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

The persistent high mortality from power failure resulting from myocardial infarction has stimulated an intensive search for methods of reducing infarct size, which has been shown to relate directly to the occurrence of power failure. By analyzing the time course of myocardial injury during ischemia, the reversibility of lesions with reperfusion, and the characteristics of reversibly injured tissues along the border zone of ischemic areas, concepts have been formulated regarding the possibility of salvaging marginally injured cells. Measures designed to diminish myocardial oxygen consumption, to increase blood flow or oxygen supply to ischemic areas, to increase substrate availability, or to change the degree of swelling and autolysis of injured cells have all been tested in experimental animals with some success. These methods are just beginning to be tested in the clinical setting, and, if successful, will no doubt usher in a new era in medical therapy for acute myocardial infarction.
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PMID:Modification of infarct size. 81 57

Nitroglycerin (NTG) traditionally has bben avoided in the treatment of pain caused by acute myocardial infarction because of the belief that NTG-induced decrease in arterial pressure and concomitant reflex increase in heart rate might extend the ischemic process. However, recent experimental and clinical investigations cast doubt on this concept. For example, when the left anterior descending coronary artery is acutely occluded in normal dogs or in dogs when chronic coronary occlusions and extensive collaterals, NTG reduces ST-segment evevation (and presumably myocardial ischemia). This salutary effect occurs despite lowering of systemic arterial pressure, as long as excessive reflex tachycardia does not result; the magnitude of ischemia reduction is potentiated when methoxamine or phenylephrine are administered simultaneously to abolish the NTG -induced hypotension and reflex tachycardia. NTG and methoxamine treatment also results in 1) reduction of infarct size as (as assessed by gross morphologic examinations and myocardial CPK levels) in dogs subjected to 5 hours of coronary occlusion, and 2) increase in ventricular fibrillation (VF) threshold and reduction of the incidence of spontaneously occurring VF in dogs with acute coronary occlusion. Finally, the effectiveness of NTG during acute myocardial iinfarction (AMI) in man has been studied. Multiple precordial electrodes were used to measure changes in the degree of ST-segment elevation; these changes were used as an index of alterations in myocardial ischemic injury. Patients with normal pulmonary capillary wedge pressures ( less than 15 mm Hg) did not benefit consistently from NTG alone; however, when phenylephrine was administered with NTG (to abolish NTG-induced arterial pressure reduction and reflex increase in heart rate), ST-segment elevation diminished consistently. In patients with elevated wedge pressures ( greater than 15 mm Hg), NTG alone consistently reduced ischemia; addition of phenylephrine often partially reversed this benefit. Thus, administration of NTG, alone or with phenylephrine, appears to reduce myocardial ischemic injury during AMI in man; however, the response to phenylephrine depends upon the presence or absence of LV failure prior to treatment. These experimental and clinical results suggest this form of therapy may be use in reducing infarct size in man, although additional studies are necessary to determine the functional significance of these acute electrophysiologic alterations.
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PMID:Protection of ischemic myocardium by nitroglycerin: experimental and clinical results. 81 59

Echocardiographic septal and posterior wall thicknesses and the percent change with systole were measured in 146 patients with the following diagnoses: acute myocardial infarction (40), chronic coronary artery disease (49), congestive cardiomyopathy (8), atrial septal defect (20), and no cardiac disease (29). Mean diastolic thicknesses for the groups of patients with coronary artery disease and congestive cardiomyopathy were not significantly different from normal although there were abnormal values for individual patients within each group. Mean diastolic thickness of the septum was greater than normal for the group with atrial septal defect (P less than 0.02). Wall thinning with systole was associated with acute infarction or ischemia (P less than 0.0001); decreased thickening (less than normal) commonly occurred in patients with acute myocardial infarction, chronic coronary artery disease, and congestive cardiomyopathy. Patients with atrial septal defect had normal thickening with abnormal motion. Results of this study show that 1) systolic thinning is indicative of an acute event; 2) abnormal changes in systolic wall thickening occur commonly in patients with coronary artery disease or congestive cardiomyopathy; and 3) abnormal wall motion may occur without abnormal wall thickening, as the echoes of patients with atrial septal defect indicate.
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PMID:Systolic thickening and thinning of the septum and posterior wall in patients with coronary artery disease, congestive cardiomyopathy, and atrial septal defect. 83 Jan 97

