Cardiovascular effects of levodopa in Parkinson's disease

Levodopa is one of the most effective symptomatic treatment options for Parkinsonism with a favorable safety and tolerability profile. In some patients, particularly those suffering from orthostatic intolerance, the hypotensive effect of levodopa limits its therapeutic use. We used continuous noninvasive cardiovascular and ventilatory monitoring in 17 patients suffering from moderate Parkinson's disease to quantify the hypotensive effect of levodopa and to determine whether this effect is rather vasodepressor or cardioinhibitory. Oral administration of 200 mg levodopa/50 mg benserazide induced a significant decrease in mean arterial pressure (-15%, p < 0.001), cardiac stroke volume (-13%, p < 0.01) and measures of cardiac contractility (dP/dt: -18%, p < 0.001). Systemic vascular resistance, heart rate and ventilatory parameters remained preserved. Our data indicate that the hypotensive blood pressure response to levodopa is caused primarily by a negative inotropic mechanism rather than peripheral vasodilation. Whether this effect is triggered peripherally at the level of the heart or is mediated via central sympathoinhibition remains unsolved.