Cellular Electrophysiological Changes in Rats with Heart Failure and Ventricular Arrhythmias - in Vitro-in Vivo Correlations

Journal of Clinical and Basic Cardiology 2005; 8 (1-4): 23-28

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Keywords: Herzinsuffizienz,  Kardiologie,  Studie,  ventrikuläre Arrhythmie,  cardiology,  heart failure,  ventricular arrhythmia

Aim of the study: During heart failure (HF), mechanisms of ventricular arrhythmias are poorly understood. The clinical relevance of elementary mechanisms suggested by in vitro experiments has to be questioned, since in vivo correlations are often lacking. We compared action potential (AP) characteristics, occurrence of automaticity, and triggered activity with in vivo arrhythmic, morphologic, and haemodynamic data in post myocardial infarction (PMI) rats. Methods and results: Telemetric ECG, morphologic, and haemodynamic data were obtained from 16 live PMI and 13 sham rats, at one and five months after surgery. Action potentials (AP) were studied on the papillary muscle in different solutions, and at different pacing rates. Spontaneous ventricular premature beats (VPBs) were frequent in PMI and were bradycardia-dependent. Abnormal automaticity was the most common in vitro observed mechanism. Time after infarction was related to EAD/DAD in vitro distribution but not with in vivo data. HF induced major alterations of filling pressures and of AP characteristics. AP duration was strongly correlated with the size of infarction but not with the arrhythmic density, in contrast with AP amplitude, resting potential, and Vmax. Conclusion: In PMI rats, abnormal automaticity was the major mechanism of in vitro recorded arrhythmias, consistently with the bradycardiadependence of in vivo observed VPBs. Delay after infarction influenced only EAD/DAD proportion. In this model, AP prolongation could be a simple marker of HF not involved in arrhythmogenic mechanisms. Heterogeneity of the pathobiology of arrhythmias in HF warrants further in vitro-in vivo correlations.