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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent publications purporting to show that calcium antagonists, when used for the treatment of hypertension or in the post myocardial infarction patient, would paradoxically increase the rate of heart attack and mortality have cast doubts on the safety and efficacy of this drug class. All three studies are retrospective, and have various drawbacks. Specifically, the metaanalysis of Furberg et al is fraught with mistakes, of borderline significance, and based on old data pertaining to short-acting nifedipine only (which should not be given in patients who have suffered an acute heart attack). The case control study of Psaty et al suggested that hypertensive patients who were treated with short-acting verapamil, diltiazem, and nifedipine had an excessive rate of myocardial infarction when compared with patients who were treated with diuretics. Two out of the three calcium antagonists that were used in this study were not approved for the treatment of hypertension by the US Food and Drug Administration. Some patients were taking these drugs only once a day whereas, because of their short duration of action, at least a three or four times daily regimen would be required to achieve an acceptable blood pressure control throughout a 24-h period. The cohort study of Pahor et al suggested distinct differences among various calcium antagonists with regard to survival. Blood pressure was controlled in < 40% of all patients, and in some patients blood pressure was never even measured. Recent studies, such as the Prospective Randomized Amlodipine Survival Evaluation (PRAISE), the third Vasodilator-Heart Failure Trial (VHeFT-III), the second Doppler Flow and Echocardiography in Functional Cardiac Insufficiency Assessment of Nisoldipine Therapy (DEFIANT II), the Angina Prognosis Study in Stockholm (APSIS), and the Shanghai Trial of Nifedipine in the Elderly (STONE), attest to the safety and efficacy of the newer long-acting calcium antagonists in patients with a wide spectrum of heart disease. Several ongoing trials including the Antihypertensive and Lipid Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) with amlodipine, the International Nifedipine-GITS Study: Intervention as a Goal in Hypertension Treatment (INSIGHT) with nifedipine, the Hypertension Optimal Treatment study (HOT) with felodipine, the Systolic Hypertension in the Elderly in Europe Trial (SYST-EUR) with nicardipine, the Second Swedish Trial in Old Patients with Hypertension (STOP II) with felodipine, and Nordic Diltiazem Study (NORDIL) with diltiazem, will give us morbidity and mortality data in patients with high blood pressure within the next few years. Until these results are available, we can be confident that the lowering of blood pressure and providing relief of patients with symptomatic angina can be achieved safely and efficiently with the presently available long-acting calcium antagonists.
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PMID:What, if anything, is controversial about calcium antagonists? 896 30

The incidence of hospitalizations, lengths of stay, and per-diem costs were determined for 421 patients (amlodipine, 209; placebo, 212) with nonischemic cardiomyopathy in the first Prospective Randomized Amlodipine Survival Evaluation (PRAISE) study to assess the impact of amlodipine on hospital use and to compare the costs of hospitalization with the cost of amlodipine treatment. Treatment with amlodipine versus placebo significantly delayed the mean (+/- SD) time to first hospitalization (447 +/- 26 d vs 315 +/- 18 d, respectively; P = 0.0139). Both treatment groups showed a similar number of hospital admissions per patient per year. The overall hospital length of stay was 1.17 days less per year with amlodipine than with placebo, at a cost of $1098 less per person per year although these differences were not statistically significant. Significantly fewer amlodipine patients were admitted for unexplained cardiac arrest (odds ratio, 0.235; P = 0.002) and ventricular arrhythmias (odds ratio, 0.497; P = 0.004). These findings are consistent with clinical reports from PRAISE of prolonged survival and a reduction in sudden cardiac death among patients with severe heart failure due to nonischemic heart disease. This analysis suggests that in patients with nonischemic cardiomyopathy, treatment with amlodipine can delay the time to hospitalization and may reduce the number of hospital admissions related to ventricular arrhythmias. The estimated reduction in hospital costs of $1098 per year would more than offset the amlodipine treatment cost of approximately $700 per year.
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PMID:Hospital use and costs among patients with nonischemic cardiomyopathy in the first prospective randomized amlodipine survival evaluation study. 1046 22

Our previous study found that angiotensin-converting enzyme (ACE) inhibitors and amlodipine induce NO release from coronary microvessels through a kinin-dependent mechanism. The goal of this study was to determine whether amlodipine could potentiate NO formation during ACE inhibition. Coronary microvessels were isolated from 16 mongrel dogs. Nitrite, the hydration product of NO, from coronary microvessels was quantified by using the Griess reaction. Bradykinin and kallikrein all significantly increased nitrite release from coronary microvessels in a concentration-dependent manner. The ACE inhibitor, ramiprilat, potentiated these effects. Amlodipine also markedly potentiated nitrite production by ramiprilat. For instance, amlodipine (10(-10) M) enhanced nitrite release induced by ramiprilat (10(-7) M) from 122 +/- 9 to 168 +/- 14 pmol/mg (p < 0.05 vs. ramiprilat). Nitrite release potentiated by ramiprilat and amlodipine was entirely blocked by N(omega)-nitro-L-arginine methyl ester (L-NAME, an inhibitor of NO synthase), HOE 140 (Icatibant, a specific B2-kinin receptor antagonist), and dichloroisocoumarin (DCIC, a serine protease inhibitor that blocks local kinin formation). These results clearly show that there is a synergistic effect on NO formation when amlodipine is combined with ACE inhibition. Our data suggest that kinin-mediated coronary NO production may contribute importantly to the beneficial therapeutic action of ACE inhibitors, especially in combination with amlodipine in the treatment of heart disease.
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PMID:Amlodipine enhances NO production induced by an ACE inhibitor through a kinin-mediated mechanism in canine coronary microvessels. 1067 50

This research highlights high clinical affectivity of Amlodipine in patients with essential hypertension complicated by ishemic heart disease. Monotherapy with Amlodipine doesn't deteriorate contractive quality of the left ventricle. Therapy with Amlodipine considerably improves the diastolic function of the left ventricle and adjusts it. These positive changes are expressed in decreasing preload, end-diastolic pressure of the left ventricle.
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PMID:[Clinical hemodynamic effects of amlodipine in patients with hypertension associated with angina pectoris]. 1705 17