J B Park1, E L Schiffrin. 1. Multidisciplinary Research Group on Hypertension, Clinical Research Institute of Montreal, University of Montreal, Quebec, Canada.
Abstract
BACKGROUND: The heart and blood vessels are exposed to elevated blood pressure (BP) in hypertensive patients, but their changes in response to BP or non-hemodynamic stimuli may be different, and occur with different time-courses. To evaluate this, we studied the prevalence of structural and functional alterations of resistance arteries and cardiac hypertrophy in patients with mild essential hypertension. METHODS: Resistance arteries were dissected from gluteal subcutaneous tissue from 38 hypertensive patients (47 +/- 1 years; 71% male; BP 148 +/- 2/99 +/- mmHg), studied on a pressurized myograph, and compared to those from 10 normotensives (44 +/- 3 years; 40% male; BP 113 +/- 4/76 +/- 2 mmHg). RESULTS: The prevalence of abnormal structure (media-to-lumen ratio, M/L) and impaired endothelial function (maximal acetylcholine response) was 97 and 58% (abnormal was defined as greater than mean + 1 SD of normotensives), or 63 and 34% (abnormal defined as greater than mean +/- 2SD). Thirty four percent of hypertensive patients exhibited left ventricular hypertrophy by echocardiography. When grouped into tertiles according to increasing ambulatory systolic BP (SBP), the highest BP tertile showed increased M/L (P< 0.01) and left ventricular mass index (LVMI, P < 0.05) and marginally decreased endothelial function (P= 0.07). LVMI was greatest in the tertile of patients with highest M/L (P< 0.05). Endothelial function was decreased in the tertile with greatest vascular stiffness (P< 0.01). By multivariate analysis, M/L correlated with ambulatory SBP (beta = 0.40, P= 0.02), and LVMI correlated with ambulatory SBP (beta = 0.41, P = 0.001) and body mass index (beta = 0.30, P< 0.05). Female sex influenced endothelial function negatively (beta = -0.63, P< 0.01). CONCLUSION: Structural alterations of resistance arteries were demonstrated in most hypertensive patients, followed by endothelial dysfunction and cardiac hypertrophy in a smaller number of hypertensives. Small artery structural remodeling may precede most clinically relevant manifestations of target organ damage in mild essential hypertension.
BACKGROUND: The heart and blood vessels are exposed to elevated blood pressure (BP) in hypertensivepatients, but their changes in response to BP or non-hemodynamic stimuli may be different, and occur with different time-courses. To evaluate this, we studied the prevalence of structural and functional alterations of resistance arteries and cardiac hypertrophy in patients with mild essential hypertension. METHODS: Resistance arteries were dissected from gluteal subcutaneous tissue from 38 hypertensivepatients (47 +/- 1 years; 71% male; BP 148 +/- 2/99 +/- mmHg), studied on a pressurized myograph, and compared to those from 10 normotensives (44 +/- 3 years; 40% male; BP 113 +/- 4/76 +/- 2 mmHg). RESULTS: The prevalence of abnormal structure (media-to-lumen ratio, M/L) and impaired endothelial function (maximal acetylcholine response) was 97 and 58% (abnormal was defined as greater than mean + 1 SD of normotensives), or 63 and 34% (abnormal defined as greater than mean +/- 2SD). Thirty four percent of hypertensivepatients exhibited left ventricular hypertrophy by echocardiography. When grouped into tertiles according to increasing ambulatory systolic BP (SBP), the highest BP tertile showed increased M/L (P< 0.01) and left ventricular mass index (LVMI, P < 0.05) and marginally decreased endothelial function (P= 0.07). LVMI was greatest in the tertile of patients with highest M/L (P< 0.05). Endothelial function was decreased in the tertile with greatest vascular stiffness (P< 0.01). By multivariate analysis, M/L correlated with ambulatory SBP (beta = 0.40, P= 0.02), and LVMI correlated with ambulatory SBP (beta = 0.41, P = 0.001) and body mass index (beta = 0.30, P< 0.05). Female sex influenced endothelial function negatively (beta = -0.63, P< 0.01). CONCLUSION: Structural alterations of resistance arteries were demonstrated in most hypertensivepatients, followed by endothelial dysfunction and cardiac hypertrophy in a smaller number of hypertensives. Small artery structural remodeling may precede most clinically relevant manifestations of target organ damage in mild essential hypertension.