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)

11 coronary patients, 8 with mild hypertension, were treated with clonidine, at a dose of 75 micrograms b.i.d. per os for a week. The effect of the drug on coronary heart disease was assessed by means of a symptom-limited multistage exercise test on the cycloergometer. Clonidine was effective in reducing the exercise-induced increases in blood pressure (by 15.5 +/- 6.1%), the double product (by 34.8 +/- 20.8%) and the electrocardiographic ischemic changes. In 2/4 patients, effort related ventricular extrasystoles were reduced by greater than 50% after clonidine. The drug worsened the anginal pain in 3 and relieved the pain in 3 patients. However, it reduced the exercise-induced ST-T segment downsloping in 7 patients. The tolerance was good, since only 3/11 patients reported slight dry mouth, sedation and pyrosis. In view of the electrocardiographic effect, further studies with clonidine on myocardial ischemia should be performed.
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PMID:The therapeutic value of clonidine in patients with coronary heart disease. 49 82

In patients with chest pain somatic pain (thoracic wall pain) has to be differentiated from visceral pain (organ pain). History and careful physical examination are diagnostic in most cases. Presented are rare and not well-known diseases like valvular aortic stenosis, idiopathic hypertrophic subaortic stenosis and the mitral valve prolapse syndrome. Not seldom they are masked by angina pectoris-like symptoms, although in general the coronary arteries are normal. In acute chest pain differential diagnostic considerations have to include lung embolism, acute pericarditis, spontaneous pneumothorax, acute dissecting aneurysm of the aorta and diseases of the gastrointestinal tract as well. Only after exclusion of any organic cause the diagnosis of "effort syndrome" may be made.
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PMID:[Chest pain: differential diagnosis in general practice]. 49 63

The early postprandial changes in 10 patients with angiographically proven coronary artery disease and history of postprandial angina were studied by the continuous recording on magnetic tape of the electrocardiogram and haemodynamic variables. The significant changes 20 minutes after a meal not followed by angina included increases in cardiac index and stroke index, with a decrease in systemic vascular resistance. When angina developed after a meal, there were significant increases in mean systemic arterial blood pressure, heart rate, pulmonary capillary wedge pressure, and systemic vascular resistance with decreases in stroke index at the onset of pain rather than at the onset of ischaemic electrocardiographic abnormalities. The first haemodynamic variable to change was pulmonary capillery wedge pressure which tended to increase coincident in time with the electrocardiographic abnormalities. In all cases, postprandial angina occurred within 25 minutes after a meal. In every instance, there was little or no change in the product of heart rate and systolic arterial blood pressure at the onset of the ischaemic electrocardiographic abnormalities at a time when the pulmonary capillary wedge pressure had begun to rise. Postprandial angina, like many cases of rest angina, may rise on the basis of a primary decrease in myocardial perfusion, the nature of which is unclear but merits further investigation.
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PMID:Haemodynamic and electrocardiographic accompaniments of resting postprandial angina. 50 70

Twenty-six patients underwent arterial counterpulsation for refractory heart failure without shock complicating acute myocardial infarction. Patients were divided into a group of 12 with continuing myocardial ischaemia, evidenced by anginal pain associated with abnormal ST segment elevation, and a group of 14 without continuing ischaemia. Clinical features (apart from pain) and prognostic indices were similar in the two groups when counterpulsation was started but short- and long-term results were different. Hospital survival was 92 per cent (11/12) and 43 per cent (6/14), respectively, in the groups with and without ischaemia and four-year survival was 73 per cent and 7 per cent. Counterpulsation is of greatest value in acute infarction when used to relieve myocardial ischaemia.
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PMID:Arterial counterpulsation in continuing myocardial ischaemia after acute myocardial infarction. 51 82

Cardiogenic shock and severe left ventricular failure after acute myocardial infarction, refractory angina pectoris at rest either of new onset or superimposed on stable angina pectoris, or occurring in the post infarct (less than 2 weeks) period, and the suspicion of a slowly evolving infarction are the main indications for intra-aortic balloon pumping at the Thoraxcenter. 76 patients were treated with intra-aortic balloon pumping for cardiogenic shock after acute myocardial infarction and left ventricular failure, 42/76 (55%) could be weaned, 9 (12%) died within 3 months, 33 (43%) survived over 3 months, to date 29 are alive. 42 patients with refractory angina at rest were treated with intra-aortic balloon pumping. Pain relief was prompt in 41 (98%), who subsequently underwent coronary artery bypass grafting. Total myocardial infarction rate was 11% (5/42), total mortality rate was 7%. Perioperative myocardial infarction rate was 8% (4/42) and perioperative mortality was 7% (3/42). Pain relief was prompt in 14/17 patients (82%) with post infarct refractory angina. In 3 patients pain persisted despite intra-aortic balloon pumping, all sustained a myocardial infarction, 1 died, 2 other patients were excluded for surgery. 12 patients underwent coronary artery bypass grafting, none died, none developed acute myocardial infarction, 3 have mild stable angina. In 8 patients a slowly evolving myocardial infarction was suspected. Pain relief was prompt in 7/8 (88%) after institution of intra-aortic balloon pumping. Intra-aortic balloon pumping improves prognosis in cardiogenic shock after myocardial infarction, and abolishes refractory ischemic pain.
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PMID:Intra-aortic balloon pumping in coronary artery disease. 52 Sep 98

