Ventricular Function, Left
Ventricular Dysfunction, Left
Dose-Response Relationship, Drug
Myocardial uptake of digoxin in chronically digitalized dogs. (1/9164)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)
Ventricular pressure-volume curve indices change with end-diastolic pressure. (2/9164)Many indices have been proposed to describee the diastolic pressure-volume curve mathematically and permit quantification of the elastic properties of the myocardium itself in hopes that changes in the muscle caused by disease would b.e reflected in the diastolic pressure-volume curve. To date, none of the proposed indices has been shown convincingly to discriminate one group of patients from another. While this situation in part arises from the relatively large amount of noise introduced by the technical difficulties of measuring synchronous pressures and volumes during diastole in man, ther is a more fundamental difficulty. In practice, one can measure only a short segment of the entire pressure-volume curve, and the values of all diastolic pressure-volume curve parameters investigated change significantly when one uses different segments of the same pressure-volume curve to compute them. These results were derived from relatively noise-free pressure-volume curves obtained by filling nine excised dog left ventricles at a known rate and monitoring pressure-volume curve used to compute the parameter. Merely increasing measurement fidelity will not resolve this problem, because none of these parameters accurately characterizes the entire diastolic pressure-volume curbe from a segment like that which one can reasonably expect to obtain from humans. (+info)
The effect of cardiac contraction on collateral resistance in the canine heart. (3/9164)We determined whether the coronary collateral vessels develop an increased resistance to blood flow during systole as does the cognate vascular bed. Collateral resistance was estimated by measuring retrograde flow rate from a distal branch of the left anterior descending coronary artery while the main left coronary artery was perfused at a constant pressure. Retrograde flow rate was measured before and during vagal arrest. We found that in 10 dogs the prolonged diastole experienced when the heart was stopped caused no significant change in the retrograde flow rate, which indicated that systole has little effect on the collateral resistance. However, when left ventricular end-diastolic pressure was altered by changing afterload or contractility, a direct relationship between end-diastolic pressure and collateral resistance was noted. (+info)
Evaluation of the force-frequency relationship as a descriptor of the inotropic state of canine left ventricular myocardium. (4/9164)The short-term force-frequency characteristics of canine left ventricular myocardium were examined in both isolated and intact preparations by briefly pertubing the frequency of contraction with early extrasystoles. The maximum rate of rise of isometric tension (Fmas) of the isolated trabeculae carneae was potentiated by the introduction of extrasystoles. The ratio of Fmas of potentiated to control beats (force-frequency ratio) was not altered significantly by a change in muscle length. However, exposure of the trabeculae to isoproterenol (10(-7)M) significantly changed the force-frequency ratio obtained in response to a constant frequency perturbation. Similar experiments were performed on chronically instrumented conscious dogs. Left ventricular minor axis diameter was measured with implanted pulse-transit ultrasonic dimension transducers, and intracavitary pressure was measured with a high fidelity micromanometer. Atrial pacing was performed so that the end-diastolic diameters of the beats preceding and following the extrasystole could be made identical. Large increases in the maximum rate of rise of pressure (Pmas) were seen in the contraction after the extrasystole. The ratio of Pmax of the potentiated beat to that of the control beat was not changed by a 9% increase in the end-diastolic diameter, produced by saline infusion. Conversely, isoproterenol significantly altered this relationship in the same manner as in the isolated muscle. Thus, either in vitro or in situ, left ventricular myocardium exhibits large functional changes in response to brief perturbations in rate. The isoproterenol and length data indicate that the force-frequency ratio reflects frequency-dependent changes in the inotropic state, independent of changes in length. (+info)
