Digoxin
Digitoxin
Cardenolides
Cardiotonic Agents
Cardiac Glycosides
Medigoxin
Eleutherococcus
Nerium
Digitalis Glycosides
Anti-Arrhythmia Agents
Drug Interactions
Ouabain
Radioimmunoassay
P-Glycoprotein
Myocardial uptake of digoxin in chronically digitalized dogs. (1/952)
1 The time course of myocardial uptake of digoxin, increase in contractility and changes in myocardial potassium concentration was studied for 90 min following an intravenous digoxin dose to long-term digitalized dogs. 2 Nineteen dogs were investigated by the use of a biopsy technique which allowed sampling before and after administration of digoxin. 3 Ten minutes after administration of digoxin the myocardial concentration increased from 60 to 306 nmol/kg tissue, the myocardial concentration of digoxin was significantly lower (250 nmol/kg tissue) after 30 min and then increased again. 4 The transmural myocardial distribution of digoxin was uniform before and 90 min after administration of digoxin in long-term digitalized dogs but at 10 min after administration, both the subepicardial and the subendocardial concentration of digoxin were significantly lower than that of the mesocardial layer. 5 During the first 10 min the dp/dtmax increased to 135% of the control level. The increase remained unchanged during the rest of the study. 6 Myocardial potassium decreased throughout the study. 7 The M-configuration of the myocardial uptake curve and the non-uniformity of myocardial distribution of digoxin observed at 10 min after administrating digoxin to long-term digitalized dogs indicate that the distribution of myocardial blood flow may be changed during chronic digitalization. (+info)Fetal tachycardias: management and outcome of 127 consecutive cases. (2/952)
OBJECTIVE: To review the management and outcome of fetal tachycardia, and to determine the problems encountered with various treatment protocols. STUDY DESIGN: Retrospective analysis. SUBJECTS: 127 consecutive fetuses with a tachycardia presenting between 1980 and 1996 to a single tertiary centre for fetal cardiology. The median gestational age at presentation was 32 weeks (range 18 to 42). RESULTS: 105 fetuses had a supraventricular tachycardia and 22 had atrial flutter. Overall, 52 fetuses were hydropic and 75 non-hydropic. Prenatal control of the tachycardia was achieved in 83% of treated non-hydropic fetuses compared with 66% of the treated hydropic fetuses. Digoxin monotherapy converted most (62%) of the treated non-hydropic fetuses, and 96% survived through the neonatal period. First line drug treatment for hydropic fetuses was more diverse, including digoxin (n = 5), digoxin plus verapamil (n = 14), and flecainide (n = 27). The response rates to these drugs were 20%, 57%, and 59%, respectively, confirming that digoxin monotherapy is a poor choice for the hydropic fetus. Response to flecainide was faster than to the other drugs. Direct fetal treatment was used in four fetuses, of whom two survived. Overall, 73% (n = 38) of the hydropic fetuses survived. Postnatally, 4% of the non-hydropic group had ECG evidence of pre-excitation, compared with 16% of the hydropic group; 57% of non-hydropic fetuses were treated with long term anti-arrhythmics compared with 79% of hydropic fetuses. CONCLUSIONS: Non-hydropic fetuses with tachycardias have a very good prognosis with transplacental treatment. Most arrhythmias associated with fetal hydrops can be controlled with transplacental treatment, but the mortality in this group is 27%. At present, there is no ideal treatment protocol for these fetuses and a large prospective multicentre trial is required to optimise treatment of both hydropic and non-hydropic fetuses. (+info)Ventriculo-atrial time interval measured on M mode echocardiography: a determining element in diagnosis, treatment, and prognosis of fetal supraventricular tachycardia. (3/952)
