Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A study was undertaken in order to compare the effects of Diltiazem, Nifedipine and Verapamil on 11 male adults (aged 44 to 70 yrs: mean age 60 yrs) affected by effort angina with a stable exercise threshold. The study was carried out according to a 4 week double-blind randomized protocol. Diltiazem (300 mg/die), Nifedipine (50 mg/die), Verapamil (400 mg/die) and placebo were administered each for 7 day periods. An ergometric test was performed on the last of each therapeutic cycle in order to evaluate the effects of the treatments. The three active drugs globally provoked an increased tolerance to physical effort with respect to placebo (p less than 0.01); no significant differences, as regards physical performance, could be detected among the three drugs. Treatment with Nifedipine significantly increased heart rate at rest (p less than 0.05), under submaximal (p less than 0.05) and maximal load (p less than 0.05), with respect to treatment with Diltiazem and Verapamil. Systolic and diastolic arterial blood pressure did not vary significantly with any of the three drugs. Rate pressure product under submaximal load (p less than 0.05) and at the end of the exercise (p less than 0.05) was higher with Nifedipine than with the other two drugs. These results show that patient response to Nifedipine is different from that to Verapamil and Diltiazem and suggest that the three drugs exert their anti ischemic effect through different mechanisms. The evaluation of individual response revealed that only one patient showed no increased tolerance to physical effort with any of the drugs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Comparative evaluation of 3 calcium antagonist drugs in patients with stable angina of effort. Double-blind placebo-controlled randomized study]. 330 5

Of 576 patients with non-Q-wave acute myocardial infarction enrolled in the Diltiazem Reinfarction Study, 246 (43%) had 1 or more episodes of angina at rest or with minimal effort during 10.5 days of treatment with either diltiazem (90 mg every 6 hours) or placebo. Reinfarction (12.2% vs 3.6%, p less than 0.0001) or death (6.1% vs 1.5%, p = 0.003) was more likely to occur within 2 weeks of randomization in patients with postinfarction angina than in those without angina. Based on serial electrocardiographic data, 115 of the 246 patients with angina had transient ST-T changes and 131 did not. Comparison of the 14-day event rates in these 2 groups showed that the 115 patients with electrocardiographic evidence of ischemia had a higher frequency of reinfarction (20% vs 5.3%, p less than 0.001), more extensive damage as assessed by peak MB-creatine kinase levels (91 +/- 76 vs 37 +/- 19 IU/liter, p = 0.059 [Wilcoxon rank sum]) and a higher mortality rate (11.3% vs 1.5%, p = 0.001). Angina associated with transient ST-T changes occurred in 70 of the 289 patients in the placebo group but in only 45 of the 287 patients in the diltiazem group--a 28% reduction in cumulative life-table incidence (p = 0.0103 [2-tail, log rank]; 95% confidence interval, 9.3 to 53.8%). It is concluded that patients with early postinfarction angina are at increased risk of reinfarction and death, and angina associated with transient electrocardiographic changes identified a very high risk subset. This subset appeared to have a larger area of viable but jeopardized myocardium and benefited from prophylactic therapy with diltiazem.
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PMID:Prognostic significance and beneficial effect of diltiazem on the incidence of early recurrent ischemia after non-Q-wave myocardial infarction: results from the Multicenter Diltiazem Reinfarction Study. 330 86

The safety and efficacy of a sustained-release preparation of diltiazem (diltiazem-SR), with dose levels of 240 and 360 mg/day, were assessed in 18 patients with stable angina of effort. A double-blind, placebo-controlled, randomized, crossover protocol was used. Diltiazem-SR, when given twice daily, reduced the frequency of weekly anginal attacks from 9.3 +/- 10.4 with placebo to 3.7 +/- 4.7 with 240 mg/day and to 3.1 +/- 4.7 with 360 mg/day (both p less than 0.01 compared with placebo). Treadmill time was increased from 410 +/- 180 seconds during the placebo phase to 519 +/- 177 seconds during the 240-mg/day dose and to 506 +/- 182 seconds during the 360-mg/day dose of diltiazem-SR (both p less than 0.01 compared with placebo). The time to the onset of angina and ischemic ST-segment depression were similarly prolonged by both doses of diltiazem-SR. The beneficial effects of diltiazem-SR appeared partly due to a reduction in the heart rate during submaximal exercise. Diltiazem-SR is effective and safe for the treatment of angina of effort when given twice daily.
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PMID:Efficacy and safety of sustained-release diltiazem in stable angina pectoris. 351 May 25