Adenoviral gene transfer of the human V2 vasopressin receptor improves contractile force of rat cardiomyocytes. (5/9164)BACKGROUND: In congestive heart failure, high systemic levels of the hormone arginine vasopressin (AVP) result in vasoconstriction and reduced cardiac contractility. These effects are mediated by the V1 vasopressin receptor (V1R) coupled to phospholipase C beta-isoforms. The V2 vasopressin receptor (V2R), which promotes activation of the Gs/adenylyl cyclase system, is physiologically expressed in the kidney but not in the myocardium. Expression of a recombinant V2R (rV2R) in the myocardium could result in a positive inotropic effect via the endogenous high concentrations of AVP in heart failure. METHODS AND RESULTS: A recombinant adenovirus encoding the human V2R (Ad-V2R) was tested for its ability to modulate the cardiac Gs/adenylyl cyclase system and to potentiate contractile force in rat ventricular cardiomyocytes and in H9c2 cardiomyoblasts. Ad-V2R infection resulted in a virus concentration-dependent expression of the transgene and led to a marked increase in cAMP formation in rV2R-expressing cardiomyocytes after exposure to AVP. Single-cell shortening measurements showed a significant agonist-induced contraction amplitude enhancement, which was blocked by the V2R antagonist, SR 121463A. Pretreatment of Ad-V2R-infected cardiomyocytes with AVP led to desensitization of the rV2R after short-term agonist exposure but did not lead to further loss of receptor function or density after long-term agonist incubation, thus demonstrating resistance of the rV2R to downregulation. CONCLUSIONS: Adenoviral gene transfer of the V2R in cardiomyocytes can modulate the endogenous adenylyl cyclase-signal transduction cascade and can potentiate contraction amplitude in cardiomyocytes. Heterologous expression of cAMP-forming receptors in the myocardium could lead to novel strategies in congestive heart failure by bypassing the desensitized beta-adrenergic receptor signaling. (+info)
Myocardial oxygenation during high work states in hearts with postinfarction remodeling. (6/9164)BACKGROUND: Postinfarction left ventricular remodeling (LVR) is associated with reductions in myocardial high-energy phosphate (HEP) levels, which are more severe in animals that develop overt congestive heart failure (CHF). During high work states, further HEP loss occurs, which suggests demand-induced ischemia. This study tested the hypothesis that inadequate myocyte oxygen availability is the basis for these HEP abnormalities. METHODS AND RESULTS: Myocardial infarction was produced by left circumflex coronary artery ligation in swine. Studies were performed in 20 normal animals, 14 animals with compensated LVR, and 9 animals with CHF. Phosphocreatine (PCr)/ATP was determined with 31P NMR and deoxymyoglobin (Mb-delta) with 1H NMR in myocardium remote from the infarct. Basal PCr/ATP tended to be decreased in postinfarct hearts, and this was significant in animals with CHF. Infusion of dobutamine (20 microg x kg-1 x min-1 IV) caused doubling of the rate-pressure product in both normal and LVR hearts and resulted in comparable significant decreases of PCr/ATP in both groups. This decrease in PCr/ATP was not associated with detectable Mb-delta. In CHF hearts, rate-pressure product increased only 40% in response to dobutamine; this attenuated response also was not associated with detectable Mb-delta. CONCLUSIONS: Thus, the decrease of PCr/ATP during dobutamine infusion is not the result of insufficient myocardial oxygen availability. Furthermore, in CHF hearts, the low basal PCr/ATP and the attenuated response to dobutamine occurred in the absence of myocardial hypoxia, indicating that the HEP and contractile abnormalities were not the result of insufficient oxygen availability. (+info)
Hemodialysis with high-calcium dialysate impairs cardiac relaxation. (7/9164)BACKGROUND: During hemodialysis (HD), serum ionized calcium is directly related to the dialysate calcium concentration. We have recently shown an acute induction of hypercalcemia to impair left ventricular (LV) relaxation. In the current study we sought to establish whether changes in serum Ca++ also affect LV function during HD. METHODS: We echocardiographically examined the LV relaxation and systolic function of 12 patients with end-stage renal disease before and after three HD treatments with dialysate Ca++ concentrations of 1.25 mmol/liter (dCa++1.25), 1.5 mmol/liter (dCa++1.50), and 1.75 mmol/liter (dCa++1.75), respectively. Age- and sex-matched healthy controls were also examined echocardiographically. RESULTS: The LV posterior wall thickness and the interventricular septum thickness, and the LV end-diastolic dimension and the end-systolic dimensions were significantly greater in the patients when compared with the controls, and the LV fractional shortening, the ratio of peak early to peak late diastolic velocities (E/Amax), and the isovolumic relaxation time (IVRT) showed impairment of LV relaxation and systolic function in the patients. Serum ionized calcium increased significantly during the dCa++1.5 HD (1.24 +/- 0.10 vs. 1.34 +/- 0.06 mmol/liter, P = 0. 