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J Am Coll Cardiol, 1995; 26:1692-1698
© 1995 by the American College of Cardiology Foundation
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Central blood volume: a determinant of early cardiac adaptation in arterial hypertension?

RE Schmieder, HP Schobel, and FH Messerli

Department of Medicine, Universitat Erlangen-Nurnberg, Germany.

OBJECTIVES. This study was undertaken to assess the influence of the fluid volume state on cardiac adaptation to hypertension. BACKGROUND. Left ventricular hypertrophy is an important predictor of hypertensive complications. We analyzed volume status and its impact on cardiac structural changes in early hypertension. METHODS. In 33 normotensive subjects, 40 patients with borderline hypertension and 63 patients with established essential hypertension, mean arterial pressure was measured invasively; total blood volume was measured by iodine-125-labeled plasma albumin and hematocrit; central blood volume by indocyanine green dye dilution curve; and diastolic diameter and left ventricular mass by two-dimensional-guided M-mode echocardiography. RESULTS. Central blood volume was approximately 20% higher in patients with stage I borderline hypertension than in normotensive subjects ([mean +/- SD] 3,001 +/- 663 vs. 2,493 +/- 542 ml, p < 0.05), whereas total blood volume was similar in all three groups. This shift in intravascular volume toward the cardiopulmonary circulation was accompanied by a significant increase in diastolic diameter (5.29 +/- 0.80 vs. 4.86 +/- 0.77 cm, p < 0.05) and in left ventricular mass (239.4 +/- 90.6 vs. 183.5 +/- 68.8 g, p < 0.05) in patients with borderline hypertension compared with subjects with normotension. In patients with established essential hypertension, volume status of stroke volume and diastolic dimension returned to normal values, whereas left ventricular mass increased further. CONCLUSIONS. We conclude that the early phase of hypertension is characterized by centripetal distribution of intravascular volume, leading to an increased preload to the left ventricle. This change in volume status appears to be related to cardiac structural adaptation to an increase in arterial pressure.


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