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)

Impaired diastolic function of the hypertrophied and stiffened left ventricle is a characteristic feature of hypertrophic cardiomyopathy (Figure 1). Altered left ventricular filling dynamics and reduced left ventricular distensibility or increased left ventricular diastolic chamber stiffness are associated with reduced left ventricular stroke volume, increased left ventricular filling pressures and compressive effects on the coronary microcirculation. These factors contribute importantly to the clinical presentation of many patients, including symptoms of fatigue, dyspnea and angina pectoris. Reduced distensibility results both from factors determining the passive elastic properties of the ventricular chamber (including severity of hypertrophy, fibrosis and cellular disarray) and from factors influencing the rate and extent of active left ventricular relaxation (Figure 2). The factors contributing to impaired relaxation in hypertrophic cardiomyopathy are mediated via either inactivation dependent or load-dependent mechanisms. In laboratory animals, compromise of myocardial inactivation results in a persistent increase in intracellular calcium concentration and in prolonged interaction of the contractile proteins. Additionally, there is evidence for an increased number of active receptors for calcium antagonists and, lastly, for myocardial ischemia (Figure 3). Load-dependent mechanisms include diminished wall tension at the opening of the mitral valve, changes in afterload, contractility and coronary flow. Other factors are nonuniform and asynchronous regional ventricular function due to differing increases in thickness of the ventricular walls and ischemia (Figure 4). Calcium channel blockers exert a favorable influence on left ventricular relaxation and filling (Figure 5); verapamil and diltiazem are preferable to nifedipine. Verapamil increases left ventricular stroke volume without an increase in the end-diastolic pressure (Figure 6), reduces regional asynchrony if present, and leads to a more homogeneous regional diastolic filling (Figure 4).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Left ventricular diastolic function in hypertrophic cardiomyopathy. 202 81

We present a case of association of apical hypertrophic cardiomyopathy of the Japanese type and coronary arteriovenous fistula in a 56-year-old male who presented with anginal symptoms. Both cardiopathies can produce myocardial ischemia and angina, and their association could aggravate the ischemia. In our patient the symptoms were adequately controlled with Verapamil. The coexistence of these two rare entities in the same patient has recently been described in 2 other cases, allowing us to speculate on a possible etiological relation between the 2 abnormalities, probably both been originated in a common developmental error.
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PMID:[Apical hypertrophic cardiomyopathy and coronary arteriovenous fistula]. 206 59

Forty one patients with ischaemic heart disease (IHD) of the age 60 +/- 12.3 years were hospitalized and treated two weeks with Curantyl (Dipyridamol) which was applied per os in a dose of 75 mg 3 times, and after another two weeks 34 of them wass applied Isoptin (Verapamil) in a dose of 40 mg 3 times daily. The heat conductivity (J.m-1, sec-1.degree C.10(-2), HC) and skin temperature (degree C, ST) were examined at the isothermic level 2 cm above the inner ankle by the apparatus Fluvograph 2 of Hartmann and Braun A. G. (BRD). The HC after Isoptin application above the left and right ankle was in 34 patients increased significantly (p less than 0.001). In patients with IHD after Curantyl application the HC and ST was significantly decreased above the left and right ankle in 9 (21.9%) and in 12 (30.0%), respectively. Curantyl could deteriorate HC and so to worsen legs ulceration healing and to point ap ischemia in patients with associated chronic postphlebitic syndrome with ulcera crurium.
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PMID:Heat conductivity and skin temperature at the treatment of ischemic heart disease with curantyl and isoptin. 207 72

1. The hypothesis that early verapamil (VP) treatment in acute myocardial ischemia can enhance the effects of subsequent reperfusion was tested in open-chest dogs submitted to 3 h of left anterior descending artery occlusion and 2 h of reperfusion. 2. Arterial pressure and heart rate were monitored continuously. The area at risk (AR) was determined by left atrial injection of 99technetium-labeled microspheres soon after occlusion. The area of necrosis (AN) was identified histologically with triphenyl tetrazolium chloride and calculated as percent of AR. Myocardial preservation is reported as percent of AR spared from necrosis (AR-AN) x 100/AR. 3. Fourteen dogs received 0.2 mg VP, iv, 15 min after occlusion and 9 untreated dogs served as controls. Verapamil significantly reduced heart rate but did not affect blood pressure or the pressure-heart rate product. 4. Myocardial preservation was significantly greater in verapamil-treated dogs than in control animals (51 +/- 20 vs 31 +/- 19%, mean +/- SD). However, area at risk (%) in the left ventricle was not significantly different in treated and control animals (31 +/- 12 vs 32 +/- 4%). 5. These data indicate that verapamil protects the ischemic myocardium in this occlusion/reperfusion model and that the mechanism of protection is probably related to a non-hemodynamic, metabolic activity of verapamil.
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PMID:Myocardial protection by verapamil and reperfusion following coronary occlusion. 209 44

