Copyright © 1993 by the European Society of Cardiology.
© 1993 The Europen Society of Cardiology
Interrelation of cardiac and vascular structure in young men with borderline hypertension
Hypertension Section, Departments of Medicine and Clinical Physiology, Östra Hospital, University of Göteborg Göteborg, Sweden
Received 17 December 1992; revised 24 March 1993; .
Correspondence Dr Anders Bergbrant, Department of Medicine. CK, Östra Hospital, S-416 85 Göteborg, Sweden.
Abstract
It is not established whether left ventricular hypertrophy and structural vascular changes are primary phenomena or secondary consequences of raised blood pressure. In this study we investigated 54 borderline hypertensive men (BH) (SBP 140–160 mmHg and/or DBP 84–95 mmHg) and 20 normotensive men (NC) (SBP 110–130 mmHg and DBP 60–80 mmHg), recruited from an unbiased population sample (age 20 ± 2 years). Blood pressure (BP) levels were confirmed by i.a. BP recordings. Left ventricular mass (LVM) was determined with M-mode echocardiography and minimal vascular resistance (Rmin) was calculated from the blood flow in the calf and forearm after maximal ischaemic work. Central haemodynamics were assessed by intra-arterial blood pressure recordings and cardiac output determinations by the dye dilution technique. In the BH group, LVM and Rmin were strongly correlated to body size, especially weight and body surface area. However, LVM and Rmin were only weakly correlated to blood pressure. In the normokinetic BH subgroup (NBH) (n = 38) minimal forearm vascular resistance was significantly higher than in the hyperkinetic BH individuals (HBH) (n = 16), indicating the presence of structural vascular changes in the former. Furthermore, in the NBH group there was a significant correlation between LVM and Rmin both in the calf (r = 0.490 P = 0002) and in the forearm (r = 0.520 P = 0.001). This association remained after correction for body size. No such correlation was seen in the HBH subgroup or in the NC group. The present study does give long-reaching conclusions as regards the aetiological factors underlying the cardiovascular remodelling. However, our data show that (1) cardiovascular changes appear early in the course of blood pressure elevation, (2) the cardiac and vascular changes develop in parallel, and (3) structural remodelling is not solely explained by the degree of blood pressure elevation since blood pressure was similar in the two BH subgroups. Thus, other factors than blood pressure appear to be important determinants of structural adaptation in mildly hypertensive states.
Key Words: Borderline hypertension • structural changes • left ventricular mass • minimal resitance • haemodynamics
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