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)

Several hypotheses, developed in the early years of arrhythmology, and frequently used for the explanation of many types of clinical tachyarrhythmias, are often based on experiments on unusual models, unphysiologic interventions, or, in some instances, on erroneously interpreted histologic findings. However, it can be demonstrated that several of these hypotheses are valid. Focal activity, unidirectional block, extremely slow conduction velocity, differences in conduction velocity in closely adjacent regions, reentry of the excitation wave, circulating excitation waves in small or large regions of the heart and other postulated mechanisms as, for example, entrance and exit block, local ventricular fibrillation, appear to be involved in the causative mechanisms of clinical tachyarrhythmias. A multicausal genesis of at least some of these must be considered seriously, particularly those which occur in acute or chronic coronary heart disease. A recent suggestion that the injury current might be involved in the genesis of ventricular tachyarrhythmias in acute myocardial ischemia and infarction is supported by observations on several properties of this current. Progress has been made in recent years but large gaps in our knowledge of mechanisms causing arrhythmias are still present.
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PMID:Mechanisms of tachyarrhythmias, past and present. 8 Nov 32

Three patients with ischaemic heart disease died suddenly while being monitored with an ambulatory tape recorder. Two had terminal ventricular fibrillation initiated by paired bidirectional ventricular ectopic beats against a background of scattered ectopic activity; both had had ventricular tachycardia during routine treadmill exercise testing in the week before death. The third patient developed bizarre ventricular complexes followed by asystole. Sudden death may be due to ventricular fibrillation initiated by paired ventricular ectopic beats with changing morphology, or asystole following bizarre ventricular complexes. Exercise testing may have an important predictive value.
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PMID:Sudden death during ambulatory monitoring. 8 92

The effect of nitroglycerin on vulnerability to ventricular fibrillation was examined in 44 chloralose-anesthetized dogs. In 19 animals ventricular fibrillation threshold was measured before and during a 10 minute period of occlusion of the left anterior descending coronary artery followed by abrupt release of occlusion. Fibrillation threshold was determined using the single stimulus and train of stimuli methods. The influence of nitroglycerin on vulnerability was assessed with and without prevention of the drug's hypotensive effect by intravenous injection of phenylephrine. In the nonischemic myocardium, infusion of nitroglycerin alone or in combination with phenylephrine did not alter the ventricular fibrillation threshold. However, during both coronary occlusion and reperfusion, administration of nitroglycerin alone afforded partial protection against vulnerability to ventricular fibrillation. Nearly complete protection was imparted by combined administration of nitroglycerin and phenylephrine. The incidence of spontaneous ventricular fibrillation during reperfusion was significantly reduced by combined administration of nitroglycerin and phenylephrine. It is concluded that infusion of nitroglycerin decreases susceptibility to ventricular fibrillation during both acute myocardial ischemia and reperfusion and that this beneficial action is substantially enhanced when the drug's hypotensive effect is prevented.
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PMID:Effect of nitroglycerin on vulnerability to ventricular fibrillation during myocardial ischemia and reperfusion. 10 8

Although myocardial ischemia may occur in thyrotoxic patients with normal coronary arteries, the mechanism remains unclear. This report describes a woman with hyperthyroidism who had ventricular fibrillation during an apisode of myocardial ischemia. The event was documented with continuous ambulatory electrocardiography. Subsequent angiography revealed normal coronary anatomy with spasm of the right coronary artery that disappeared after ingestion of one sublingual nitroglycerin tablet. The angina, electrocardiographic evidence of myocardial ischemia, ventricular arrhythmias and the patient's need for nitroglycerin were eliminated after she became euthyroid. These findings suggest that coronary spasm may be associated with myocardial ischemia and arrhythmias in a hyperthyroid patient.
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PMID:Coronary spasm with ventricular fibrillation during thyrotoxicosis: response to attaining euthyroid state. 10 11

Continuously recorded bipolar electrograms were obtained simultaneously from epi-, endo-, and mid-myocardial regions of the ischemic and normal zones of cat left ventricle in vivo after coronary occlusion, analyzed by computer, and compared to regional cyclic AMP levels. Regional cyclic AMP content was used as an index of the combined local effects of: (a) efferent sympathetic nerve discharge; (b) release of myocardial catecholamines due to ischemia; and (c) circulating catecholamines. Ischemia resulted in a progressive increase in pulse width and rise time and a decrease in rate of rise of voltage (dV/dt) of the local electrograms from ischemic zones reaching a maximum within 2.4+/-0.3 min (mean+/-SE) at the time of onset of severe ventricular dysrhythmias, all of which returned toward control before the cessation of the dysrhythmia (33.5+/-1.5 min after coronary occlusion). Increases in cyclic AMP in ischemic zones preceded corresponding increases in the frequency of premature ventricular complexes (PVCs). Propranolol inhibited the increases in cyclic AMP and reduced the frequency of PVCs in animals without ventricular fibrillation. In animals with ventricular fibrillation, cyclic AMP was significantly elevated in normal and ischemic zones compared to animals with PVCs only. Electrical induction of PVCs or ventricular fibrillation in ischemic and nonischemic hearts failed to increase cyclic AMP. The results suggest that the changes in regional adrenergic stimulation of the heart may contribute to perpetuation of ventricular dysrhythmia and the genesis of ventricular fibrillation early after the onset of myocardial ischemia.
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PMID:Mechanisms contributing to malignant dysrhythmias induced by ischemia in the cat. 20 67

