Fhh. Leenen et Bx. Yuan, Mortality after coronary artery occlusion in different models of cardiac hypertrophy in rats, HYPERTENSIO, 37(2), 2001, pp. 209-215
Citations number
32
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Chronic treatment with minoxidil induces cardiac trophic and sympathetic re
sponses, which may increase the propensity for lethal arrhythmias. To test
this hypothesis, acute coronary artery occlusion was performed in conscious
normotensive rats treated for 2 or 5 weeks with minoxidil with the use of
a 2-stage approach to cause a myocardial infarction. For comparison, rats w
ith aortocaval (A-V) shunts and spontaneously hypertensive rats (SHR) were
studied. Minoxidil increased left ventricular and right ventricular weights
by 15% to 20%, and the A-V shunt increased these weights by 30% to 40%. In
SHR, left ventricular weight was increased by 50%, and right ventricular w
eight was increased by 25%. In rats treated with minoxidil for 5 weeks, cor
onary artery occlusion caused a rapid and marked mortality, and 4 hours aft
er myocardial infarction, only 18% of these rats were alive versus 61% of t
he control rats. In rats with the A-V shunt, coronary artery occlusion was
also associated with increased mortality, and after 6 hours, 33% were still
alive compared with 59% of the control rats. In contrast, SHR with marked
hypertension and cardiac hypertrophy showed only a minor increase in mortal
ity (survival rates were 53% versus 60% in SHR versus Wistar-Kyoto rats, re
spectively). Mortality was preceded by high arrhythmia scores, and ventricu
lar fibrillation was the cause of death. Discontinuation of minoxidil for 1
week, sympathetic blockade with nadolol or clonidine, or blockade of the r
enin-angiotensin system with enalapril or losartan did not improve minoxidi
l-induced excess mortality. We conclude that ventricular stretch and other
mechanisms (eg, cardiac vagal activity) in rats appear to be more potent th
an hypertension-induced left ventricular hypertrophy in predisposing for le
thal arrhythmias in the setting of acute ischemia.