004) and dCa++1.75 HD (1.19 +/- 0.10 vs. 1.47 +/- 0.06 mmol/liter, P = 0.002), and plasma intact parathyroid hormone decreased significantly during the dCa++1.75 HD (medians 8.2 vs. 2.7 pmol/liter, P = 0.002). LV systolic function was not altered during any of the treatments. The changes in E/Amax and IVRT suggested impairment of relaxation during all sessions, but only during the dCa++1.75 HD was the impairment statistically significant (E/Amax 1. 153 +/- 0.437 vs. 0.943 +/- 0.352, P < 0.05; IVRT 147 +/- 29 vs. 175 +/- 50 msecond, P < 0.05). CONCLUSION: HD with high-calcium (dCa++1. 75 mmol/liter) dialysate impairs LV relaxation when compared with lower calcium dialysate (dCa++1.25 and dCa++1.5 mmol/liter) treatments. (+info)
Simultaneous assessment of effects of coronary vasodilators on the coronary blood flow and the myocardial contractility by using the blood-perfused canine papillary muscle. (8/9164)Effects of 6 coronary vasodilators on the coronary blood flow and the contractile force of the ventricular muscle were examined simultaneously by injecting these drugs to the arterially blood-perfused canine papillary muscle preparation. All compounds produced a dose-dependent increase in blood flow rate, and relative potencies determined on the basis of doses producing a 100% increase in blood flow rate, ED100, were in the descending order : nifedipine greater than verapamil greater than diltiazem greater than dilazep greater than dipyridamole greater than carbochromen, and approximately 1 : 1/12 : 1/26 : 1/100 : 1/300 : 1/500. All drugs except for dipyridamole caused a dose-dependent decrease in the developed tension of the papillary muscle, although nifedipine and diltiazem in low doses produced a slight increase. Relative potencies determined on the basis of doses producing a 50% decrease in developed tension, ID50, were as follows: nifedipine (1), verapamil (1/13), diltiazem (1/40), dilazep (1/100), and carbochromen (1/270). Ratios of the ID50 to ED100 were as follows: diltiazem (5.2), nifedipine (3.5), verapamil (3.5), dilazep (2.5), and carbochromen (1.8). The higher the value the more predominant on the coronary vascular bed or the less depressant on the myocardial contractility were their actions. (+info)
There are several potential causes of LVD, including:
1. Coronary artery disease: The buildup of plaque in the coronary arteries can lead to a heart attack, which can damage the left ventricle and impair its ability to function properly.
2. Heart failure: When the heart is unable to pump enough blood to meet the body's needs, it can lead to LVD.
3. Cardiomyopathy: This is a condition where the heart muscle becomes weakened or enlarged, leading to impaired function of the left ventricle.
4. Heart valve disease: Problems with the heart valves can disrupt the normal flow of blood and cause LVD.
5. Hypertension: High blood pressure can cause damage to the heart muscle and lead to LVD.
6. Genetic factors: Some people may be born with genetic mutations that predispose them to developing LVD.
7. Viral infections: Certain viral infections, such as myocarditis, can inflame and damage the heart muscle, leading to LVD.
8. Alcohol or drug abuse: Substance abuse can damage the heart muscle and lead to LVD.
9. Nutritional deficiencies: A diet lacking essential nutrients can lead to damage to the heart muscle and increase the risk of LVD.
Diagnosis of LVD typically involves a physical exam, medical history, and results of diagnostic tests such as electrocardiograms (ECGs), echocardiograms, and stress tests. Treatment options for LVD depend on the underlying cause, but may include medications to improve cardiac function, lifestyle changes, and in severe cases, surgery or other procedures.
Preventing LVD involves taking steps to maintain a healthy heart and reducing risk factors such as high blood pressure, smoking, and obesity. This can be achieved through a balanced diet, regular exercise, stress management, and avoiding substance abuse. Early detection and treatment of underlying conditions that increase the risk of LVD can also help prevent the condition from developing.