OBJECTIVE: To determine whether M mode echocardiography can differentiate fetal supraventricular tachycardia according to the ventriculo-atrial (VA) time interval, and if the resulting division into short and long VA intervals holds any relation with clinical presentation, management, and fetal outcome. DESIGN: Retrospective case series. SUBJECTS: 23 fetuses with supraventricular tachycardia. MAIN OUTCOME MEASURES: A systematic review of the M mode echocardiograms (for VA and atrioventricular (AV) interval measurements), clinical profile, and final outcome. RESULTS: 19 fetuses (82.6%) had supraventricular tachycardia of the short VA type (mean (SD) VA/AV ratio 0.34 (0.16); heart rate 231 (29) beats/min). Tachycardia was sustained in six and intermittent in 13. Hydrops was present in three (15.7%). Digoxin, the first drug given in 14, failed to control tachycardia in five. Three of these then received sotalol and converted to sinus rhythm. All fetuses of this group survived. Postnatally, supraventricular tachycardia recurred in three, two having Wolff-Parkinson-White syndrome. Four fetuses (17.4%) had long VA tachycardia (VA/AV ratio 3.89 (0.82); heart rate 226 (10) beats/min). Initial treatment with digoxin was ineffective in all, but sotalol was effective in two. Heart failure caused fetal death in one and premature delivery in one. All three surviving fetuses had recurrences of supraventricular tachycardia after birth: two had the permanent form of junctional reciprocating tachycardia and one had atrial ectopic tachycardia. CONCLUSIONS: Careful measurement of ventriculo-atrial intervals on fetal M mode echocardiography can be used to distinguish short from long VA supraventricular tachycardia and may be helpful in optimising management. Digoxin, when indicated, may remain the drug of choice in the short VA type but appears ineffective in the long VA type. (+info)Common variant in AMPD1 gene predicts improved clinical outcome in patients with heart failure. (4/952)
BACKGROUND: This study was undertaken to identify gene(s) that may be associated with improved clinical outcome in patients with congestive heart failure (CHF). The adenosine monophosphate deaminase locus (AMPD1) was selected for study. We hypothesized that inheritance of the mutant AMPD1 allele is associated with increased probability of survival without cardiac transplantation in patients with CHF. METHODS AND RESULTS: AMPD1 genotype was determined in 132 patients with advanced CHF and 91 control reference subjects by use of a polymerase chain reaction-based, allele-specific oligonucleotide detection assay. In patients with CHF, those heterozygous (n=20) or homozygous (n=1) for the mutant AMPD1 allele (AMPD1 +/- or -/-, respectively) experienced a significantly longer duration of heart failure symptoms before referral for transplantation evaluation than CHF patients homozygous for the wild-type allele (AMPD1 +/+; n=111; 7.6+/-6.5 versus 3.2+/-3.6 years; P<0.001). The OR of surviving without cardiac transplantation >/=5 years after initial hospitalization for CHF symptoms was 8.6 times greater (95% CI: 3.05, 23.87) in those patients carrying >/=1 mutant AMPD1 allele than in those carrying 2 wild-type AMPD1 +/+ alleles. CONCLUSIONS: After the onset of CHF symptoms, the mutant AMPD1 allele is associated with prolonged probability of survival without cardiac transplantation. The mechanism by which the presence of the mutant AMPD1 allele may modify the clinical phenotype of heart failure remains to be determined. (+info)Penetration of digoxin into cerebrospinal fluid. (5/952)
The concentration of digoxin in the cerebrospinal fluid (CSF) of ten patients receiving conventional oral doses of this cardiac glycoside has been measured by a radioimmunoassay technique. Digoxin was undetected in eight patients and barely detectable in two, suggesting the presence of a significant blood-CSF barrier for digoxin. The implication of these findings is discussed. (+info)Clinical practice guidelines for heart failure. (6/952)
Development of guidelines can be a difficult process; each organization or institution must establish the rules and criteria for including specific therapies and the level of complexity needed. Specific outcomes must be incorporated, including maintenance of comfort and functionality, freedom from hospitalization, and survival. In existing guidelines for the management of heart failure, angiotensin-converting enzyme (ACE) inhibitor therapy is clearly the gold standard. However, there is still a high mortality with ACE inhibitor therapy; the key may be choosing the right patients. Current guidelines reflect the uncertainty regarding digoxin before the Digitalis Investigation Group (DIG) trial; obviously, these guidelines should be revisited. Clinical practice guidelines for the management of heart failure need to be revised to include a better consensus on beta-blockade, the new data on digoxin, emerging data on angiotensin II receptor antagonists, and current thinking on anticoagulant therapy. (+info)Cost of heart failure to the healthcare system. (7/952)
