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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

"Painless" or silent myocardial ischemia is common and may be associated with all types of coronary insufficiency. Repeated ischemia impairs the functional and anatomical status of the ventricle and the aim of the treatment of coronary insufficiency must be to reduce not only pain, when present, but also ischemia. A distinction must be drawn between: 1) Painless ischemia after myocardial infarction occurring in a high risk group. This requires investigation of the patient, medical treatment and, according to results, angioplasty or surgery. 2) Painless ischemia associated with stable or unstable angina. It is known that in stable angina 50 per cent of ischemia attacks are painless and that complete treatment must seek to reduce the duration of ischemia. Treatment is adjusted on the basis of the results of investigations and the severity of ischemia. 3) Silent ischemia alone which requires precise diagnostic evaluation and assessment of risk based upon the patient's condition.
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PMID:[Silent ischemia. Therapeutic strategy]. 178 31

Beat-to-beat fluctuations of the spatial QRS-T angle, which are reported to be greater in patients with ischemic heart disease than in healthy subjects, are thought to be a helpful factor in diagnosing ischemic heart disease. In this study, we assessed the usefulness of the standard deviation of the spatial QRS-T angle per beat as an index of magnitude of the fluctuations. The subjects consisted of 27 patients with effort angina, 14 with vasospastic angina, 18 with the "chest pain syndrome" and 36 normal controls. The standard deviations of the spatial QRS-T angle were obtained for 10 consecutive stable beats at rest using Frank's orthogonal X, Y, Z scalar electrocardiogram. The results were compared with those of coronary angiography and exercise tolerance tests. Treadmill exercise tests were performed in all patients using Bruce's protocol to observe decreased ST levels and delta ST/HR indices. QRS-T angle deviation values were 8.10 +/- 8.64 degrees (mean +/- SD) in the effort angina group, 3.63 +/- 1.26 degrees in the vasospastic angina group, 4.13 +/- 1.70 degrees in the "chest pain syndrome" group, and 2.35 +/- 0.85 degrees in the normal control group; the groups of patients with heart disease showed significantly higher values (all p < 0.01) than did the control group. The effort angina group showed a significantly higher value than did the vasospastic angina group and the "chest pain syndrome" group (all p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Ischemic heart disease detected by the standard deviation of the spatial QRS-T angle and by treadmill exercise test]. 184 6

Prolonged ECG-recording with Holter's technique facilitated detection of heart ischemic episodes without accompanying anginal pain. It is estimated that ischemic heart disease without anginal pain involves about 20% of all patients with IHD, and the episodes of heart ischemia with and without anginal pain occur in 30% of these patients. A course of ischemic heart disease without anginal pain may be due to decreased sensitivity to pain stimuli caused by the lesions to sensory afferent nerves or by the increased serum endorphins. The majority of experiments has shown that asymptomatic ischemic heart disease increases the risk of sudden death. It may be explained by increased physical exercise attempted by these patients and not compliance with anti-sclerotic therapeutical and preventive measures. The treatment of asymptomatic ischemic heart disease is similar to that in symptomatic froms of this diseases.
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PMID:[Ischemic heart disease without anginal pain]. 184 71

