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[Coronary spasm in angina pectoris].
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[Iso Mack Retard 40 mg. Coronary drug for long term therapy and prophylaxis in coronary circulation disorders (angina pectoris)].
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[Trimetazidine in the treatment of stable angina pectoris TRIADA-(trimetazidine in stable angina twice daily)].
The primary objective of the national study TRIADA was to evaluate the efficacy and tolerability of Preductal MR (trimetazidine) at a dose of 35 mg twice daily which was added to current therapy involving the maximum of two antianginal drugs. The outcome was evaluated after 12 weeks of therapy and compared with baseline data. The study included 74 patients with stable exertional angina pectoris (AP) and positive exercise testing results. Trimetazidine (Preductal MR) at a dose of 35 mg twice daily was added to their current therapy involving two drugs at most. TRIADA confirmed that the use of trimetazidine in a new pharmacological form is effective and well tolerated in the treatment of angina pectoris. The study also confirmed a beneficial effect of trimetazidine on the incidence of angina pectoris paroxysms and objective manifestations of ischaemia during exercise testing. Holter monitoring clearly showed that metabolic therapy added to standard antianginal therapy would reduce the incidence of symptomatic and asymptomatic ischaemia. In addition, 12-week therapy with trimetazidine helped improve all end points of quality of life of AP patients evaluated using a questionnaire for AP patients (The Seattle Angina Questionnaire).
Angina pectoris in presumably healthy middle-aged men. Validation of two questionnaire methods in making the diagnosis of angina pectoris.
In 2014 presumably healthy men aged 40-59 yr the prevalence of previously undiagnosed angina pectoris was assessed by two angina questionnaires: (1) World Health Organization Questionnaire (WHO-Q) and (2) Greater New York Health Insurance Plan Survey Questionnaire (NY-Q). The angina prevalence given by the questionnaires singly or in combination varied between 1.15 and 4.7% (lowest prevalence by the WHO-Q interview version (WHO-Qi) and highest by the WHO-Q self-administered version and the NY-Q in combination), indicating a considerable variation in prevalence with variation in criteria used. Validation of the questionnaires by means of (1) coronary angiography, and (2) follow-up in selected cases, indicated NY-Q superiority over WHO-Q in predicting the presence of coronary heart disease (CHD). WHO-Qi had a particularly low sensitivity without being more specific. However, CHD-risk factor patterns in subgroups of individuals classified as angina-positive or -negative by the respective questionnaires were similar.
Guidelines on the management of stable angina pectoris: executive summary: The Task Force on the Management of Stable Angina Pectoris of the European Society of Cardiology.
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[Success and complication rates of coronary angioplasty in the unstable angina pectoris stage after myocardial infarct--a comparison with percutaneous transluminal coronary angioplasty in the acute infarct stage and unstable angina pectoris without preceding myocardial infarct].
To evaluate whether there is a difference in terms of the success and complication rates of PTCA in patients (pts) with unstable angina pectoris (UAP) after myocardial infarction (group I) and patients with myocardial infarction (group II), as well as in patients with UAP without preceding myocardial infarction (group III), we analyzed the data of 188 patients retrospectively. Acute PTCA was performed in 42 patients of group I, 55 patients of group II, and 91 patients of group III. The primary success rate was comparable in all three groups (group I: 74%; group II: 76%; group III: 77%). The incidence of acute ACVB operation was comparable in group I (5 pts: 9%) and group III (10 pts: 11%). One patient was operated during an acute myocardial infarction. Five patients of group I (9%) and seven patients of group III (8%) developed a myocardial infarction. Three patients of group I (7%) and three patients of group II (5%) died during hospitalization. PTCA performed during acute myocardial ischemia has the highest complication rate in patients with UAP after myocardial infarction and is considerably higher than in patients with UAP without preceding infarction.
Usefulness of oral nisoldipine for stable angina pectoris. The Nisoldipine Multicenter Angina Study Group.