We performed a multicenter, double-blind, randomized study to evaluate the effect of diltiazem on reinfarction after a non-Q-wave myocardial infarction. Nine centers enrolled 576 patients: 287 received diltiazem (90 mg every six hours) and 289 received placebo. Treatment was initiated 24 to 72 hours after the onset of infarction and continued for up to 14 days. The primary end point, reinfarction, was defined as an abnormal reelevation of MB creatine kinase in plasma within 14 days. Reinfarction occurred in 27 patients in the placebo group (9.3 percent) and in 15 in the diltiazem group (5.2 percent)--a 51.2 percent reduction in cumulative life-table incidence (P = 0.0297; 90 percent confidence interval, 7 to 67 percent). Diltiazem reduced the frequency of refractory postinfarction angina (a secondary end point) by 49.7 percent (P = 0.0345; 90 percent confidence interval, 6 to 73 percent). Mortality was similar in the two groups (3.1 and 3.8 percent, respectively, in the placebo and diltiazem groups), but adverse drug reactions (most of which were mild) were more common in the diltiazem group. Nevertheless, the drug was well tolerated, despite concurrent treatment with beta-blockers in 61 percent of the patients. We conclude that diltiazem was effective in preventing early reinfarction and severe angina after non-Q-wave infarction and that it was also safe and generally well tolerated.
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PMID:Diltiazem and reinfarction in patients with non-Q-wave myocardial infarction. Results of a double-blind, randomized, multicenter trial. 352 51

Fifteen patients with coronary artery spasm completed a double-blind placebo-controlled trial comparing diltiazem and nifedipine. Increasingly, higher daily doses (diltiazem, 90 to 360 mg; nifedipine, 30 to 120 mg) were administered to achieve optimal clinical effects. Daily diaries and ambulatory electrocardiographic recordings were used to assess efficacy and side effects. Both drugs significantly decreased angina frequency compared with that in the preceding placebo period (diltiazem 1.4 +/- 0.4 [mean +/- SEM] to 0.4 +/- 0.2 episodes per day; nifedipine 1.4 +/- 0.3 to 0.4 +/- 0.1 episodes per day; both p less than 0.05). Ambulatory electrocardiographic recordings showed fewer ST shifts than were expected during all treatment periods (0.02/h recorded during placebo, none during diltiazem and 0.02/h during nifedipine therapy). Although some patients responded better to one drug than the other, neither drug resulted in a clearly superior clinical response. Diltiazem was discontinued in one patient because of urticaria, but the total number of side effects was higher with nifedipine (12 of 15 patients) than with diltiazem (5 of 15, p less than 0.01). Nine patients remained symptomatic on single drug treatment and entered open label treatment with the combination of diltiazem and nifedipine. Three patients did not tolerate the combination because of important side effects; the other six also had side effects, but these were relatively minor. Four patients received no more benefit from the combination than from a single agent; the condition of two patients improved. Both diltiazem and nifedipine provide effective antianginal therapy for coronary spasm, but diltiazem has fewer side effects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of diltiazem and nifedipine alone and in combination in patients with coronary artery spasm. 354 92

We evaluated the protective effect of Diltiazem from pacing-induced myocardial ischemia in 9 patients (pts) with coronary heart disease (CAD) and stable effort angina by studying the changes in systemic and coronary hemodynamics during pacing. Hemodynamic parameters were evaluated at baseline and at peak pacing before and after Diltiazem, 25 mg i.v. Diltiazem prevented angina in 6 of 7 pts who presented angina in the control pacing. This beneficial effect was accompanied at peak pacing rate by a significant fall in ST depression, arterial pressure, rate-pressure product and left ventricular (LV) end-diastolic pressure, while no significant changes were observed in LV dp/dt max, coronary blood flow and coronary vascular resistance. Therefore, Diltiazem exerts a protective effect from pacing-induced myocardial ischemia in pts with CAD and stable effort angina, without impairing LV function. This beneficial effect is due to a reduction in myocardial metabolic requirements, rather than to an improvement of blood supply to the ischemic myocardium.
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PMID:[Beneficial effects of diltiazem in exertion stable angina. Evaluation of coronary hemodynamics during cardiac pacing]. 355 41

Ten patients four men and six women aged 35 to 78 years (mean, 57) who had been admitted to a coronary care unit because of unstable angina, received intravenous infusions of diltiazem for three to ten days after a 24-hour observation period. During the observation and treatment periods, the patients were monitored daily for number of attacks of angina, nitroglycerin intake, blood pressure, and ECG parameters. Routine laboratory tests were performed before and after diltiazem therapy. Two patients did not respond to treatment, but administration of diltiazem controlled anginal pain in eight patients, without producing side effects. In one case the dose had to be reduced because of atrioventricular dissociation; in three cases there was a modest increase in SGPT. Diltiazem was found to be a safe and effective drug for controlling anginal attacks in patients with unstable angina.
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PMID:Intravenous diltiazem in the treatment of unstable angina: a study of efficacy and tolerance. 366 54