From an economic, mortality, and functional standpoint, heart failure is clearly a disease that needs to be targeted. We can develop a model for heart failure to determine the impact that specific management strategies will have on the overall cost to the system, which by itself can tell us some interesting things because we're currently spending twice as much on transplantation as on digoxin therapy. We can then use this model to assess the impact of different strategies, such as greater use of angiotensin-converting enzyme (ACE) inhibitors or digoxin therapy. (+info)The effect of steady-state ropinirole on plasma concentrations of digoxin in patients with Parkinson's disease. (8/952)
AIMS: The aim of this single-blind study was to assess the effect of ropinirole, a novel treatment for Parkinson's disease, on the steady-state pharmacokinetics and safety of digoxin in 10 patients with Parkinson's disease. METHODS: There were three parts to the study: digoxin once daily plus placebo three times daily for 1 week; digoxin once daily plus ropinirole three times daily for 6 weeks; and digoxin once daily plus placebo three times daily for 1 week. Serial blood samples were collected over 24 h at the end of each part of the study for pharmacokinetic assessment. Pre-dose blood samples were collected on specific days throughout the study to assess the attainment of steady-state plasma levels of digoxin. The primary endpoints were AUC(0, tau) and Cmax for digoxin. RESULTS: There was a mean decrease of 10% in digoxin AUC (0, tau) (90% CI: 0.79, 1.01) and a 25% decrease in digoxin Cmax (90% CI: 0.58, 0.97) when ropinirole was co-administered, compared with digoxin alone Cmin plasma values for digoxin, however, were fairly constant throughout the study (point estimates 0.99, 95% CI: 0.85, 1.15). Changes in trough levels of digoxin are believed to be the most reliable way of assessing steady-state concentrations of digoxin, and therefore the clinical significance of an interaction. Changes in Cmax are too readily influenced by other factors. CONCLUSIONS: These results therefore indicate that on pharmacokinetic grounds no dose adjustment is necessary for digoxin co-administered with ropinirole. (+info)Digoxin is a medication that belongs to a class of drugs called cardiac glycosides. It is used to treat various heart conditions, such as heart failure and atrial fibrillation, by helping the heart beat stronger and more regularly. Digoxin works by inhibiting the sodium-potassium pump in heart muscle cells, which leads to an increase in intracellular calcium and a strengthening of heart contractions. It is important to monitor digoxin levels closely, as too much can lead to toxicity and serious side effects.
Digitoxin is a cardiac glycoside drug that is derived from the foxglove plant (Digitalis lanata). It is used in the treatment of various heart conditions, particularly congestive heart failure and certain types of arrhythmias. Digitoxin works by increasing the force of heart muscle contractions and slowing the heart rate, which helps to improve the efficiency of the heart's pumping action.
Like other cardiac glycosides, digitoxin inhibits the sodium-potassium pump in heart muscle cells, leading to an increase in intracellular calcium levels and a strengthening of heart muscle contractions. However, digitoxin has a longer half-life than other cardiac glycosides such as digoxin, which means that it stays in the body for a longer period of time and may require less frequent dosing.
Digitoxin is available in tablet form and is typically prescribed at a low dose, with regular monitoring of blood levels to ensure safe and effective use. Common side effects of digitoxin include nausea, vomiting, diarrhea, and dizziness. In rare cases, it can cause more serious side effects such as arrhythmias or toxicity, which may require hospitalization and treatment with medications or other interventions.
