Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Verapamil, at a dose of 1 mg/kg, was given intravenously to anesthetized cats one hour after coronary artery occlusion. Verapamil significantly reduced mean arterial blood pressure, but produced an increase in heart rate, partially offsetting the reduction in myocardial oxygen demand resulting from the reduction in pressure. Verapamil failed to prevent the elevations in the S-T segment of the electrocardiogram observed in cats subjected to myocardial ischemia (MI) and given only the vehicle for verapamil (i.e., 0.9% NaCl). Moreover, verapamil also did not prevent the accumulation of creatine phosphokinase (CPK) activity in the circulating blood after MI. Nevertheless, verapamil significantly prevented the loss in CPK and in amino-nitrogen observed in the ischemic region of the myocardium, indicating some protective effect on myocardial integrity. The major effects of verapamil on electrolyte content of ischemic myocardial tissue were a decrease in sodium and an increase in potassium. However, calcium gain by the heart was not prevented by verapamil. Verapamil, therefore, exerts a partial degree of protection of the ischemic myocardium but exerts some other effects which do not help prevent the spread of ischemic damage in the myocardium.
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PMID:Influence of verapamil on cellular integrity and electrolyte concentrations of ischemic myocardial tissue in the cat. 52 60

The effect of verapamil on ST changes was evaluated in 10 selected patients with acute myocardial infarction admitted to the Coronary Care Unit within 8 hours after the onset of symptoms. To evaluate the extent of ischemia it has been used the magnitude and direction of the ST vector derived from X, Y and Z leads of the Frank vector system. After a control period of 2 hours, during which the changes of the ST vector magnitude were assessed, each patient received 0.1 mg/Kg verapamil intravenously, ST vector magnitude (STVM), ST azimuth (STAZ), ST elevation (STEL), heart rate, systemic blood pressure and pressure-rate product were assessed 5, 15, 30, 45, 60, 75, 90, 105 and 120 minutes after the administration of the drug. Verapamil produced a significant progressive decrease in STVM (from a mean of 254 +/- 44 muV at the end of the control period, to 139 +/- 25 muV after 2 hours; P < 0.01). Systolic blood pressure decreased significantly throughout the trial; the most significant decrease was registered immediately after the infusion of verapamil (from a mean of 134 +/- 3 mmHg to 121 +/- 3 mmHg; P < 0.001). Pressure-rate product declined slightly. No significant change in STVM was observed in 10 control patients with acute myocardial infarction examined over a 4 hours period. The apparent protective effect of verapamil in myocardial ischemia is discussed in relation to its calcium-antagonistic properties in excitable tissues.
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PMID:[Effects of acute infusion of verampil on the ST segment elevation measured with the Frank orthogonal leads in patients with acute myocardial infarct]. 54 89

The effect of verapamil, a calcium antagonist and antiarrhythmic and anti-anginal actions, were studied on the size of infarct in open-chest anesthetized dogs with left anterior descending coronary artery occlusion. Hemodyamic functions were monitored by standard techniques, and infarct size was assessed by epicardial electrocardiography. Myocardial blood flow was measured by radioactive microspheres, and regional metabolism was studied by measuring lactate concentration in the venous drainage of the ischemic myocardium. Verapamil produced a significant reduction to ST segment elevation in the epicardial electrocardiogram and prevented the hemodynamic deterioration seen in the control animals in which ST segment elevation persisted. The drug had no effect on either total collateral blood flow or on the relative distribution of flow to the inner and outer halves of the ventricular wall. No significant differences were found between the levels of coronary venous lactate in the control animals and those in the verapamil-treated group. The results raise the possibility that the apparent protective effect of verapamil in myocardial ischemia may be due to its electrophysiological action on the cardiac membrane in relation to its calcium-antagonistic properites in excitable tissues.
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PMID:Reduction in infarct size following experimental coronary occlusion by administration of verapamil. 81 84

The effects of verapamil, nifedipine, propranolol, and combinations of nifedipine+propranolol and nifedipine+verapamil were studied in 60 patients with stable angina pectoris. Verapamil was found to have a pronounced antianginal activity against all types of myocardial ischemia, whereas nifedipine relieved mainly painful ischemic episodes. By the end of 12-week therapy with propranolol, the agent lost its antiischemic effect in a third of patients, which was accompanied by an increase in the number and severity of silent ischemic episodes.
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PMID:[Effect of various antianginal agents on the frequency and duration of myocardial ischemic episodes in patients with stable angina pectoris]. 129 87