Myocardial infarction diagnosis
Premature ventricular contraction
Pressure-volume loop analysis in cardiology
Management of heart failure
Cardiac magnetic resonance imaging
Coronary perfusion pressure
Acute cardiac unloading
Discovery and development of beta-blockers
Cardiac contractility modulation
Cardiac conduction system
List of cardiology mnemonics
William B. Kouwenhoven
Congenital heart defect
Creatine phosphate shuttle
G beta-gamma complex
Glossary of diabetes
COVID-19 pandemic in the San Francisco Bay Area
Myosin binding protein C, cardiac
Omega-6 fatty acid
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- Acute myocardial infarction and pulmonary. (nih.gov)
- Myocardial ischaemia, infarction and ventricular dysfunction are described. (inchem.org)
- A heart attack or acute myocardial infarction (MI) occurs when one of the arteries that supplies the heart muscle becomes blocked. (medlineplus.gov)
- The bowel demonstrates spastic contraction in the early phase of the disease, followed by adynamic ileus caused by ischemic tissue damage, including muscular and neurologic infarction. (appliedradiology.com)
- Exercise, depression, and mortality after myocardial infarction in the ENRICHD trial. (duke.edu)
- myocardial infarction. (stanford.edu)
- The current status of stem cell therapies for patients with myocardial infarction is discussed from a bioengineering and biomaterial perspective in this review. (nature.com)
- We describe (a) the current status of clinical trials of human pluripotent stem cells (hPSCs) compared with clinical trials of human adult or fetal stem cells, (b) the gap between fundamental research and application of human stem cells, (c) the use of biomaterials in clinical and pre-clinical studies of stem cells, and finally (d) trends in bioengineering to promote stem cell therapies for patients with myocardial infarction. (nature.com)
- These conditions are (1) spinal cord injury, (2) diabetes, (3) acute myocardial infarction (AMI), and (4) macular degeneration (namely Stargardt macular dystrophy and age-related macular degeneration). (nature.com)
- Here, we have described the current status of stem cell therapies using hPSCs for patients with myocardial infarction (MI), focusing on the bioengineering aspects of these therapies. (nature.com)
- Now everybody who is taking care of a patient is able to communicate on one platform much earlier, even when the paramedic is still in the patient's home," said Alina Capatina, MSN, program coordinator for acute coronary syndrome and ST-elevation myocardial infarction (STEMI) at Baystate Medical Center and the study's lead author. (eurekalert.org)
- The origin of electrical behavior in post-myocardial infarction scar tissue is still under debate. (frontiersin.org)
- Following this myocardial infarction (MI), ischemia of the underlying muscle causes necrosis of cardiomyocytes and vasculature. (frontiersin.org)
- GTN GlycerylTriNitrate in Commonwealth countries) safe for treating prehospital suspected STEMI (ST segment Elevation Myocardial Infarction) patients? (roguemedic.com)
- (4) This raises concern for use in inferior ST-segment elevation myocardial infarction (STEMI) in the prehospital setting, since many inferior STEMI result from proximal right coronary artery (RCA) occlusion and 50% involve the right ventricle. (roguemedic.com)
- 28. How does measuring the level of cardiac enzymes help detect a myocardial infarction (MI)? (weber.edu)
- Mr. Dixon was diagnosed with having a myocardial infarction. (weber.edu)
- The aim of this study was to clearly define the hemodynamic efficiency of the EHAM system in myocardial tissue perfusion during its application in acute animal experiment. (iospress.com)
- [ 9 ] The manifestations of toxicity are generally extensions of the drugs' pharmacologic and therapeutic effects and often include hypotension, bradycardia, conduction block, and myocardial depression. (medscape.com)
- Calcium plays an integral role in myocardial function and is necessary for automaticity, conduction, contraction, and vascular tone. (medscape.com)
- Through this system, under physiological conditions, the frequency of heart beating is determined by the pacemaker cells of the sinoatrial node that give rise to spontaneous action potentials that spread through the conduction fibers of atria and ventricles triggering the contraction [ 3 - 6 ]. (hindawi.com)
- Christian Arvei Moen (2013) "Myocardial deformation during ischemia and reperfusion. (uib.no)
- Mitochondrial Ca2+ transients in cardiac myocytes during the excitation-contraction cycle: effects of pacing and hormonal stimulation. (nih.gov)
- It causes excitation-contraction uncoupling in various myocardial tissues without changes in the configuration of the action potential. (nih.gov)
- Thus, the interaction of the myofilament proteins, myosin and actin supported by other sarcomeric proteins, would not be possible without the crucial role of Ca 2+ in the excitation-contraction (E-C) coupling mechanism [ 7 , 8 ]. (hindawi.com)
