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PubMed1980

Nocturnal angina pectoris. Comparison between angina with ST segment elevation and depression documented by continuous orthogonal ECG recording.

In 30 patients with nocturnal angina, the night-time ECGs were continuously recorded, and the time and duration of attack, cyclic character of attacks, the relation of chest pain to ischemic ECG changes and arrhythmias during attack were compared between 18 cases with ST elevation and 12 cases with ST depression during attack. In cases with ST elevation, 1) attacks occurred between 2:00 and 8:00 a.m., being most frequent between 4:00 and 5:00 a.m. 2) the duration of attack measured from the duration of ischemic ECG changes was less than 5 min in 88% of the attacks, 3) the attack often recurred with intervals less than 30 min and ECG changes were often unaccompanied bt chest pain, 4) the attack was complicated with various kinds of arrhythmias. These features were in marked contrast to the cases with ST depression, in which attacks were evenly distributed over the night-time, of longer duration, sporadic in occurrence and far less complicated with arrhythmias. These data suggest that the difference of mechanisms causing attacks between both groups.

Adult↗
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↗
PubMed2000

Sexual intercourse and stable angina pectoris.

Stable angina pectoris is a common condition associated with chest pain predictable for a given level of exercise. Sexual intercourse does not lead to exaggerated heart rate or blood pressure responses and is interpreted by the heart as one of many forms of activity that may take place in a 24-hour period. Stable angina patients optimally treated are not at significantly increased cardiovascular risk during sexual intercourse. Erectile dysfunction (ED) increases with age and shares similar cardiovascular risk factors with stable angina. Sildenafil citrate can be safely prescribed for stable patients with ED providing they are not taking oral, topical, or sublingual nitrates. Sexual relationships should not be constrained by the diagnosis of angina pectoris provided appropriate medical advice is given on risk status. Family physicians and specialists are able to provide this advice based on their knowledge of the patient and the social circumstances. Impersonal advice is potentially dangerous and should be vigorously discouraged.

Angina Pectoris↗
PubMed1991

[Simultaneous measurement of end-diastolic pressure in the left ventricle and transmitral flow before and after nitroglycerin in patients with angina pectoris].

In angina pectoris, left ventricular diastolic function evaluated by end-diastolic pressure (LVEDP) on catheterization and transmitral flow (TMF) on Doppler echocardiography is abnormal. As a parameter describing TMF, the ratio between peak flow velocities of the two filling phases in diastole (PE/PA) can be used. We examined 22 patients with angina pectoris and measured LVEDP and PE/PA simultaneously and found positive correlation (r = 0.60). Nitroglycerin (0.8 mg sublingually) reduced LVEDP and PE/PA significantly, and correlation between reductions was positive (r = 0.52). None of the correlation analyses permitted LVEDP to be calculated from PE/PA, but Doppler echocardiography and TMF will probably be used increasingly in evaluation of ischemic heart disease with medical intervention.

Adult↗
PubMed2001

Trimetazidine for stable angina pectoris.

Stable angina pectoris, a symptom of coronary heart disease (CHD), manifests as stress-induced ischaemic episodes resulting in severe chest pain. Therapeutic aims are to improve quality of life by decreasing anginal attacks and to prevent myocardial infarction (MI) and death. Current anginal medications include beta-blockers and calcium antagonists, which decrease ischaemic severity by reducing cardiac workload, and nitrates, which increase coronary blood flow. A new therapeutic approach is the use of metabolic agents, such as trimetazidine, which are cytoprotective during ischaemia. Results of several clinical trials demonstrated that trimetazidine, at the standard dose of 20 mg t.i.d., increased exercise capacity, decreased anginal incidence and decreased left-ventricular (LV) dysfunction compared to placebo. Trimetazidine was also as effective as propranolol (120 - 160 mg/day) and nifedipine (40 mg/day) in decreasing anginal episodes and improving exercise parameters. Trimetazidine improved anginal frequency and symptoms in patients in which treatment with diltiazem, nifedipine, propranolol, pindolol, oxprenolol or long-acting nitrates had failed. Trimetazidine was also more effective than isosorbide dinitrate (30 mg/day) as an adjunct to propranolol. Despite efficacy being equivalent to that of beta-blockers and calcium antagonists, trimetazidine does not depress cardiac function and, correspondingly, is not contraindicated in any condition. Adverse effects of trimetazidine are mild and infrequent. In summary, clinical data indicate that trimetazidine is a safe, effective treatment for the symptoms of stable angina pectoris when used either as a monotherapy or an adjunctive therapy. Longer-term trials are necessary to determine whether trimetazidine will be effective in reducing rates of mortality and MI.

Adrenergic beta-Antagonists↗
PubMed1987

The sensitivity of the symptom angina pectoris as a marker of transient myocardial ischaemia in chronic stable angina pectoris.

Therapeutic decisions in patients with angina pectoris are traditionally based on the history reported by the patient, since objective evidence of myocardial ischaemia during daily life is often not available. In this study, ambulatory ST segment monitoring was performed in 60 patients with a history of chronic stable angina pectoris, positive exercise test and/or positive coronary angiography, and a correlation was made between the episodes of chest pain and ST segment change. The patients were grouped according to the results of exercise testing and coronary arteriography, and one group was studied with and without antianginal medication. Overall, 195 episodes of angina were noted, only 94 of which (48%) were accompanied by ST segment depression. Pain and ST segment changes were best correlated in patients with a positive exercise test, positive angiography and who were not receiving antianginal medication. In 101 episodes of chest pain, ST segment change could not be identified; in 18 (18%) there was sinus tachycardia, in 12 (12%) ventricular premature beats, and in 71 (70%) sinus rhythm solely. Thus, anginal pain appears not to be the reliable indicator of transient myocardial ischaemia as was previously thought, a finding which supports the use of objective methods in identifying episodes of transient myocardial ischaemia in daily life.

