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At least 73 records · Page 4Linked to original sources
PubMed1991

Comparison of celiprolol and propranolol in stable angina pectoris. Celiprolol International Angina Study Group.

The comparative antianginal effects and safety of propranolol and celiprolol, a highly beta 1-selective adrenoceptor blocker with selective partial beta 2-adrenoceptor agonist activity, were assessed in an international multicenter, placebo run-in, active control, double-blind, randomized, titration-to-effect study of 140 patients with stable, exercise-induced angina pectoris. At baseline, all patients received placebo for 2 weeks, then titrated doses of once-daily celiprolol (200, 400, 600 mg) or twice-daily propranolol (total daily dose 80, 160, 320 mg) over 4 weeks, followed by a 2-week maintenance period. Heart rate and blood pressure, at rest and with exercise, weekly anginal attack frequency, nitroglycerin consumption and symptom-limited treadmill exercise times (modified Bruce protocol) were assessed. Compared with their respective baselines, both celiprolol and propranolol reduced anginal attack and nitroglycerin consumption rates to a comparable degree, while improving exercise tolerance (p less than 0.05). Treatment with propranolol compared with celiprolol, however, was associated with a significantly lower heart rate at rest (p less than 0.01). The double-product at the conclusion of exercise testing was significantly reduced by both drugs. Celiprolol and propranolol had similar effects on blood pressure, and were well tolerated. More symptomatic bradycardia occurred with propranolol. Despite the differences in their hemodynamic actions, once-daily celiprolol is as effective as twice-daily propranolol in the treatment of patients with stable angina pectoris.

Adrenergic beta-Antagonists↗
PubMed1994

The prognostic significance of post-infarction angina pectoris and the effect of verapamil on the incidence of angina pectoris and prognosis. The Danish Study Group on Verapamil in Myocardial Infarction.

The prognostic significance of angina pectoris and the effect of intervention with verapamil on the incidence of angina pectoris were studied in patients recovering from myocardial infarction and included in the Danish Verapamil Infarction Trial II. During the second week after admission patients were doubly-blindly randomized to treatment with verapamil 360 mg.day-1 or placebo. Treatment was continued for up to 18 months. At discharge angina pectoris was reported in 11% of 869 patients randomized to verapamil and in 12% of 888 randomized to placebo (ns). One month after discharge a significant increase in the prevalance of angina pectoris was reported in both the verapamil (33%) (P < 0.001) and the placebo groups (39%) (P < 0.001). The one month prevalence of angina pectoris (P = 0.03) and the 18 months overall incidence of angina pectoris (P = 0.002) were both significantly lower in the verapamil group compared with placebo. Stable angina pectoris during the first month of follow-up was a significant predictor of major events (i.e. death or reinfarction) (hazard ratio = 1.45; 95% confidence limits: 1.10, 1.89). As verapamil significantly reduced the incidence of angina pectoris during daily activities, and thereby the number of patients at high risk, the beneficial effect of verapamil in reducing major events in patients recovering from myocardial infarction is likely to be due to abolishing myocardial ischaemia.

Adult↗
PubMed1976

The variant form of angina pectoris.

Variant angina pectoris, usually not precipitated by exertion or emotional stress, often is more severe and lasts longer than classic angina. The pain tends to recur at about the same time each day. Arrhythmias, usually ventricular, occur in about 50% of cases during the peak of pain. Electrocardiograms show a characteristic ST segment elevation during pain, which is in contrast to the ST segment depression of classic angina pectoris. Pain may be due, at least in some cases, to a temporary increase in tonus of a single, large, narrowed coronary artery. Chemical changes in the myocardium and plasma catecholamine changes differ from those occurring in classic angina pectoris. The course of the disease is highly variable but the prognosis must be regarded as grave, since single large vessel disease, present in most cases, is associated with severe myocardial ischemia. Patients with variant angina pectoris should be studied early with coronary arteriography and considered for coronary artery bypass surgery if appropriate.

Angina Pectoris↗
PubMed1995

Clinical validation of a quality of life questionnaire in angina pectoris patients.

