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Coronary microcirculation in essential hypertension: a quantitative myocardial contrast echocardiographic approach
V Di Bello1, R Pedrinelli, D Giorgi
1Cardiac and Thoracic Department, University of Pisa, Italy. vdibello@med.unipi.it
Insights
Hypertensive patients with left ventricular hypertrophy exhibit impaired coronary microcirculation vasodilation compared to healthy controls. Quantitative myocardial contrast echocardiography reveals reduced response to dipyridamole, suggesting endothelial dysfunction.
Area of Science:
- Cardiovascular Research
- Medical Imaging
- Hypertension Research
Background:
- Essential hypertension is associated with left ventricular hypertrophy (LVH).
- Coronary microcirculatory function in hypertensive individuals with LVH requires further investigation.
- Assessing coronary flow reserve is crucial for understanding cardiovascular risk.
Purpose of the Study:
- To evaluate coronary microcirculatory function using quantitative myocardial contrast echocardiography (MCE).
- To compare the vasodilatory response to dipyridamole between hypertensive patients with LVH and healthy controls.
- To determine if MCE can detect alterations in coronary flow induced by vasodilation.
Main Methods:
- A case-control study involving 10 hypertensive males with mild LVH and 10 age-matched healthy males.
- Quantitative myocardial contrast echocardiography was performed at rest and after dipyridamole infusion.
- Analysis focused on microbubble appearance, peak intensity, and disappearance parameters to assess coronary flow.
Main Results:
- Hypertensive patients showed a significantly lower microbubble appearance area and time to peak compared to controls.
- While peak intensity at rest was higher in hypertensives, the percentage increase after dipyridamole was significantly lower (+31% vs +71%).
- The percentage increase in microbubble disappearance area after dipyridamole was also significantly lower in hypertensives (+90% vs +124%).
Conclusions:
- Coronary microcirculation in hypertensive patients with LVH demonstrates reduced vasodilation capacity in response to dipyridamole.
- Findings suggest potential impairment of endothelium-dependent vasodilation in this patient group.
- Myocardial hypertrophy may be associated with a mismatch between capillary supply and myocardial mass (rarefaction).
Aims:
The aims of the present study were: (a) to demonstrate whether quantitative myocardial contrast echocardiography can detect the increase in coronary flow induced by dipyridamole infusion vasodilation through the myocardial opacification due to the transit of microbubbles, both at rest and after dipyridamole induced vasodilation; (b) to explore the coronary microcirculatory function before and after dipyridamole in two different models: asymptomatic and relatively young hypertensive patients with a mild degree of left ventricular hypertrophy, and healthy controls.
Methods And Results:
Two groups of strictly age-matched males were studied (case-control study): 10, relatively young and asymptomatic essential hypertensive patients with a mild degree of left ventricular hypertrophy with a normal left ventricular function, and 10 healthy controls. The main findings were: the microbubbles' appearance area was significantly lower in hypertensive patients than in controls (P<0.05) because of a significantly lower time to peak. The peak intensity at rest was higher in hypertensives than in controls (P<0.05); but the per cent increase after vasodilatory stimulus was significantly higher in controls (+71% in controls vs +31% in hypertensives; P<0.05). The microbubbles' disappearance area was comparable in both groups at rest; the per cent increase of this parameter after dipyridamole was significantly higher in controls (+124%) than in hypertensives (+90%) (P<0.05). The results achieved in this study documented that the coronary microcirculation in hypertensive patients presenting a mild degree of left ventricular hypertrophy, explored with quantitative myocardial contrast echocardiography, showed a different behaviour in comparison with controls, in the vasodilatory response to dipyridamole.
Conclusion:
The coronary microcirculation in hypertensives showed a reduced vasodilation capacity of the resistance arterioles under dipyridamole induced vasodilatation, and a possible impairment of the endothelium dependent vasodilation. This happened despite an increase in the left ventricular mass, where the relation between capillary bed distribution and hypertrophied myocardium (rarefaction phenomenon) is not completely respected.