Myocardial 201Tl uptake and regional blood flow by the microsphere technique were determined in anesthetized dogs undergoing either 20 min of coronary occlusion and 100 min of reperfusion (N = 10) or 120 min of occlusion (N = 4). In both groups, 201Tl was injected intravenously after 10 min of occlusion. In transiently occluded dogs, regional flow at the time of 201Tl administration was reduced to 8 +/- 3% of normal flow in endocardial layers of the central ischemic zone. After 100 min of reperfusion, flow values were not significantly different from normal. 201Tl activity after reperfusion rose to 56 +/- 5% of normal, demonstrating that redistribution of the radionuclide occurred during the reflow period. In animals with persistent occlusion, there was a significant relationship between 201Tl uptake and flow (r = 0.95) and no evidence of redistribution of 201Tl during the two hour occlusion period. In another five dogs receiving 201Tl, serial gamma camera images obtained during reperfusion showed increasing uptake of the tracer in apical defects which returned to normal by 4 hours of reflow. Thirteen patients with stable angina received 2 mCi of 201Tl intravenously at peak exercise, and multiple gamma camera images obtained serially. All demonstrated zones of diminished 201Tl uptake 10 min after exercise. Defects which partially or completely disappeared within 1-6 hours postexercise corresponded to areas supplied by coronary arteries with significant stenoses. Persistent defects were present in regions of old myocardial infarction. Six additional patients with acute myocardial infarction demonstrated 201Tl myocardial defects which showed no significant change over 6 hours. Thus, redistribution of 201Tl into ischemic myocardium was demonstrated during transient coronary occlusion in dogs and after exercise stress in man. Sequential imaging after a single dose of 201Tl at the time of exercise may provide a means for distinguishing between transient perfusion abnormalities or ischemia and myocardial infarction of scar.
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PMID:Differentiation of transiently ischemic from infarcted myocardium by serial imaging after a single dose of thallium-201. 83 45

Six men, clinically diagnosed as having coronary heart disease, had postexertional ventricular fibrillation after maximal exercise testing. The common featureof their treadmill performance was "exertional hypotension," that is, a decrease or a limited increase (10 mm Hg) in systolic blood pressure. All six men were successfully resuscitated with electircal defibrillation. The major indication for electrocardiographic monitoring is the detection of major ventricular arrhythmias and changes in QRS-ST-T of acute myocardial infarction or severe ischemia, all of which are urgent indications for stopping exertion. Close supervision both during and after exercise testing is essential, particularly in men with severe coronary artery disease; monitoring of changes in systolic pressure during and shortly after exercise testing is as important as searching for changes in the -S-T segment.
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PMID:Exertional hypotension and postexertional ventricular fibrillation in stress testing. 86 Jun 95

Because of their potential role in the pathogenesis of sudden death, cardiac arrhythmias in patients with coronary artery disease have become the subject of increasing concern and investigation. A series of studies on the problem of ventricular ectopy as it relates to the entire spectrum of sudden death in coronary disease were carried out utilizing continuous portable electrocardiographic monitoring systems. Evaluation of arrthymias during the entire 3 week in-hospital period after acute myocardial infarction in 83 patients revealed that absence of premature ventricular contractions, including their serious forms (multifocal, paired, R on T phenomenon, frequency 5/min or greater) and ventricular tachycardia in the coronary care unit did not exclude their high incidence rate (premature ventricular contractions 30 percent, serious forms 41 percent, ventricular tachycardia 6 percent) in the late hospital phase. Because late hospital serious forms of ventricular ectopy correlated with arterial hypoxia and elevated left ventricular filling pressure in the coronary care unit and with persistent S-T abnormalities, the extent of left ventricular dysfunction and ischemia with acute myocardial infarction appeared precursors to these arrhythmias. Study of ventricular ectopy in the late hospital phase of acute myocardial infarction indicated that ventricular ectopy and particularly its serious forms and prognostic significance relative to subsequent sudden death after discharge; the extent of predischarge S-T segment alterations was greater in subjects who died suddenly than in survivors, suggesting that persistent ischemia or segmental dyssynergy, or both, predisposed to lethal arrhythmias. Among 86 patients with chronic coronary disease documented by catheterizerization, 87 percent had ventricular ectopy and 62 percent serious ventricular arrhythmias, in contrast to 34 percent and 9 percent, respectively in normal subjects; frequency of serious forms of ventricular ectopy was related to extent of coronary atherosclerosis. Correlation of standard electrocardiograms with continuous Holter electrocardiograms in 101 patients with chronic coronary disease over 24 months revealed that the former modality was insensitive in arrhythmia detection; patients free of ventricular ectopy by serial standard electrocardiograms had a 62 percent incidence rate of serious forms of ventricular ectopy and 6 percent ventricular tachycardia on portable continuous monitoring. Additional studies of patients with chronic coronary disease showed that assessment of both the type of ventricular ectopy and the setting in which it occurs provides the most meaningful characterization of risk of sudden death. These systematic series of observations identify premature ventricular ectopic beats as important and separate risk factors in coronary disease...
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PMID:Identification of sudden death risk factors in acute and chronic coronary artery disease. 87 Nov 8

