OBJECTIVES: This study sought to evaluate the effect of dynamic exercise on coronary vasomotion in hypertensive patients in the presence and absence of coronary artery disease. BACKGROUND: Endothelial dysfunction with abnormal coronary vasodilation in response to acetylcholine has been reported in patients with arterial hypertension. METHODS: Coronary artery dimensions of a normal and stenotic vessel segment were determined in 64 patients by biplane quantitative coronary arteriography at rest and during supine bicycle exercise. Patients were classified into two groups: 20 patients without evidence of coronary artery disease (10 normotensive, 10 hypertensive [group 1]) and 44 patients with coronary artery disease (26 normotensive, 18 hypertensive [group 2]). Both groups were comparable with regard to clinical characteristics, serum cholesterol levels, body mass index, exercise capacity and hemodynamic data. RESULTS: Mean aortic pressure was significantly higher in hypertensive than normotensive patients. Exercise-induced vasodilation of the normal vessel segment was similar in normotensive and hypertensive patients without coronary artery disease (group 1), namely, +19% versus +20%. However, in hypertensive patients with coronary artery disease, exercise-induced vasodilation was significantly less in both normal and stenotic vessel segments than in normotensive subjects (+1% vs. +20% for normal [p < 0.003] and -20% vs. -5% for stenotic vessels [p < 0.025]). Administration of 1.6 mg of sublingual nitroglycerin at the end of exercise led to a normalization of the vasodilator response in normotensive as well as hypertensive patients. However, this response became progressively abnormal in group 2 when coronary artery disease was present. CONCLUSIONS: In the absence of coronary artery disease, the vasomotor response to exercise is normal in both normotensive and hypertensive patients. However, in hypertensive patients with coronary artery disease, an abnormal response of the coronary vessels can be observed, with a reduced vasodilator response to exercise in normal arteries but an enhanced vasoconstrictor response in stenotic arteries. This behavior of the epicardial vessels during exercise suggests the occurrence of endothelial dysfunction (i.e., functional defect) that is not evident in the absence of coronary artery disease. Nitroglycerin reverses impaired coronary vasodilation, but this effect is blunted in the presence of coronary artery disease (i.e., structural defect).
OBJECTIVES: This study sought to evaluate the effect of dynamic exercise on coronary vasomotion in hypertensivepatients in the presence and absence of coronary artery disease. BACKGROUND: Endothelial dysfunction with abnormal coronary vasodilation in response to acetylcholine has been reported in patients with arterial hypertension. METHODS: Coronary artery dimensions of a normal and stenotic vessel segment were determined in 64 patients by biplane quantitative coronary arteriography at rest and during supine bicycle exercise. Patients were classified into two groups: 20 patients without evidence of coronary artery disease (10 normotensive, 10 hypertensive [group 1]) and 44 patients with coronary artery disease (26 normotensive, 18 hypertensive [group 2]). Both groups were comparable with regard to clinical characteristics, serum cholesterol levels, body mass index, exercise capacity and hemodynamic data. RESULTS: Mean aortic pressure was significantly higher in hypertensive than normotensive patients. Exercise-induced vasodilation of the normal vessel segment was similar in normotensive and hypertensivepatients without coronary artery disease (group 1), namely, +19% versus +20%. However, in hypertensivepatients with coronary artery disease, exercise-induced vasodilation was significantly less in both normal and stenotic vessel segments than in normotensive subjects (+1% vs. +20% for normal [p < 0.003] and -20% vs. -5% for stenotic vessels [p < 0.025]). Administration of 1.6 mg of sublingual nitroglycerin at the end of exercise led to a normalization of the vasodilator response in normotensive as well as hypertensivepatients. However, this response became progressively abnormal in group 2 when coronary artery disease was present. CONCLUSIONS: In the absence of coronary artery disease, the vasomotor response to exercise is normal in both normotensive and hypertensivepatients. However, in hypertensivepatients with coronary artery disease, an abnormal response of the coronary vessels can be observed, with a reduced vasodilator response to exercise in normal arteries but an enhanced vasoconstrictor response in stenotic arteries. This behavior of the epicardial vessels during exercise suggests the occurrence of endothelial dysfunction (i.e., functional defect) that is not evident in the absence of coronary artery disease. Nitroglycerin reverses impaired coronary vasodilation, but this effect is blunted in the presence of coronary artery disease (i.e., structural defect).
Authors: J D Schuijf; D Poldermans; L J Shaw; J W Jukema; H J Lamb; A de Roos; W Wijns; E E van der Wall; J J Bax Journal: Eur J Nucl Med Mol Imaging Date: 2006-01 Impact factor: 9.236
Authors: Viola Vaccarino; John Votaw; Tracy Faber; Emir Veledar; Nancy V Murrah; Linda R Jones; Jinying Zhao; Shaoyong Su; Jack Goldberg; J Paolo Raggi; Arshed A Quyyumi; David S Sheps; J Douglas Bremner Journal: Arch Intern Med Date: 2009-10-12
Authors: Christophe A Wyss; Pascal Koepfli; Mehdi Namdar; Patrick T Siegrist; Thomas F Luscher; Paolo G Camici; Philipp A Kaufmann Journal: Eur J Nucl Med Mol Imaging Date: 2004-07-31 Impact factor: 9.236