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)

A case is reported of the variant form of Prinzmetal angina, occurring two months after effort angina, in which the electrocardiogram revealed a Q wave in V2 in addition to ST segment elevation in precordial leads all of which disappeared in a few minutes. Several hours later, the ECG changes were suggestive of antero-septal infarction. However, four days later an R wave was present in lead V2, and 12 days after the acute episode, the tracing became entirely normal. Cinecoronary angiography revealed severe obstruction of the anterior descending artery, and a moderate obstruction of the left circumflex artery. The possibilities of spasm and/or coronary thrombosis, of spontaneous recanalization and of reperfusion due to thrombolysis are discussed, in addition to interpreting the abnormal Q waves as presumably due to severe myocardial ischemia resulting from acute coronary insufficiency. The present case exemplifies the concept that the syndromes of acute coronary heart disease cannot always be precisely differentiated, since they often overlap and are difficult to identify.
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PMID:[Unstable angina, Prinzmetal's variant and transient Q waves. Report of a case]. 259 1

During ergonovine-induced vasospastic angina, U wave inversion without significant ST segment deviation on the precordial electrocardiograms was documented in four patients. Coronary angiography revealed incomplete spastic obstruction of the left anterior descending artery without delayed filling and runoff in three patients. In the remaining patient, the proximal left anterior descending artery was totally occluded and there were well-developed collaterals from the non-spastic artery. Thus, ergonovine-induced U wave inversion was related to the presence of coronary vasospasm, and angiography demonstrated less severe myocardial ischemia in such patients than in cases with ST segment elevation or depression, which is usually associated with subtotal or total obstruction of a major coronary artery without adequate collaterals. In their clinical courses, two patients had episodes of angina with ST segment elevations or depressions. It was suggested that vasospastic angina with U wave inversion alone is one aspect of a continuous spectrum of vasospastic myocardial ischemia.
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PMID:[Coronary angiography in patients with U wave inversion during coronary artery spasm]. 264 70

The primary purpose of the present study was to evaluate the role of lipid and glucose metabolism in vasospastic angina. A group of 93 patients in whom the presence of ischemic heart disease was suggested, were classified into the control (C) group, consisting of 30 patients; the coronary artery disease (CAD) group, consisting of 47 patients; and the vasospastic angina (VSA) group, consisting of 16 patients. Among these three groups, age, total cholesterol (TC), triglyceride (TG), HDL-cholesterol (HDL-C), atherogenic index (AI), apolipoproteins and the prevalence of diabetes mellitus were compared. No age difference was seen among the three groups. The TC was the highest in the CAD group, followed by the VSA and C groups. A significant difference in TC was noted between the C and CAD groups and the C and VSA groups. TG levels were higher in the CAD group than in the C and VSA groups, without a significant difference among the three groups. The AI was significantly higher in the CAD group than in the C and VSA groups. No significant difference was noted in the prevalence of diabetes mellitus among the three groups. Apolipoprotein A-I (apo A-I) levels were higher in the VSA group than in the C and CAD groups, and the difference between the VSA and CAD groups was significant. Apolipoprotein A-II (apo A-II) levels were significantly higher in the VSA group than in the C and CAD groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Study on lipid and glucose metabolism in patients with vasospastic angina. 266 90

Calcium antagonists are often prescribed for treatment of ischemic heart disease. Therapeutic activity is achieved by reducing myocardial oxygen requirements and by increasing blood supply in ischemic heart disease associated with coronary artery spasms. The efficacy of calcium antagonists depends on the type and clinical presentation of ischemic heart disease: (1) in vasospastic angina (variant angina, short episodes of angina at rest), first-line therapy with calcium antagonists will reduce the number of ischemic episodes and improve long-term prognosis. (2) In effort angina the efficacy of calcium antagonists is comparable with that of beta blockers. (3) In unstable angina the use of calcium antagonists is controversial. Large-scale studies with nifedipine showed no benefit when it was given alone but an additive effect in patients pretreated with beta blockers. In contrast, diltiazem and verapamil appear to have comparable efficacy to beta blockers in patients with unstable angina. (4) After myocardial infarction the results of treatment with calcium antagonists have been disappointing. Nifedipine and verapamil did not reduce mortality or the incidence of reinfarction. In one study diltiazem significantly reduced the rate of reinfarction in patients who had had a non-Q wave infarction, but in a recent large-scale multicenter trial it had no effect on mortality and cardiac events in patients with evidence of both Q- and non-Q wave infarctions. Other secondary preventative measures against reinfarction, such as the use of beta-blockers and aspirin, appear to be more effective than calcium antagonists. The most frequently prescribed calcium antagonists, verapamil, diltiazem, and nifedipine, each of which represents a different chemical class, have in general similar efficacy in vasospastic and effort angina. Their different pharmacologic profile, such as the slowing of heart rate with verapamil or diltiazem and a more marked vasodilatation with nifedipine and other dihydropyridines, may become clinically relevant in individual patients. The new dihydropyridine derivatives have a pharmacologic profile comparable to that of nifedipine but some of these compounds, especially amlodipine, have more favorable pharmacokinetics, such as a prolonged elimination half-life. These agents may offer the advantage of a more practical dosage regimen for long-term treatment in patients with ischemic heart disease.
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PMID:The role of calcium antagonists in the treatment of myocardial ischemia. 268 2

