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

Myocardial ischemia causes a series of anatomic and physiologic abnormalities that can be detected and quantified by assessment of myocardial perfusion, mechanical function, electrophysiology, and metabolism. These methods of assessment vary widely in sensitivity, specificity, relevance, cost, and ease of application. Although occasionally the appropriate choice of diagnostic procedures is clinically difficult, the demonstrated potential of coronary artery bypass surgery to reverse both acute and chronic myocardial ischemia makes the detection of ischemia an important effort in the care of patients with coronary artery disease.
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PMID:Detection of myocardial ischemia. 33 74

Physiologic concepts relating to reperfusion of ischemic areas of myocardium may be applied both to acute coronary insuficiency, manifested by angina pectoris, and to restoration of coronary blood flow by coronary bypass procedures, currently employed both in acute myocardial infarction and in chronic myocardial ischemia for relief of angina pectoris. Of the information currently available from experimental studies, much may be applicable to the clinical situation. After acutr transient coronary occlusion mechanical and electrical properties of the ischemic area rapidly return to normal, but there is prolongation of tension development and occurrence of ventricular arrhythmias; implications of these phenomena for clinical coronary ischemia deserve exploration. Following more prolonged coronary ischemia, results of experimental reperfusion appear to be variable and, although restoration of function following several hours of ischemia is possible, certain deleterious effects are often observed in the form of myocardial edema and hemorrhage. Clinical use of bypass procedures in acute myocardial infarction suggests that results may be good, but that deleterious effects are occasionally observed; occurrence of the later requires definition and explanation. Restoration of myocardial blood flow in the presence of normal left ventricular function in chronic coronary artery disease, and failure to reverse functional abnormalities when left ventricular damage has already ensued in the clinical situation, appears to be well established; however, better methods to assess the potential for recovery of function following revascularization are needed in both acute and chronic coronary artery diseases. It is anticipated that more careful exploration of pathophysiology both in the catheterization laboratory and in the operating room may aid this process.
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PMID:Effect of reperfusion in acute ischemia and infarction. 115 38

Recent studies suggest that granulocytes (PMNs) play a role in the pathogenesis of acute and chronic myocardial ischemia and extension of myocardial injury. Granulocytes can release a variety of molecules mediating tissue injury which act synergistically with other molecules and cells. The aim of our investigation was to evaluate the granulocyte function in patients affected by coronary artery disease (CAD) and during coronary angioplasty (PTCA). We studied 20 patients suffering from CAD. The PMN's aggregating activity was greater in the coronary sinus than in the aorta (P < 0.01). The increase in aggregating activity was evident in patients who were smokers: their cells release significantly lower quantities of leukotriene C4 (P < 0.025). In the 20 patients who underwent coronary angioplasty we analyzed superoxide release after stimulation with phorbol-myristate-acetate (PMA). The results showed a greater decrease of PMN's superoxide production in the coronary sinus than in the aorta (P < 0.05). In all patients affected by CAD we evaluated the PMN's expression of CD11b/CD18 membrane integrins. In these patients the increase in expression of CD11b/CD18 was statistically significant in comparison with the controls (P < 0.01). This increase in expression correlates with a higher aggregation (r = 0.87, P < 0.001). The potential role of leukocytes, oxygen radicals, leukotrienes and granulocyte enzymes in the pathophysiology of myocardial injury due to regional ischemia and reperfusion is an area of intense investigation. This paper presents studies carried out in vivo which have been instrumental in demonstrating the role of granulocytes as mediators of myocardial ischemia.
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PMID:Phagocyte activation in coronary artery disease. 136 45

The efficacy of amlodipine, a long half-life dihydropyridine calcium antagonist, at the dosage of 5-10 mg/day in a single daily administration, has been compared with that of nifedipine R, a short half-life dihydropyridine, at the dosage of 20-40 mg b.i.d. in 29 patients with chronic ischemic heart disease. After a one week placebo period, patients were assigned to the treatment with amlodipine or nifedipine R, according to a randomized sequence and a cross-over, single-blind design, for two control periods of four weeks and without a wash-out interval between these two phases. During the stress test, a significant increase from baseline in test duration and in time to onset of ischemia and of angina have been obtained with both treatments; moreover amlodipine increased significantly the time to onset of ST segment deviation (-1 mm) and the time to maximum ST segment deviation compared with nifedipine R changes. Also with Holter monitoring and in the angina diary there was a significant reduction of anginal episodes. As regards safety profile, amlodipine treatment was associated with a significantly lower incidence of side effects compared with nifedipine R. This is probably due to the particular pharmacokinetics of amlodipine which, besides the long half-life which allows a single daily administration, shows a retarded peak (between the 6th and the 12th hour) with consequent reduction of phenomena connected with fast and excessive peripheral vasodilatation. In conclusion, amlodipine was as effective in reducing the signs of ischemia as nifedipine R, but compliance was better due to the single daily administration and so was tolerability.
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PMID:Amlodipine versus nifedipine retard in the treatment of chronic ischemic heart disease. 138 15