Eighty-eight patients undergoing percutaneous transluminal coronary angioplasty (PTCA) of 100 stenoses were studied for the presence of factors deemed significant in the etiology of silent myocardial ischemia. Thirty-two patients were asymptomatic during balloon dilations of 36 arteries, and 56 patients had angina during PTCA of 64 arteries. There were no differences in age, sex, prior anginal history, antianginal regimen, extent of coronary artery disease and number or duration of inflations between the 2 study groups. Previous infarction (33 vs 12%, p less than 0.02), Q waves in the target area (31 vs 7%, p less than 0.005) and diabetes mellitus (36 vs 17%, p less than 0.05) were present more often in the asymptomatic group. Sixty-four% of all asymptomatic patients had either diabetes or previous infarction in the target territory. Collateral circulation was more frequent in asymptomatic patients, probably reflecting the ability of collateral arteries to ameliorate ischemia. During 2-vessel PTCA, patients without angina during dilation of only 1 of the 2 treated arteries (discordant responders) had previous infarction in that artery's territory (5 of 5, 100%), whereas patients without previous infarction were either symptomatic or asymptomatic (concordant responders) during PTCA of both arteries. This study shows that asymptomatic ischemia occurs frequently during PTCA in patients with symptomatic coronary disease. Prior Q-wave infarction and diabetes mellitus are important, independent factors associated with painless ischemia. It is suggested that infarction produces a localized dysfunction of afferent cardiac pain fibers, whereas diabetes can cause a global cardiac sensory neuropathy.
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PMID:Asymptomatic myocardial ischemia during percutaneous transluminal coronary angioplasty and importance of prior Q-wave infarction and diabetes mellitus. 189 79

A significant minority of patients with chest pain who undergo cardiac catheterization are found to have angiographically normal coronary arteries. Over the past 25 years, several studies have shown that a subset have demonstrable abnormalities in coronary flow and cardiac function; however, only a minority of these patients have convincing evidence for myocardial ischemia during stress, and alternative mechanisms have been explored to explain the frequent and debilitating symptoms of pain experienced by the majority of these patients undergoing study. Abnormal visceral nociception appears to be a fundamental abnormality in this population, whether or not demonstrable abnormalities in coronary flow or cardiac function can be demonstrated.
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PMID:Microvascular angina. Cardiovascular investigations regarding pathophysiology and management. 189 8

Transcutaneous electrical stimulation was reintroduced into medical practice in the early 1970s. Since that time, numerous studies, both controlled and uncontrolled, have suggested its utility for the treatment of pain related to acute musculoskeletal injury, postoperative pain, pain of peripheral vascular origin, pain of myocardial ischemia and chronic pain of a variety of causes. Pain of labor in delivery is affected equivocally. Pain complicating cancer has not been reliably relieved. A small number of controlled studies fail to demonstrate benefit, but the preoponderance of evidence suggests that electrical stimulation of the peripheral nervous system is a useful adjunct in the management of many pain states. Most studies indicate that the resultant analgesia is not opioid-dependent. Pain threshold and perception both appear to be reduced. The physiological mechanism by which pain is affected is not defined; local neural blockade, branch block in the dorsal horn and activation of a central inhibitory system have all been postulated.
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PMID:Fifteen years of transcutaneous electrical stimulation for pain control. 194 98

Angina pectoris is the cardinal symptom of coronary heart disease and is a symptom with which physicians are very familiar. The clinical diagnosis of ischaemic heart disease is often based largely on a history of typical chest or arm pain, and the major therapeutic endeavour in such patients is directed towards abolition or amelioration of angina. Indeed physicians have, at least up until recently, been confident in assuming that angina is a reliable marker of ongoing ischaemia and that success of medical or surgical treatment of coronary heart disease can be accurately gauged according to improvement or disappearance of anginal symptoms (Cohn & Braunwald, 1988). However, the results of a number of important clinical studies, reported over that last 10 to 15 years, appear to challenge these traditional medical assumptions. In many patients with coronary heart disease, acute episodes of myocardial ischaemia are frequently unaccompanied by angina, often referred to as "silent myocardial ischaemia" (Epstein et al., 1988; Fox, 1988; Cohn, 1985; Maseri, 1985). It has to be pointed out that not all painless ischaemic episodes are truly silent. Instead of experiencing pain during some episodes of acute myocardial ischaemia, patients may, on occasion, instead report symptoms such as dyspnoea or palpitations (these symptoms being known as "anginal equivalents") (Cohn & Braunwald, 1988). Nevertheless, the great majority of painless ischaemic episodes are, truly silent and not accompanied by "anginal equivalents", which has led to the trend in the recent literature to regard the terms "silent" and "painless" myocardial ischaemia as synonymous.
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PMID:Silent ischaemia: an update on current concepts. 195 49

