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The effect of cardiac hypertrophy on the coronary collateral circulation
Insights
Hypertension and left ventricular hypertrophy do not alter coronary collateral resistance in dogs or patients. This suggests that increased infarct size in these conditions is not due to impaired collateral circulation.
Area of Science:
- Cardiovascular Physiology
- Cardiac Surgery
- Renal Hypertension
Background:
- Previous studies suggest hypertension and left ventricular hypertrophy (LVH) increase infarct size.
- A potential explanation is higher collateral resistance, but human postmortem studies show increased collaterals in LVH.
- This study investigates the relationship between LVH, hypertension, and coronary collateral resistance.
Purpose of the Study:
- To test the hypothesis that left ventricular hypertrophy is associated with alterations in coronary collateral resistance.
- To determine if hypertension and LVH impact collateral resistance in dogs.
- To assess functional evidence of collateral circulation in patients with LVH.
Main Methods:
- Used an isolated, adenosine-vasodilated, blood-perfused cardiac preparation in dogs to measure pressure-flow relationships using radioactive microspheres.
- Assessed collateral and normal zone resistance in nine dogs with renal hypertension and LVH and 17 controls.
- Monitored systolic wall thickening via echo transducer during transient left anterior descending artery occlusions in patients with and without LVH during cardiac surgery.
Main Results:
- Collateral resistance was similar in dogs with and without renal hypertension and LVH (4.0 ± 0.7 vs. 3.9 ± 0.4 mm Hg/ml/min/100 g).
- Normal zone resistance was also not different between canine groups.
- Systolic thickening reduction during coronary occlusion was comparable in patients with and without LVH, indicating similar ischemia severity.
Conclusions:
- Coronary collateral resistance is not altered by hypertension and left ventricular hypertrophy.
- Left ventricular hypertrophy in patients is not associated with functional evidence of an enhanced collateral circulation.
- The increased infarct size observed in hypertension and LVH is likely not due to impaired collateral function.
Abstract:
We have previously shown that dogs with renal hypertension and left ventricular hypertrophy have larger infarcts (per risk area size) than do control animals. A potential explanation for this is that collateral resistance is higher in these dogs. Paradoxically, previous postmortem studies in human hearts with left ventricular hypertrophy have suggested that coronary collaterals are actually increased in this condition. To test the hypothesis that left ventricular hypertrophy is associated with alterations in coronary collateral resistance, studies were performed in dogs with renal hypertension and left ventricular hypertrophy and in patients with aortic valvular disease at the time of cardiac surgery. With an isolated, adenosine-vasodilated, blood-perfused cardiac preparation, collateral and normal zone pressure-flow relationships were established by means of radioactive microspheres in nine dogs with renal hypertension and left ventricular hypertrophy and in 17 controls. Collateral resistance calculated from these pressure-flow relationships were similar in both groups (4.0 +/- 0.7 in dogs with renal hypertension and left ventricular hypertrophy and 3.9 +/- 0.4 mm Hg/ml/min/100 g in controls). In addition, normal zone resistance was not different between groups (transmural resistances 0.17 +/- 0.01 in controls and 0.18 +/- 0.02 in dogs with renal hypertension and left ventricular hypertrophy. In five patients with aortic valve disease, left ventricular hypertrophy, and normal coronary arteries and in six patients without left ventricular hypertrophy who had normal left anterior descending coronary arteries, a 7 MHz suction-mounted echo transducer was used to monitor systolic wall thickening during transient occlusions of the left anterior descending artery at the time of cardiac surgery. Because noncollateralized myocardium ceases to contract promptly after coronary occlusion, this approach provides an indirect index of collateral perfusion. Twenty seconds after the onset of coronary occlusion, systolic thickening had markedly decreased in both groups (15 +/- 10% of control values in nonhypertrophied hearts and 10 +/- 10% in hearts with left ventricular hypertrophy; p = NS between groups). Thus the severity of contraction abnormality induced during transient coronary occlusion in these two groups of patients was similar, suggesting that the degree of severity of ischemia was comparable between the two groups. We conclude that collateral resistance is not altered by hypertension and left ventricular hypertrophy and that left ventricular hypertrophy in patients is not associated with functional evidence of an enhanced collateral circulation.(ABSTRACT TRUNCATED AT 400 WORDS)