Symptoms, signs, hemodynamic and electrocardiographic responses of 12 patients with acute myocardial infarction were studied before, during and after three activities: activity I, sitting upright; activity II, walking to the adjacent toilet; and activity III, walking on a treadmill set at 1.2 mph (1.9 km/hr) at 0, 3 and 6% successive gradients. The three activities were studied respectively at three, six and ten days (means) after infarction. Weakness was the most commonly occurring symptom. Mean systolic blood pressure fell 9 mm Hg upon assumption of the upright position (activity I) and was sustained for the five minutes of sitting. The systolic blood pressure drop was only 3.5 mm Hg with activity II. During activity III, one patient developed angina. Between rest and the 6% treadmill gradient, systolic blood pressure, heart rate and pressure-rate product rose 29 mm Hg, 26 beats/minute and 64 units, respectively. Electrocardiographic evidence of ischemia was observed in two patients during activity I, in two patients during activity II, and in one patient during activity III, but was insufficient for stopping the activities. Similarly, two patients developed minor arrhythmias, one with activity I and one with activity III. The use of this low-level treadmill test before discharging the patient from the hospital proved to be safe and feasible for obtaining objective data to assess the patients' ability to perform activities requiring equal exertion at home. Successful performance of these three activities before leaving the hospital should provide useful criteria for discharge of a patient with myocardial infarction.
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PMID:Progressive ambulation and treadmill testing of patients with acute myocardial infarction during hospitalization: a feasibility study. 87 Dec 37

Fifty patients with acute myocardial infarction were studied serially to evaluate the extent and nature of functional cardiovascular impairment and the time course of recovery. Reinfarction or death occurred in six patients. Peak workload during bicycle exercise in a subgroup of 25 patients with maximal initial test and complete follow-up increased from 334 to 409 kpm/min (P less than 0.01) bwtween three and six weeks. There was further significant (P less than 0.01) improvement between three and six months from 438 to 488 kpm/min. The incidence of ischemia at a constant workload decreased between three and six weeks without any significant changes in heart rate or blood pressure. Mean cardiac output during exercise at three months was 6.5 and at six months 7.8 L/min (P less than 0.05). Corresponding values for stroke volume were 61 and 72 ml (P less than 0.05). The data suggest that in clinically stable patients there is an early improvement of the relation between myocardial oxygen supply and demand and a late improvement of functional capacity associated with increased stroke volume and cardiac output.
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PMID:Cardiovascular function during early recovery from acute myocardial infarction. 92 62

In 12 patients affected by acute myocardial infarction complicated only by ventricular extrasystoles, verapamil was highly effective in the control of the arrhythmias. This result is in agreement with the experimental finding that ischemia inactivates partially or totally early Na+ inward currents, so that fast fibers become slow fibers. The efficacy of verapamil stresses the importance of these fibers which have acquired a slow response in the genesis of arrhythmias due to acute coronary attacks and opens interesting therapeutical prospects.
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PMID:[The antiarrhythmic effects of verapamil in acute myocardial infarction. Considerations on the possible action mechanism (author's transl)]. 92 57

The degree of vectorcardiographic ST-segment elevation was employed as an index of myocardial ischemic injury in a study of 27 patients after acute myocardial infarction (AMI). The ST-segment vector magnitude (STVM) was derived from the continuously recorded modified Frank vectorcardiogram and was plotted serially by hours after onset of AMI. The STVM in normal subjects was 51.1 +/- 7.1 muV (mean +/- SE). A standard deviation of the pooled variance of 15.2 muV was obtained in a group of control patients and a change of more than 2 SD (greater than 30 muV) in an individual STVM was considered to be significant. The STVM progressively decreased in patients who survived without clinical complications while it remained elevated in those with congestive heart failure. A modest, sustained re-elevation of STVM was observed in patients who developed pericarditis, and a significant late average increase of 64 muV occurred in survivors with infarct extension. In contrast, STVM underwent a major increase in patients who died. In five of these six patients without associated pericarditis a mean increase of 164 muV was recorded in the last 5-12 hours of life. While death was clinically predictable in two patients with cardiogenic shock, it was not so for the four other patients who died. Thus, major increases in STVM frequently suggested significant new ischemic injury and were often premonitory to sudden death after AMI. The increases preceding death implied that not only ventricular extopy but also lethal conduction abnormalities after AMI might be ischemia-related.
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PMID:ST-segment variations after acute myocardial infarction. Relationship to clinical status. 97 71


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