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At least 19 recordsLinked to original sources
PubMed1992

Double-blind trial of aspirin in primary prevention of myocardial infarction in patients with stable chronic angina pectoris. The Swedish Angina Pectoris Aspirin Trial (SAPAT) Group.

Clinical trials have demonstrated a prophylactic role for aspirin in myocardial infarction and in unstable angina pectoris. The Swedish Angina Pectoris Aspirin Trial (SAPAT) is the first prospective study of aspirin in stable angina. 2035 patients were randomised double-blind to treatment with aspirin 75 mg daily or placebo. All patients were treated with sotalol for control of symptoms. The median duration of follow-up was 50 months. Compared with the placebo+sotalol group, the aspirin+sotalol group had a 34% (81 vs 124 patients) reduction in primary outcome events (myocardial infarction and sudden death; 95% confidence interval 24-49%; p = 0.003) and the reduction observed in secondary outcome events (vascular events, vascular death, all cause mortality, stroke) ranged from 22% to 32%. Treatment withdrawal caused by adverse events occurred in 109 patients in the aspirin+sotalol group and 100 in patients in the placebo+sotalol group; major bleeds, including haemorrhagic stroke, occurred in 20 and 13 patients, respectively (not significant). The addition of a low dose of aspirin to sotalol treatment showed significant benefit in terms of cardiovascular events, including a significant reduction in the incidence of first myocardial infarction in patients with symptoms of stable angina pectoris.

Aged↗
PubMed1978

Haemodynamic effects on the myocardial blood flow supply/oxygen demand ratio in pacing induced angina pectoris.

Angina pectoris results from an imbalance between oxygen supply and demand in the subendocardium. The haemodynamic effects contributing to this imbalance have been studied in 10 patients with coronary artery disease. Myocardial oxygen demand was estimated from the tension time index (TTI), potential subendocardial flow from a diastolic pressure time index (DPTI), and the oxygen supply/demand ratio from (DPTI/TTI. With progressively increasing pacing rates up until induction of angina, no significant change in TTI was found whereas a significant fall in DPTI and DPTI/TTI occurred (P less than 0.001). During pacing runs with induction of angina DPTI/TTI reached a minimum value 5 s before,and at the onset of angina. No such relationship was seen for TTI or DPTI alone. A significant rise in LVEDP (P less than 0.05) and fall in dP/dt min (P less than 0.01) occurred at angina both contributing to a further reduction in DPTI and DPTI/TTI. Changes in DPTI/TTI may then reflect changes in the myocardial blood flow supply/oxygen demand ratio in the presence of coronary artery disease and haemodynamic changes before and at the induction of angina lead to a further reduction of this ratio.

Angina Pectoris↗
PubMed1976

The medical treatment of angina pectoris.

Angina pectoris is a subjective symptom recognized primarily by a careful history. It must be differentiated from nonatherosclerotic chest pain. Arteriography should be performed when the diagnosis is in doubt or when the stable from becomes unstable. Management must include: attention to risk factors; awareness of precipitating factors; treatment of other illnesses such as hypertension and diabetes, and the use of drugs: nitroglycerin and, for long-term therapy, propranolol. If this regimen fails, patients should be considered for surgery.

Adult↗
PubMed1976

Clinical analysis of angina pectoris and angina-like pain --With special reference to ECG during attack, "cervical spondylosis" and selective coronary arteriography.

In a series of 63 patients, 60 with angina pectoris and 3 with cervical spondylosis and "thoracic spondylosis" showing angina like pain detailed assessments were made of the mode of onset of attack, including electrocardiography during attacks, X-ray examination of the thoracic and cervical vertebrae and neurological examinations, along with coronary arteriography in some cases, with the following results: 1. The cases of angina pectoris were classifiable grossly into two groups according to mode of onset of chest pain: Group A: Angina began with pain in the anterior chest (39 cases); Group B: Angina in the anterior chest was preceded by "pain" occurred elsewhere in the chest (21 cases). The cases in group B were further classified under two categories, types BI and BII, the former being characterized by a sudden onset of "pain" in a somatic area or areas other than the anterior chest where there is usually no dysesthesia, followed by development of retrosternal or precordial pain (6 cases), while the latter type of angina began with paroxysmal exacerbation of preexistent dysesthesia in the nape, shoulder and arms and eventuated in pain in the anterior chest (15 cases). There were two subtypes in the type BII angina viz. types BIIa and BIIb. There was no ECG evidence of ischemic changes at exacerbation of the nucha-omo-brachial dysesthesia in type BIIa while significant ischemic ECG changes were evident in association of aggravation of dysesthesia in the type BIIb patients. 2. Concomitant "cervical spondylosis" with radiographic evidence of abnormalities in cervical vertebrae and associated subjective symptoms accounted for 22.9% of group A and for 71.4% of group B. In no case of type BI was there evidence of such complication whilst all the cases of type BII had this complication. 3. The mode of appearance of pain in patients with cervical spondylosis showing angina like pain resembled to that of angina pectoris in type BII but ECG during attack did not reveal any significant ischemic changes. 4. As for interrelation between findings by selective coronary angiography (26 cases of angina pectoris) and complication of "cervical spondylosis", the complication of "cervical spondylosis" was higher in incidence in the group of cases with low-grade coronary arterial changes (degree of occlusion less than 50%) than in the group with greater arterial changes (degree of occlusion over 50%). The findings described suggest the possibility that the mode of manifestation of anginal attack may be modified by the concomitant presence of "cervical spondylosis".

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↗
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↗
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↗
PubMed1976

Unstable angina pectoris.