The ECG is an indirect and non-specific test of myocardial ischemia, which means that the limits in respect to sensitivity and specificity must be evaluated. The dynamic Holter ECG is a useful method, particularly if pain appears during the recording time. The exercise test as an example of additional stress is of great general interest, especially in man; stress-testing is particularly useful in explaining the origin of atypical anginal pain. Hence the interpretation criteria must be closely followed rather than enlarged as long as the indication for diagnostic coronary-angiography is limited by the result of exercise testing. When other non-invasive methods are not readily available it should be possible to broaden the diagnostic criteria to increase sensitivity; by the same token, the number of false positive tests will be controlled by these complementary non-invasive methods.
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PMID:[Electrocardiographic manifestations of myocardial ischemia]. 53 52

18 patients with angina pectoris participated in a double blind trial with atenolol (100 mg and 200 mg once daily, or 100 mg twice daily) and propranolol (80 mg twice daily). The number of anginal attacks (NAP), the number of days free of pain (NAFT), consumption of sublingual nitroglycerin (NNT) and bicycle ergometry data (EFE) were recorded. Atenolol given in a dose of 100 g twice daily significantly reduced NAP and NNT as compared with the other dose schedules for atenolol and propranolol. There was, however, no difference between NAFT and EFE under any of the treatment schedules mentioned above. Only with 100 mg atenolol twice daily was it possible to reduce heart rate at rest and immediately after exercise testing, and also diastolic blood pressure (at rest, upright and after stress testing). In spite of the long plasma T 1/2 (= 24 hours) reported by others, atenolol given twice daily seems to be the most effective schedule. It is concluded that atenolol (100 mg twice daily) has a more potent anti-anginal effect than propranolol (80 mg twice daily). In addition, atenolol has the advantage of being cardioselective.
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PMID:[Atenolol in the treatment of angina pectoris]. 53 63

The person who has asymptomatic myocardial ischemia is at high risk because he does not have the benefit of the warning signals afforded by the substernal pain that tells most patients with angina to stop what they are doing.
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PMID:Prevention of heart disease in the normal subject with a positive exercise test. 58 14

The haemodynamic effects of distending the small intestine (with a balloon in the lumen) were examined in cats anaesthetised with chloralose. Particular attention was paid to blood flow changes in localised areas of the left ventricular wall (as assessed using the heated thermocouple technique). Intestinal distension led to an increase in systemic blood pressure but usually to a reduction in myocardial blood flow; no cardiac dysrhythmias were observed. When the effect of increased systemic (perfusion) pressure on blood flow was eliminated (using partial correlation coefficients) flow then bore a negative relationship to intestinal pressure, probably indicating constriction of the myocardial blood vessles. This may indicate that distension of hollow organs can lead to a visceral-cardiac reflex. The resulting coronary vasospasm might be one cause of pain in certain patients with angina pectoris.
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PMID:The effects of distension of the small intestine on myocardial blood flow in anaesthetised cats: possible relevance to coronary vasospasm. 58 99

The effect of nifedipine on effort angina was investigated by means of exercise tests with bycicle ergometer and compared, in the same patients, with the effects of a nitroderivative and a betablocking agent. Five patients with stable effort angina entered the study, after an hemodynamic and contrasto-graphic control. According to the protocol of a latin square 5 X 5, all the patients received in a random sequence the following treatments: placebo, 1 c. orally; isosorbide dinitrate, 5 mg sublingually; propranolol, 40 mg orally; nifedipine, 10 mg sublingually; nifedipine, 10 mg orally. No significant change of any of the considered parameters was observed after the placebo. Isosorbide dinitrate and nifedipine produced significant increases of the duration of work before appearance of pain and EKG positivity, and of total work performed before anginal pain. Only the duration of work before EKG positivity was improved by propranolol. The comparisons between treatments showed no significant difference of the effects of the administered doses of isosorbide dinitrate and nifedipine. The improvements observed after propranolol were significantly lower than that observed after isosorbide dinitrate and oral nifedipine. On the basis of the observed changes of cardiac rate, maximal arterial pressure, ejection time index and triple product, the authors evaluate the possible mechanism of action of nifedipine.
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PMID:[Effectiveness of nifedipine on exercise tolerance in patients with angina pectoris. Comparison with a nitroderivative and a beta-blocking agent]. 59 35


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