Reperfusion arrhythmia: A marker of restoration of antegrade flow during intracoronary thrombolysis for acute myocardial infarction

Goldberg, Sheldon; Greenspon, Arnold J.; Urban, P.; Muza, Barbara; Berger, Bruce C.; Walinsky, Paul; Maroko, Peter R.

doi:10.1016/0002-8703(83)90274-0

Cited by 253 publications

(68 citation statements)

References 20 publications

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“…Various studies have shown the association of sinus bradycardia and accelerated idioventricular rhythm with the occurrence of myocardial reperfusion, 8,9 as well as the lack of specificity of the ventricular arrhythmias as reperfusion markers. [10][11][12] However, it is not completely clear whether VT is a marker of inadequate myocardial perfusion after thrombolysis; 13 therefore, a more aggressive attitude has been recommended in these patients based on their high mortality rate.…”

Section: Discussion Sustained Ventricular Tachycardia As a Marker Of mentioning

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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Section: Discussion Sustained Ventricular Tachycardia As a Marker Of mentioning

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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“…4 whom serious ventricular arrhythmias occurred shortly after spontaneous relief of episodes of coronary spasm-induced silent ischaemia (Tzivoni et al, 1983), or in whom persistent arrhythmias followed successful thrombolysis (Goldberg et al, 1983), or during reperfusion of the whole heart after a period of surgically-induced ischaemic arrest (Rubin et al, 1985). Despite the potential importance of post-ischaemic reperfusion arrhythmias, the effects of pharmacological K ATP activation on these arrhythmias have been reported infrequently, especially in the absence of arrhythmias during the preceding phase of ischaemia (Ferdinandy et al, 1995;Tosaki et al, 1993;Tanaka et al, 1996).…”

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confidence: 99%

A KATP channel opener inhibited myocardial reperfusion action potential shortening and arrhythmias

Workman

Mackenzie

Northover

2001

European Journal of Pharmacology

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Low concentrations of certain K ATP openers have been reported to exert a moderate inhibitory effect on arrhythmias during post-ischaemic early myocardial reperfusion, but the accompanying effects on the time course of changes in action potentials in intact hearts have not yet been studied.We report that, in rat isolated hearts reperfusion following 10 min of regional no-flow ischaemia was associated with both an acute, marked, but transient, shortening of ventricular repolarisation (by 63%) during reperfusion, and a high incidence (90%) of ventricular tachyarrhythmias. The K ATP opener Ro 31-6930 [2-(6-cyano-2,2-dimethyl-2H-1-benzopyran-4-yl)-pyridine 1-oxide] delivered prior to ischaemia at a relatively low concentration (0.5 µM), significantly reduced the incidence and duration of reperfusion arrhythmias, and prevented the associated acute action potential shortening during reperfusion, each in a glibenclamide (1 µM)-sensitive manner (P<0.05, n=10-15 hearts). This was associated with a moderate, and non-arrhythmogenic, action potential shortening during ischaemia (a potentially "cardioprotective" effect). However, these data highlight the potential harm these drugs may cause, since a higher concentration of Ro 31-6930 caused marked shortening of action potentials and significant pro-arrhythmia during ischaemia. KeywordsATP-sensitive potassium channel; Reperfusion; Isolated heart; Action potential; Ventricular arrhythmias. 1: IntroductionCardiac adenosine triphosphate-sensitive K + (K ATP ) channels, first identified in the sarcolemma (Noma, 1983), and more recently in the mitochondria (Inoue et al., 1991) are thought to remain closed under physiological conditions. It is well recognised that under certain pathological conditions, such as myocardial ischaemia, however, opening of sarcolemmal K ATP channels may contribute to the shortening of action potential duration (Wilde and Janse, 1994; Wilde, 1997). We recently reported (Workman et al., 2000) that in the rat isolated heart, ischaemia in the presence (but not the absence) of pharmacological K ATP activation, caused action potential shortening of a sufficient degree to cause ventricular tachyarrhythmias.It is also recognised that K ATP activation-induced action potential shortening, under certain conditions may help to protect the myocardium from the injury caused by excessive Ca 2+ influx and ATP consumption [see (Grover and Garlid, 2000) for recent review]. Several studies have highlighted the protective effects on the myocardium of pharmacological K ATP activation. In many cases such protection was demonstrated during post-ischaemic reperfusion. For example, K ATP openers have been shown, during reperfusion, to improve recovery of contractile function (Docherty et al., 1997), to restrain the rise in the intracellular Ca 2+ concentration, [Ca 2+ ] i (Behling and Malone, 1995), to enhance the restoration of high energy phosphates (Tanonaka et al., 1999), as well as limiting the extent of myocardial infarction after reperfusion (Grover et al., 1...

