Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The risk of instantaneous death due to ventricular fibrillation was compared in resting and exercised dogs. Three weeks before testing, all dogs had bipolar left ventricular stimulating electrodes implanted and a reversible snare was placed around the anterior descending coronary artery. The dogs were randomly assigned to either an exercise (13 dogs) or a control (12 dogs) group. We measured ventricular fibrillation thresholds (VFTs) in all dogs before and after inducing ischemia by tightening the snare while the dogs stood at rest. The next day, nonischemic and ischemic VFTs were redetermined for control dogs at rest and for the exercise group during a treadmill run. No statistically significant changes were noted within and between groups in nonischemic or in ischemic VFTs at rest. In five exercise dogs, spontaneous ventricular fibrillation occurred during the first 8 minutes of the ischemic run, For the eight other exercise dogs, running increased the mean drop in VFTs during coronary occlusion by 23% (p less than 0.01). These data suggest that moderate dynamic exercise may greatly enhance the risk of ventricular fibrillation and sudden death in the presence of myocardial ischemia. In the absence of ischemia, exercise does not appear to increase vulnerability to ventricular fibrillation.
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PMID:Effect of submaximal exercise on vulnerability to fibrillation in the canine ventricle. 47 84

Five patients with ischemic heart disease were resuscitated after experiencing ventricular fibrillation in a medically supervised exercise program. Four subsequently had successful myocardial revascularization (three prior to hospital discharge), and three have returned to an exercise prescription of reduced intensity. Multivessel operative coronary disease is common in patients experiencing ventricular fibrillation. Ventricular fibrillation may occur unpredictably (two to 48 months) in duration of exercise. Exercise fitness centers for such patients should be medically supervised and equipped with a defibrillator and appropriate drugs.
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PMID:Ventricular fibrillation in a medically supervised cardiac exercise program. Clinical, angiographic, and surgical correlations. 57

The presented analysis concerns the clinical and electrocardiographic data of dynamic examinations of 15 patients in whom ECG recorded a deep and wide ("gigantic") inverted T-wave. In 5 cases the clinical and electrocardiographic data were compared with the anatomic ones. It was demonstrated that a wide and deep inverted T-wave is common in ischaemic heart disease and inflammatory lesions. Focal myocardial lesions (predominantly in the ventricular septum) combined with atrioventricular conductivity disorders in the His-Purkinje system were found to play a definite role in the genesis of the "gigantic" T-wave. In some cases the wide T-wave may develop due to a fusion of T and U-waves. Patients with such ECG alterations suffer severe rhythm disorders in the form of frequent polytopic extrasystoles, paroxysmal ventricular tachycardia, ventricular fibrillation.
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PMID:[Origin of the deep and wide T-wave in myocardial diseases]. 59 83

To study the action of aspirin upon the myocardium per se, independent of thrombosis, coronary occlusion with a balloon catheter was induced in 53 anesthetized dogs divided into two groups. One group (N = 20) was treated daily with aspirin (600 mg/dog) for seven days and another (N = 33) was untreated. Left ventricular hemodynamics and precordial ECG mapping were used to assess the influence of myocardial ischemia over a four hour period. There were no significant differences in left ventricular function or extent of injury as judged by ECG mapping between the two groups. However, there was a significant decrease in the incidence of ventricular fibrillation in the treated dogs (5% vs 39%). Serial plasma samples for free fatty acid determination showed a significant rise in the untreated group. Aspirin blocked the FFA increment in the treated animals. Tissue samples from the ischemic area of left ventricle exhibited a significant reduction of the sodium and water increments, as well as a lesser potassium loss in the treated animals compared to the controls and may have been the basis for the lower incidence of arrhythmias. Since infusion of 51Cr labelled platelets showed no myocardial accumulation of platelets in either group, microthrombi did not appear to contribute to the observed differences.
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PMID:Antiarrhythmic effects of aspirin during nonthrombotic coronary occlusion. 63 Jun 76