The duration and extent of antianginal effects of nisoldipine, a dihydropyridine calcium antagonist, were assessed in 178 patients with chronic stable angina pectoris. Using a placebo run-in, placebo-controlled, randomized, parallel study design, patients received placebo twice daily for 2 to 3 weeks and were then randomized to receive either placebo (n = 42), nisoldipine 10 mg once daily (n = 44), nisoldipine 10 mg twice daily (n = 47) or nisoldipine 20 mg once daily (n = 45) for 5 weeks. Frequency of angina and nitroglycerin consumption were assessed by weekly patient diaries. Exercise tolerance time was assessed at baseline and at weeks 1, 3 and 5 in the double-blind phase. Peak effects after 5 weeks of double-blind medication showed significant or nearly significant improvements with nisoldipine over placebo in time-to-termination of exercise, time to onset of angina, and time to onset of 1 mm ST-segment depression. There were no significant improvements in trough effects with nisoldipine. Also, placebo was not significantly different from nisoldipine in either the number of anginal attacks or nitroglycerin consumed. Although significantly more drug-related, adverse effects were observed with the nisoldipine regimen, 20 mg once daily, compared with placebo, nisoldipine appears to be an effective and well-tolerated antianginal drug. However, its duration of antianginal action, as measured by exercise stress testing, is relatively short. The drug needs to be examined using shorter dosing intervals and higher daily doses, or in a longer-acting sustained-release formulation.
Regional myocardial blood flow redistribution as a cause of postprandial angina pectoris.
BACKGROUND: Postprandial angina pectoris has been recognized for more than two centuries and can be identified in up to 10% of patients with chronic ischemic heart disease. Redistribution of myocardial blood flow, from a region supplied by a severely stenotic coronary artery to those supplied by less diseased or normal vessels, is a potential mechanism of postprandial angina. METHODS AND RESULTS: To test this hypothesis, we have determined the effects of a standard liquid meal on whole heart and regional myocardial blood flow, measured by means of dynamic positron emission tomography (PET) with 15O-labeled water in 14 patients with a reproducible history of postprandial angina and 7 matched control subjects. The standard liquid meal precipitated angina pectoris in all patients. Baseline whole heart blood flow was similar and increased normally after the meal in patients (0.97+/-0.14 to 1.14+/-0.25 mL.min(-1).g(-1), P<.04) as in control subjects (0.92+/-0.12 to 1.02+/-0.13 mL.min(-1).g(-1), P<.02). In contrast, the coefficient of variation of blood flow increased significantly after the standard liquid meal in patients (34+/-9%, P<.05 versus baseline) but not in control subjects (17+/-7%, P=NS versus baseline). In patients, analysis of regional myocardial blood flow demonstrated decreased myocardial blood flow in territories supplied by stenotic arteries (1.01+/-0.35 to 0.76+/-0.27 mL.min(-1).g(-1), P<.03), but there was an increase in blood flow in territories supplied by normal arteries (0.89+/-0.16 to 1.34+/-0.25 mL.min(-1).g(-1), P<.001) after the meal. CONCLUSIONS: The standard liquid meal induced angina pectoris in patients with coronary artery disease. Although whole heart blood flow increased appropriately for the greater cardiac work, there was a redistribution of regional blood flow from territories supplied by severely stenosed coronary arteries to those supplied by less diseased or normal arteries. This redistribution may be the cause of myocardial ischemia in postprandial angina.
[Therapy of angina pectoris].
Treatment of angina pectoris should follow the clinical course: Stable angina is most often responding to nitropreparations, betablockers or calciumantagonists; differentialtherapy should consider the basic state of the patient: age, heart-rate, hypo- or hypertension, cardiac failure or asthma bronchiale etc. Unstable angina needs more attention and should be transferred to a coronary care unit. Analgetics, sedatives, oxygen and nitrates should be applied under hemodynamic monitoring. Only in rare cases with cardiac failure or with rapid atrial fibrillation glycosides will be necessary. In extreme bradiacardias a pacemaker can be helpful. Captopril might be a new substance in nonresponders.
Guidelines on the management of stable angina pectoris: executive summary: the task force on the management of stable angina pectoris of the European society of cardiology.
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[Angina pectoris: progress in diagnosis and treatment. III. Progress in treatment. 5. Coronary artery intervention for angina pectoris].
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Continuous twenty-four hour vasodilation in the treatment of angina pectoris; time-disintegration capsules containing pentaerythritol tetranitrate reduced the severity and frequency of angina pectoris attacks.
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Selection of medical treatment in stable angina pectoris: results of the International Multicenter Angina Exercise (IMAGE) Study.
