Sublingual nitroglycerin delays arterial wave reflections despite increased aortic "stiffness" in patients with hypertension: A Doppler echocardiography study

Venodilatation with consequent reduction in left ventricular filling and en d-diastolic wall stress is an important mechanism for the beneficial effect s of nitroglycerin in ischemic heart disease and in left ventricular failur e. The effects of sublingual nitroglycerin on arterial pulsatile hemodynami cs are less well defined. Doppler echocardiography and the calibrated subcl avian artery pulse tracing were used to assess hemodynamics in subjects wit h sustained arterial hypertension (n = 25) before and 5 to 10 minutes after sublingual deposition of 0.5 mg glyceryl trinitrate. Aortic characteristic impedance was calculated by averaging the modulus of the input impedance ( ratio of pressure to now) at high frequencies and by calculating the ratio of pressure and now increments during upstroke. The pressure wave was split into forward and backward components, and the reflection coefficient (the ratio of backward to forward pressures) was calculated. Parameters of the a rterial bed were estimated by using 2- and 3-element Windkessel models. Nit roglycerin delayed the return of arterial wave reflections by 17% (P =.02) and increased aortic characteristic impedance by 20% (P =.01), but it did n ot influence total arterial compliance. Mean arterial pressure decreased 7% (P = .0001), but pulse pressure did not change. Stroke volume and the acce leration time of aortic root flow decreased by 13% (P = .0001) and 8% (P = .01), respectively. Cardiac output decreased 7% (P =.01), despite an increa se in heart rate of 10% (P = .0001). Peripheral resistance tended to decrea se (4%, P = .06). Thus, in subjects with sustained hypertension, sublingual nitroglycerin dilates peripheral, predominantly muscular arteries with a s ubsequent delayed return of reflected pressure waves. Reflex activation of the sympathetic nervous system with consequent increased acceleration of le ft ventricular ejection seems to counteract the effect of reduced mean arte rial pressure (distending pressure) with respect; to the "stiffness" of the aorta.