During the four year period from 1972 to 1975, eleven patients, eight with recurrent and three with first attacks of ventricular fibrillation, underwent aortocoronary bypass graft and/or resection of ventricular aneurysm. All patients had old myocardial infarction from seven weeks to six years. Left ventricular angiography demonstrated discrete aneurysm of the anterior wall of the left ventricle in nine of the patients and akinesis or hypokinesis of the anterior and posterior wall of the left ventricle in the remaining two. Coronary angiography was carried out in ten patients and revealed significant disease of the left anterior descending and right coronary arteries in ten and nine patients, respectively. There was no operative mortality, and there were two late deaths. Eight patients have improved significantly and have had no further sign of ventricular irritability. The present study indicates that aortocoronary bypass graft and/or resection of ventricular aneurysm is an effective method of therapy for patients with repeacted ventricular fibrillation who have ventricular aneurysm and ischemic heart disease.
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PMID:The treatment of patients with recurrent ventricular fibrillation. 30 May 71

Bretylium tosylate (Bretylol) has recently been approved for parenteral use against resistant ventricular arrhythmias. The pharmacologic action of bretylium is complex, and its antiarrhythmic action differs significantly from other drugs. Bretylium is an adrenergic neuronal blocking agent taken up selectively at peripheral adrenergic nerve terminals, where it initially releases norepinephrine (sympathomimetic effect) and then produces adrenergic neuronal blockade. It has direct cardiac membrane effect to prolong action potential duration and effective refractory period but, unlike other membrane active antiarrhythmic agents, does not depress conduction velocity or automaticity. Bretylium increases ventricular fibrillation threshold and prevents the decrease in ventricular fibrillation threshold associated with myocardial ischemia. It does not depress myocardial contractility. Clinical studies have shown parenteral bretylium to be effective in suppressing ventricular arrhythmias, particularly recurrent, drug resistant ventricular tachycardia or ventricular fibrillation.
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PMID:Bretylium tosylate: a newly available antiarrhythmic drug for ventricular arrhythmias. 38 Apr 36

The systemic hemodynamic and myocardial effects of potent vasodilators administered directly into the left coronary artery were determined and compared with the actions of contrast material in 10 anesthetized dogs in the normal state and in the presence of segmental myocardial ischemia. Contrast material (Renografin 76) caused systemic hypotension, rise in left ventricular diastolic pressure and decreases in LV dp/dt and dp/dt/LVP in both states. Doses of ATP (7.2 microgram/kg and 20 microgram/kg/min) which are maximally effective in augmenting coronary blood flow caused only mild arterial hypotension and minimal inotropic effects in both states. Nitroglycerin (3 microgram/kg and 10 microgram/kg/min) induced no inotropic effects but slightly greater arterial hypotension than ATP in both states. On the other hand, papaverine HCl (300 microgram/kg and 800 microgram/kg/min) induced profound increases in LV dp/dt and dp/dt/LVP, decreases in LVEDP and arterial hypotension in the non-ischemic state. In the presence of segmental ischemia, papaverine HCl caused significantly less increases in LV dp/dt and dp/dt/LVP, paradoxical increases in LVEDP in 5 dogs and ventricular fibrillation in 3 dogs. Thus, maximally effective vasodilatory doses of ATP causes only small alterations in hemodynamics and myocardial contractile state of the normal and ischemic heart. Similar doses of papaverine induce profound positive inotropic effects which are apparently deleterious to the ischemic heart.
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PMID:Comparative hemodynamic effects of coronary vasodilators and contrast material on the normal and ischemic canine myocardium: determination of the optimal agent for clinical augmentation of coronary blood flow. 40 73

The overall results over three and a half years of the treatment of ventricular fibrillation secondary to ischaemic heart disease in the Royal Sussex County Hospital were reviewed. Records of all patients who were brought to hospital by resuscitation ambulances or who were admitted to the coronary care unit from any source were analysed. Eighty-seven of the 174 patients (50%) who developed ventricular fibrillation were discharged. The survivors included 13 out of 61 patients (21%) in whom fibrillation was secondary to cardiogenic shock or severe left ventricular failure. The presence of resuscitation equipment and nursing staff trained to use it in the general wards and emergency areas ensured a uniformly high success rate throughout the hospital, similar to that achieved in the coronary care unit. Prompt defibrillation in the general wards and the accident and emergency department may improve overall survival.
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PMID:Hospital resuscitation from ventricular fibrillation in Brighton. 44 62

A 60-year-old patient with variant angina was shown to have myocardial ischemia in two different regions supplied by separate major coronary arteries. Neither artery had significant coronary atherosclerotic obstruction. Ventricular fibrillation was noted during ST-segment elevation in anteroseptal leads. The attacks of pain and arrhythmias disappeared during nifedipine therapy.
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PMID:Multivessel coronary artery spasm. 44 62


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