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Coronary vasodilator capacity and epicardial vessel remodeling in physiological and hypertensive hypertrophy
M Kozàkovà1, F Galetta, L Gregorini
1Institute of Clinical Physiology, CNR, University of Pisa, Italy.
Insights
Physiological hypertrophy from exercise preserves coronary vasodilator capacity, unlike hypertensive hypertrophy. Athletes maintain normal coronary flow and oxygen demand relationships, while hypertensive patients show impaired vasodilation.
Area of Science:
- Cardiology
- Physiology
- Exercise Science
Background:
- Left ventricular hypertrophy (LVH) can result from physiological (athlete's heart) or pathological (hypertensive) causes.
- Understanding the impact of different LVH types on coronary circulation is crucial for cardiovascular health assessment.
Purpose of the Study:
- To compare coronary blood flow, myocardial oxygen demand, and vasodilator capacity in individuals with physiological, exercise-induced, and hypertensive left ventricular hypertrophy.
- To investigate the relationship between resting coronary flow and determinants of oxygen demand across different hypertrophy types.
Main Methods:
- Utilized transesophageal and transthoracic Doppler echocardiography to assess coronary flow velocity and artery dimensions.
- Measured coronary flow velocity in the left anterior descending artery and left main artery cross-sectional area at rest and during dipyridamole-induced vasodilation.
- Estimated myocardial oxygen demand using rate-pressure product, left ventricular wall stress, and inotropic function.
Main Results:
- Athletes with physiological hypertrophy demonstrated preserved coronary flow reserve and normal minimum coronary resistance, comparable to sedentary individuals.
- Hypertensive subjects exhibited decreased coronary flow reserve and increased minimum coronary resistance.
- Left main artery dilation was significantly greater in athletes compared to sedentary and hypertensive groups, indicating enhanced macrocirculation vasodilator capacity.
Conclusions:
- Coronary microcirculation vasodilator capacity is not impaired in athletes with physiological hypertrophy, contrasting with hypertensive hypertrophy.
- The relationship between resting coronary flow velocity and oxygen demand determinants is maintained in physiological hypertrophy but lost in hypertensive hypertrophy.
- Exercise-induced adaptations enhance coronary macrocirculation vasodilator capacity in trained individuals.
Abstract:
The aim of this study was to compare resting coronary flow velocity, determinants of myocardial oxygen demand, and coronary vasodilator capacity in subjects with physiological, exercise-induced, and hypertensive left ventricular hypertrophy. Sixteen healthy sedentary men, 16 endurance athletes, and 16 hypertensive subjects (mean+/-SEM for left ventricular mass index: 94.9+/-5.5, 184.6+/-8.4, 154.4+/-9.5 g/m(2), respectively) were studied by transesophageal and transthoracic Doppler echocardiography. Coronary flow velocity in left anterior descending artery and cross-sectional area of left main artery were assessed at rest and during dipyridamole-induced vasodilation. Myocardial oxygen demand was estimated through rate-pressure product, left ventricular wall stress, and inotropic function. Coronary flow reserve and minimum coronary resistance were comparable to those of sedentary men in athletes (mean+/-SEM: 3. 23+/-0.16 versus 3.60+/-0.18 and 0.96+/-0.06 versus 1.04+/-0.04 mm Hg. s. cm(-1)), while in hypertensive subjects they were decreased and increased, respectively (mean+/-SEM: 2.31+/-0.08 and 1.21+/-0.10 mm Hg. s. cm(-1); P:<0.05 for both). Resting flow velocity was directly related to rate-pressure product in sedentary men and athletes and also to wall stress in athletes, while these correlations were absent in hypertensives. Dilation of left main artery after dipyridamole was significantly higher in athletes than in sedentary men and hypertensive subjects (mean+/-SEM for area change: 32.9+/-3.7% versus 12.8+/-2.5% and 6.4+/-3.3%; P:<0.05 and 0.01). These data indicate that vasodilator capacity of coronary microcirculation is not impaired in athletes with physiological hypertrophy, in contrast to hypertensive patients. The relationship between resting flow velocity and determinants of oxygen demand is preserved in physiological hypertrophy but missing in hypertensive hypertrophy. Furthermore, the vasodilator capacity of coronary macrocirculation is also enhanced in exercise-trained subjects.