Arterial mechanical properties in dilated cardiomyopathy. Aging and the response to nitroprusside.

J D Carroll; S Shroff; P Wirth; M Halsted; S I Rajfer

doi:10.1172/JCI115058

Arterial mechanical properties in dilated cardiomyopathy. Aging and the response to nitroprusside.

J D Carroll, S Shroff, P Wirth, M Halsted, and S I Rajfer

Published March 1, 1991 - More info

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Abstract

The effects of aging on arterial mechanical properties and the response to nitroprusside were examined in 25 patients with dilated cardiomyopathy. High-fidelity pressures were recorded with a multisensor catheter. Pulse wave velocity was determined between two sensors in the thoracic aorta. Arterial compliance was determined by an analysis of the diastolic waveform and cardiac output. At baseline, despite a similar systemic vascular resistance, the pulsatile load (e.g., arterial compliance) and wave transmission characteristics (e.g., pulse wave velocity) were altered with aging. Arterial compliance was reduced in older (greater than 50 yr, n = 8) versus younger (less than 35 yr, n = 8) patients (0.51 +/- 0.17 vs. 1.33 +/- 0.63 ml/mmHg, P less than 0.01) and intermediate in those 35-50 yr of age (n = 9, 0.72 +/- 0.40 ml/mmHg). There was a positive correlation between age and pulse wave velocity (r = +0.90). Nitroprusside infusion decreased resistance, increased arterial compliance, and lowered pulse wave velocity in all groups. Yet, advancing age was associated with a greater fall in wave velocity for a given fall in aortic pressure. The slope (K) of the relation between pulse wave velocity and aortic diastolic pressure progressively increased with age (0.01 +/- 0.03, 0.06 +/- 0.02, and 0.09 +/- 0.03 m/s-mmHg). Multiple linear regression analysis revealed a significant relation between K and age. These data demonstrate that in older patients with dilated cardiomyopathy the left ventricle is coupled to an arterial circulation that has a greater pulsatile load, despite a similar steady load. Furthermore, these age-related changes in the arterial system affect the hemodynamic response to pharmacologically-induced vasodilatation.