Short‐Term Hemodynamic Effects of Intravenous Methyldopa in Patients with Congestive Heart Failure

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Abstract
The acute hemodynamic effects of intravenous methyldopa were studied in six patients with chronic congestive heart failure (New York Heart Association class IV) at 4–6 hours after a 750-mg bolus (period A) and 6–12 hours after a maintenance infusion of 1–2 mg/minute (period B). For period A, the most consistent and striking finding was a significant (48%) fall in pulmonary wedge pressure (33 ± 6 to 17 ± 2 mm Hg; p < 0.05). Stroke volume increased 39% (23 ± 3 to 32 ± 4 ml/m2; p < 0.05), while peripheral vascular resistance decreased 15% (3331 ± 363 to 2841 ± 241 dynes·s·cm−5; p < 0.05). Heart rate fell from 97 ± 7 to 76 ± 3 beats/minute (p < 0.05) with a nonsignificant decline in mean right atrial pressure (18 ± 4 to 9 ± 1 mm Hg). These hemodynamic changes were either sustained or enhanced during period B. Concomitant clinical improvement was also noted. As an agent with potent vasodilatory and antiadrenergic properties, methyldopa permitted a rise in stroke volume by virtue of unloading and possible inhibition of sympathetic activity that led to increased density of beta-adrenergic receptors of the heart (up-regulation). Significant reduction of ventricular filling pressure was attributed to venodilation and probable improved diastolic function. In selected patients with severe congestive heart failure, particularly underscored by excessive sympathetic tone, methyldopa may be considered as an alternative agent to improve cardiac performance and clinical symptomatology.