Angina pectoris impairs patients' quality of life. In order to assess its impact on quality of life, a questionnaire was developed using a literature review and interviews with patients and clinicians. It consisted of a general profile (SF-36) which measured functional status, well-being, perceived health, and a specific index, the Angina Pectoris Quality of Life Questionnaire, supplemented by new items. The acceptability, internal consistency reliability and clinical validity of this 70-item questionnaire were analysed in a cross-sectional study. Of 197 coronary patients approached, 93% (n = 184) agreed to participate and 86% (n = 170) returned the mailed questionnaire. Mean age of patients was 67 years (+/- 10); 79% were male and 70% were retired. Sixty patients were asymptomatic and 110 reported anginal crises (Canadian Cardiovascular Society Classification: class I: 48; II: 37; III: 13; IV: 0; V: 12). Globally, angina pectoris was found to affect each quality of life concept measured: physical functioning, well-being, and perceived health. Quality of life profiles worsened in accordance with increasing severity of the condition, as stratified by angina pectoris class. Asymptomatic patients reported better general and specific profiles. These results support the feasibility and usefulness of evaluating quality of life using the questionnaire. The validation of the data is very encouraging and enables the questionnaire to be used in clinical trials.

Adult↗
PubMed2006

[New data in the diagnosis and treatment of stable angina pectoris].

Stable angina pectoris is a manifestation of ischemic heart disease which frequently leeds to acute coronary syndrome. The patient has a short effort or stress situation induced retrosternal pain which is easing after the elimination of its cause, or taking nitroglycerin. Several new data have appeared in the literature about the pathogenesis and diagnosis of stable angina pectoris. Due to the international guidelines using the new drugs and revascularisation techniques, the primary and secondary prevention of stable angina pectoris was improved.

Acute Disease↗
PubMed1995

Hemostatic factors and the risk of myocardial infarction or sudden death in patients with angina pectoris. European Concerted Action on Thrombosis and Disabilities Angina Pectoris Study Group.

BACKGROUND: Increased levels of certain hemostatic factors may play a part in the development of acute coronary syndromes and may be associated with an increased risk of coronary events in patients with angina pectoris. METHODS: We conducted a prospective multicenter study of 3043 patients with angina pectoris who underwent coronary angiography and were followed for two years. Base-line measurements included the concentrations of selected hemostatic factors indicative of a thrombophilic state or endothelial injury. The results were analyzed in relation to the subsequent incidence of myocardial infarction or sudden coronary death. RESULTS: After adjustment for the extent of coronary artery disease and other risk factors, an increased incidence of myocardial infarction or sudden death was associated with higher base-line concentrations of fibrinogen (mean +/- SD, 3.28 +/- 0.74 g per liter in patients who subsequently had coronary events, as compared with 3.00 +/- 0.71 g per liter in those who did not; P = 0.01), von Willebrand factor antigen (138 +/- 49 percent vs. 125 +/- 49 percent, P = 0.05), and tissue plasminogen activator (t-PA) antigen (11.9 +/- 4.7 ng per milliliter vs. 10.0 +/- 4.2 ng per milliliter, P = 0.02). The concentration of C-reactive protein was also directly correlated with the incidence of coronary events (P = 0.05), except when we adjusted for the fibrinogen concentration. In patients with high serum cholesterol levels, the risk of coronary events rose with increasing levels of fibrinogen and C-reactive protein, but the risk remained low even given high serum cholesterol levels in the presence of low fibrinogen concentrations. CONCLUSIONS: In patients with angina pectoris, the levels of fibrinogen, von Willebrand factor antigen, and t-PA antigen are independent predictors of subsequent acute coronary syndromes. In addition, low fibrinogen concentrations characterize patients at low risk for coronary events despite increased serum cholesterol levels. Our data are consistent with a pathogenetic role of impaired fibrinolysis, endothelial-cell injury, and inflammatory activity in the progression of coronary artery disease.

Adult↗
PubMed1997

[The medical therapy of angina pectoris].

