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Am J Physiol Heart Circ Physiol 280: H142-H150, 2001;
0363-6135/01 $5.00
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Vol. 280, Issue 1, H142-H150, January 2001

Myocardial remodeling and arrhythmogenesis in moderate cardiac hypertrophy in rats

Donatella Stilli1, Andrea Sgoifo1, Emilio Macchi1, Massimiliano Zaniboni1, Sergio De Iasio2, Elisabetta Cerbai3, Alessandro Mugelli3, Costanza Lagrasta4, Giorgio Olivetti4, and Ezio Musso1

1 Dipartimento di Biologia Evolutiva e Funzionale-Sezione Fisiologia, 2 Dipartimento di Biologia Evolutiva e Funzionale-Sezione Biologia Umana, and 4 Istituto di Anatomia Patologica, Università degli Studi di Parma, 43100 Parma; and 3 Dipartimento di Farmacologia Preclinica e Clinica, Università degli Studi di Firenze, 50134 Florence, Italy

In 47 male adult Wistar rats with 4-wk aortic coarctation (AC) and 39 age-matched sham-operated rats (SO) chronically instrumented for telemetry electrocardiogram recording, we investigated the mechanisms of arrhythmogenesis in moderate cardiac hypertrophy, with an approach from "in vivo" toward the cellular level, analyzing 1) stress-induced cardiac arrhythmias in all rats and 2) myocardial fibrosis in 35 animals and action potential duration and density of hyperpolarization-activated current in 19 others at the ventricular level. Aortic banding increased arterial blood pressure, cardiac weight, and ventricular myocyte volume by 11, 25, and 14%, respectively (P < 0.001-0.05). Ventricular arrhythmias occurred at similar rates in AC and SO rats throughout the stress procedure. Action potential duration and hyperpolarization-activated current were about twice as great and myocardial fibrosis about four times greater in AC animals (P < 0.005-0.05). Electrocardiogram data also revealed more supraventricular arrhythmias in AC rats during the baseline period and after stress and fewer atrioventricular block episodes after stress (P < 0.05). Thus stress-induced supraventricular and atrioventricular nodal, but not ventricular, arrhythmias were affected in moderate cardiac hypertrophy when ventricular morphofunctional alterations were evident.

mechanisms of cardiac arrhythmias; myocardial fibrosis; membrane potential; hyperpolarization-activated current; social stress


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