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“…Even among clinical studies, varied incidence of reperfusion arrhythmias has been demonstrated. 2,[27][28][29][30][31] These results suggest that mechanisms responsible for AIVR and VT in clinical cases might be somewhat different from those observed in experimental models. In the present study, we clinically demonstrated for the first time that AIVR and VT that occur after reperfusion are probably cAMP-mediated arrhythmias and are therefore likely to be triggered arrhythmias.…”

Section: Electrophysiological Mechanisms Of Reperfusion Arrhythmiasmentioning

confidence: 81%

“…[1][2][3] Reperfusion arrhythmias, in addition to their importance as a marker of successful reperfusion of an occluded coronary artery, require special attention because hemodynamics may rapidly deteriorate during VT or ventricular fibrillation (Vfib). It is therefore important clinically to establish the mechanism and treatment of such reperfusion arrhythmias.…”

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confidence: 99%

Antiarrhythmic Efficacy of Dipyridamole in Treatment of Reperfusion Arrhythmias

et al. 2000

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Background-Intracellular calcium overload is believed to play an important role in development of reperfusion arrhythmias. Dipyridamole, an inhibitor of cellular uptake of adenosine, may prevent or terminate reperfusion arrhythmias by reducing intracellular calcium overload. Methods and Results-First, we tested for a preventive effect of dipyridamole. Sixty-one patients who underwent primary PTCA for treatment of acute anterior wall myocardial infarction were enrolled in this prospective study. Patients were divided into dipyridamole (DP) and nondipyridamole (non-DP) groups. The 2 groups had similar baseline characteristics. In the DP group, dipyridamole 0.5 mg/kg was infused intravenously for 3 minutes immediately before reperfusion during primary PTCA. Arrhythmias after reperfusion were analyzed from continuous ECG recordings. None of the patients in the DP group (nϭ23) had accelerated idioventricular rhythms (AIVR) or ventricular tachycardia (VT). In contrast, 7 (18.4%) had AIVR and 3 (7.9%) had VT in the non-DP group (nϭ38; PϽ0.01). Second, we tested for a termination effect of dipyridamole. Dipyridamole 0.5 mg/kg was infused intravenously while continuous ECG recordings were obtained in 9 patients who had either sustained AIVR (nϭ7) or sustained VT (nϭ2) after reperfusion of occluded coronary artery. Arrhythmias were terminated in all patients. Conclusions-These results indicate that administration of dipyridamole can prevent and terminate reperfusion arrhythmias such as AIVR and VT. cAMP-mediated triggered activity may, at least in part, be responsible for reperfusioninduced AIVR and VT. (Circulation. 2000;101:624-630.)

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Reperfusion arrhythmia: A marker of restoration of antegrade flow during intracoronary thrombolysis for acute myocardial infarction

Cited by 253 publications

References 20 publications

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

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

A KATP channel opener inhibited myocardial reperfusion action potential shortening and arrhythmias

Antiarrhythmic Efficacy of Dipyridamole in Treatment of Reperfusion Arrhythmias

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