The role of blood platelets in ischemia- and reperfusion-induced arrhythmias and the efficacy of three calcium blocking drugs (verapamil, diltiazem, and nicardipine) in preventing the arrhythmias were investigated. Using anesthetized rats, we measured platelet count (Pc) continuously in vivo with a Technicon autocounter. Thromboxane B2 (TxB2) and 6-keto-PGF1 alpha levels in blood from coronary sinus were determined by radioimmunoassay (RIA). Myocardial ischemia and arrhythmias were monitored from lead I ECG during and after occlusion of the left anterior descending coronary artery (LAD) for 7 min. Ischemia-induced arrhythmias were mainly ventricular ectopic contractions (VECs), whereas reperfusion produced VECs, ventricular tachycardia (VT), and reversible and irreversible ventricular fibrillation (VF). Both ischemia and reperfusion decreased platelet count and increased TxB2 level in blood from the coronary sinus. The effects of the CEBs were determined at two dose levels (0.1 and 0.3 mg/kg). Each calcium entry blocker (CEB), at both dose levels, significantly inhibited ischemia-induced arrhythmias. Verapamil and diltiazem significantly reduced reperfusion-induced VECs, prevented VT and irreversible VF, and reduced the number of animals with reversible VF. Nicardipine in preventing arrhythmias was not very effective at either dose. The CEBs also inhibited both ischemia- and reperfusion-induced decreases in PC with a moderate increase (up to 7%) as compared with levels in sham-operated controls. The CEBs also significantly reduced TxB2 levels in blood from the coronary sinus. These results indicate that ischemia and postischemic reperfusion both induce platelet aggregation in rats. Aggregating platelets release biologically active substances including thromboxane A2 (TxA2) which exacerbates existing ischemia and facilitates generation of arrhythmias. CEBs inhibit platelet aggregation and TxA2 release and enhance PGI2 synthesis, thereby preventing arrhythmias.
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PMID:Occlusion and reperfusion-induced arrhythmias in rats: involvement of platelets and effects of calcium antagonists. 169 43

Recent studies have improved our understanding of the beneficial actions of calcium antagonists on myocardial microcirculation and metabolism. The effect of calcium antagonists on the microcirculation of the left ventricular rat myocardium was studied using in vivo microscopic techniques. Intravenous verapamil 0.3 mg/kg and nifedipine 75 micrograms/kg produced a 15 to 18% increase in the diameter of larger A1 and A2 coronary arterioles (range 31 to 300 microns); diameters of terminal (A4) arterioles and capillaries did not change significantly. Furthermore, verapamil significantly (p less than 0.001) increased the ratio of capillaries filled with red cells to those containing plasma alone. Verapamil pretreatment produced a similarly selective dilatation of larger coronary arterioles and protected against the ischaemia-induced fall in capillary red cell content. Spectroscopic data show that verapamil also produces an increase in myocardial phosphocreatine and preservation of adenosine triphosphate (ATP) during ischaemia in the Langendorff-perfused heart. In patients with exercise-induced angina, gallopamil decreased global myocardial 201Tl and 123I phenylpentadecanoic acid (IPPA) uptake due to a reduction in myocardial oxygen consumption. Regional 201Tl and IPPA uptake as well as IPPA clearance in post-stenotic areas tended to rise after gallopamil treatment. Thus, the beneficial effects of calcium antagonists such as verapamil or gallopamil in patients with ischaemic heart disease may result from dilatation of predominantly larger arterioles. Consequently, there is an improvement in regional perfusion and free fatty acid utilisation in reversibly ischaemic regions.
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PMID:Calcium antagonists and myocardial microperfusion. 171 89

The effect of verapamil on death and reinfarction after an acute myocardial infarction was studied in two double-blind, randomized, placebo-controlled multicenter trials, the Danish Verapamil Infarction Trials I and II (DAVIT I and II). The studies demonstrated that verapamil 360 mg/day from the 2nd week after an acute myocardial infarction, prevented death and reinfarction. Meta-analyses of the results of DAVITs I and II resulted in a reduction of pooled ratios of 22% (95% confidence limits 1-37, p = 0.04) for death, 21% (5-35, p = 0.02) for first major events (first reinfarction or death), and 27% (6-43, p = 0.02) for first reinfarctions. The effect of verapamil was to prevent myocardial ischemia and reduce sudden death and reinfarction. It is concluded that long-term treatment with verapamil after an acute myocardial infarction may be recommended with the object of reducing overall mortality, major events and reinfarction.
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PMID:Treatment with verapamil during and after an acute myocardial infarction: a review based on the Danish Verapamil Infarction Trials I and II. The Danish Study Group on Verapamil in Myocardial Infarction. 172 12