Cardenolides are a type of steroid compound that are found in certain plants and animals. These compounds have a characteristic structure that includes a five-membered lactone ring, which is attached to a steroid nucleus. Cardenolides are well known for their toxicity to many organisms, including humans, and they have been used for both medicinal and poisonous purposes.
One of the most famous cardenolides is digitoxin, which is derived from the foxglove plant (Digitalis purpurea). Digitoxin has been used as a medication to treat heart conditions such as congestive heart failure, as it can help to strengthen heart contractions and regulate heart rhythm. However, because of its narrow therapeutic index and potential for toxicity, digitoxin is not commonly used today.
Other cardenolides include ouabain, which is found in the seeds of the African plant Acokanthera ouabaio, and bufadienolides, which are found in the skin and parotid glands of toads. These compounds have also been studied for their potential medicinal uses, but they are not widely used in clinical practice due to their toxicity.
It is important to note that cardenolides can be highly toxic to humans and animals, and exposure to these compounds can cause a range of symptoms including nausea, vomiting, diarrhea, seizures, and even death. As such, it is essential to use caution when handling or coming into contact with plants or animals that contain cardenolides.
Cardiotonic agents are a type of medication that have a positive inotropic effect on the heart, meaning they help to improve the contractility and strength of heart muscle contractions. These medications are often used to treat heart failure, as they can help to improve the efficiency of the heart's pumping ability and increase cardiac output.
Cardiotonic agents work by increasing the levels of calcium ions inside heart muscle cells during each heartbeat, which in turn enhances the force of contraction. Some common examples of cardiotonic agents include digitalis glycosides (such as digoxin), which are derived from the foxglove plant, and synthetic medications such as dobutamine and milrinone.
While cardiotonic agents can be effective in improving heart function, they can also have potentially serious side effects, including arrhythmias, electrolyte imbalances, and digestive symptoms. As a result, they are typically used under close medical supervision and their dosages may need to be carefully monitored to minimize the risk of adverse effects.
Cardiac glycosides are a group of naturally occurring compounds that have a toxic effect on the heart. They are found in certain plants, including foxglove and lily of the valley, as well as in some toads and beetles. The most well-known cardiac glycoside is digoxin, which is derived from the foxglove plant and is used as a medication to treat heart failure and atrial arrhythmias.
Cardiac glycosides work by inhibiting the sodium-potassium pump in heart muscle cells, leading to an increase in intracellular calcium levels. This increases the force of heart contractions, which can be beneficial in treating heart failure. However, if the dose is too high, cardiac glycosides can also cause dangerous arrhythmias and even death.
It's important for healthcare professionals to carefully monitor patients taking cardiac glycosides, as the therapeutic and toxic doses are very close together. Additionally, certain medications and medical conditions can interact with cardiac glycosides and increase the risk of toxicity.
I'm sorry for the confusion, but there seems to be a typo in your request. The correct name for the medication you might be asking about is "Digoxin." Digoxin is a type of medication known as a cardiac glycoside, which is used to treat various heart conditions such as heart failure and atrial fibrillation.
Here's a medical definition of Digoxin:
Digoxin is a cardiac glycoside derived from the digitalis plant, which is used in the treatment of heart failure and atrial fibrillation. It works by increasing the force of contraction of the heart muscle and slowing the heart rate, thereby improving the efficiency of the heart's pumping action. Digoxin is available in oral and injectable forms and is typically administered in divided doses throughout the day. Common side effects include nausea, vomiting, and diarrhea, while more serious side effects may include arrhythmias and cardiac toxicity. Close monitoring of serum digoxin levels is necessary to ensure safe and effective use of this medication.
Eleutherococcus is a genus of shrubs in the family Araliaceae, native to Northeastern Asia. The most well-known species is Eleutherococcus senticosus, also known as Siberian ginseng or ciwujia. This plant has been used in traditional medicine in Russia and China for centuries, and it is believed to have adaptogenic properties, which means it can help the body resist stress and promote overall well-being.
