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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

When severely ischemic myocardium is reperfused, prolonged myocardial dysfunction--a phenomenon named myocardial stunning--frequently occurs. Stunning also occurs in a variety of other situations. These include myocardium located adjacent to infarcted tissue, transient increase in myocardial O2 demands in the presence of incomplete coronary obstruction, during both systole and diastole, in isolated perfused hearts rendered ischemic or anoxic, and in a variety of clinical situations, such as following ischemic arrest in cardiac surgery, thrombolytic reperfusion, and after episodes of severe ischemia in Prinzmetal's angina or unstable angina. Although the fundamental mechanism(s) responsible for myocardial stunning has not been elucidated, in experimental preparations calcium antagonists, free-radical scavengers, and neutrophil depletion have each been found to be helpful in minimizing it.
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PMID:Stunning of the myocardium: an update. 175 30

To clarify the prognostic implications of exercise induced silent myocardial ischemia (SMI) in patients with angina pectoris, the clinical characteristics and long-term prognosis after coronary angiography in 379 patients without prior myocardial infarction were investigated. According to the results of treadmill testing and/or Tl-201 exercise imaging after medical treatment, 50 patients with negative for ischemia were classified as control group, 110 patients with exercise induced SMI were classified as the SMI group, and 187 patients with painful ischemia formed the PI group. Thirty-two patients were excluded because of inconclusive exercise results. Single vessel disease and vasospastic angina were more frequent in the control group than in the SMI and PI groups. But there were no differences in baseline characteristics and extent of coronary lesions between the latter two groups. Heart rate, systolic blood pressure and rate-pressure product at end point in treadmill testing were higher in the control and SMI groups than in the PI group. The mean follow-up period was 4.8 years, and follow-up was completed in every case. Cardiac events, including cardiac death, nonfatal myocardial infarction and readmission from severe angina, occurred in 25 patients of the SMI group, 43 of the PI group and 7 of the control group. Cumulative cardiac event curves did not show any statistically significant difference between the SMI and PI groups. We conclude the presence or absence of angina during exercise test is no longer the principal prognostic index for determining a patient's risk of cardiac events.
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PMID:[Prognostic implications of exercise induced silent myocardial ischemia in patients with angina pectoris]. 192 5

A number of tests are used for the noninvasive detection of coronary stenosis, which results from the combination of different stimuli (exercise, pacing, dobutamine, dipyridamole, etc.) and different signals and methodologies (ECG, echocardiography, scintigraphy). In this article, the theoretical assumptions for and the methodological limitations of the functional evaluation of the degree of coronary stenosis are considered within the framework of pathophysiology. In particular, the issues of dilating coronary circulation by either increasing myocardial O2 demand or infusing dipyridamole and of assessing coronary reserve by either flow- or ischemia-related techniques are examined. In addition, the hypotheses of a physiological blood steal during exercise, a decrement of exercise ischemic threshold secondary to additional pharmacological vasodilation, and coronary vasospasm in Prinzmetal's angina patients, following the sequence dipyridamole-aminophylline, are discussed on the basis of preliminary studies.
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PMID:Pathophysiological basis for noninvasive functional evaluation of coronary stenosis. 202 43

Among the clinical manifestations of ischemic heart disease, right coronary artery (RCA) disease offers a wide variety of right and left ventricular ischemic involvement, including prevalent right ventricular dysfunction and severe cardiac failure. Whether the right ventricular impairment is dependent primarily on ischemia of the right ventricle or requires a concomitant left ventricular dysfunction remains debatable. To assess the pathophysiology and clinical relevance of RCA-related ischemia, a systematic study of patients with single RCA disease (either vasospastic angina at rest or typical stable angina) was undertaken by radionuclide ventriculography. A high incidence of ischemia-induced right ventricular dysfunction was observed (93% and 95% in angina at rest and on effort, respectively), either alone or associated with left ventricular impairment. These results were compared with those obtained in a control population with isolated left anterior descending artery disease and either primary or secondary angina pectoris. We infer that the impairment of the right ventricle was related primarily to right ventricular ischemia and that left ventricular dysfunction alone did not cause an important depression of right ventricular systolic function. In conclusion, the clinical manifestations of RCA disease can be protean; the right ventricle can be the target of ischemia, and recognition of its impairment poses diagnostic problems. Radionuclide ventriculography and two-dimensional echocardiography, together with stressors of coronary flow reserve, are reliable techniques for assessing RCA-related ischemia.
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PMID:Right coronary artery disease. Pathophysiology, clinical relevance, and methods for recognition. 202 49