Treatment of patients with heart failure due to major ventricular systolic dysfunction should aim not only at symptomatic but also at prognostic improvement. If correction of the underlying problem is not possible, treatment should slow down the progression of cardiac failure and eliminate triggers for sudden cardiac death due to electromechanical dissociation or arrhythmias. In every patient with chronic congestive heart failure screening for myocardial ischemia and complete revascularization is mandatory, if possible. In patients with coronary artery disease and diminished systolic function, beta-blockade may improve prognosis by reducing ischemic events and sudden cardiac death. The incidence of life-threatening arrhythmias in patients with heart failure may be reduced by eliminating facilitating factors like electrolyte disturbances, altered autonomic tone and raised intracardiac pressure rather than by antiarrhythmic medical treatment itself. One of the most important prognostic aspects in treatment is the interference with the development of the cardiomyopathy of overload, uniformly observed in chronic congestive heart failure. Modification of mechanical and neuroendocrine stimuli may postpone myocardial hypertrophy and interstitial hyperplasia as a consequence of altered gene expression. Early treatment with ACE inhibitors and in certain patients with betablockers are the most promising strategies to delay the progression of the disease. In contrast, positive inotropic drugs, including digitalis and phosphodiesterase inhibitors, do not improve prognosis. Calcium antagonists should also be used with restriction, as Verapamil and Diltiazem, but also Nifedipine may adversely affect the outcome in congestive heart failure patients.
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PMID:[Prognostic aspects in the treatment of chronic heart insufficiency]. 173

Verapamil is a calcium-channel blocking agent with antianginal and antiarrhythmic properties that have been widely studied. Its myocardial depressant effect is well known. The purpose of this study was to examine the effects of verapamil on the training response in patients with ischemic heart disease. The study group consisted of 41 male patients with a mean age of 53.3 +/- 7.2 years who had suffered a myocardial infarction or had undergone coronary artery bypass surgery 8 to 12 weeks previously. They were chosen on a consecutive basis from eligible patients entering a cardiac rehabilitation program. With use of a double-blind technique, 21 patients were assigned to receive verapamil, 120 mg three times daily, while the other 20 were given an identical placebo. Each patient underwent exercise stress testing in the untreated state to permit comparison between tests performed on commencement and completion of training. The training effect was determined by comparing exercise response before and after the eight-week program. There was an increase in exercise duration (p less than 0.001) and a decrease in functional aerobic impairment (p less than 0.001), without difference between the two groups. Energy expenditure increased in both groups, but the highest level was achieved by those receiving active treatment (p less than 0.02). Heart rate for equal workload was significantly reduced after training (p less than 0.001), although this was lower in the placebo patients (p less than 0.001) and the patients who had a recent myocardial infarction (p less than 0.01). It appears that treatment with verapamil does not impair the development of a training effect in patients with ischemic heart disease who are undergoing organized training.
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PMID:The effects of verapamil on training in patients with ischemic heart disease. 173 64

We compared the effects of cicletanine (10 mg/kg i.v.) and verapamil (0.1 mg/kg i.v.) on heart rate, ventricular effective refractory period, systolic and diastolic arterial blood pressure and overpacing-induced ST-segment elevation detected by right ventricular intracavital electrogram in conscious rabbits. Cicletanine significantly reduced overpacing-induced ST-segment elevation, which is an indicator of myocardial ischemia, and heart rate, but did not influence blood pressure and ventricular effective refractory period. Verapamil did not significantly influence ventricular effective refractory period, blood pressure or heart rate, but reduced the ST-segment elevation induced by frequency loading. These results suggest that acute treatment with cicletanine induces an anti-ischemic effect in the overpaced heart of conscious rabbits.
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PMID:Effect of cicletanine on overpacing-induced ST-segment elevation in conscious rabbits. A comparison with verapamil. 191 86


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