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 + 1SD 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 (β = 0.40, P = 0.02), and LVMI correlated with ambulatory SBP (β = 0.41, P = 0.001) and body mass index (β = 0.30, P < 0.05). Female sex influenced endothelial function negatively (β =− 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.
aMultidisciplinary Research Group on Hypertension, Clinical Research Institute of Montreal, University of Montreal, Montreal, Quebec, Canada and bSamsung Cheil Hospital, Sungkyunkwan University School of Medicine, Seoul, Korea.
Received 23 October 2000
Revised 14 December 2000
Accepted 27 December 2000
Sponsorship: This study was supported by grant 13570 to ELS and a Group grant to the Multidisciplinary Research Group on Hypertension, both from the Medical Research Council of Canada (now the Canadian Institutes of Health Research).
Correspondence and requests for reprints to Ernesto L. Schiffrin, MD, PhD, FRCPC, Clinical Research Institute of Montreal, 110 Pine Avenue West, Montreal, Quebec, Canada H2W 1R7. Tel: +1 514 987 5528; fax: 1 514 987 5602; email: email@example.com