In rat models of cardiac hypertrophy (moderate aortic coarctation: ACm, n =
18; severe aortic coarctation: ACs, n = 27; aging: OLD, n = 25; spontaneou
s chronic hypertension: SHR, n = 18) and properly matched control animals (
C-ACm, n = 17; C-ACs n = 19; C-OLD,C- n = 24; C-SHR, n = 22), we investigat
ed the relative contribution of intense autonomic activity and cardiac stru
ctural damage to ventricular arrhythmogenesis. We used an "in vivo" to tiss
ue level approach, by correlating in the same animal: (i) social stress-ind
uced ventricular arrhythmias, telemetrically recorded, and (ii) left ventri
cular weights (LVW) and amount and geometrical properties of myocardial fib
rosis (MF). Arterial blood pressure was significantly higher in ACm (+ 11%)
, ACs (+ 28%) and SHR (+ 34%) than in controls. LVW were approximately 20%
greater in ACm, ACs and OLD and 50% greater in SHR. MF was about twice as g
reat and characterized by more frequent occurrence of microscopic scarring
in ACm and ACs. and eight times greater and associated with both a higher n
umber and a larger size of fibrotic foci in OLD and SHR compared to control
s. Social stress increased ventricular arrhythmia vulnerability in all mode
ls of cardiac hypertrophy. as well as in controls. The arrhythmogenic actio
n of stress was facilitated in ACs, OLD and SHR. A correlation between stru
ctural cardiac remodeling and ventricular arrhythmias was found only in SHR
and OLD, which exhibited the greatest increase in LVW: and/or MF. Social s
tress proved to be a valuable tool for analyzing the combined effects of au
tonomic stimulation and altered myocardial substrate on the genesis of pote
ntially life-threatening arrhythmias in social animals. (C) 2001 Elsevier S
cience Inc. All rights reserved.