Nine hundred and sixty-nine coronary care patients with acute myocardial infarction were followed for one year. Atrial fibrillation was documented in 107 patients. Compared with patients without atrial fibrillation, those with this arrhythmia were older, had clinically more severe infarction, and had a higher frequency of ventricular fibrillation or tachycardia, and right bundle-branch block. They had similar past histories of ischaemic heart disease and coronary risk factors. Patients with atrial fibrillation had a higher total mortality at 3 months and 12 months. The presence of atrial fibrillation was not associated with any significant increase in mortality within any decade of age or within any subgroup of clinical severity of infarction. The frequency of atrial fibrillation was similar in anterior and inferior infarction. Multiple episodes of atrial fibrillation occurred in 52 patients and episodes usually lasted for over 1 hour. In 50% of patients with single episode of atrial fibrillation the initial ventricular rate was greater than 120 beats per minute.
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PMID:Effects of atrial fibrillation on prognosis of acute myocardial infarction. 63 85

The prognostic implications of a past history of ischaemic heart disease, site of infarction, ectopic ventricular dysrhythmias (ventricular premature beats (VPB) more than one in 10 sinus beats, and/or ventricular tachycardia (VT), ventricular fibrillation (VF), atrioventricular blocks (AVB), bundle branch blocks (BBB)) and the occurrence of electrical and/or mechanical complications during stay in the Coronary Care Unit (CCU) were analysed in 154 women with definte (WHO Class 1) acute myocardial infarction, admitted sequentially to the CCU over a four-year period. The prognosis in these women was then compared with the prognosis in a group which represented the general male population in the CCU and an age-matched group of men. The results showed that the long-term prognosis in women with acute myocardial infarction is remarkably similar to age-matched groups of men.
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PMID:Acute myocardial infarction in women. The influence of age on complications and mortality. 65 40

Among 1,118 admissions for acute ischemic heart disease to St. Luke's Hospital in Malta during 1963-72, there were 945 (84.5%) cases of acute myocardial infarction (AMI) and 173 (15.5%) cases of acute coronary insufficiency (ACI). The ratio of AMI to ACI was higher among diabetic than among nondiabetic patients, especially among women. In comparison with the nondiabetic AMI patients, the diabetics, especially women, had a significantly longer interval between onset of symptoms and hospitalization and more often had painless infarcts, both of which resulted in delay of adequate treatment; the diabetics with AMI han more complications and a significantly higher case fatality rate (20.8vs. 14.3% for nondiabetics; in diabetic women the rate was 24.1%). in fatal cases of AMI the mean age at death was lower among diabetics than among nondiabetics. In fatal cases among diabetics death was more often associated with an anteroseptal AMI site, and was the result of one or more of the following: left heart failure (61.6%), shock (38.3%), sudden death from ventricular fibrillation (13.3%), atrioventricular block (8.3%), or systemic or pulmonary arterial thromboembolism (6.5%); it was very rarely the result of diabetic ketosis.
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PMID:Effect of diabetes on the course of acute myocardial infarction in Malta. 66 18

The sequence of localized changes in ventricular repolarization time during and after temporary coronary artery occlusion was studied in 10 open chest dogs. Immediately after the onset of coronary occlusion functional refractory periods (FRPs) prolonged slightly in the ischemic area, then shortened with continued occlusion. Within the first minute following release of occlusion, FRPs underwent a further brief decrease in duration. By varying the period of occlusion from 1 1/2 to 6 1/2 min, evidence was obtained that the post-release shortening of RFPs was temporally related to release of the clamp and not to the onset of occlusion. Ventricular fibrillation occurred in 2 dogs, in each instance soon after release of the coronary artery occlusion. The possible relationship of these experimental FRP changes to waveform abnormalities and arrhythmias in ischemic heart disease is discussed.
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PMID:Changes in ventricular recovery properties during and after temporary coronary artery occlusion. 69 Dec 76

Alterations of autonomic tone appear to have important effects on the electrical stability of the heart. Since altered electrical stability, ventricular fibrillation, is the cause of death in the majority of patients who die from ischemic heart disease, the effects of the autonomic nervous system on ventricular electrical stability have been examined. Increased vagal tone increases the electrical stability of the heart and reduces the incidence of spontaneous ventricular fibrillation after coronary occlusion. These salutary effects of increased cholinergic tone appear to be mediated by cholinergic innervation of the ventricular conducting system. Conversely, increased adrenergic tone decreases the electrical stability of the heart and increases the propensity of the heart to develop ventricular arrhythmias during coronary occlusion. The interaction of the adrenergic and cholinergic system during myocardial ischemia may be one of the important determinants of survival in patients with coronary artery disease and acute myocardial infarction.
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PMID:Neural basis for the genesis and control of arrhythmias associated with myocardial infarction. 78 2

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


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