The situation of absent pain with silent myocardial ischemia is highly difficult to define. There are probably several reasons for the lack of pain. Partly, nerve ways may be destroyed, partly, myocardial ischemia as peripheral pain stimulus may be to weak and beyond threshold, however, additionally, there are a lot of clues for the participation of endogenous pain modification systems therein. A certain amount of myocardial ischemia is a necessary, but not sufficient precondition for anginal pain. Myocardial ischemia is only felt painfully if the peripheral nociceptive impulse rate is high enough to pass the actual inhibitory pain threshold, and if the nerve ways are intact. It is generally accepted that the endogenous opiate system, to some extent, takes part in the endogenous analgesia system. A range of examinations in recent years hinted at the fact that endorphins are in relation to the absence of pain in silent ischemia. Patients with symptomatic and asymptomatic myocardial ischemia are significantly different in plasma beta-endorphin levels at rest and during physical exercise. A relation between peripheral endogenous opiates and suffering behavior can, at present, only be indicated correlatively. It is likely that the intensive overlaying of the cardiovascular and pain regulating systems is related to the absence of pain in silent myocardial ischemia.
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PMID:Influence of opiate systems in pain transmission during angina pectoris. 196 35

The definition, pathogenesis, incidence and characteristics, detection, treatment, and prognosis of silent myocardial ischemia (SMI) are reviewed. SMI is the occurrence of myocardial ischemia for which there is objective evidence (electrophysiological, hemodynamic, and metabolic changes) but no angina. Patients with SMI are classified as type 1 (completely asymptomatic), type 2 (SMI after myocardial infarction), and type 3 (both symptomatic and silent ischemia). Episodes of SMI are true ischemic events. The absence of pain may be due to defects in pain perception, an altered physiological response to ischemia, or a lesser degree of ischemia. The incidence of SMI is 2-5% in totally asymptomatic patients, 20-30% in patients who have suffered myocardial infarction, and 44-84% in patients who have symptomatic ischemia. SMI can be detected by exercise testing, portable electrocardiographic monitoring, or imaging techniques. Patients with SMI have more frequent adverse cardiac events (except death) than patients without SMI. The frequency of adverse cardiac events is similar in patients with angina and patients with SMI. SMI has been treated with nitrates, calcium-channel blockers, and beta blockers. Beta blockers appear to be the most consistent in reducing the number and duration of episodes. Combination therapy with beta blockers and nifedipine may be more effective than therapy with either agent alone. Because of the limited number of studies and the possible contribution to the results of spontaneous variability in the occurrence of SMI, no definite conclusions can be drawn about drug efficacy. There is no evidence that the prognosis of patients with SMI is altered by drug therapy; routine treatment with anti-ischemic drugs cannot be recommended. Patients must be evaluated individually, with aggressive management being reserved for those at high risk for myocardial infarction or other serious cardiac events.
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PMID:Current concepts of silent myocardial ischemia. 197 45

Pediatric chest pain usually occurs in benign conditions. However, this case portrays the dramatic electrocardiographic appearance of acute myocardial ischemia in a boy with biopsy-proven myocarditis who had only mild chest pain. This underscores the need for eliciting a detailed history when evaluating a patient with chest pain. If the pain cannot be clearly attributed to chest wall phenomena, or if there are historical or physical findings suggestive of an arrhythmia or angina, then further investigation with a chest radiograph and a 12-lead electrocardiogram is recommended. Myocarditis must be considered in the differential diagnosis of any child whose electrocardiogram is indistinguishable from an acute myocardial infarction. Finally, endomyocardial biopsy allows early diagnosis and institution of therapy, which may have beneficial effect on decreasing morbidity and mortality. Further follow-up and research is still needed to evaluate the effect of early treatment of myocarditis on long-term myocardial function and the development of chronic cardiomyopathy.
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PMID:Acute myocarditis simulating myocardial infarction in a child. 198 39


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