylglutaryl coenzyme-A (HMG Co-A) reductase inhibitors (or statins) are widely prescribed, and any class-specific side effect has the potential to affect many thousands of patients. (mja.com.au)
  • Pitavastatin calcium, a novel member of the medication class of statins , is a calcium salt formulation of pitavastatin which is a highly effective HMG-CoA reductase inhibitor. (selleckchem.com)
  • These uptake mechanisms are also important for disposition and action of a broad variety of cardiovascular drugs frequently used concomitantly in patients with type 2 diabetes (e.g., statins, ACE inhibitors, and angiotensin type 1 receptor blockers) ( 12 ). (diabetesjournals.org)
  • Subjects with a clinically indicated need for statin (HMG-CoA reductase inhibitor) therapy other than atorvastatin or other concomitant therapy with known lipid altering effects on LDL-C and HDL-C including fibrates and nicotinic acid. (clinicaltrials.gov)
  • The primary outcome was whether a patient reported taking a goal dose of beta-blocker, statin, and angiotensin-converting enzyme (ACE) inhibitor/angiotensin-receptor blocker (ARB) at 12 months after AMI. (acc.org)
  • Twelve months after AMI, only 60-70% of patients reported taking any dose of beta-blocker, statin, or ACE inhibitor/ARB. (acc.org)
  • At 12 months after AMI, only 12%, 26%, and 32% of eligible patients were of goal doses of beta-blockers, statin, and ACE inhibitors/ARBs, respectively. (acc.org)
  • May be used alone or combined with a hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor (i.e., statin). (drugs.com)
  • Lovastatin is used for the treatment of hypercholesterolemia ( 11 ) because it inhibits hydroxymethyl-glutaryl (HMG)-CoA reductase, and thus prevents HMG-CoA's conversion into mevalonic acid ( 12 , 13 ). (pnas.org)
  • The hydroxymethylglutaryl-CoA reductase inhibitor lovastatin is used widely to treat hypercholesterolemia and has been shown to have cell cycle-specific effects. (aacrjournals.org)
  • Lovastatin, a hydroxymethylglutaryl-CoA reductase inhibitor, has traditionally been used to treat hypercholesterolemia ( 1 , 2 ). (aacrjournals.org)
  • Simvastatin, the methylated form of lovastatin, is an oral antilipemic agent which inhibits HMG-CoA reductase. (pharmacycode.com)
  • Lovastatin is an inhibitor of hydroxymethyl glutaryl (HMG)-CoA reductase, the rate-limiting enzyme in cholesterol synthesis. (pnas.org)
  • Previously, we reported that lovastatin can be used to arrest cultured cells in the G 1 phase of the cell cycle, resulting in the stabilization of the cyclin-dependent kinase inhibitors (CKIs) p21 and p27. (pnas.org)
  • We show that while the lovastatin open-ring form and pravastatin (a lovastatin analogue, 100% open ring) inhibit the HMG-CoA reductase enzyme, lovastatin pro-drug inhibits the proteasome but does not inhibit HMG-CoA reductase. (pnas.org)
  • A derivative of LOVASTATIN and potent competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES), which is the rate-limiting enzyme in cholesterol biosynthesis. (bioportfolio.com)
  • The cytotoxicity of lovastatin is evidenced in that lovastatin can induce cell cycle arrest in vitro in both G 1 and G 2 -M. The G 1 effect has been the most closely examined and is associated with lovastatin-induced decreases in cyclin A, D, and E levels ( 9 ) and increases in cyclin-dependent kinase inhibitors ( 10 ). (aacrjournals.org)
  • Lovastatin lowers hepatic cholesterol synthesis by competitively inhibiting HMG-CoA reductase, the enzyme that catalyzes the rate-limiting step in the cholesterol biosynthesis. (nextbio.com)
  • Lovastatin is structurally similar to the HMG, a substituent of the endogenous substrate of HMG-CoA reductase. (nextbio.com)
  • Like mevastatin, lovastatin is structurally similar to hydroxymethylglutarate (HMG), a substituent of HMG-Coenzyme A (HMG-CoA), a substrate of the cholesterol biosynthesis pathway via the mevalonic acid pathway. (drugbank.ca)
  • Lovastatin is a competitive inhibitor of HMG-CoA reductase with a binding affinity 20,000 times greater than HMG-CoA. (drugbank.ca)
  • Lovastatin is an inhibitor of HMG-CoA reductase with IC50 of 3.4 nM in a cell-free assay, used for lowering cholesterol (hypolipidemic agent). (selleckchem.com)
  • oxidoreductase acting on donor CH-OH group, NAD + or NADP + acceptor) inhibitor that inhibits HMG-CoA reductases. (ebi.ac.uk)
  • Fluvastatin Sodium inhibits HMG-CoA reductase activity with IC50 of 8 nM in a cell-free assay. (selleckchem.com)
  • Clinofibrate inhibits hydroxymethylglutaryl coenzyme A reductase (HMGCR) with IC50 of 0.47 mM, is a lipid-lowering agent used for controlling high cholesterol and triacylglyceride levels in the blood. (selleckchem.com)
  • Pravastatin is a lipoprotein-lowering drug via reversibly inhibiting hydroxymethylglutaryl-CoA (HMG-CoA) reductase and the synthesis of very-low-density lipoproteins. (selleckchem.com)
  • Pravastatin sodium is an HMG-CoA reductase inhibitor against sterol synthesis with IC50 of 5.6 μM. (selleckchem.com)
  • Members of the OATP family transport a variety of anionic endogenous substances and drugs, including hydroxymethylglutaryl-CoA reductase inhibitors, such as fluvastatin, pitavastatin, pravastatin, and rosuvastatin ( 12 , 13 ). (diabetesjournals.org)
  • Atorvastatin is a hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitor demonstrated to be effective in reducing both cholesterol (CHOL) and triglyceride (TG) levels in humans. (unboundmedicine.com)
  • Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) can reduce heart enlargement and increase the chance of survival for many people. (merckmanuals.com)
  • It is a competitive inhibitor of hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase , the rate-determining enzyme in cholesterol biosynthesis via the mevalonate pathway. (selleckchem.com)
  • Rosuvastatin is an inhibitor of HMG-CoA reductase , an enzyme that catalyzes the rate-limiting step in cholesterol biosynthesis, with Ki value (inhibition constant) of approximately 0.1 nM. (selleckchem.com)
  • A dose-response study with simvastatin, a specific inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, was conducted in four treatment groups of FHC animals exhibiting TC≥250 mg/dL. (tudelft.nl)
  • The ubiquitin pathway also regulates the levels of cyclin-dependent kinase inhibitors (CKIs) p27 and p21 ( 5 - 7 ). (pnas.org)
  • In addition, many of the properties of proteasome inhibition by the pro-drug are the same as the specific proteasome inhibitor lactacystin. (pnas.org)
  • Hydroxymethylglutaryl-CoA reductase inhibition not only depletes cells of mevalonic acid, a necessary precursor for the synthesis of cholesterol, but also limits the availability of isoprenyl metabolites such as farnesyl PP i and geranylgeranyl PP i for the posttranslational modification of cellular proteins, many of which are critical for cell proliferation ( 7 ). (aacrjournals.org)
  • The purpose of this study was to comprehensively investigate this substrate-dependent inhibition of OATP1B1 using clinically relevant OATP1B1 inhibitors and substrate drugs. (aspetjournals.org)
  • Subjects taking any drugs known to be associated with an increased risk of myositis in combination with HMG-CoA reductase inhibitors. (clinicaltrials.gov)
  • Hydroxymethylglutaryl-CoA Reductase Inhibitors" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (umassmed.edu)
  • The hydrolyzed lactone ring mimics the tetrahedral intermediate produced by the reductase allowing the agent to bind with 20,000 times greater aff. (nextbio.com)
  • Atorvastatin Calcium is an inhibitor of HMG-CoA reductase used as a cholesterol-lowering medication that blocks the production of cholesterol. (selleckchem.com)
  • Hydroxymethylglutaryl-CoA reductase inhibitors have been shown to lower directly cholesterol synthesis. (ebi.ac.uk)
  • Rosuvastatin Calcium is a competitive inhibitor of HMG-CoA reductase with IC50 of 11 nM in a cell-free assay. (selleckchem.com)
  • cholesterol absorption inhibitor Ezetimibe 10 mg and simvastatin 80 mg, when split into 4 using a tablet splitter, versus a whole simvastatin 20 milligram tablet. (bioportfolio.com)
  • Rifampicin (RIF) was chosen as an inhibitor for Oatp in both uptake and IPRL studies. (aspetjournals.org)
  • We previously reported that in vitro inhibitory potencies of several inhibitors on OATP1B1 depend on the substrates when prototypical substrates, estradiol-17 β -glucuronide (E 2 G), estrone-3-sulfate, and sulfobromophthalein were used as test substrates. (aspetjournals.org)
  • Treating modifiable CHD risk factors (such as blood pressure and lipids) and using ACE inhibitors and aspirin reduce mortality in diabetes ( 21 - 25 ), which is now considered a CHD equivalent ( 26 ). (diabetesjournals.org)
  • 100 mg/dl if CHD or multiple risk factors were present, as well as prophylactic use of aspirin and blood pressure control with an ACE inhibitor to delay progression to microalbuminuria ( 28 ). (diabetesjournals.org)
  • This graph shows the total number of publications written about "Hydroxymethylglutaryl-CoA Reductase Inhibitors" by people in this website by year, and whether "Hydroxymethylglutaryl-CoA Reductase Inhibitors" was a major or minor topic of these publications. (umassmed.edu)
  • Studies involving FTIs and geranylgeranyl transferase inhibitors have indicated that geranylgeranylated proteins, but not farnesylated proteins, may be required for the G 1 to S-phase transition ( 11 ). (aacrjournals.org)
  • Furthermore, other natural products that have been shown to possess the potential to inhibit hydroxymethylglutaryl-CoA reductase are also reviewed with respect to their chemical structures. (eurekaselect.com)
  • Similarly, components of AP-1 that synergize with YAP ( FOSL1 ), growth factors (TGFα, EPEG, and HBEGF), a specific integrin ( ITGA2 ), heptahelical receptors ( P2Y 2 R , GPR87 ) and an inhibitor of the Hippo pathway ( MUC1 ), all of which stimulate YAP activity, are associated with unfavorable survival of PDAC patients. (nature.com)
  • Do not stop taking his or her life as a preservative since the beginning of the body attacks its own is likely multifactorial in origin, the em- 108 industrial poisoning: Information and control taking an ace inhibitor drug. (childbirthsolutions.com)
  • Simvastatin is a competitive inhibitor of HMG-CoA reductase with K i of 0.1-0.2 nM in cell-free assays. (selleckchem.com)
  • It has been found to accumulate in urine of patients suffering from HMG-CoA lyase (3-hydroxy-3-methylglutaryl-CoA lyase, EC 4.1.3.4) deficiency. (ebi.ac.uk)
  • If using lamivudine/raltegravir (Dutrebis ), consider that lactic acidosis and severe hepatomegaly with steatosis, including fatalities, reported in patients receiving HIV nucleoside reverse transcriptase inhibitors (NRTIs) in conjunction with other antiretrovirals. (drugs.com)