Recent studies suggest that granulocytes (PMNs) play a role in the pathogenesis of acute and chronic myocardial ischemia and extension of myocardial injury. A positive correlation was also found between leukocyte count and severity of coronary artery disease. Rabbit derived antiserum dependent-reduction of circulating PMNs in the dog or using monoclonal antibody anti-CD11b/CD18 of PMNs resulted in smaller myocardial infarcts. Granulocytes can release a variety of mediators tissue injury and synergize with these different mediators and other cells resulting in amplification of neutrophil stimulation and rising to additional products with enhanced endothelial injury. This paper reviews "in vivo" studies that have been instrumental in demonstrating this role of granulocytes as a mediator of myocardial ischemia. Experience in humans shows the modification of PMNs function in angina and during myocardial ischemia, and data from our group demonstrated that their aggregability is increased in the coronary sinus of patients with angiographically documented coronary disease. Upon re-perfusion PMNs accumulate and produce an inflammatory response resulting in endothelial injury. Free radicals formed during ischemia or re-perfusion produce deleterious effects on cell membranes, endothelial cell and myocardium. On the other hand the PMNs activation occurring during coronary angioplasty (PTCA) by the release of proteolytic enzymes and the generation of oxygen-free radicals, may aggravate the endothelial damage induced by PTCA and further stimulate platelets having potential implications in subsequent development of restenosis. An other aspect of PMNs function is related to leukotriene C4 release; the vasoconstrictor effect of this leukotriene on coronary arteries is synergistic with that induced by platelet-released thromboxane A2, as well as the decrease in coronary flow produced by the combination of both substances is greater than the sum of changes caused by the two eicosanoids separately administered. The potential role of leukocytes, oxygen radicals, leukotrienes and granulocyte enzymes in pathophysiology of myocardial injury due to a regional ischemia and reperfusion is an area of intense investigation. Experimental and clinical studies to elucidate these events should not only provide insights into acute and chronic pathologic tissue damage, but may also lead to the identification of important new targets of pharmacologic intervention.
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PMID:Role of granulocytes in endothelial injury in coronary heart disease in humans. 181 45

Beta-adrenoreceptor blocking agents have been used to relieve symptoms mainly in patients with ischemic heart disease. Prophylactic use of beta blockade in patients after acute myocardial infarction has shown a reduction in total mortality and also in sudden death. The overall total mortality reduction amounts to about 30%, whereas the reduction in the sudden death rate is 50%. The mechanisms behind this reduction in sudden death are probably manifold. Antiarrhythmic effects in ischemic myocardium, prevention of new ischemia, and also perhaps other factors may play a role. Apart from the prevention effect in chronic ischemic heart disease, beta blockers have also been able to reduce the sudden death rate in the long QT syndrome and are suggested for use in congestive cardiomyopathy.
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PMID:Prevention of sudden death by beta-blockade. 198 82

The association between pressure overload, left ventricular (LV) hypertrophy and failure, and abnormalities in diastolic function has been described both clinically and experimentally. The mechanisms underlying this association, however, are complex and controversial. Factors that have been implicated include mechanical alterations due to hypertrophy alone, changes in collagen type and content, alterations in beta-adrenergic responsiveness, and chronic myocardial ischemia. Studies in our laboratory have identified limitations in subendocardial flow reserve in compensated LV hypertrophy and near exhaustion in subendocardial reserve in animals with decompensated LV hypertrophy and failure. These abnormalities in coronary reserve are associated with impaired diastolic function, particularly during periods of physiological stress. For example, with pacing-induced stress, impairment in diastolic function was observed in conscious dogs with compensated LV hypertrophy. In conscious dogs with LV hypertrophy and failure, isoproterenol also resulted in altered diastolic function. Thus, in the model of severe pressure-overload hypertrophy, which is characterized by limitations in coronary reserve, the mechanism of subendocardial ischemia might be responsible in part for the impairment in diastolic function observed in response to superimposed stress.
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PMID:Reduced subendocardial coronary reserve. A potential mechanism for impaired diastolic function in the hypertrophied and failing heart. 213 53

