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

The effects on myocardial function, metabolism and ultrastructure of 60 minutes of reperfusion, instituted after 30, 60 and 90 minutes of occlusion of the left anterior descending coronary artery, were studied in 48 dogs. Twelve sham-operated dogs served as controls. Coronary occlusion for 60 or 90 minutes caused significant depression in the first derivative of left ventricular pressure (dP/dt) (P less than 0.05) that could not be reversed by reperfusion. Upon reperfusion, creatine phosphate stores in myocardium made ischemic for 30 and 60 minutes, but not for 90 minutes, returned toward control levels, but stores of adenosine triphosphate (ATP) and total nucleotides and the ATP/adenosine diphosphate ratio of myocardium subjected to 60 and 90 minutes of ischemia were further decreased. After 60 and 90 minutes of ischemia, swelling of the sarcoplasmic reticulum and mitochondrial damage (swelling, decreased matrix density and partial loss of cristae) were seen. Myofibrils were relaxed in all these groups. Reperfusion produced gross contraction of myofibrils and aggravated these changes in mitochondria and sarcoplasmic reticulum. In the hearts subjected to 90 minutes of ischemia these changes were gross. The levels of creatine phosphokinase, glutamic oxaloacetic transaminase and lactic dehydrogenase in the coronary sinus blood increased dramatically (P less than 0.05) upon reperfusion after 60 or 90 minutes of occlusion, indicating severe impairment of cell membranes. This secondary rise in serum enzyme activity during reperfusion should be taken into consideration when estimating the size of a myocardial infarct from enzyme changes alone. It appears that 60 and 90 minutes of ischemia cause severe myocardial damage that is not reversed by reperfusion maintained for 1 hour although longer periods of reperfusion may be beneficial.
Am J Cardiol 1975 Aug
PMID:Alterations in energy metabolism and ultrastructure upon reperfusion of the ischemic myocardium after coronary occlusion. 108 Mar 52

The purpose of this study was (1) to establish the maximal interval between the onset of ischemia and reperfusion that would permit a decrease in the size of infarction, and (2) to evaluate the relation between changes in infarct size and preservation of cardiac function. Studies were carried out in 19 dogs of which 13 had temporary (1 to 3 hours) occlusion of the left anterior descending coronary artery. The hospital course of 15 patients of whom 13 underwent myocardial revascularization within 8 hours of acute infarction was also reviewed. In dogs, the eventual pathologic infarct size was significantly reduced if reperfusion was performed within 2 hours of ischemia. After 2 hours of ischemia, the revascularized segment remained dyskinetic on angiographic assessment and cardiac function was depressed. After 3 hours of ischemia, in spite of a patent coronary artery, the extent of infarct and dykinesia was greater than during ligation of the left anterior descending coronary artery. In patients, small infarcts developed with revascularization performed more than 4 hours after infarction but with revascularization of the left anterior descending coronary artery the size of the dyskinetic area (as assessed with angiography) was similar to that in patients with a closed graft to the left anterior descending coronary artery but with a patent graft to its diagonal branch. In all patients after revascularization the extent of the left ventricular dyskinetic area was smaller and cardiac function was significantly better than in patient who did not receive revascularization for complete occlusion of the left anterior descending coronary artery. In spite of successful revascularization, electrocardiographic evidence of transmural infarction persisted postoperatively. It is concluded that reperfusion of an area of myocardium that has been ischemic for less than 2 hours in dogs or less than 4 hours in man may lead to a significant reduction in the extent of infarction as well as improvement in cardiac function. However, the revascularized area remains angiographically dyskinetic and electrocardiographically abnormal.
Am J Cardiol 1975 Sep
PMID:Myocardial revascularization after acute infarction. 108 Sep 50

Three noninvasive radioactive tracer techniques for evaluating patients with ischemic heart disease are described: (1) myocaridal perfusion imaging, (2) acute infarct imaging, and (3) the gated blood pool scan. Myocardial perfusion imaging with tracers that distribute in the myocardium in relation to regional blood flow allows detection of patients with transmural and nontransmural infarction by the finding of decreased tracer concentration in the affected region of the myocardium. If these tracers are injected at the time of maximal stress to patients with significant coronary arterial stenosis but without infarction, areas of transient ischemia can be identified as zones of decreased tracer concentration not found when an examination is performed at rest. Acute infarct imaging with tracers that localize in acutely damaged tissue permits separation of patients with acute myocardial necrosis from those without infarction and those with more chronic damage. The gated blood pool scan permits assessment of left ventricular function and regional wall motion. The measurement of ventricular volumes, ejection fraction and regional wall motion adds significantly to the determination of hemodynamic variables in assessing patients with acute infarction. The technique also permits detection of right ventricular dysfunction. Performance of a combination of these radioactive tracer techniques is often advantageous, particularly in patients with suspected infarction. The techniques can establish whether infarction is present, whether it is acute, where the damage is located and how extensive it is; they can also provide a measure of the effect of this damage on left ventricular function.
Am J Cardiol 1976 Apr
PMID:Myocardial imaging in the noninvasive evaluation of patients with suspected ischemic heart disease. 108 67

