Reperfusion ventricular tachyarrhythmias: Correlation with antecedent coronary artery occlusion tachyarrhythmias and duration of myocardial ischemia

Balke, C. William; Kaplinsky, Elieser; Michelson, Eric L.; Naito, Masahito; Dreifus, Leonard S.

doi:10.1016/0002-8703(81)90135-6

Cited by 122 publications

(22 citation statements)

References 24 publications

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“…28 In animal models, reperfusion arrhythmias occur after brief episodes of ischemia, ie, Ͻ10 minutes, 12,29 but are most common when the preceding ischemia lasts for 20 to 30 minutes. 30,31 The increased incidence of reperfusion arrhythmias after 20 to 30 minutes of ischemia may relate to the rapid reexpansion of the extracellular compartment, washout of the extracellular K ϩ and H ϩ , and the attendant recovery of excitability in the presence of persistent cellular uncoupling. 1,2,24,32 The persistent cellular uncoupling and concomitant recovery of excitability are anticipated to enhance electrical discontinuities [33][34][35] and contribute to heterogeneity of electrical properties, slowing of impulse conduction, the propagation of delayed afterdepolarizations, and the initiation of arrhythmia.…”

Section: Relevance To Ventricular Arrhythmiasmentioning

confidence: 99%

Electrical Properties and Conduction in Reperfused Papillary Muscle

Cascio

Yang

Johnson

et al. 2001

Circulation Research

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Abstract-The reversibility of ischemia-induced changes of extracellular K ϩ concentration ([K ϩ ] o ), resting membrane potential (E M ), and passive cable-like properties, ie, extracellular resistance and cell-to-cell electrical coupling, and their relationship to recovery of conduction and contraction is described in 25 reperfused rabbit papillary muscles. No-flow ischemia caused extracellular K ϩ accumulation, depolarization of E M , an increase in whole-tissue (r t ), external (r o ), and internal (r i ) longitudinal resistances, and failure of conduction and contraction. Muscles were reperfused 10 minutes after the onset of ischemia related cell-to-cell electrical uncoupling, ie, 26Ϯ1 minutes after arrest of perfusion. In 11 muscles, incomplete reflow occurred with only partial recovery of [K ϩ ] o and r t . In the remaining 14 muscles, reperfusion caused a rapid and parallel decrease in [K ϩ ] o , r t , and r o . When complete tissue reperfusion occurred, cell-to-cell electrical uncoupling was largely reversible. Thus, cell-to-cell electrical uncoupling did not indicate irreversible injury. Reperfusion induced a depolarizing current widening the difference between the K ϩ equilibrium potential and the E M . This difference decreased after longer periods of reperfusion. Conduction was restored and conduction velocity approached preischemic values as cell-to-cell electrical interaction was reestablished and E M recovered. The recovery of r o preceded r i , decreasing the ratio of the extracellular to intracellular resistance early in reperfusion, an effect predicted to influence the amplitude of the extracellular voltage field and electrocardiographic ST segments during reperfusion. (Circ Res. 2001;89:807-814.)

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Section: Relevance To Ventricular Arrhythmiasmentioning

confidence: 99%

Electrical Properties and Conduction in Reperfused Papillary Muscle

Cascio

Yang

Johnson

et al. 2001

Circulation Research

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“…Several experimental9' 10 and clinical studies' [1][2][3][4][5][6][7][8][9][10][11][12][13][14] have shown that the early reflow of blood to ischemic myocardium increases the creatine kinase (CK) recovery rate. Accordingly, the total amount of CK that is released into the plasma may be greater than the amount of CK released from an area of myocardial necrosis of the same size without reperfusion.…”

mentioning

confidence: 99%

Quantitative relationship between left ventricular function and serum cardiac myosin light chain I levels after coronary reperfusion in patients with acute myocardial infarction.

et al. 1987

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To estimate the extent of myocardial infarction after coronary artery reperfusion, serum levels of cardiac myosin light chain (LC) I and creatine kinase (CK) were determined serially in 49 patients with acute myocardial infarction. Intracoronary thrombolysis was successful in 25 patients (reperfusion group), and 24 patients were treated in a conventional manner (control group). The peak level of CK appeared significantly earlier in the reperfusion group (1 1.3 + 3. 1 hr, mean + SD) than in the control group (21.6 ± 7.2 hr). Cumulative release of CK was significantly related to angiographically determined left ventricular ejection fraction 1 month after the attack in both groups (r = -.50; -.45, respectively). However, the amount of cumulative release of CK in the reperfusion group was greater compared with that in those with the same left ventricular ejection fraction in the control group. Peak appearance time of LCI was almost equal in the two groups (3.8 ± 1.4 vs 3.9 ± 1.2 days). Peak levels of LCI were related to the left ventricular ejection fraction in the reperfusion group (r = -.63) and in the control group (r = -.74), and the slopes of their regression lines were similar. The cardiac index obtained on the day of onset in the two groups was related to peak levels of LCI but not to total release of CK. These results suggest that serum levels of LCI reflect the changes in left ventricular function after acute myocardial infarction, regardless of the presence of coronary reperfusion. Thus, serial determinations of LCI in serum facilitate noninvasive assessment of the effects of intracoronary thrombolysis on infarct size. Circulation 76, No. 6, 1251-1261, 1987 IT HAS BEEN SHOWN that the intracoronary infusion of thrombolytic drugs can bring about coronary artery recanalization and this has been proposed as a way of reducing the extent of acute myocardial infarction. 1, 2 Although recent clinical investigations suggest beneficial effects of intracoronary thrombolysis,-5 many laboratory studies have pointed out the deleterious effects of coronary reperfusion, including massive myocardial hemorrhage, refractory arrhythmias, or noreflow phenomenon.68 Therefore, for evaluation of salvage and damage to the myocardium after throm-

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“…There is some evidence for this from the present study since those dogs given timolol that ultimately survived reperfusion had fewer ischaemia-induced arrhythmias ( Figure 2) and less marked ST-segment changes (Table 4) than those dogs that eventually succumbed. Others have also suggested that the severity of reperfusion arrhythmias depends upon the degree of the preceding myocardial ischaemia (Balke et al, 1981) and we have ourselves shown (Coker & Parratt, 1983a) that where the area at risk is less than 30 % of the free left ventricular wall little arrhythmic activity results either during ischaemia or reperfusion.…”

Section: Discussionmentioning

confidence: 54%