Adult↗
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↗
PubMed1991

Integration of anticoagulation, thrombolysis and coronary angioplasty for unstable angina pectoris.

Unstable angina pectoris remains a challenging acute ischemic syndrome to treat despite recent randomized trials that confirm the benefit of intravenous heparin. Coronary angioplasty, which is often required to treat the underlying arterial lesion, is adversely affected by the presence of thrombus with at least a 2-fold increase in abrupt closure. Four studies with heparin treatment prior to angioplasty indicate a reduction of abrupt vessel closure from 8-33% to 0-6% with apparent reduction of morbidity; no controlled trials are thus far available for heparin pretreatment. Another therapeutic alternative, thrombolytic therapy, has had quite equivocal results with several negative small studies. When angioplasty has been performed with thrombolytic therapy, a nonfibrin-specific plasminogen activator appears to be preferable. Newer studies that focus on thrombin inhibitors that bind to clot-bound thrombin and potent antiplatelet agents are in the early phase of clinical investigation. This review offers current recommendations for the integration of heparin, thrombolysis, and coronary angioplasty for unstable angina pectoris.

Angina, Unstable↗
PubMed1983

Platelet aggregation studies in patients with angina pectoris--relationships to types of angina and coronary pathoanatomy.

Platelet aggregation was studied in patients with angina pectoris in whom coronary sclerosis was found by arteriography. The subjects consisted of 20 patients with stable angina pectoris, 12 with unstable angina pectoris and 4 with variant form of angina pectoris. Fifteen healthy subjects served as controls. ADP- and collagen-induced platelet aggregations were estimated during resting conditions before and immediately after an exercise test. In patients with unstable angina pectoris, ADP-induced as well as collagen-induced platelet aggregations during resting conditions were significantly less than those in normal subjects. After exercise, however, they significantly increased. In stable angina pectoris, they did not differ from those in the control group and their responses to exercise were also not significant. In general, platelet aggregation during resting conditions was accelerated in relation to an increase in the number of coronary arteries involved. The results demonstrate that examination of platelet aggregation during resting conditions and following exercise aids in a more accurate evaluation of the types and the stages of patients with angina pectoris.

Adult↗
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↗
PubMed1995

[Analysis of heart rhythm variability in evaluation of treatment for unstable angina pectoris].

Unstable angina pectoris is accompanied by several unfavourable autonomic disturbances. A noninvasive assessment of the autonomic cardiac control is possible by means of heart rate variability analysis (HRV). 26 patients with unstable angina pectoris were enrolled in the study. All patients received obligatory nitroglycerin and heparin intravenously within two days, and gallopamil (G) or metoprolol (M) together with aspirin or ticlopidine orally randomly, which were continued for 3 month or shorter if coronary revascularization was earlier performed. 512 R-R intervals was registered in each patient at 7th day of hospitalization and in 14th at the time of admission. Kardioassist v.1.0 system was used for heart rate variability analysis. After analog to digital conversion, with 12 bit resolution and 1000 Hz of sampling rate, seriogram of R-R intervals was obtained, and then power spectrum density was computed with the Fast Fourier Transform. Time-domain analysis provided mean (basic) R-R interval (BCL) and its standard deviation (SD-RR). In frequency-domain the following spectral variables were analysed: power spectral density (s2/Hz) of the high frequency component (aHF, 0.15-035 Hz), low frequency component (aLF, 0.05-0.15 Hz) and very low frequency component (aVLF, 0.004-0.05 Hz), percentage power of respective components (%HF, %LF and %VLF) and autonomic balance indices: aLF:aHF and %LF:%HF. These variables were compared in patients treated with G (13 patients) against those with M (13 patients). Additionally, the effects of treatment regimen was evaluated also in 14 patients, in whom HRV analysis was performed at admission and 7 days later.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Haemostasis factors in angina pectoris; relation to gender, age and acute-phase reaction. Results of the ECAT Angina Pectoris Study Group.

The ECAT Angina Pectoris Study is a European multicentre study with the aim of investigating the pathogenetic and predictive role of haemostatic factors in the progression of coronary heart disease. It is the largest study performed up to now with regard to both the number of patients with angina pectoris (n = 3043) and the number of haemostasis assays (n = 23) included. The present paper presents baseline cross-sectional data with particular reference to the relationship of haemostatic factors with each other and with the coronary risk factors age, gender and acute-phase reaction (1). Two clusters of haemostatic factors could be distinguished in which each variable was correlated (P < 0.001) to every other variable: (a) Eight fibrinolysis assays including t-PA, PAI-1 and euglobulin clot lysis time (ECLT), for which PAI-1 appeared to be the dominating factor; (b) antithrombin III, protein C, alpha 2-antiplasmin and plasminogen, the interdependence of which has no obvious explanation. (2). Twelve out of the 23 haemostasis assays were associated (P < or = 0.01) with age. Except for alpha 2-antiplasmin, these relationships indicated an increased tendency to thrombosis with increasing age. (3). Gender differences found in 14 haemostasis parameters do not indicate a consistent difference in the tendency to thrombosis between men and women. Eight haemostasis parameters were on average higher in female than in male patients in the age group over 50 years. (4). C-reactive protein, an acute-phase reactant, was positively correlated (P < 0.001) with fibrinogen, factor VIIIc, von Willebrand factor, the fibrinolysis assays t-PA, PAI-1, ECLT and plasminogen.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute-Phase Reaction↗