The antiischaemic properties of intravenous diltiazem in recommended therapeutic doses are disputed. In 17 patients with coronary artery disease the systemic and coronary haemodynamic effects of diltiazem were assessed during a high-dose infusion (0.4 mg kg-1 per 5 min, followed by 0.4 mg kg-1 per 10 min). In addition, its potential antiischaemic properties were investigated during identical pacing stress tests, 30 minutes before (P1) and immediately after diltiazem administration (P2). Diltiazem reduced left ventricular systolic pressure from 133 +/- 5 to 116 +/- 5 mmHg (P less than 0.005, means +/- SEM), persisting until after P2. It decreased systemic and coronary resistance by 32% (P less than 0.001) and 29% (P less than 0.005), respectively, with a sustained increase in cardiac output from 5.9 +/- 0.4 to 7.3 +/- 0.6 l min-1 (P less than 0.01), but a brief 20% rise in coronary flow (P less than 0.05), after the bolus infusion only. Heart rate, contractility, left ventricular filling pressure and myocardial O2 consumption remained unchanged. Despite high plasma levels (673 +/- 81 micrograms l-1) diltiazem was well tolerated. During identical maximal pacing rates diltiazem considerably reduced myocardial O2 demand (double product: 16.3 +/- 0.8 (P2) vs 21.1 +/- 1.1 (P1), P less than 0.005), due to an 18% decrease in left ventricular systolic pressure, resulting in diminished coronary flow and myocardial O2 consumption during P2 (14% and 15%, respectively, P less than 0.05 vs P1). Diltiazem also significantly reduced pacing-induced ischaemia, indicated by normalization of myocardial lactate extraction (1 +/- 8% (P2) vs -41 +/- 12% (P1), P less than 0.05), and left ventricular filling pressure (13 +/- 2 (P2) vs 27 +/- 3 mmHg (P1), P less than 0.01), less ST-segment depression (0.12 +/- 0.01 (P2) vs 0.24 +/- 0.02 mV (P1), P less than 0.01) and improved contractility (Vmax 59 +/- 5 (P2) vs 48 +/- 3 s-1 (P1), P less than 0.05). Angina was absent or less in 15 patients during pacing after diltiazem. Thus, diltiazem, in high dosages, induces continuing systemic but short lasting coronary vasodilation, improves pump function without negative chronotropic and inotropic effects and has pronounced antiischaemic properties, predominantly due to diminished myocardial O2 demand.
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PMID:Acute antiischaemic properties of high dosages of intravenous diltiazem in humans in relation to its coronary and systemic haemodynamic effects. 366 56

To investigate the mechanism of the antianginal action of diltiazem in stress-induced myocardial ischemia, we studied 12 patients with stable exertional angina and disease of the proximal left anterior descending artery by measuring great cardiac vein flow (GVCF) and calculating anterior regional coronary resistance (ARCR) during myocardial ischemia induced by atrial pacing before and after intravenous administration of diltiazem (0.25 mg/kg in a bolus dose followed by continuous infusion of 0.005 mg/kg/min). Diltiazem increased the pacing time to angina from 6.9 +/- 3.5 to 10.7 +/- 4 min (p less than .001). At peak pacing heart rate was increased after diltiazem (from 128 +/- 17 to 145 +/- 17 beats/min, p less than .005), while mean arterial pressure was decreased (from 131 +/- 19 to 113 +/- 17 mm Hg, p less than .025), leaving the double product unaltered. At peak pacing no changes were observed in GCVF (from 115 +/- 46 to 119 +/- 46 ml/min, p = NS), ARCR (from 1.3 +/- 0.4 to 1.1 +/- 0.4 mm Hg/ml/min), or myocardial oxygen consumption of the anterior region (from 14.5 +/- 4.2 to 13.4 +/- 4.7 ml/min). Reduction of myocardial oxygen demand plays a major role in the antianginal action of diltiazem in patients with stress-induced myocardial ischemia.
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PMID:Effects of diltiazem on regional coronary hemodynamics during atrial pacing in patients with stable exertional angina: implications for mechanism of action. 369 56

Patients with angina pectoris, exercise induced myocardial ischemia, normal coronary arteries and no evidence of epicardial spasm, i.e. patients with syndrome x, have been suggested to haven inadequate increase in coronary blood flow during tachycardia, possibly due to a functional disorder of small coronary vessels. To evaluate the best medical management of this syndrome we studied 13 patients who showed the above set of findings. Patients were given propranolol (160 mg daily), diltiazem (360 mg daily) and placebo for 2 weeks, using a randomized single blind protocol. Upright bicycle ergometer testing was performed at the end of each period of treatment. Compared to placebo, diltiazem significantly (p less than 0.001) prolonged exercise duration (x +/- SD: 365 +/- 86 vs 303 +/- 89 sec) and time to onset of angina (358 +/- 88 vs 276 +/- 90 sec). Angina appeared in 7 patients with diltiazem vs 13 patients with placebo and occurred at a higher rate pressure product (26.3 +/- 3.5 vs 24.1 +/- 2.8 X 10(-3); p less than 0.02). Conversely, following propranolol exercise duration and time to onset of angina were unchanged and angina appeared in all patients at a lower rate pressure product (18.3 +/- 2.9 vs 24.4 +/- 3.6 X 10(-3); p less than 0.001). The most likely explanations for these findings are: propranolol counteracts beta 2-adrenergic receptors, thus further reducing coronary reserve. This may lower the anginal threshold; Diltiazem reduces smooth muscle tone in small coronary vessels. This may result in increased coronary reserve and exercise duration.
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PMID:[Opposing effects of propranolol and diltiazem on the angina threshold during an exercise test in patients with syndrome X]. 373 15


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