Eleutherococcus senticosus contains a variety of bioactive compounds, including eleutherosides, polysaccharides, and phenolic acids, that are thought to contribute to its medicinal effects. Some studies have suggested that it may help boost physical performance, enhance immune function, and reduce fatigue, although more research is needed to confirm these benefits and establish recommended dosages.
It's worth noting that Eleutherococcus should not be confused with Panax ginseng, which is a different plant species that is also known as Asian or Korean ginseng. While both plants have some similar medicinal properties, they belong to different genera and contain different active compounds.
I am not aware of a specific medical definition for "Nerium." However, Nerium is a genus of plants in the dogwood family, and its most common species is Nerium oleander, also known as oleander. Oleander is a toxic plant that can cause serious health problems if ingested or touched. Its symptoms include nausea, vomiting, seizures, irregular heartbeat, and even death in severe cases. It's essential to keep oleander away from children, pets, and livestock and seek immediate medical attention if any part of the plant is accidentally ingested.
Digitalis glycosides are a type of cardiac glycoside that are derived from the foxglove plant (Digitalis purpurea) and related species. These compounds have a steroidal structure with a lactone ring attached to the molecule, which is responsible for their positive inotropic effects on the heart.
The two main digitalis glycosides used clinically are digoxin and digitoxin. They work by inhibiting the sodium-potassium pump in cardiac muscle cells, leading to an increase in intracellular calcium levels and a subsequent enhancement of myocardial contractility. This makes them useful in the treatment of heart failure and atrial arrhythmias such as atrial fibrillation.
However, digitalis glycosides have a narrow therapeutic index, meaning that there is only a small difference between their therapeutic and toxic doses. Therefore, they must be administered with caution and patients should be closely monitored for signs of toxicity such as nausea, vomiting, visual disturbances, and cardiac arrhythmias.
Anti-arrhythmia agents are a class of medications used to treat abnormal heart rhythms or arrhythmias. These drugs work by modifying the electrical activity of the heart to restore and maintain a normal heart rhythm. There are several types of anti-arrhythmia agents, including:
1. Sodium channel blockers: These drugs slow down the conduction of electrical signals in the heart, which helps to reduce rapid or irregular heartbeats. Examples include flecainide, propafenone, and quinidine.
2. Beta-blockers: These medications work by blocking the effects of adrenaline on the heart, which helps to slow down the heart rate and reduce the force of heart contractions. Examples include metoprolol, atenolol, and esmolol.
3. Calcium channel blockers: These drugs block the entry of calcium into heart muscle cells, which helps to slow down the heart rate and reduce the force of heart contractions. Examples include verapamil and diltiazem.
4. Potassium channel blockers: These medications work by prolonging the duration of the heart's electrical cycle, which helps to prevent abnormal rhythms. Examples include amiodarone and sotalol.
5. Digoxin: This drug increases the force of heart contractions and slows down the heart rate, which can help to restore a normal rhythm in certain types of arrhythmias.
It's important to note that anti-arrhythmia agents can have significant side effects and should only be prescribed by a healthcare professional who has experience in managing arrhythmias. Close monitoring is necessary to ensure the medication is working effectively and not causing any adverse effects.
A drug interaction is the effect of combining two or more drugs, or a drug and another substance (such as food or alcohol), which can alter the effectiveness or side effects of one or both of the substances. These interactions can be categorized as follows:
1. Pharmacodynamic interactions: These occur when two or more drugs act on the same target organ or receptor, leading to an additive, synergistic, or antagonistic effect. For example, taking a sedative and an antihistamine together can result in increased drowsiness due to their combined depressant effects on the central nervous system.
2. Pharmacokinetic interactions: These occur when one drug affects the absorption, distribution, metabolism, or excretion of another drug. For example, taking certain antibiotics with grapefruit juice can increase the concentration of the antibiotic in the bloodstream, leading to potential toxicity.