We investigated the effect that mild coronary stenosis exerts on the ability of the coronary circulation to compensate for the increased extravascular compression that occurs in the subendocardium during tachycardia. An electromagnetic flowmeter transducer and balloon cuff occluder were implanted on the left circumflex coronary artery in seven dogs, and experiments were performed 1 week later with the dogs under sedation but conscious. Stenosis of the left circumflex artery was produced by partial inflation of the cuff occluder. We determined coronary blood flow distribution by the radioactive microsphere technique, injection 200,000 15mu spheres into the left ventricular cavity during (1) a control period, (2) stenosis of the left circumflex artery and a normal heart rate, and (3) stenosis of the left circumflex artery and tachycardia. When the heart rate was normal, the degree of stenosis used caused no change in myocardial microsphere distribution but eliminated postocclusion reactive hyperemia. Thus, reserve coronary vasodilation compensated for the stenosis. With the degree of stenosis kept constant, an increase in heart rate to 196 beats/min caused a marked transmural shift in distribution of microspheres from subendocardium into subepicardium within the region of the left ventricle supplied by the left circumflex artery. There was no significant transmural shift in the region supplied by the uninvolved left anterior descending coronary artery. Myocardial lactate extraction decreased. These results suggest that when reserve coronary vasodilation has already been utilized to compensate for coronary stenosis, the increased extravascular coronary compression from tachycardia causes subendocardial ischemia and hypoxia.
Am J Cardiol 1975 Jan
PMID:Subendocardial ischemia provoked by tachycardia in conscious dogs with coronary stenosis. 110 44

The effect of regional myocardial ischemia and hypoxia on myocardial scintigraphy was studied in patients and dogs after intravenous administration of cesium-129. Seven men with angiographically proved ischemic heart disease underwent exercise testing and 129Cs was given immediately when ischemia was manifested in the electrocardiogram. Defects were not evident in the scintigrams of any patient. Failure to visualize a defect might be related to delayed uptake of 129Cs by the myocardium (maximal uptake in 45 minutes). The ischemic state was dissipated before the disparity in uptake between normal and ischemic myocardium could be visualized. Cesium-129 is useful for identifying acute myocardial infarcts but should not be used to visualize transient exercise-induced regional ischemia. Six dogs were given 129Cs after induction of regional myocardial hypoxia by perfusion of the anterior descending coronary artery with venous blood. In each, scintigraphy revealed a defect that resolved after reperfusion with arterial blood. Two other dogs were given 129Cs before perfusion with hypoxemic blood; neither dog manifested a defect. Since perfusion was maintained by a pump these results suggest that the major cause of the scintigraphically observed defect was inadequate cellular uptake of 129Cs rather than excessive cellular loss. Since regional myocardial hypoxia produced a reversible defect, scintigraphic studies might overestimate the size of an acute myocardial infarct in man by including the ischemic zone surrounding the infarct.
Am J Cardiol 1975 Feb
PMID:Effects of myocardial hypoxia and ischemia on myocardial scintigraphy. 111 85

As a prelude to a study of severe ischemic heart failure, the therapeutic response of the ischemic ventricle to epinephrine and acetylstrophanthidin in nontoxic doses was determined in 24 intact anesthetized dogs undergoing a first episode of acute regional ischemia. A thrombotic obstruction was produced in the left ventricular dysfunction. The elevation of end-diastolic pressure and reduced stroke volume in control dogs were not significantly altered by administration of strophanthidin. Epinephrine (0.05 mug/kg per min) elicited a significant reduction in end-diastolic pressure and increase in stroke volume. The latter was not attended by an increased incidence of ventricular fibrillation, whereas fibrillation occurred in half of the group given strophantihidin. Thus, the catecholamine was selected to study pump failure. Severe ischemic heart failure was assessed in two groups with scar from previous infarction for up to 4 hours. By 60 minutes of ischemia the increase in end-diastolic pressure and volume and decrease in stroke volume and ejection fraction were comparable in both groups. Thereafter, alternate animals received small doses of epinephrine (0.05 to 0.15 mug/kg per min) with graded increments at 60 minute intervals to counter tachyphylaxis and findings were compared with those in control dogs. Over the subsequent 3 hours, there was progressive deterioration of left anterior descending coronary artery, affecting ventricular function in the untreated group with an increase in end-diastolic pressure from 10 plus or minus 1 to 33 plus or minus 2.4 mm Hg. End-diastolic volume increased by 63 percent; stroke volume and ejection fraction decreased by 48 and 66 percent, respectively. The infusion of epinephrine was attended by a significantly lower end-diastolic pressure of 20 plus or minus 2.5 mm Hg, whereas end-diastolic volume, stroke volume and ejection fraction were restored to control levels after 4 hours of ischemia. Mortality in the untreated group was 62 percent by 4 hours; all seven animals in the treated group survived.
Am J Cardiol 1975 Apr
PMID:Ischemic heart failure: sustained inotropic response to small doses of I-epinephrine without toxicity. 111 1