OBJECTIVES: The present study was designed to investigate which characteristics of anginal symptoms or exercise test results could predict the favorable anti-ischemic effect of the beta-adrenergic blocking agent metoprolol and the calcium antagonist nifedipine in patients with stable angina pectoris. BACKGROUND: The characteristics of anginal symptoms and the results of exercise testing are considered of great importance for selecting medical treatment in patients with chronic stable angina pectoris. However, little information is available on how this first evaluation may be used to select the best pharmacologic approach in individual patients. METHODS: In this prospective multicenter study, 280 patients with stable angina pectoris were enrolled in 25 European centers. After baseline evaluation, consisting of an exercise test and a questionnaire investigating patients' anginal symptoms, the patients were randomly allocated to double-blind treatment for 6 weeks with either metoprolol (Controlled Release, 200 mg once daily) or nifedipine (Retard, 20 mg twice daily) according to a parallel group design. At the end of this period, exercise tests were repeated 1 to 4 h after drug intake. RESULTS: Both metoprolol and nifedipine prolonged exercise tolerance over baseline levels; the improvement was greater in the patients receiving metoprolol (p < 0.05). Multivariate analysis revealed that low exercise tolerance was the only variable associated with a more favorable effect within each treatment group. Metoprolol was more effective than nifedipine in patients with a lower exercise tolerance or with a higher rate-pressure product at rest and at ischemic threshold. None of the characteristics of anginal symptoms or exercise test results predicted a greater efficacy of nifedipine over metoprolol. CONCLUSIONS: The results of a baseline exercise test, but not the characteristics of anginal symptoms, may offer useful information for selecting medical treatment in stable angina pectoris.
Angina pectoris. III. Demonstration of a chemical origin of ST deviation in classic angina pectoris, its variant form, early myocardial infarction, and some noncardiac conditions.
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The design of proper experiments to investigate clinical angina pectoris and the importance of knowing the determinants of coronary flow in considering therapy of angina pectoris.
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Combination therapy with metoprolol and nifedipine versus monotherapy in patients with stable angina pectoris. Results of the International Multicenter Angina Exercise (IMAGE) Study.
OBJECTIVES: This study was designed to investigate whether combination therapy with metoprolol and nifedipine provides a greater anti-ischemic effect than does monotherapy in individual patients with stable angina pectoris. BACKGROUND: Combination therapy with a beta-adrenergic blocking agent (which reduces myocardial oxygen consumption) and a dihydropyridine calcium antagonist (which increases coronary blood flow) is a logical approach to the treatment of stable angina pectoris. However, it is not clear whether, in individual patients, this combined therapy is more effective than monotherapy. METHODS: Two hundred eighty patients with stable angina pectoris were enrolled in a double-blind trial in 25 European centers. Patients were randomized (week 0) to metoprolol (controlled release, 200 mg once daily) or nifedipine (Retard, 20 mg twice daily) for 6 weeks; placebo or the alternative drug was then added for a further 4 weeks. Exercise tests were performed at weeks 0, 6 and 10. RESULTS: At week 6, both metoprolol and nifedipine increased the mean exercise time to 1-mm ST segment depression in comparison with week 0 (both p < 0.01); metoprolol was more effective than nifedipine (p < 0.05). At week 10, the groups randomized to combination therapy had a further increase in time to 1-mm ST segment depression (p < 0.05 vs. placebo). Analysis of the results in individual patients revealed that 7 (11%) of 63 patients adding nifedipine to metoprolol and 17 (29%) of 59 patients (p < 0.0001) adding metoprolol to nifedipine showed an increase in exercise tolerance that was greater than the 90th percentile of the distribution of the changes observed in the corresponding monotherapy + placebo groups. However, among these patients, an additive effect was observed only in 1 (14%) of the 7 patients treated with metoprolol + nifedipine and in 4 (24%) of the 17 treated with nifedipine + metoprolol. CONCLUSIONS: The mean additive anti-ischemic effect shown by combination therapy with metoprolol and nifedipine in patients with stable angina pectoris is not the result of an additive effect in individual patients. Rather, it may be attributed to the recruitment by the second drug of patients not responding to monotherapy.
[Angina pectoris: progress in diagnosis and treatment. III. Progress in treatment. 1. Control of risk factors of angina pectoris].
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