The angina pectoris crisis should be treated with nitroglycerin S.L.. In our days as in the 19th century, the non pharmacological therapeutic approach for angina pectoris (per se and to improve the free interval between crises) is still the same. This consists of the reduction of mental and physical stress, to stop smoking, improve light exercise, reduce obesity, and control other risk factors for coronary disease. Beta blockers are the choice drugs followed by calcium antagonists and nitrates. It is recommended that no short action calcium antagonists be used. Nitrates must be given with free intervals of action to avoid tachyphylaxis. The anti-platelet therapy can not be forgotten with aspirin or ticlopidine. Patients with refractory angina pectoris should be coronariography for performed eventual revascularization process.

Angina Pectoris↗
PubMed1987

The prognostic importance of asymptomatic ischemic episodes in patients with unstable angina pectoris.

Unstable angina pectoris is a high-risk ischemic disease which is characterized by recent onset of angina, a change in preexisting stable angina pattern or the occurrence of angina at rest. In a study of 70 patients with unstable angina on treatment with a triple drug regimen of nitrates, propranolol and nifedipine, 37 patients (53%) had 205 ischemic episodes, 90% of which were asymptomatic. 33 patients (47%) had no changes in the ST-segments. Between the two groups, there were no significant differences with respect to risk factors, medical treatment or coronary angiographic findings. Only the resting ejection fraction in the former group was slightly but significantly lower than in the latter group. At one month of follow-up seven patients had developed myocardial infarction, six of whom were in the group with silent ischemia. In 13 patients, due to inadequate success of medical treatment, bypass surgery or PTCA was performed; ten of these were from the group with silent ischemia. Of patients with silent ischemia, those with episodes totaling more than 60 minutes per 24 hours had the worst outcome. Multivariate analysis showed that, with respect to prognosis, the most important parameter was silent ischemia followed by angina pectoris.

Angina Pectoris↗
PubMed1992

Comparison of the safety and efficacy of bisoprolol versus atenolol in stable exercise-induced angina pectoris: a Multicenter International Randomized Study of Angina Pectoris (MIRSA).

Bisoprolol 10 mg and atenolol 100 mg once daily were compared regarding efficacy and safety in stable effort angina in a 12-week, multicenter, double-blind, randomized, parallel-group study. Efficacy was evaluated with angina pectoris diaries and bicycle exercise tests. Spontaneously mentioned complaints and side effects were recorded at each visit. In 11 centers, 147 patients completed the study; 76 received bisoprolol 10 mg, and 71 received atenolol 100 mg. After 12 weeks, weekly anginal attack rate was reduced significantly (p less than 0.05) with bisoprolol (5 +/- 0.5 to 2 +/- 0.6) and with atenolol (4 +/- 0.4 to 1 +/- 0.2). Peak exercise capacity (in W x min) increased significantly (p less than 0.05) with bisoprolol (772 +/- 47 to 878 +/- 52) and with atenolol (891 +/- 46 to 986 +/- 53). Rate pressure product (RPP) at peak exercise (in beats/min x mm Hg) decreased significantly (p less than 0.05) with both bisoprolol (25,003 +/- 692 to 20,116 +/- 637) and atenolol (26,544 +/- 557 to 21,603 +/- 576) (all values are mean +/- SE). The differences between the groups were not statistically significant. There were no significant differences regarding nature and incidence of adverse events between the groups. Thus, bisoprolol 10 mg once daily and atenolol 100 mg once daily are equipotent in their effects on stable effort angina. Both regimens were comparable with respect to incidence and nature of side effects.

Adult↗
PubMed1988

Diltiazem, nifedipine, and their combination in patients with stable angina pectoris: effects on angina, exercise tolerance, and the ambulatory electrocardiographic ST segment.

