Reperfusion Arrhythmias in Man: Influence of Intravenous Lidocaine

Kuck, K. H.; Schofer, Joachim; Schlüter, Michael; Bleifeld, W.; Mathey, D

doi:10.1093/eurheartj/6.suppl_e.163

Cited by 11 publications

(2 citation statements)

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“…Although reperfusion is essential to prevent irreversible cellular injury and preserve ventricular function, reperfusion and the attendant recovery from ischemia-induced metabolic, ionic, and electrical changes cause ventricular arrhythmias, 26 cellular injury, 27 and sudden death. 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.…”

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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“…Arrhythmias during intracoronary streptokinase administration in humans have been described (specifically) in three studies, [22][23][24] which, unfortunately, are difficult studies to compare for the following reasons. First, the definition of "reperfusion arrhythmias" differed from study to study.…”

Section: Ment2'mentioning

confidence: 99%

Predictive value of ventricular arrhythmias for patency of the infarct-related coronary artery after thrombolytic therapy.

Six

Louwerenburg

Kingma

et al. 1991

Heart

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In animal studies reperfusion of coronary arteries is commonly accompanied by ventricular arrhythmias. It is not certain, however, whether ventricular arrhythmias can be used as a reliable non-invasive marker of reperfusion in humans. Two-channel In humans, however, some of the arrhythmias seen in the first hours after the onset of infarction can be attributed to the inherent electrical instability of the ischaemic myocardium and not to reperfusion. To investigate the difference between "infarction arrhythmias" and "reperfusion arrhythmias", we need to measure the patency rate of the infarct-related coronary artery and disorders of the heart rhythm within a well-defined interval.We therefore determined the predictive value of ventricular arrhythmias for patency of the infarct-related vessel in patients with acute transmural infarction by monitoring the heart rhythm with Holter recording from the start of streptokinase administration until angiographic visualisation of the infarctrelated vessel up to four hours later (that is, the study period). Patients and methods PATIENTSFifty seven patients with acute myocardial infarction were treated with intravenous streptokinase. We studied male and female patients below the age of 71 years with symptoms of acute myocardial infarction for less than four hours and ST segment elevation of > 1 mm in at least two leads of the standard 12 lead electrocardiogram. We excluded patients with a history of abnormal bleeding, use of anticoagulant drugs, recent surgery (<2 weeks), previous cerebral haemorrhage or injury, impaired renal function (serum creatinine concentration > 300 ymol/l), systolic blood pressure > 200 mm Hg, diastolic > 120 mm Hg, severe heart failure with pulmonary congestion on admission, any malignancy (except those of the skin), or previous treatment with streptokinase.

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