Central Inhibition of Sympathetic Overdrive by Clonidine in Acute Myocardial Infarction with Systolic Hypertension. Haemodynamic Study

Intravenous clonidine was used to treat systolic hypertension (systolic blood pressure greater than 160 mm Hg) in 15 patients with acute myocardial infarction and documented sympathetic overactivity (high plasma norepinephrine). Its effects on haemodynamics and blood gases were studied. After one hour, clonidine significantly reduced the systolic (195 +/- 7 to 137 +/- 7 mm Hg, p less than 0.01) and diastolic (81 +/- 4 to 60 +/- 3 mm Hg, p less than 0.01) blood pressures as well as the systemic vascular resistance (26 +/- 2 to 20 +/- 1 IU, p less than 0.01). The cardiac index was reduced from 2.8 +/- 0.2 to 2.4 +/- 0.2 l/min X m2, p less than 0.01. This change was related to a reduction of the heart rate (92 +/- 4 to 81 +/- 4 beats/min, p less than 0.01) as the stroke index was unchanged. Pulmonary wedge pressure (15 +/- 3 to 10 +/- 2 mm Hg, p less than 0.01) and rate pressure product (18.034 +/- 1.159 to 11.274 +/- 917 mm Hg, beats/min, p less than 0.01) were also significantly decreased. The arterial oxygen tension did not change significantly but there was a significant drop in the mixed venous oxygen saturation (63 +/- 2 to 61 +/- 2%, p less than 0.02) and oxygen transport (433 +/- 41 to 409 +/- 36, p less than 0.01). Clonidine is thus able to normalize blood pressure in acute myocardial infarction; this is accompanied by a reduction in myocardial oxygen requirements and pulmonary wedge pressure. Oxygen transport to the tissues, however, may be decreased.