Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:The variant form of angina pectoris. 76 70

In 14 of 204 consecutive cadaveric renal allograft recipients, the primary diagnosis was essential hypertension. Four patients had manifest ischemic heart disease before transplantation. Three of these patients died within 31 months of transplantation from recurrent myocardial infarction, and the fourth experienced coronary insufficiency. Cadaveric renal transplantation does not prevent the progression of coronary artery disease in patients whose renal failure was due to essential hypertension. In the presence of angina or previous myocardial infarction, these patiemts may be better treated by maintenance hemodialysis.
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PMID:Renal transplantation. Effect on the ischemic heart disease of essential malignant hypertension. 77 41

The cardiovascular system of aging people exhibits a number of morphological, functional and clinical special features. Alterations in shape, size and weight of the heart, alterations of coronary arteries, valves and aorta are accompanied by typical changes in several hemodynamics variables. The result is a diminution of the adaptation capacity to physical exertion and increased incidence of failure. However, heart failure cannot be regarded as a physiological process; it is caused by a coincidence of an increasing polypathy of the aging heart (coronary artery disease, arteriosclerosis, hypertrophy, valve-changes,disseminated degenerative changes) and the polypathy or multimorbidity of the whole aging organism. In advanced age the various forms of ischaemic heart disease (angina pectoris, infarction, failure, arrhythmias) show increasingly atypical courses, complications and a higher degree of mortality. Modern therapeutic measures like demand pacemakers or bypass operations are principally applicable. Our study of now 326 patients of very high age shows that the good state of their cardiovascular system (probably genetically determined) is mainly responsible for reaching high age.
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PMID:[The so-called aging heart in 50- to 100-year-old subjects]. 79

Although hypertension is an acknowledged risk factor in ischaemic heart disease (IHD) the question remains whether antihypertensive therapy is necessarily beneficial. A priori, because coronary atherosclerosis is probably irreversible, the time for effective intervention would seem to be well before the development of clinical manifestations. The Australian National Blood Pressure Study, a long term clinical trial of the treatment of mild hypertension, is in principle better suited than previous trials to answer the question because the trial population selected (4000 subjects aged 30-69) contains substantial proportions of younger age groups (26% below 45) and of females (37%) and none had manifest IHD at entry. Sensitivity to the emergence of IHD in the trial population is increased by including as diagnostic indices angina and ischaemic ECG changes, using suitably objective methods, as well as myocardial infarction and sudden death. Thus morbidity and mortality from IHD which currently accounts for 71% of trial end points (cf 19% for stroke) will effectively determine the outcome of the trial. The occurrence of a substantial proportion of subjects withdrawn from randomised treatment will mean that the question will be answered necessarily in two ways: firstly in respect of those subjects remaining on their assigned treatments and secondly in terms of all subjects initially assigned one treatment or other irrespective of the subsequent need to change treatment on ethical grounds or of the degree of compliance.
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PMID:The Australian National Blood Pressure Study: a test of the effectiveness of antihypertensive therapy on the incidence of ischaemic heart disease. 79 27

Twenty patients with ischemic heart disease documented by coronary angiograms or ST segment depression in the ECG during treadmill walking, were administered sublingual nitroglycerin 0.3 to 0.6 mg on one occasion and a chewable form of isosorbide dinitrate 5 mg on another occasion during treadmill walking when anginal discomfort was definitely present at a mild degree of intensity. Despite continued walking at a constant speed and grade, angina was relieved in all patients, completely in most patients, partially in a few. The average time from administration of the medication to onset to relief was 74.7 seconds for nitroglycerin and 107.6 seconds for chewable isosorbide dinitrate. Average time to complete relief or maximal incomplete relief was 190.3 seconds for nitroglycerin and 315.1 seconds for chewable isosorbide dinitrate. Ischemic electrocardiographic changes were reverted toward normal by nitroglycerin in 13 subjects and by isosorbide dinitrate in 15. The differences in onset to complete relief were all statistically significant indicating that nitroglycerin is more rapid in its action than is chewable isosorbide dinitrate.
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PMID:Effectiveness of isosorbide dinitrate and nitroglycerin in relieving angina pectoris during uninterrupted exercise. 80 37