The efficacy and safety of oral nifedipine and diltiazem were compared in 20 patients with stable angina pectoris with use of a placebo run-in, randomized, double-blind titration to maximal effect crossover protocol. The effects of treatment withdrawal were also analyzed. All patients received placebo for 2 weeks and were then randomly assigned to receive either diltiazem or nifedipine. A 2 week drug titration phase in which patients received either diltiazem (180 to 360 mg/day) or nifedipine (30 to 120 mg/day) in three divided doses was followed by a 1 week maintenance phase. Patients then received placebo for 1 to 2 weeks, followed by crossover to the other treatment regimen and a second placebo washout period of 1 week. Patients (n = 13) who remained symptomatic on both diltiazem and nifedipine during the monotherapy periods entered a 3 week combination treatment phase, followed by a final 1 week placebo washout period. Frequency of angina, nitroglycerin consumption, exercise tolerance (Naughton protocol), and frequency of daily episodes of ST segment deviations on the electrocardiogram (1 mm of ST segment depression persisting for at least 1 min with and without chest pain) on an ambulatory electrocardiographic monitor were assessed during the baseline placebo, active monotherapy, placebo withdrawal, and combination treatment phases. Plasma drug levels were also measured. Compared with initial placebo values, the frequency of angina and the amount of nitroglycerin treatment were reduced by both diltiazem (p less than .001) and nifedipine (p less than .02). Diltiazem was more effective than nifedipine in reducing angina (p less than .02). Exercise duration increased with both drugs (p less than .0001). Diltiazem was significantly better than nifedipine in reducing the episodes of ST segment depression on the ambulatory monitor (p less than .01). Diltiazem reduced the resting heart rate (p less than .01); both drugs reduced the resting blood pressure and rate-pressure product. Overall, combination therapy was more effective in patients who did not maximally respond to diltiazem or nifedipine alone with respect to anginal and exercise variables and in reducing blood pressure at rest and during exercise. Plasma drug levels could not predict an individual patient's treatment response. Diltiazem may increase nifedipine drug levels when the drugs are combined. Fewer side effects were observed with diltiazem than nifedipine; the most side effects were seen with combination treatment. There were no apparent withdrawal effects observed with either treatment regimen.(ABSTRACT TRUNCATED AT 400 WORDS)

Angina Pectoris↗
PubMed1975

Left and right heart haemodynamics during spontaneous angina pectoris. Comparison between angina with ST segment depression and angina with ST segment elevation.

The function of both right and left sides of the heart was studied during spontaneous attacks of angina pectoris at rest in 7 patients showing ST depression (type I) and 4 showing ST elevation (type II) during the attack. In none of the 44 type I attacks and 29 type II attacks which were recorded did circulatory changes; the latter were different in the two groups. Type I attacks showed: a) a brief fall in arterial pressure, accompanied by b) a rise of right atrial and pulmonary wedge pressures and c) a decrease of cardiac output, right and left stroke work, the mean rate of systolic ejection, and indirect left ventricular pre-ejection dP/dt. In the course of the attack a hypertensive phase followed, which was paralleled by an increase of heart rate, cardiac output, left and right stroke work, and mean systolic ejection rate, left dP/dt; right atrial pressure and wedge pressure remained raised. All of the circulatory functions started to revert towards the pre-attack levels coincident with the waning phase of the electrocardiographic alteration, the latter occurring either spontaneously or after nitroglycerin. Type II attacks for the entire duration of the electrocardiographic changes showed: a) a reduction of arterial pressure, cardiac output, right and left stroke work, mean systolic ejection rate, and left dP/dt, b) a rise of right atrial and wedge pressures, and c) quite small changes of heart rate. When the electrocardiogram started to revert to the pre-attack aspect, the cardiac function rapidly improved and, after a supernormal phase, returned to the basal levels in about 2 minutes. It is concluded: 1) that no circulatory factor interfering with the mechanical effort of the heart is responsible for eliciting spontaneous angina: 2) that in type I attacks right and left ventricular impairment occurs which recovers rapidly, possibly through a sympathetic compensation; 3) that in type II attachs dysfunction of both sides of the heart occurs and persists throughout the episode of electrocardiographic alteration; 4) that the dynamic impairment is probably more severe in type I than in type II angina.

Angina Pectoris↗