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Coronary reserve is depressed in postmyocardial infarction reactive cardiac hypertrophy
Insights
Following myocardial infarction (MI), surviving heart muscle hypertrophies but shows reduced blood flow and vasodilator reserve. This study investigated coronary blood flow in hypertrophied heart muscle after MI in rats.
Area of Science:
- Cardiovascular Physiology
- Cardiac Remodeling
- Myocardial Infarction Research
Background:
- Compensatory reactive hypertrophy occurs in surviving myocardium post-myocardial infarction (MI).
- Coronary perfusion is critical for cardiac function after MI, but data on myocardial blood flow in reactive hypertrophy are lacking.
Purpose of the Study:
- To measure coronary blood flow and reserve in surviving myocardium exhibiting reactive hypertrophy after MI in a rat model.
Main Methods:
- Radioactive microspheres were used to measure coronary blood flow and reserve in rats 4 weeks post-MI.
- Maximal coronary vasodilation was induced using Carbochrome.
- Sham-operated rats served as controls.
Main Results:
- Infarcted animals exhibited significant reactive hypertrophy (30%) of surviving left ventricular myocardium.
- Coronary flow and vasodilator reserve in the surviving myocardium were depressed post-MI.
- Maximal coronary blood flow was significantly lower, and minimal coronary resistance was significantly higher in the MI group compared to controls.
Conclusions:
- Surviving myocardium after MI demonstrates compensatory hypertrophy but has impaired coronary blood flow and vasodilator capacity.
- These findings highlight a critical deficit in perfusion to hypertrophied heart muscle, potentially impacting cardiac function post-MI.
Abstract:
After a myocardial infarction (MI), the remaining myocardium undergoes a compensatory reactive hypertrophy. Although coronary perfusion to the surviving myocardium can be an important determinant of cardiac function in this setting, there are no available data regarding myocardial blood flow in reactive hypertrophy. Accordingly, we measured coronary blood flow and reserve using radioactive microspheres in rats 4 weeks after induction of an MI by ligation of the left coronary artery. Maximal coronary dilation was induced by Carbochrome, a potent coronary vasodilator, infused at a rate of 0.45 mg/kg/min up to a total dose of 12 mg/kg. Sham-operated rats served as controls. All animals in the infarct group had a large MI affecting 30-51% (average, 41%) of the left ventricle. Left ventricular end-diastolic pressure was significantly elevated (30 +/- 6.5 vs. 8.0 +/- 2.5 mm Hg in sham-operated rats, p less than 0.01) and baseline hemodynamic indexes of cardiac performance were significantly (p less than 0.01) reduced in this group. Myocyte cross-sectional area measurements were used as an index to quantify the degree of reactive hypertrophy and indicated that the infarcted animals had, on average, a 30% hypertrophic response of the surviving left ventricular myocardium. In the infarcted animals, both coronary flow and vasodilator reserve in the surviving myocardium were depressed. Maximal coronary blood flow in the remaining myocardium was significantly lower than that measured in the sham-operated animals (839 and 1,479 ml/min/100 g, respectively; p less than 0.001). Similarly, minimal coronary resistance was significantly higher in the MI group as compared with the sham group (0.12 vs. 0.07 mm Hg/ml/min/100 g, respectively; p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)