In 10 patients without and 20 patients with various degrees of angiographically proven CAD 93 pacing runs were studied. Changes of PAm, of ECG, and of anginal pain serving as parameters of myocardial ischemia were correlated to the rate-pressure-product. In patients without CAD no correlations could be ascertained. In each patient with CAD determination of ischemia was achieved reproducibly. Ischemia threshold is represented by a sharp increase of PAm. Ischemia threshold seems a parameter to be preferred as compared to pain threshold. The extent of CAD (angiographically estimated) correlates well with the pacing test especially when collaterals are taken into account. After NG no substantial improvement of ischemia can be detected: Ischemia threshold before and after NG was reached at same rate pressure in each case. We conclude the atrial pacing test to be an excellent test for the provocation of myocardial ischemia. The test is also useful for estimation of the extent of CAD.
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PMID:Pacing-induced myocardial ischemia in spite of nitroglycerin. Correlations regarding the extent of coronary artery disease. 80 82

Despite widespread clinical application of propranolol (P) in angina pectoris, convincing evidence of its efficacy has been incomplete, thereby resulting in continued controversy. Its antianginal effectivess was investigated in 20 patients with documented coronary heart disease in a 44-wk study incorporating a prolonged 12-wk lead-in period, individualization of P dosage in a 6-wk dose-finding period, and a 24-wk doule-blind crossover phase. On double-blind placebo, patients had 10.5 +/- 2.1 anginal attacks and consumed 12.8 +/- 3.0 nitroglycerin tablets (NTG) each week compared to 6.6 +/- 1.5 anginal episodes (- 37%, p less than 0.001) and 8.0 +/- 1.7 NTG (-38%, p less than 0.001) when on P. No patient experienced more angina with P than with placebo. In addition, time to onset of chest pain during treadmill exercise was prolonged by P from 190 +/- 16 to 248 +/- 22 sec (+31%, p less than 0.02) and ST depression was reduced from 1.7 +/- 0.21 to 0.99 +/- 0.18 mm (-42%, p less than 0.05). There was correlation (r = 0.64 p less than 0.01) between per cent declines in anginal frequency and resting double product with P. Thus, propranolol favorably altered several indices of myocardial ischemia in severe coronary heart disease. This investigation clearly documents the clinical efficacy of optimal beta adrenergic blockade in coronary disease and provides objective justification for the judicious application of propranolol in treatment of angina pectoris.
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PMID:Efficacy of beta adrenergic blockade in coronary heart disease: propranolol in angina pectoris. 81 Feb 95

A 40-year-old man with severe angina had electrocardiographic changes typical of Prinzmetal angina during his attacks of chest pain. ST segment elevations in leads II, III, and aVF occurred intermittently with elevations in leads I and aVL, and with T wave flattening in V1, suggesting myocardial ischemia in areas supplied by the right coronary artery and by the circumflex branch of the left coronary artery. However, the coronary arteries appeared normal when arteriograms were made, suggesting that a reversible event caused the attacks.
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PMID:Prinzmetal angina. Normal arteries and multifocal electrocardiographic changes. 81 19

The long-term efficacy of lidoflazine was investigated in 40 patients with a longer history of angina pectoris and well-documented ischemic heart disease over a whole range of 18 months in double-blind technique. Significant improvement occurs to frequency and severity of angina pectoris, related to reduction in consumption of nitro-compounds and in the extent of ST-segmental depression under resting and cycloergometric test conditions. Increase in cardiac work capacity is evident. There are no changes in heart rate, blood pressure and AV-interval in the ECG. The mode of action of lidoflazine may be an increase in the formation of coronary collaterals, whereas its acute vasodilating properties, experimentally verified in the dog, does not play any important part in the treatment of human coronary insufficiency. The introduction of lidoflazine in the treatment of coronary heart disease appears to be justified as an additive medication.
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PMID:[Efficacy of lidoflazine in angina pectoris. A long-term double-blind study]. 81 96

In patients with ischemic heart disease the evaluation of regional myocardial perfusion by 133Xenon intracoronary injection using a gamma camera computer system allows the detection of regional alterations of myocardial perfusion. While at rest a minority of the patients studied shows large alterations, during pacing induced angina a severe reduction of regional myocardial perfusion can be evidenced both in initial distribution scintigrams, when the injection is performed during angina, and on the washout curves when angina is induced immediately after the injection, during the course of the washout.
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PMID:Methods for the study of regional myocardial perfusion in patients with atherosclerotic coronary artery disease: findings at rest after nitroglycerin and during angina pectoris. 81 88


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