The records of 12 patients with aortic stenosis previously studied by Fallen et al. in 1967 before and after infusion of isoproterenol were reviewed to assess the value of hemodynamic indexes in predicting myocardial ischemia--defined as less than 5 percent transmyocardial lactate extraction or lactate production. Potential subendocardial blood supply was estimated from a diastolic pressure-time index (DPTI), calculated from the tension-time index (TTI). The ratio DPTI/TTI was used to estimate the supply/demand relation. Of eight patients with aortic stenosis but without associated coronary artery disease, four (Group A) metabolized lactate normally after administration of isoproterenol, and four (Group B) had biochemical evidence of ischemia. Three of four patients (Group C) with aortic stenosis and associated coronary artery disease had abnormal glycolysis after administration of isoproterenol. Calculated aortic valve areas were comparable in all groups. In patients with aortic stenosis alone, abnormal lactate metabolism occurred whenever DPTI/TTI was less than 0.30 (P smaller than 0.01) (Group B). Two of three patients with aortic stenosis and associated coronary artery disease (Group C) showed abnormal lactate metabolism when DPTI/TTI was greater than 0.6; this ratio was below 0.3 in the third patient. These results suggest that the supply/demand relation calculated from these readily obtained indexes may be useful (1) in predicting in which patients with aortic stenosis ischemia will develop, (2) in distinguishing the role played by associated coronary artery disease, and (3) as an adjunct to calculation of valve area since the quantitation of associated aortic regurgitation is not necessary.
Am J Cardiol 1975 Jun
PMID:Ischemia in aortic stenosis: hemodynamic prediction. 113 Feb 86

The relationship of left ventricular relaxation and compliance to the mechanism of elevation of left ventricular enddiastolic pressure during ischemia was investigated. Isovolumic left ventricular contraction, relaxation, and diastolic pressure-volume relationship were studied in controls and in coronary heart disease patients. Patients were studied at similar heart rates during ergometric exercise and pacing. Diastolic aortic, left ventricular systolic, and incisural pressure were not significantly different in both groups at rest, pacing, and exercise. Left ventricular dP/dtmax increased during pacing and exercise in controls (P smaller than 0.05; P smaller than 0.01) and in coronary heart disease patients (P smaller than 0.01 for both); whereas left ventricular dP/dtmin increased only in controls during exercise (P smaller than 0.01). Peak measured velocity of shortening (Vpm) and of lengthening (Vpmr) of the contractile elements was calculated as (dP/dt)/p. Vpm and Vpmr increased in controls during both pacing (P smaller than 0.05; P smaller than 0.02) and exercise (P smaller than 0.01 for both). In coronary heart disease patients Vpm increased during pacing (P smaller than 0.01) while Vpmr did not differ significantly. During exercise both Vpm and Vpmr were unchanged. In patients with coronary heart disease paced to angina, diastolic logarithmic pressure-volume relationship showed change in slope (P smaller than 0.05) of the regression line and upward shift in intercept b (+0.25; P smaller than 0.001). Ischemia produced an impaired contractile state, delayed relaxation and generation of active diastolic tone in the intact ventricle.
Eur J Cardiol 1975 Jun
PMID:Left ventricular contraction and relaxation in patients with coronary heart disease. 113 9

The pathological processes underlying the symptom of mitral insufficiency appearing during the course of acute myocardial infarction are reviewed. The mitral valve apparatus can be considered as being composed of fibrous elements (the annulus fibrosus, the valve leaflet and the chordae tendineae), the left atrial endocarduim and the muscular elements (the papillary muscles together with their supporting myocardium). Since the fibrous elements are avascular, it is concluded that they are unlikely to be directly affected by ischemia. For this and other reasons dilatation of the mitral annulus is not considered a cause of incompetence. It is suggested that muscular involvement is the most likely cause of mitral incompetence during acute myocardial infarction. The syndrome of 'papillary muscle dysfunction' is therefore reviewed under the headings of (1) conditions producing abnormal spatial orientation of the muscles, (2) conditions producing abnormal or absent contraction of the muscles and (3) conditions producing improper timing of muscular contraction. Cases are illustrated which demonstrated generalized dilatation of the left ventricle, localized dilatation and both complete and imcomplete papillary muscle rupture. Mitral insufficiency under these circumstances may ensue from either improper orientation or improper functioning of the muscular elements of the mitral valve apparatus, or from both. It is also emphasized that direct involvement of the papillary muscles by the ischemic process is not necessary for incompetence to occur, and that most cases of mitral incompetence complicating the acute stage of myocardial infarction are of transient nature, resolving during the recovery phase.
Eur J Cardiol 1975 Jan
PMID:Mitral insufficiency complicating acute myocardial infarction. 114 72

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.
Adv Cardiol 1975
PMID:Effect of reperfusion in acute ischemia and infarction. 115 38


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