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Query: UMLS:C0022116 (ischemia)
 91,303 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

The antiarrhythmic activity of the aminosteroid Org 6001 was investigated in young pigs (20-28 kg). Ventricular arrhythmias were induced by restriction of the flow in the left anterior descending coronary artery (LAD) to 25% of its control value during a period of 30 minutes. Nine out of 30 control animals died in this period due to ventricular fibrillation. None of the 19 animals treated with Org 6001 (5-10 mg/kg) or the 12 animals treated with lidocaine (2.75-3.50 mg/kg) fibrillated. Moreover, the number of premature ventricular beats was greatly reduced in pretreated groups compared with the untreated group (P less than .001). The first derivative of left ventricular pressure decreased with 25% (P less than 0.001) after administration of Org 6001. However, during 30 minutes of LAD flow reduction to 25% of control, the adverse effects of Org 6001 were less than those of lidocaine. Myocardial lactate production indicated some delay in onset of ischemia. However, there was no indication that this beneficial effect was long-lasting. When after 30 minutes of LAD flow reduction to 25% of control, the LAD was completely occluded between its second and third branch, all untreated animals fibrillated within 120 minutes, whereas 4 of the 19 animals treated with Org 6001 and 3 of the 12 treated with lidocaine survived. It is concluded that Org 6001 has antiarrhythmic properties in the ischemic pig heart which compare favorably with those of lidocaine.
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PMID:Antiarrhythmic, metabolic and hemodynamic effects of Org 6001 (3alpha-amino-5alpha-androstan-2beta-ol-17-one-hydrochloride) after coronary flow reduction in pigs. 63 69

Ventricular dimensions by surface echocardiography and intraventricular pressures were monitored in 27 dogs before and during ventricular fibrillation (VF) induced by coronary embolization (nine dogs), potassium infusion (nine dogs) and calcium infusion (nine dogs). Left ventricular diameter (LVD) fell by an average of 10.3 mm during the first 30 s after the onset of VF induced by ischemia or potassium and remained smaller than the prefibrillation end-diastolic LVD during the ensuing 10 min. LVD fell during calcium infusion, and after the onset of VF it remained only slightly larger than the preinfusion end-systolic LVD. Right ventricular (RV) diameter increased progressively for the first 2 min during VF an average of 15.9 mm. The failure of LV size to increase during VF was explained by a pressure gradient inhibiting LV filling during the early phase of VF. Despite progressive RV filling, pressure in the more compliant RV remained lower than in the LV, which exhibited reduced compliance during VF. Therefore, cardiac dilation during VF appears to be confined to the RV, and inhibition to LV filling is an important feature of the syndrome.
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PMID:Left and right ventricular dimensions during ventricular fibrillation in the dog. 68 90

New-generation high-performance aircraft can produce levels of high sustained +Gz which may exceed man's physiological capacity to withstand such stress. The severity of this stress has led to concern that sudden incapacitation due to coronary heart disease could occur during sustained +Gz. This report presents results obtained from an apparently asymptomatic miniature swine with a severe stenosis of the left anterior descending branch of the left coronary artery. Regional coronary blood flow was measured with the radiolabeled microsphere technique using 9 +/- 0.8 microgram diameter microspheres. Under resting conditions, myocardial blood flow was marginally depressed in the areas distal to the coronary stenosis. When the animal was exposed to +7 Gz, a large portion of the heart became acutely ischemic due to a redistribution of coronary blood flow. After 49 x of exposure to +7 Gz, the animal developed fatal ventricular fibrillation. Histologically, the areas of myocardium supplied by the stenosed vessel showed a variety of ischemia-induced lesions, including infarction and patchy myocardial fibrosis.
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PMID:Regional coronary blood flow at rest and during high sustained +Gz in a miniature swine with subclinical, ischemic, coronary heart disease due to coronary stenosis. 71 74

Subendocardial ischemia develops in hearts that are fibrillated during cardiopulmonary bypass when: (1) the normal ventricle is fibrillated with a sustained electrical stimulus, (2) the hypertrophied ventricle is allowed to fibrillate spontaneously, (3) the fibrillating heart becomes distended, or (4) the perfusion pressure is reduced to approximately 50 mm Hg. Myocardial hypothermia reduces cardiac oxygen requirements during fibrillation but does not prevent ischemia when perfusion pressure falls to levels frequently attained during clinical open-heart operations. The ischemia occurs because flow cannot rise sufficiently to meet the metabolic demands of ventricular fibrillation. The forces interacting to impede adequate flow to the subendocardium during ventricular fibrillation are: (1) the compressive forces exerted on subendocardial muscle by the strength of fibrillation, (2) the compressive forces resulting from raised intracavitary pressure due to occlusion or malfunction of the ventricular vent, and (3) the evolution of myocardial edema as ischemia is prolonged. We have abandoned the use of ventricular fibrillation in clinical open-heart operations and now allow the heart to beat continually with adequate perfusion pressure. We have not needed to use inotropic drugs postoperatively after aortic or mitral valve replacement since adopting this technique.
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PMID:Ventricular fibrillation. Its effect on myocardial flow, distribution, and performance. 80 60