To investigate the relation between basal coronary artery diameter and development of coronary artery spasm, the diameters of the proximal, middle and distal segments of the three major coronary artery branches, together with that of the left main trunk, were measured on a control angiogram and after ergonovine and nitrate administration in 30 patients with vasospastic angina without significant organic stenosis, and in 35 patients without ischemic heart disease. The percent change in coronary diameter after ergonovine and nitrate administration compared with the control diameter was used as an index of coronary vasoreactivity. In patients with vasospastic angina, coronary artery responses to both ergonovine and nitrate were greater in the spastic segments than in the other segments (p less than 0.05), and those of the coronary arteries without spasm were greater than those of the coronary arteries in patients without ischemic heart disease (p less than 0.01). There were no significant differences between the coronary artery diameters in the two groups after nitrate administration, and the control diameters were less in patients with vasospastic angina than in patients without ischemic heart disease. These observations indicate that a coronary vasomotion disorder, which involves increased basal coronary artery tone and hypersensitivity to vasoconstrictive stimuli, not only at a localized segment but also in the entire coronary artery tree, is present in patients with vasospastic angina. Clinically, evaluation of basal coronary artery tone may be useful for predicting the occurrence and location of coronary artery spasm.
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PMID:Significance of coronary artery tone in patients with vasospastic angina. 276 10

Previous attempts to define the etiology of coronary arterial spasm have been focused on mechanisms such as autonomic nervous dysfunction and/or enhanced platelet activation. In the present study, humoral regulation was investigated in patients with vasospastic angina and scintigraphically documented transient myocardial perfusion abnormalities after a peripheral cold pressor test. Serial changes in angiotensin II, epi- and norepinephrine as well as thromboxane B2 (the stable derivate of thromboxane A2), and malondialdehyde were determined at baseline (I), immediately after 5 minutes cold water hand immersion (II), and following 10 minutes recovery (III). Angiotensin II and epinephrine remained unchanged during observation (I vs II, II vs III: P = NS). Norepinephrine was elevated after cold (I vs II: P less than 0.001) and normalized after 10 minutes (I vs III: P = ns). Thromboxane B2 and malondialdehyde increased continuously (I vs III: P less than 0.05 and I vs III: P less than 0.002, respectively). Further radiothin-layer chromatography results indicate an activation of platelet function during myocardial ischemia. Our results do not establish a cause-effect relationship but, together with other evidence, they may suggest that thromboxane A2 is unlikely to be the cause of spasm. It might, however, play an important role in the maintenance of vasoconstriction.
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PMID:Humoral regulation during cold-induced coronary arterial spasm. 280 8

A group of 53 with angina pectoris-like chest pain and normal coronary arteriography was studied. Nine of these patients had a positive ergonovine test and were diagnosed as coronary spasm or vasospastic angina. In four of these nine patients there was evidence of an accessory esophageal disease responsible for the chest pain. In 44 patients organic or functional ischemic heart disease was excluded. The possible esophageal origin of the pain was studied by means of esophageal manometry and acid and endofonium provocation. The final results were that 15 patients had pain of an esophageal origin and 13 had an esophageal disease that made the esophagus a likely, or at least possible, source of pain.
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PMID:[Thoracic pain of esophageal origin]. 281 15

Knowledge of the pathophysiology of myocardial ischemia has been greatly enhanced recently by new information on coronary artery spasm. This phenomenon accounts for the mechanism underlying the attacks of resting chest pain in Prinzmetal's angina and plays a role in almost all aspects of ischemic heart disease. The diagnosis of coronary artery spasm can be made presumptively with noninvasive methods, but definitive documentation is usually obtained in the cardiac catheterization laboratory. The nitrate derivatives and the calcium antagonists provide a safe and effective approach to therapy.
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PMID:Coronary artery spasm. What is its role in ischemic heart disease? 286 79

Monitoring of the electrocardiogram during normal daily activity yields data regarding silent myocardial ischemia and its relation to heart rate in addition to the detection of cardiac arrhythmias. In recent years various techniques have been developed to quantify the frequency and duration of ischemic episodes in patients with ischemic heart disease. Of particular importance are the newer frequency-modulated recording techniques, which ensure adequate low frequency response, and the computerized digital analysis used to define the role of ST-segment monitoring in the clinical and research setting. The techniques used for acquiring artifact-free signals, the methods of data analysis and the clinical role of ambulatory Holter monitoring of ST-segment changes in the diagnosis of Prinzmetal's angina, in chronic stable angina and in the detection of calcium antagonist withdrawal syndrome in angina are discussed. The data indicate the particular utility of Holter monitoring to analyze the variability of heart rate in defining the effects of calcium-channel blockers, beta-adrenergic blocking agents and their combined use in pharmacologic therapy of ischemic myocardial syndromes.
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PMID:Clinical and research applications of ambulatory Holter ST-segment and heart rate monitoring. 287 42

Silent myocardial ischemia is common in the clinical spectrum of coronary disease. Ambulatory electrocardiographic monitoring has provided the most objective evidence of silent ischemia, but the phenomenon has also been detected in patients with coronary artery disease through analysis of exercise-induced ischemic ST-segment alterations, scintigraphic myocardial perfusion defects and left ventricular wall motion abnormalities. Silent myocardial ischemia frequently occurs in patients with stable angina, unstable angina, myocardial infarction and completely asymptomatic coronary artery disease. In each of these groups, silent ischemia has been associated with an increased risk of subsequent cardiac events. However, it remains unclear whether silent ischemia is directly involved in the occurrence of these events, possibly by provoking ventricular arrhythmias. Only limited data are available on the relation between silent ischemia and arrhythmias in myocardial infarction, vasospastic angina, coronary angioplasty, exercise testing and ambulatory electrocardiography. However, fortuitous ambulatory monitoring coincident with sudden death has detected ischemia associated with lethal arrhythmias in some individual cases. This suggests that an ischemia-arrhythmia association may be important in certain patients at certain times, possibly in combination with other factors.
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PMID:Relation of silent myocardial ischemia to ventricular arrhythmias and sudden death. 305 16


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