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Effects of cardiac hypertrophy secondary to hypertension on the coronary circulation
Insights
Cardiac hypertrophy, often caused by hypertension, can impair coronary circulation. Animal studies show reduced blood flow and abnormal distribution in hypertrophied ventricles, suggesting potential issues in humans.
Area of Science:
- Cardiovascular physiology
- Cardiac hypertrophy research
Background:
- Clinicians have long suspected inadequate coronary circulation in hypertrophied ventricles.
- Recent studies indicate normal resting flow per gram but increased coronary vascular resistance in hypertensive left ventricular hypertrophy.
Purpose of the Study:
- To investigate the impact of cardiac hypertrophy on coronary circulation using animal models.
- To assess regional myocardial perfusion and maximal coronary vasodilatation in hypertrophied hearts.
Main Methods:
- Utilized labeled microspheres to assess regional myocardial perfusion in dogs with left ventricular hypertrophy.
- Examined coronary vascular resistance and maximal coronary vasodilatation in various animal models of cardiac hypertrophy.
Main Results:
- Coronary vascular resistance is significantly increased when hypertension causes left ventricular hypertrophy.
- Transmural distribution of myocardial perfusion is often abnormal in dogs with left ventricular hypertrophy.
- Maximal coronary vasodilatation is substantially limited in hypertrophied hearts, frequently leading to endocardial underperfusion during stress.
Conclusions:
- Animal studies strongly suggest that cardiac hypertrophy adversely affects the coronary circulation.
- New human techniques for coronary blood flow estimation may allow similar studies in patients.
Abstract:
For many years clinicians have suspected that hypertrophied ventricles have an inadequate coronary circulation. Recent studies have confirmed early observations that flow per gram in hypertrophied ventricles is normal at rest. However, coronary vascular resistance is greatly increased when hypertension is the cause of left ventricular hypertrophy. Studies that have employed labeled microspheres to assess regional myocardial perfusion have shown that the transmural distribution of myocardial perfusion is often abnormal in dogs with left ventricular hypertrophy. In addition, studies of cardiac hypertrophy in many animal models have shown that maximal coronary vasodilatation is limited substantially. Furthermore, when hypertrophied hearts are subjected to a physiologic stress that induces coronary vasodilatation, endocardial underperfusion occurs frequently. Thus, studies in animals suggest that cardiac hypertrophy adversely affects the coronary circulation. The availability of new techniques for estimating phasic and transmural coronary blood flow in man should make it possible to extend these studies to patients with cardiac hypertrophy.