Delayed Development of Ventricular Ectopic Rhythms following Experimental Coronary Occlusion

Harris, Andrew

doi:10.1161/01.cir.1.6.1318

Cited by 673 publications

(200 citation statements)

References 28 publications

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“…A second surge of ventricular arrhythmias occurred 12-20 min following occlusion. This pattern of ventricular arrhythmias occurring after coronary occlusion was essentially similar to that described by previous workers (Harris, 1950;Kaplinsky et al, 1979). On reperfusion of the LAD there was an immediate phase of ventricular tachyarrhythmias The incidence of arrhythmias in all groups of animals was not significantly different during the occlusion period.…”

Section: Introductionsupporting

confidence: 88%

BW A256C, a chemically novel class 1 antiarrhythmic agent. A comparison of in vitro and in vivo activity with other class 1 antiarrhythmic agents

Allan¹,

Donoghue

Follenfant

et al. 1986

British J Pharmacology

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1 BW A256C (5(3)-amino-6-(2,3-dichlorophenyl)-2,3(2,5)-dihydro-3(5)-imino-2-isopropyl-1,2,4-triazine) is a novel class 1 antiarrhythmic agent designed to combine the features ofpotency with reduced central nervous system penetration. 2 BW A256C reduced the maximum rate of depolarization of guinea-pig ventricle and dog Purkinje fibres in vitro (EC5o, 2.2 x 10-6 M and 1.8 x 10-6 M, respectively), being significantly more potent than quinidine, lidocaine, disopyramide and flecainide. BW A256C was also more potent than these agents at inhibiting aconitine-induced arrhythmias in anaesthetized rats; however, unlike these agents, BW A256C was devoid of hypotensive activity at antiarrhythmic doses. 3 In anaesthetized dogs, intravenous administration of BW A256C (0.25-1 mg kg-') caused a dosedependent suppression of ventricular arrhythmias that occurred on reperfusion of an occluded coronary artery. 4In conscious dogs, intravenous infusion (total dose, 1.5 mg kg 1) or oral administration of BW A256C (1.25-5mg kg-') caused dose-dependent suppression of the ventricular ectopic activity that occurred following 20-24 h of permanent coronary artery ligation. 5In the conscious dog, BWA256C was approximately 7 times more potent and was also longer acting than flecainide. 6 Administration of BW A256C was not associated with any evidence of peripheral or CNS toxicity. However, plasma levels 3-4 times greater than the antiarrhythmic levels were associated with a proarrhythmic activity.

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Section: Introductionsupporting

confidence: 88%

BW A256C, a chemically novel class 1 antiarrhythmic agent. A comparison of in vitro and in vivo activity with other class 1 antiarrhythmic agents

Allan¹,

Donoghue

Follenfant

et al. 1986

British J Pharmacology

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“…Under isoflurane anesthesia (30 mg/kg), myocardial infarction was produced by a two-step total occlusion of the left coronary artery using the Harris procedure. 6 Forty-eight hours after occlusion, infarcted hearts were used for the myocyte study.…”

Section: This Investigation Conforms With the Guide For The Care And mentioning

confidence: 99%

2APB- and JTV519(K201)-sensitive micro Ca2+ waves in arrhythmogenic Purkinje cells that survive in infarcted canine heart

Boyden

Dun²,

Barbhaiya³

et al. 2004

Heart Rhythm

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Objectives/Background-Studies from several laboratories have implicated intracellular Ca 2+ dynamics in the modulation of electrical activity. We have reported that abnormal Ca 2+ wave activity is the underlying cause of afterdepolarization-induced electrical activity in subendocardial Purkinje cells that survive in the 48-hour infarcted canine heart. These cells form the focus of arrhythmias at this time postcoronary artery occlusion.Methods-We studied the effects of agonists and antagonists on the abnormal Ca 2+ release activity of Purkinje cell aggregates dispersed from the subendocardium 48 hours postcoronary artery occlusion (IZPCs). Studies were completed using epifluorescent microscopy of Fluo-3 loaded Purkinje cells.Results-Similar to our previous report, highly frequent traveling micro Ca 2+ transients(μCaiTs) and cell-wide Ca 2+ waves were seen in IZPCs in the absence of any drug. Isoproterenol (ISO) increased μCaiTs and cell-wide Ca 2+ waves in Purkinje cells dispersed from the normal heart (NZPCs). In IZPCs, ISO increased cell-wide wave frequency but had no effect on the already highly frequent micro Ca 2+ wave transient activity, suggesting that ISO lowers the threshold of cell-wide generators responding to micro Ca 2+ transients. Drugs that block inward sodium or calcium currents (verapamil, tetrodotoxin) had no effect on Ca 2+ activity in Purkinje cells. Antagonists of intracellular Ca 2+ release channels [ryanodine, JTV519(K201)] greatly suppressed spontaneous Ca 2+ release events in IZPCs. 2APB, an agent that blocks IP 3 receptors, greatly reduced the frequency of Ca 2+ events in IZPCs.Conclusions-In arrhythmogenic Purkinje cells that survive in the infarcted heart, agents that block or inhibit intracellular Ca 2+ release channel activity reduced Ca 2+ waves and could be antiarrhythmic.

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“…31 After this time, arrhythmias gradually decrease in frequency, but the action potential remains, which makes the occurrence of reentry arrhythmias possible. 20 …”

Section: Possible Mechanism Of Ventricular Tachycardiamentioning

confidence: 99%

Sustained ventricular tachycardia as a marker of inadequate myocardial perfusion during the acute phase of myocardial infarction

Sala

Bárcena

Rota

et al. 2002

Clinical Cardiology

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SummaryBackground: Sustained ventricular tachycardia (VT) complicating the acute phase of myocardial infarction (AMI) is a quite rare event but with short-term unfavorable prognosis. The clinical characteristics as well as the therapeutic implications have not yet been well defined.Hypothesis: This paper attempts to prove that VT may be considered a marker of inadequate myocardial perfusion after thrombolysis.Methods: To assess the clinic-electroangiographic characteristics and prognosis of patients with VT occurring within the first 4 days of an AMI, a case-control study was carried out in 23 patients from a total of 1,100 patients (1.9%) hospitalized with AMI between March 1993 and July 1997. These patients were compared with a control group of 131 patients hospitalized consecutively. A statistical analysis was made using the chi-square test, t-test, and logistic regression.Results: There were no differences among groups with regard to age, gender, and area of necrosis. Average time for the onset of VT was 26 h (range 0-92 h). Sixteen patients underwent coronary angiography: 4 patients had left main coronary artery disease, 2 had single-vessel disease, 8 had lesions in two vessels, and 2 had triple-vessel disease. Univariate analysis showed that patients with VT had a higher incidence of crea-

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Delayed Development of Ventricular Ectopic Rhythms following Experimental Coronary Occlusion

Cited by 673 publications

References 28 publications

BW A256C, a chemically novel class 1 antiarrhythmic agent. A comparison of in vitro and in vivo activity with other class 1 antiarrhythmic agents

BW A256C, a chemically novel class 1 antiarrhythmic agent. A comparison of in vitro and in vivo activity with other class 1 antiarrhythmic agents

2APB- and JTV519(K201)-sensitive micro Ca2+ waves in arrhythmogenic Purkinje cells that survive in infarcted canine heart

Sustained ventricular tachycardia as a marker of inadequate myocardial perfusion during the acute phase of myocardial infarction

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