• Cardiovascular research · Sep 1990

    Comparative Study Clinical Trial

    Effects of nifedipine on systemic hydraulic vascular load in patients with hypertension.

    • K C Chang, K S Hsieh, T S Kuo, and H I Chen.
    • Department and Institute of Electrical Engineering, National Taiwan University, Taipei, Republic of China.
    • Cardiovasc. Res. 1990 Sep 1;24(9):719-26.

    Study ObjectiveThe aim of the study was (1) to determine the difference in aortic input impedance and derived parameters between hypertensives and normotensives; and (2) to assess the acute effects of nifedipine on the aortic impedance, compliance, and resistance in patients with hypertension.DesignA high fidelity multisensor catheter (Millar) was used to obtain the aortic pressure and flow signals for impedance analysis. The acute effects of nifedipine on the impedance parameters were evaluated at steady state before and after (10-30 min) a sublingual dose of 10 mg.PatientsThe patients included seven normotensive (mean blood pressure, 97 mm Hg) and nine hypertensive (mean blood pressure, 135 mm Hg), age matched, ethnic Chinese. Patients with clinical evidence of heart failure and valvular or congenital heart diseases were excluded.Measurements And Main ResultsPulsatile aortic flow and pressure were measured by Millar catheter inserted into the ascending aorta. Cross sectional area of aorta was estimated by echocardiograms. Cardiac output was determined by Fick principle with an oximeter. These data were subjected to Fourier analysis for impedance spectra. In comparison with normotensives, hypertensives had increased peripheral vascular resistance R, at 2751(705) v 1651(363) dyne.s.cm-5; increased characteristic impedance Zc, at 193(64) v 122(27) dyne.s.cm-5; and increased first zero crossing frequency of impedance phase angle fo, at 4.8(0.9) v 3.4(0.7) Hz. Arterial compliances corresponding to peak systolic pressure Cs were lower, at 0.32(0.19) v 0.90(0.32) ml.mm Hg-1, as was mean pressure Cm, at 0.55(0.25) v 1.24(0.38) ml.mm Hg-1, and end diastolic pressure Cd, at 0.83(0.29) v 1.65(0.44) ml.mm Hg-1. Although the values of external ventricular hydraulic power were higher in hypertensive subjects, the difference was not statistically significant. Nifedipine administration in 7/9 hypertensives significantly reduced R, from 2806(721) to 2433(664) dyne.s.cm-5; mean aortic pressure Pm, from 138(22) to 112(12) mm Hg; total external ventricular power Wt, from 1452(306) to 1121(135) mW; and steady external power Ws, from 1251(310) to 939(119) mW; but did not reduce Zc, fo, Cs, Cm, Cd, and oscillatory external power Wo.ConclusionsThe results indicate that (1) the stiffness of proximal aorta and vascular tone of peripheral arterioles are higher in hypertensives than in normotensives; (2) in hypertensive subjects, sublingual administration of nifedipine reduces the arterial pressure and peripheral arteriolar tone, but not the stiffness of proximal aorta; (3) the decrease in total external ventricular power in hypertensives treated with nifedipine results from a reduction in the steady, but not the oscillatory, component of hydraulic external ventricular power.

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