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Effects of coronary artery occlusion in animals with hypertension and left ventricular hypertrophy
K C Dellsperger1, J L Clothier, S Koyanagi
1Department of Internal Medicine, College of Medicine, University of Iowa, Iowa City 52242.
Insights
Chronic hypertension and left ventricular hypertrophy accelerate myocardial infarction progression and increase mortality. Beta-blockade may reduce sudden death in these high-risk patients during acute coronary artery occlusion.
Area of Science:
- Cardiovascular Physiology
- Myocardial Infarction Research
- Hypertension Studies
Background:
- Chronic hypertension (HT) and left ventricular hypertrophy (LVH) are known risk factors for increased morbidity and mortality in acute myocardial infarction (AMI).
- Previous studies indicated a 3.5-fold increase in mortality and a 35% larger infarct size in animals with HT-LVH subjected to acute coronary artery occlusion (CAO).
Purpose of the Study:
- To investigate the effect of HT-LVH on the progression of myocardial infarction.
- To determine if normalizing blood pressure or chronic beta-adrenergic blockade can mitigate adverse outcomes during CAO in HT-LVH models.
Main Methods:
- Created a renovascular hypertension model in dogs, inducing HT-LVH.
- Subjected HT-LVH and control animals to 1 or 3 hours of CAO.
- Measured infarct size (triphenyltetrazolium chloride) and area at risk (barium angiography).
- Assessed mortality rates and electrophysiological abnormalities during CAO.
Main Results:
- The wavefront of myocardial infarction was accelerated in animals with HT-LVH.
- Normalizing blood pressure with nitroprusside 1 hour post-CAO markedly retarded infarction progression.
- Animals with HT-LVH exhibited a higher incidence of sudden death (65%) during CAO compared to controls (27%).
Conclusions:
- HT-LVH accelerates myocardial infarction development and significantly increases mortality risk during CAO.
- Interventions like blood pressure normalization and potentially chronic beta-adrenergic blockade show promise in reducing infarct size and sudden death in this vulnerable population.
Abstract:
Chronic arterial hypertension (HT) and left ventricular hypertrophy (LVH) increase the morbidity and mortality of acute myocardial infarction in patients. In this article, we discuss earlier studies from Koyanagi et al. in our laboratory that showed that when animals with chronic HT and LVH (HT-LVH) were subjected to acute coronary artery occlusion (CAO), there was a 3.5-fold increase in mortality and a 35% increase in infarct size expressed as a percent of the area at risk. We subsequently determined the effect of HT-LVH on the wavefront of myocardial infarction. Dogs were made hypertensive using a single-kidney, single-clip model of renovascular hypertension that produced mean arterial blood pressure (BP) = 141 +/- 3 mm Hg and left ventricular:body weight = 5.8 +/- 0.1 g/kg (p less than 0.05 vs. control animals). Conscious animals with HT-LVH and control animals were subjected to 1 or 3 h of CAO. Infarct and risk areas were measured using triphenyltetrazolium chloride (TTC) stain and barium angiography, respectively. The results suggested that the wavefront of infarction was accelerated in animals with HT-LVH. Further studies suggested that the wavefront of myocardial infarction could be markedly retarded by normalizing blood pressure (nitroprusside) 1 h following CAO. Recent studies in an animal model of HT-LVH suggested that electrophysiological abnormalities occur when these animals were subjected to CAO. Sixty-five percent of animals with HT-LVH had sudden death during CAO compared to 27% of the control group. We studied whether chronic beta-adrenergic blockade would reduce mortality associated with CAO in animals with HT-LVH.(ABSTRACT TRUNCATED AT 250 WORDS)