Circulation, Vol 65, 1192-1197, Copyright © 1982 by American Heart Association
S Koyanagi, C Eastham and ML Marcus
When acute myocardial infarction occurs in patients with hypertension and
left ventricular hypertrophy (LVH), the incidence of sudden cardiac death
increases markedly. Possible explanations include increased size of the
occluded vascular bed secondary to more extensive atherosclerotic coronary
vascular disease in the presence of hypertension, decreased coronary
reserve secondary to LVH, and intrinsic electrophysiologic abnormalities in
hypertrophied cardiac muscle. To explore these possibilities, we produced
acute circumflex coronary occlusion during the resting, conscious state in
32 control dogs and in 28 dogs with hypertensive LVH. Before coronary
occlusion, mean arterial pressure was 96 +/- 0.1 mm Hg in control dogs and
125 +/- 5 mm Hg in dogs with hypertensive LVH (p less than 0.01). The
control left ventricular/body weight ratio was 4.5 +/- 0.1 g/kg, compared
with 6.1 +/- 0.1 g/kg in hypertensive LVH (p less than 0.01). Cumulative
mortality at 6, 24 and 48 hours was 9%, 13% and 16% in control dogs and
32%, 43% and 54%, respectively, in dogs with hypertensive LVH (all p less
than 0.01 vs control). The perfusion fields of the occluded vessel defined
by postmortem coronary angiography were similar in the two groups (31 +/-
2% of left ventricular mass for control vs 29 +/- 2% for hypertensive LVH).
Thus, the increased incidence of sudden cardiac death after coronary artery
occlusion in hypertensive LVH dogs cannot be explained by increased size of
the occluded vascular bed and is probably related to the decreased coronary
reserve or intrinsic electrophysiologic abnormalities that characterize
pressure-induced hypertrophied cardiac muscle.
ARTICLES
Effects of chronic hypertension and left ventricular hypertrophy on the incidence of sudden cardiac death after coronary artery occlusion in conscious dogs
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