BACKGROUND: In patients with essential arterial hypertension (EAH) the left heart ventricular hypertrophy (LVH) causes structural and functional alterations of the coronary vessels that can alter the coronary blood flow reserve. The aim of this study is to evaluate in hypertensive patients with or without LVH versus normotensive subjects, the blood flow and the coronary vasodilatation capability and the coronary blood flow reserve in basal conditions and during dipiridamole i.v. infusion. METHODS: Eighty patients have been selected by ECG, echo color Doppler, transesophageal echocardiography: 50 were hypertensive patients with and without LVH, from mild to moderate to severe and 30 were normotensive subjects. The enrolled patients underwent a first transesophageal echocardiography, before and during infusion of 0.86 mg/kg of dipiridamole in growing doses, 0.56 in four minutes followed after three minutes by 0.30 mg/kg. The observation lasted 18 months, and no patients left the study. RESULTS: The coronary resistances in hypertensive patients were significintally reduced during dipiridamole infusion, maintaining their level higher compared to the normal controls. The reduced coronary vasodilatation capability in hypertensive subjects could be due to an increase of the basal vessel tone and/or a reduced compliance of the coronary resistances. The coronary blood flow reserve is significantly reduced in all hypertensive studied, included those without LVH. It is suggested that this is secondary to increase of the coronary blood flow and tone. CONCLUSIONS: In conclusion essential arterial hypertension is the cause of early anatomical and functional coronary alterations leading hypertensive subjects to risk for coronary events before LVH.
BACKGROUND: In patients with essential arterial hypertension (EAH) the left heart ventricular hypertrophy (LVH) causes structural and functional alterations of the coronary vessels that can alter the coronary blood flow reserve. The aim of this study is to evaluate in hypertensivepatients with or without LVH versus normotensive subjects, the blood flow and the coronary vasodilatation capability and the coronary blood flow reserve in basal conditions and during dipiridamole i.v. infusion. METHODS: Eighty patients have been selected by ECG, echo color Doppler, transesophageal echocardiography: 50 were hypertensivepatients with and without LVH, from mild to moderate to severe and 30 were normotensive subjects. The enrolled patients underwent a first transesophageal echocardiography, before and during infusion of 0.86 mg/kg of dipiridamole in growing doses, 0.56 in four minutes followed after three minutes by 0.30 mg/kg. The observation lasted 18 months, and no patients left the study. RESULTS: The coronary resistances in hypertensivepatients were significintally reduced during dipiridamole infusion, maintaining their level higher compared to the normal controls. The reduced coronary vasodilatation capability in hypertensive subjects could be due to an increase of the basal vessel tone and/or a reduced compliance of the coronary resistances. The coronary blood flow reserve is significantly reduced in all hypertensive studied, included those without LVH. It is suggested that this is secondary to increase of the coronary blood flow and tone. CONCLUSIONS: In conclusion essential arterial hypertension is the cause of early anatomical and functional coronary alterations leading hypertensive subjects to risk for coronary events before LVH.