- Coronary blood flow and myocardial energetics were assessed after the administration of a parenteral inotrope (dobutamine hydrochloride) and an oral vasodilator agent (hydralazine) in 10 patients with nonischemic congestive heart failure. (nih.gov)
- Dobutamine, demonstrating a balanced effect on the coronary circulation, induced a proportional increase in coronary blood flow and myocardial oxygen consumption, with the arterial-venous oxygen difference across the coronary vascular bed remaining unchanged. (nih.gov)
- Dobutamine, a positive inotropic agent, elicited a balanced effect on the coronary circulation while hydralazine, a vasodilator agent, induced a greater increase in coronary flow than in myocardial oxygen demand. (nih.gov)
- Interruption of myocardial blood flow due to narrowing or blocking of coronary arteries leads to cell damage and death in the areas of tissue supplied by these vessels. (frontiersin.org)
- Istaroxime is a positive inotropic agent that increases myocardial contractility through inhibition of Na+/K+- ATPase with a complimentary mechanism that facilitates myocardial relaxation through activation of the SERCA2a calcium pump on the sarcoplasmic reticulum enhancing calcium reuptake from the cytoplasm. (biospace.com)
- Chronic hypertension in the SHR is often associated with cardiac remodeling and impaired myocardial contractility. (ku.ac.ae)
- Abnormalities in the handling of calcium can facilitate arrhythmias and may contribute to poor myocardial remodeling as the disease progresses. (biospace.com)
- Diltiazem has been shown to produce increases in exercise tolerance, probably due to its ability to reduce myocardial oxygen demand. (nih.gov)
- Knut Matre (1988) "Invasive ultrasound for assessment of cardiac function: application of transit-time ultrasound for evaluation of myocardial contraction, and Doppler ultrasound for measurement of cardiac output. (uib.no)
- The publication emphasizes the interest in SERCA2a as a target in treating heart failure because it is instrumental in calcium management, critically important in heart muscle contraction and relaxation. (biospace.com)
- The contraction process is triggered by an initial calcium ion (Ca 2+ ) influx due to the opening of calcium channels located on the plasmatic membrane and activated by the electric signals. (hindawi.com)
- Myocardial tissue perfusion was measured by using Omega flow laser fiber attached to the surface of the heart. (iospress.com)
- During the EHAM compression, and increase in blood pressure and myocardial tissue perfusion was observed in all animals when compared with pre-assisted mode. (iospress.com)
- To conclude, EHAM effectively improves myocardial tissue perfusion and increases the pressure on the initiation of direct cardiac compression immediately. (iospress.com)
- The blockage results in damaged tissue and a permanent loss of contraction of this portion of the heart muscle. (medlineplus.gov)
- The main feature of cardiac tissue is the force generation through contraction. (hindawi.com)
- One reason for the poor prognosis in patients with both diabetes and ischemic heart disease seems to be an worsened myocardial function leading to accelerated heart failure (diabetic cardiomyopathy). (nih.gov)
- Before adopting the app, clinicians typically only had about five minutes of advance notice when a heart attack patient was en route, even if the patient had traveled a long distance. (eurekalert.org)
- 31. Which cardiac enzyme is the preferred marker for myocardial injury? (weber.edu)
- first described a specific type of cardiomyopathy related to diabetes, suggesting that this myocardial disease exists as an independent clinical entity. (nih.gov)
- 24. On an ECG tracing, when does atrial contraction or systole occur? (weber.edu)
- It is possible that STRN does not function normally in the contraction of hypertrophied and/or dilated hearts. (ku.ac.ae)
- Lowering blood pressure reduces the risk of fatal and nonfatal cardiovascular events, primarily strokes and myocardial infarctions. (nih.gov)
- Striatin (STRN) is a protein that is expressed in cardiac myocytes and plays an important role in maintaining normal contraction. (ku.ac.ae)
- At depths greater than approximately 300 μm, myocardial structures were evident that supported normal APs and CaTs. (frontiersin.org)
- Both forms of therapy elicited a significant increase in myocardial oxygen consumption. (nih.gov)
- In cardiomyocytes, the functional activity is characterized by a rhythmic contraction ensured by an interplay among myofilaments, intracellular Ca 2+ variations (modulated by channels and pumps), and mitochondrial activity. (hindawi.com)
- Capatina will present the study, "Reducing EMS-to-Balloon Time - There's an App for That," on Saturday, May 15, at 12 p.m. (eurekalert.org)