3. Food-drug interactions: Some drugs may interact with specific foods, affecting their absorption, metabolism, or excretion. An example is the interaction between warfarin (a blood thinner) and green leafy vegetables, which can increase the risk of bleeding due to enhanced vitamin K absorption from the vegetables.
4. Drug-herb interactions: Some herbal supplements may interact with medications, leading to altered drug levels or increased side effects. For instance, St. John's Wort can decrease the effectiveness of certain antidepressants and oral contraceptives by inducing their metabolism.
5. Drug-alcohol interactions: Alcohol can interact with various medications, causing additive sedative effects, impaired judgment, or increased risk of liver damage. For example, combining alcohol with benzodiazepines or opioids can lead to dangerous levels of sedation and respiratory depression.
It is essential for healthcare providers and patients to be aware of potential drug interactions to minimize adverse effects and optimize treatment outcomes.
Ouabain is defined as a cardiac glycoside, a type of steroid, that is found in the seeds and roots of certain plants native to Africa. It is used in medicine as a digitalis-like agent to increase the force of heart contractions and slow the heart rate, particularly in the treatment of congestive heart failure and atrial fibrillation. Ouabain functions by inhibiting the sodium-potassium pump (Na+/K+-ATPase) in the cell membrane, leading to an increase in intracellular sodium and calcium ions, which ultimately enhances cardiac muscle contractility. It is also known as g-strophanthin or ouabaine.
Radioimmunoassay (RIA) is a highly sensitive analytical technique used in clinical and research laboratories to measure concentrations of various substances, such as hormones, vitamins, drugs, or tumor markers, in biological samples like blood, urine, or tissues. The method relies on the specific interaction between an antibody and its corresponding antigen, combined with the use of radioisotopes to quantify the amount of bound antigen.
In a typical RIA procedure, a known quantity of a radiolabeled antigen (also called tracer) is added to a sample containing an unknown concentration of the same unlabeled antigen. The mixture is then incubated with a specific antibody that binds to the antigen. During the incubation period, the antibody forms complexes with both the radiolabeled and unlabeled antigens.
After the incubation, the unbound (free) radiolabeled antigen is separated from the antibody-antigen complexes, usually through a precipitation or separation step involving centrifugation, filtration, or chromatography. The amount of radioactivity in the pellet (containing the antibody-antigen complexes) is then measured using a gamma counter or other suitable radiation detection device.
The concentration of the unlabeled antigen in the sample can be determined by comparing the ratio of bound to free radiolabeled antigen in the sample to a standard curve generated from known concentrations of unlabeled antigen and their corresponding bound/free ratios. The higher the concentration of unlabeled antigen in the sample, the lower the amount of radiolabeled antigen that will bind to the antibody, resulting in a lower bound/free ratio.
Radioimmunoassays offer high sensitivity, specificity, and accuracy, making them valuable tools for detecting and quantifying low levels of various substances in biological samples. However, due to concerns about radiation safety and waste disposal, alternative non-isotopic immunoassay techniques like enzyme-linked immunosorbent assays (ELISAs) have become more popular in recent years.
P-glycoprotein (P-gp) is a type of membrane transport protein that plays a crucial role in the efflux (extrusion) of various substrates, including drugs and toxins, out of cells. It is also known as multidrug resistance protein 1 (MDR1).
P-gp is encoded by the ABCB1 gene and is primarily located on the apical membrane of epithelial cells in several tissues, such as the intestine, liver, kidney, and blood-brain barrier. Its main function is to protect these organs from harmful substances by actively pumping them out of the cells and back into the lumen or bloodstream.
In the context of pharmacology, P-gp can contribute to multidrug resistance (MDR) in cancer cells. When overexpressed, P-gp can reduce the intracellular concentration of various anticancer drugs, making them less effective. This has led to extensive research on inhibitors of P-gp as potential adjuvants for cancer therapy.
In summary, P-glycoprotein is a vital efflux transporter that helps maintain homeostasis by removing potentially harmful substances from cells and can impact drug disposition and response in various tissues, including the intestine, liver, kidney, and blood-brain barrier.