Ambulatory 24-h Holter monitoring was carried out in 198 patients who had been admitted because of suspected acute myocardial infarction (AMI) due to chest pain, but in whom AMI was not confirmed. During a follow-up period of 12-24 months (median 14 months) 16 cardiac events (i.e., nonfatal AMI or cardiac death) occurred. Ventricular premature beats (VPBs) were found in 65.2% of the patients, complex VPBs in 28.8%. Pairs of VPBs which were seen in 10.0% of the patients were the only important type of VPBs significantly related to an impaired prognosis. Thallium-201 scintigraphy was performed in 144 of the patients. VPBs were significantly related to scar formation (i.e., to permanent defects, but not to ischemia, specifically, to transient defects). It is concluded that ventricular arrhythmias in this patient category indicate presence of chronic ischemic heart disease, and that pairs of VPBs seem to identify patients at risk for cardiac events.
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PMID:Ventricular premature beats on Holter monitoring in patients admitted with chest pain, in whom acute myocardial infarction is not confirmed. The prognostic value and relationship to scars or ischemia on thallium-201 scintigraphy. 243 44

In animal studies, amiodarone has substantial and immediate antiarrhythmic/antifibrillatory action during acute myocardial ischemia. The magnitude of this effect is discordant with the minor degree of prolongation of ventricular action potential duration (APD) and refractoriness which occurs immediately after acute drug administration. However, amiodarone's early onset of antiadrenergic activity and inhibition of inward slow calcium channel currents may be important when arrhythmogenesis is dependent on increased sympathetic tone. Because ventricular arrhythmia substrate may differ in acute and chronic ischemic heart disease, we investigated the acute electrophysiologic and antiarrhythmic/antifibrillatory effects of intravenously (i.v.) administered amiodarone in nine chronically infarcted cats. Amiodarone caused significant decreases (-17%) in mean heart rate (HR) and increases (+10%) in mean ventricular effective refractory period (ERP), which occurred promptly after drug administration. Increases in mean ventricular fibrillation (VF) threshold also occurred (11 +/- 3.4 and 12.5 +/- 2.4 mA for right and left ventricular sites before drug as compared with 45.5 +/- 13.2 and 42 +/- 13.9 mA after drug). Despite these changes, no significant reduction in the incidence of malignant ventricular arrhythmias induced by programmed stimulation was noted (63% of animals with arrhythmia induced before drug were still inducible after drug). In addition, no change in the increased degree of mean dispersion of refractoriness between infarcted and normal myocardial sites occurred following amiodarone (22.8 +/- 3.9 ms before vs. 30.2 +/- 2.5 ms after drug). In chronic myocardial infarction without superimposed acute ischemia, early onset of amiodarone's antiadrenergic and calcium channel blocking activities may play only a minor role in preventing ventricular arrhythmias inducible by programmed stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute electrophysiologic effects and antiarrhythmic/antifibrillatory activity of intravenous amiodarone in a chronic feline infarction model. 247 17

The effect of hypertension, hyperlipidemia, and the combination of both on acute and chronic myocardial ischemia were evaluated in a total of 30 male rabbits. After preliminary hypertension and/or hyperlipidemic load by loading of the abdominal aorta and/or cholesterol feeding, acute ischemia was produced by clipping of the left coronary artery. The banding produced elevation of carotid arterial pressure and left ventricular hypertrophy. Cholesterol feeding resulted in severe atheromatous changes in all sizes of coronary arteries. The intimal thickening was due to foam cell accumulation in all arteries examined. Animals pretreated with the combination of hypertension and hyperlipidemia displayed the most severe cardiolmegaly with advanced coronary atherosclerosis and chronic ischemic lesions of the myocardium, i.e., perivascular patchy fibrosis in the subendocardial area. Furthermore, electron microscopic detection of ultrastructural myocardial damage, involving glycogen depletion, sarcoplasmic edema, mitochondrial swelling, and contractile abnormalities, was also most frequent in this group. These changes were quantitated using the ischemic score. These results confirm the hypothesis that fatal ischemic injuries may occur clinically in human hearts with coronary insufficiency due to coexistence of hypertensive cardiomegaly and severe coronary atherosclerosis. They offer a model for further study of these combined effects.
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PMID:An ultrastructural study on ischemic lesions in rabbits' hearts with pressure overload and hyperlipidemia. 315 60


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