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

A man with known coronary heart disease underwent treadmill exercise testing to determine his functional capacity. The test was negative for ischemia. Ventricular ectopic activity was noted at rest and in the recovery period. On the same day, while viewing a sporting event at home, the patient died suddenly. An ambulatory electrocardiographic recording documented ventricular fibrillations as the terminal mechanism. Ventricular ectopic activity and heart rate increased in the two hours prior to death, and ischemic ST-segment depression was noted at the time of the terminal arrhythmia. It is postulated that myocardial ischemia and catecholamine response lowered the threshold to ventricular fibrillation, thus facilitating the emergence of the fatal arrhythmia.
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PMID:Sudden death during ambulatory monitoring. Clinical and electrocardiographic correlations. Report of a case. 83 Feb 11

Sympathetic discharges to the heart were recorded from the left inferior cardiac nerve of 16 dogs. Inferior cardiac nerve activity (ICNA) under normal conditions consisted of grouped discharges, synchronous with the cardiac cycle and modulated by respiration. After ligation of the circumflex branch of the left coronary artery, ICNA declined concomitant with a decline in heart rate and mean aortic pressure. After 30 minutes, when arterial pressure tended to recover toward control values (six dogs), ICNA remained low; in contrast, when arterial pressure dropped to shock levels (three dogs), ICNA increaed. When aortic pressure fell precipitously as a result of ventricular fibrillation, even during the first 30 minutes of ischemia (seven dogs), ICNA immediately increased greatly. The results of this study suggest that acute coronary occlusion produces a cardiocardiac depressor reflex with attenuation of sympathetic discharge to the heart. This reflex, under the experimental conditions studied, gives way to the baroreceptor reflex when aortic pressure drops to critically low levels.
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PMID:Attenuation of cardiac sympathetic drive in experimental myocardial ischemia in dogs. 83 14

Alternans of the elevated ST segment (STEA) was found in 8 of 21 patients (38%) with Prinzmetal's variant angina. In addition to STEA, all eight patients had varying cardiac arrhythmias: multiple premature ventricular depolarizations in eight, ventricular tachycardia in five, and ventricular fibrillation in three. There was no consistent temporal relationship between the occurrence of STEA and the cardiac arrhythmias. Alternans occurred during periods when no arrhythmias were present. All eight patients underwent coronary angiography. Spontaneous coronary artery spasm was documented angiographically in three patients including two who had minimal or no coronary atherosclerotic disease. Six patients had severe, fixed, occlusive coronary artery disease. Possible mechanisms for STEA include: 1) failure of regions of myocardium to depolarize on alternate beats due to variation in conduction and refractoriness between ischemic and nonischemic zones of myocardium, and 2) electrical alternans of the transmembrane action potential during phase 2 and 3 (repolarization) caused by changes in the rate and extent of electrolyte transfer across cell membranes during ischemia. It is postulated that STEA is an electrocardiographic sign in the surface ECG of a dysequilibrium of refractory periods during ischemia and reflects an unstable electrical state of the myocardium.
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PMID:Alternans of the ST segment in Prinzmetal's angina. 83 98

Dispersion of the effective refractory period was measured in anesthetized dogs using a computerized system and bipolar epicardial electrodes or, alternatively, transmural plunge electrodes. Measurements were made at 1 minute intervals during short (5 minute) and long (15 minute) periods of coronary arterial ligation and for 3 to 5 minutes after release of the ligatures. Both transepicardial and transmural temporal dispersion of refractoriness correlated well with the increased vulnerability to spontaneous ventricular fibrillation during short periods of ligation and the relative electrical stability observed toward the end of the longer periods of ligation. During reperfusion, transmural dispersion increased somewhat after ligature release in the longer-term experiments but the increase did not appear adequate to explain the associated large incidence of spontaneous arrhythmias after release. Effective refractory periods measured at one nonischemic and five ischemic electrode sites at intervals as short as 20 seconds revealed abrupt shortening of the refractory period at all ischemic sites during the 1st minute of reperfusion, resulting in a large but short-lived electrical gradient between the ischemic and nonischemic myocardium. This increased dispersion between the ischemic and nonischemic myocardium occurred at a time of maximal vulnerability to reperfusion arrhythmias. However, this increased dispersion was greater after the 5 minute than after the 15 minute periods of ligation and thus does not fully explain the greater incidence of reperfusion arrhythmias after ligature release in the longer-term studies. Although arrhythmias of acute ischemia are associated with increased dispersion of refractoriness within theischemic segment and reperfusion arrhythmias with dispersion between ischemic and nonischemic segments, other electrophysiologic alterations probably play an important role in the genesis of the arrhythmias of reperfusion.
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PMID:Dispersion of effective refractory period during abrupt reperfusion of ischemic myocardium in dogs. 84 60


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