We investigated the clinical and pathophysiologic characteristics in patients with vasospastic angina who developed syncope and/or experienced aborted sudden death (SD). Vasospastic angina was diagnosed using the methylergonovine test. Syncope was found in 32 (10.4%) patients among 309 who were admitted to our institute in a one-year period. The most frequent cause of syncope was ventricular tachycardia which was found in 10 (31.2%) of the 32 patients. The next important cause of syncope was vasospastic angina which was found in 7 patients (21.8%). Among the 7 patients with vasospastic angina who experienced one or more syncopal episodes, there were 3 patients with aborted SD, 3 with syncope and one with shock. Cardiovascular collapse was observed in 4. Interior wall ischemia was found in 5 and anterior wall ischemia in 2 during the methylergonovine test. None of the 7 patients had significant coronary stenosis. Two patients had no prodromal symptom such as chest pain. Our results suggest that coronary artery spasm may be one of the most frequent cardiovascular diseases that causes syncope which is not always accompanied by a prodromal symptom. Therefore, coronary spasm should be distinguished in patients with unexplained syncope or aborted SD.
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PMID:Clinical characteristics and possible role of coronary artery spasm in syncope and/or aborted sudden death. 207 44

Coronary artery disease may present as silent ischemia, chronic typical angina pectoris, unstable angina, Prinzmetal angina, acute myocardial infarction, and sudden cardiac death. These manifestations can usually be differentiated by the clinical history. Each of them has its own pathophysiology and, accordingly, therapy and prognosis are different. Myocardial ischemia is common to all of the manifestations and this can be assessed by history taking, ECG stress-testing, ambulatory monitoring, myocardial perfusion scanning, or radionuclide angiography (RNA). The diagnostic accuracy of these diagnostic procedures varies from 70% (history) to 81% (RNA).
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PMID:[Clinical presentation and diagnosis of coronary heart disease]. 231 79

The peak incidence of ventricular fibrillation in acute myocardial infarction usually occurs during the first hours after the onset. Electrophysiological changes immediately after the onset have been studied in animal models, but are still incompletely understood in humans. For clarification of the characteristic features of ventricular arrhythmias during acute myocardial ischemia, ventricular arrhythmias were studied in 81 patients with vasospastic angina pectoris induced by ergonovine. Ventricular arrhythmias occurred in 45 of these patients, including ventricular tachycardia in 15, and ventricular fibrillation requiring repeated DC defibrillation in two patients. Most ventricular extrasystoles occurred before the ST segment reached maximum elevation, while reperfusion arrhythmias were less common. In many patients the coupling intervals varied, and the configuration was multiform. It is concluded that ventricular arrhythmias occurring during ergonovine-induced coronary spasm show different characteristics from those occurring during chronic ischemia. As the arrhythmias in this study seem, in some ways, to resemble arrhythmias occurring at the onset of myocardial infarction, the results might provide useful information on ventricular arrhythmias in myocardial ischemia in humans.
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PMID:The nature of ventricular arrhythmias during ergonovine-induced vasospastic angina pectoris. 244 15

Persistent intercoronary and intracoronary communications were observed on cineangiograms in four patients having vasospastic angina without significant coronary narrowings. On provocation of coronary spasm using ergonovine maleate, these communications seemed to protect myocardium from ischemia, at least partially.
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PMID:Intercoronary and intracoronary communications in four cases of vasospastic angina. 291 14

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

Dipyridamole testing represents an alternative to exercise stress testing for documentation of ischemia related to coronary artery disease (CAD). In such a case, ischemia is attributed to maldistribution of coronary flow during dipyridamole-induced vasodilation. The present study evaluated the potential role of dipyridamole testing in producing ischemia through a vasospastic mechanism, following rapid withdrawal of vasodilation induced by aminophylline. The possibility was tested in 36 in-hospital patients with variant angina pectoris who underwent dipyridamole infusion (up to 0.84 mg/kg over 10 minutes) with continuous 12-lead electrocardiographic and 2-dimensional echo monitoring. Medications were withdrawn from all patients. The test was pharmacologically stopped with the dipyridamole antidote (aminophylline, 80 to 240 mg intravenously over 1 to 3 minutes) in all patients. Two to 6 minutes after starting aminophylline infusion, 10 patients (28%) developed (greater than 0.10 mV) ST-segment elevation (2.9 +/- 0.8 mm from baseline), always accompanied by obvious asynergy detected by echocardiography, in the same electrocardiographic leads showing spontaneous or ergonovine-induced ST-segment elevation. Nitrates promptly resolved ischemia in all patients. At coronary angiography, 5 of these 10 patients showed significant CAD (greater than 70% lumen diameter reduction of at least 1 major coronary artery), whereas 5 had nonsignificant CAD. The rate pressure product at the onset of ST-segment elevation (after dipyridamole plus aminophylline) was considerably less than that recorded at peak exercise stress test in these patients (9,600 +/- 2,200 vs 18,400 +/- 4,900, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Aminophylline termination of dipyridamole stress as a trigger of coronary vasospasm in variant angina. 342 Nov 66


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