Ventricular fibrillation resulting from ischemia at a site remote from previous myocardial infarction

Patterson, Eugene; Holland, Kurt J.; Eller, Brian T.; Lucchesi, Benedict R.

doi:10.1016/0002-9149(82)90484-2

Cited by 91 publications

(19 citation statements)

References 23 publications

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“…It may be the sole cause in the absence of a previous MI or it may trigger VF in its presence. Experimental studies have suggested an increased propensity to VF if ischaemia was induced at a site remote from a previous infarction [64] . However, in another series, macroscopically visible coronary artery thrombus was reported in only 13·4% of 500 cases of SCD due to coronary artery disease, and yet another study has reported acute coronary thrombus in 49% of 206 cases of SCD suspected of being ischaemic in origin [6,65] .…”

Section: Autopsy Datamentioning

confidence: 99%

Task Force on Sudden Cardiac Death of the European Society of Cardiology

Priori

Aliot

Blomström‐Lundqvist

et al. 2001

European Heart Journal

775

445

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Section: Autopsy Datamentioning

confidence: 99%

Task Force on Sudden Cardiac Death of the European Society of Cardiology

Priori

Aliot

Blomström‐Lundqvist

et al. 2001

European Heart Journal

775

445

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“…Although the clinical relevance of this model for producing sudden death merits further investigations it seems useful for the preclinical evaluations of pharmacologic interventions designed to prevent fibrillation (5,20). It can also be indicated that compounds which increase the availability of endogenous PGI2 may serve as an approach toward the improvement of the clinical situation of patients at risk for ventricular fibrillation.…”

Section: Discussionmentioning

confidence: 99%

“…This could contribute to postinfarction angina pectoris (4) and sudden coronary death if the myocardial fibrillation threshold had been lowered by the previous pathologic event. Accordingly, a conscious canine model of sudden death was used similarly to a recent publication (5). This model consists of provocation of ventricular fibrillation as the conse-…”

Section: Introductionmentioning

confidence: 99%

Prostacyclin prevents ventricular fibrillation in a canine model of sudden cardiac death

Fiedler

Mardin

1986

Basic Res Cardiol

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The antifibrillatory, antithrombotic and hemodynamic properties of intraventricular prostacyclin (PGI2) application were studied in conscious canine model of sudden cardiac death. In anesthetized dogs, a wire electrode was implanted into the left circumflex coronary artery (LCX) and acute myocardial ischemia was produced by 90 min occlusion of the left anterior descending coronary artery (LAD) followed by reperfusion. An intracardiac pressure transducer measured ventricular pressure, heart rate, filling pressure and dP/dt. The ECG was obtained from subcutaneous chest needles. Six days later while in ambulatory state, a 180 microA DC current was applied for 4 h to the LCX intimal lining in Tris-HCl (n = 10) and PGI2-treated dogs (50 and 100 ng/kg/min, 11 and 12 dogs, respectively). Myocardial injury and coronary thrombosis induced by electrical stimulation produced ventricular fibrillation in all vehicle-treated dogs at 145 +/- 33 min (mean +/- S.D.). In PGI2-treated hearts only 2 animals fibrillated at 150 +/- 29 min and 180 +/- 52 min following 50 and 100 ng/kg/min of the prostanoid, respectively. Thus, 18/23 PGI2-treated dogs survived 4 h electrical stimulation of the artery. Within the LAD perfusion zone infarction was observed of equal volumes in vehicle and PGI2-treated animals. No ischemia occurred distal to the LCX coronary thrombosis. Ventricular pressure fell in all groups. Heart rate increased in the controls and those animals treated with 50 ng/kg/min PGI2 while 100 ng/kg/min PGI2 increased heart rate by 22 +/- 5% (p less than 0.05). Filling pressure increased in controls but fell in the PGI2-treated hearts. The results indicate that PGI2 can prevent ventricular fibrillation resulting from acute ischemia at a site distant to previous myocardial ischemia with superimposed intimal injury and coronary thrombosis. The PGI2 properties are due to prevention of coronary thrombosis and the occlusion of the artery. Antifibrillatory effects of the prostanoids are suggested.

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“…Lucchesi and co-workers [Patterson et al, 1982;Lucchesi, 1984;Lynch and Lucchesi, 19871 advocated a conscious dog model of sudden death in which a second ischemia zone (resulting from thrombosis in the circumflex coronary artery) was produced at a distance from a previously infarcted zone (by occlusion and reperfusion of the LAD coronary artery). A PES procedure could also be incorporated in the testing.…”

Section: Rational Approach and Urgent Need For Better Antiarrhythmic/mentioning

confidence: 99%

Current concepts and animal models of sudden cardiac death for drug development

Chan¹,

Cervoni²

1990

Drug Development Research

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Chan, P.S., and P. Cervoni: Current concepts and animal models of sudden cardiac death for drug development. Drug Dev. Res. 19:199-207, 1990.Sudden cardiac death (SCD) or sudden coronary death, occurring in patients with unstable angina (angina at rest), myocardial ischemia with or without myocardial infarction (MI), and congestive heart failure (CHF), emerges as one of the most important challenges in cardiovascular medicine at present. Of the 1.5 million cases of myocardial infarction that occur each year in the U.S., about 540,000 patients will die and more than 300,000 of these will die before they reach a hospital, mostly due to ventricular fibrillation (VF) and/or SCD. About 4.8 million people alive in the U.S. have a history of myocardial infarction, angina pectoris, or both and are prime candidates for SCD. About 3 million people in the U.S. have congestive heart failure (CHF) and about 400,000 new cases are reported each year. One year mortality due to CHF is 33-58% and about 45% of the deaths are sudden. These patients were not those who had deleterious hemodynamic parameters whose demise could be predicted; they were those that died suddenly and unexpectedly of VF. Current pharmacological intervention in patients with a documented myocardial infarction with marketed antiarrhythmic agents has not reduced the overall mortality of SCD significantly. This suggests that an efficacious antiarrhythmic/antifibrillatory agent for the prevention of SCD does not exist at present and that there is an urgent need for such an agent.

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Ventricular fibrillation resulting from ischemia at a site remote from previous myocardial infarction

Cited by 91 publications

References 23 publications

Task Force on Sudden Cardiac Death of the European Society of Cardiology

Task Force on Sudden Cardiac Death of the European Society of Cardiology

Prostacyclin prevents ventricular fibrillation in a canine model of sudden cardiac death

Current concepts and animal models of sudden cardiac death for drug development

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