Unstable angina is a syndrome which comprises a spectrum of symptomatic manifestations of coronary artery disease which lies between stable angina pectoris and acute myocardial infarction. Patients fall into three groups: angina of recent onset (4 weeks), angina of changing pattern, and angina occurring at rest (longer than 15 minutes). The syndrome may presage acute myocardial infarction or sudden death, or may itself be the manifestation of a myocardial infarction. The pathophysiology may involve primary cardiac events or extracardiac precipitating factors, and does not appear to be the consequence of a particular anatomic pattern of coronary artery disease. Pain may occur as a result of regional reduction of coronary flow to pressure-dependent areas of myocardium during states of increased myocardial oxygen demand. Persisting ischemia leads to infarction via a series of events which may include myocardial edema formation, increased beta-sympathetic tone, and others which have been experimentally modified by interventions designed to limit infarct size. Although the incidence of acute myocardial infarction and death was high in early studies, in recent reports acute infarction occurs in under 15.5 per cent and death in under 2 per cent. Patients at high risk are those pain persists with bed rest, and those with preceding stable angina pectoris or myocardial infarction. Prognostic differences among Groups 1, 2, and 3 may exist but cannot be assessed from available studies. Studies of the management of unstable angina have generally been uncontrolled. Hospitalization, bed rest, and short- and long-acting nitrates are generally employed in Groups 2 and 3 patients and the marked reduction in myocardial infarction rates from early to recent studies tends to support these approaches. Anticoagulants are less used now than formerly. Propranolol can produce a significant reduction of myocardial oxygen consumption and may redirect coronary flow to ischemic areas. The drug has effectively controlled pain in several studies and is now widely used to manage unstable angina. Aortocoronary bypass surgery has been extensively employed but there is only one preliminary report of a controlled study available. The role of surgery is not yet defined. The optimal approach to therapy may eventually involve the use of medical therapy, including beta-blockade to stabilize patients, with delayed semielective coronary angiography and surgery in those who respond. Emergency angiography and surgery might then be reserved for the high-risk group of patients whose pain persists during optimal medical therapy.

Angina Pectoris↗
PubMed1992

Treatment of unstable angina pectoris.

Unstable angina pectoris may be manifested as new-onset angina, a change in the anginal pattern, pain at rest with associated electrocardiographic (ECG) changes, or postinfarction angina. Of these, pain at rest with ischemic ECG changes is known to be associated with the poorest prognosis. The pathogenesis of unstable angina pectoris involves a combination of a fixed atherosclerotic obstruction and a dynamic component related to coronary vasoconstriction, thrombus formation, or both. Long-acting nitrates, inhibitors of platelet aggregation, beta blockers, and calcium antagonists are among the agents that have been shown to be effective in the medical management of unstable angina. A study now in progress is evaluating the routine use of thrombolytic therapy for this indication. Although alleviation of symptoms and prevention of death and myocardial infarction are important therapeutic goals, the overall efficacy of a particular medical therapy can best be assessed by objective evaluation of its ability to control ischemia, using such techniques as exercise scintigraphy and ambulatory ECG monitoring. Cardiac catheterization and revascularization are indicated for patients with unstable angina who continue to experience symptoms or who show evidence of silent ischemia despite medical therapy. A study is under way to determine the advisability of routine revascularization of such patients. Revascularization will provide symptomatic relief in most patients with unstable angina and may prolong survival and improve left ventricular function in certain subsets.

Angina, Unstable↗
PubMed1992

The relationship between hemostatic tests and cardiovascular risk factors in patients with angina pectoris. European Concerted Action on Thrombosis and Disabilities (ECAT) Angina Pectoris Group.

Baseline data are presented of the ECAT Angina Pectoris Study. Both plasminogen activator inhibitor and fibrinogen were positively associated with a number of cardiovascular risk factors such as smoking, body mass index, and also with the presence of coronary stenosis. Results indicate a role of the hemostatic system in the progress of coronary arteriosclerosis.

Angina Pectoris↗
PubMed1992

Role of nitrates in unstable angina pectoris.

Unstable angina pectoris is a clinically heterogeneous process with patient symptoms varying between reduced threshold for exertional angina and the occurrence of multiple episodes of rest pain. The major factors in the pathogenesis of unstable angina appear to be intracoronary platelet aggregation and thrombus formation secondary to fissuring or rupture of atheromatous plaques, with associated coronary vasoconstriction due to release of constrictor materials from aggregating platelets and deficiency of endothelium-related vasodilator activity. The latter factor is of particular interest in view of the similar biochemical mechanisms of action of nitroglycerin (NTG) and endothelium-derived relaxing factor (EDRF). The efficacy of NTG in limiting platelet aggregation is also of particular interest in this condition. Medical therapy in patients with unstable angina usually requires use of multiple agents. In the short term, there is a strong case for the use of intravenous heparin both to relieve pain and to reduce the risk of acute myocardial infarction. Aspirin is perhaps less effective in the short term, but very useful in long-term treatment of such patients. Despite their widespread clinical use, beta-adrenoceptor antagonists are probably only marginally beneficial, whereas dihydropyridine calcium antagonists such as nifedipine are potentially harmful as monotherapy and of questionable use in combination with other drugs. Other agents that are effective in relieving ischemic symptoms are the nondihydropyridine calcium antagonists verapamil and diltiazem and the oxygen-sparing agent perhexiline maleate. Despite a paucity of controlled trial data, nitrates are used in the vast majority of patients with unstable angina.

Acetylcysteine↗
PubMed1977

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.

Adult↗