The appearance of impaired left ventricular diastolic function in chronic ischemic heart disease often precedes systolic dysfunction. Myocardial ischemia and increased calcium loading have been implicated in the genesis of increased left ventricular stiffness. We have assessed the effects of long-term therapy with different classes of calcium channel-blocking drugs on left ventricular peak filling rate in patients with chronic stable angina and congestive heart failure secondary to ischemic heart disease. Therapeutic effects of nicardipine (30 mg t.i.d.), nisoldipine (10 mg b.i.d.), and verapamil (120 mg t.i.d.) (4 weeks) have been assessed on radionuclide left ventricular diastolic filling parameters in patients with chronic stable angina using placebo-controlled studies. All three drugs significantly improved exercise capacity as compared with placebo. Verapamil produced significant improvements in peak filling rate (p less than 0.005), time to peak filling rate (p less than 0.01), and first one-third filling fraction (p less than 0.005), whereas nicardipine only improved peak filling rate (p less than 0.005); neither drug altered the mean ejection fraction (n = 20). Nisoldipine did not significantly alter diastolic filling parameters or ejection fraction (n = 10). Nisoldipine and digoxin were also assessed in congestive heart failure (New York Heart Association [NYHA] classes II and III) associated with ischemic heart disease (n = 26) (open parallel design). Neither produced significant alterations in peak filling rate and ejection fraction after 3 months of therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of long-term treatment with calcium antagonists on left ventricular diastolic function in stable angina and heart failure. 240 36

Verapamil was shown to be able to recover a significantly depressed actomyosin ATPase activity of the unaffected left ventricular area in experimental myocardial ischemia. The drug also increased Ca-sensitivity of the ATPase reaction, with the amount of actomyosin components (Tn-1, LCM-1, LCM-2, Tn-C) almost reaching the control level. The possibility of direct interaction of verapamil with Ca-binding sites on actomyosin macromolecule is suggested. Its influence on metabolism and gene expression is not excluded.
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PMID:[Effect of verapamil on the molecular characteristics of myocardial actomyosin in experimental ischemia]. 241 42

The effects of AQ-A39, a selective bradycardic agent, on cardiovascular responses to beta-adrenergic stimulation with isoproterenol were investigated in open-chest, anesthetized dogs. Verapamil and timolol were also studied and compared with AQ-A39. All three compounds decreased basal heart rate and significantly decreased the chronotropic potency of isoproterenol. At 1.0 and 3.0 mg/kg, AQ-A39 reduced the relative potency of isoproterenol on heart rate to 0.730 and 0.312, respectively (control potency = 1.0). AQ-A39 enhanced the isoproterenol-mediated increases in cardiac output without affecting the potency of isoproterenol on mean arterial blood pressure or left ventricular dP/dtmax. Timolol reduced the potency of isoproterenol on all parameters studied. Verapamil decreased the left ventricular dP/dtmax response but did not change the mean arterial blood pressure or cardiac output responses to isoproterenol. Therefore, AQ-A39 demonstrated greater selectivity for inhibiting the chronotropic responses to beta-adrenergic stimulation in vivo than verapamil or timolol. Selective inhibition of positive chronotropic but not positive inotropic responses, as observed with AQ-A39, could be beneficial in the treatment of ischemic heart disease.
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PMID:Influence of AQ-A39, a bradycardic agent, on cardiovascular responses to isoproterenol in the anesthetized dog. 243 7

The effect of drugs on eicosanoid production and on the development of atherogenic index was investigated in canine myocardial ischemia. Iloprost, verapamil, the trapidil derivative AR 12463 or 0.9% NaCl solution were administered 60 min after coronary artery ligation in anaesthetized dogs. Both iloprost and AR 12463 reduced the thromboxane A2/prostacyclin (TXA2/PGI2) ratio in coronary sinus plasma in comparison to controls. The atherogenic index was significantly decreased in the iloprost as well as in the AR 12463-treated group in comparison to the control group. Verapamil had no influence on the investigated parameters.
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PMID:Influence of drugs on the TXA2/PGI2 balance and on the atherogenic index in myocardial ischemia in dogs. 247 Mar 53

The daily ECG monitoring was used in 20 patients with stable functional class II-III angina pectoris to study the antianginal and anti-ischemic effects of verapamil and nifedipine during the cross use of the drugs. Verapamil and nifedipine applied in the effective doses provoked a significant decrease of the number and total depth of painful depressions of the ST segment. The effect of verapamil on painful episodes of ST segment depressions was significantly more pronounced than that of nifedipine. At the same time nifedipine significantly reduced the number and total depth of painless episodes of myocardial ischemia whereas verapamil did not cause any significant lowering of these indicators. In cases where the drugs appeared ineffective, verapamil provoked a significant increase of the number of painless episodes of myocardial ischemia. This indicates that the painful threshold of sensitivity may change with the occurrence of myocardial ischemia in patients suffering from angina pectoris. In turn, nifedipine produced no significant effect on the number and intensity of painless episodes of myocardial ischemia.
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PMID:[Evaluation of the efficacy of a course of verapamil and nifedipine in patients with stable stenocardia by daily monitoring of the electrocardiogram]. 259 89

Seven healthy male volunteers were studied at the end of 7 days placebo period and after 7 days treatment with verapamil (120 mg twice daily). Verapamil increased significantly plasma renin activity and urinary excretion of 6-keto prostaglandin F1 alpha without significant modification of plasma aldosterone. Metoclopramide (10 mg i. v.) induced a significant increase of plasma aldosterone with the peak values 15 min after the injection of the drug. The results indicate that verapamil does not lead to secondary hyperaldosteronism which is characteristic of most other vasodilators. The increase of prostacyclin, measured as 6-keto prostaglandin F1 alpha can contribute to the efficacy of verapamil in patients with ischemic heart disease and hypertension. The present study suggests that the aldosterone response to metoclopramide is not directly dependent on calcium, but an indirect effect of calcium through renin-angiotensin system cannot be excluded.
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PMID:Effect of verapamil on renin-angiotensin-aldosterone system, urinary 6-keto prostaglandin F1 alpha and aldosterone response to metoclopramide in normal man. 263 2


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