Hemodynamic effects of clonidine in patients with acute myocardial infarction complicated by hypertension.

Arterial hypertension complicating acute myocardial infarction (AMI) may aggravate myocardial damage, possibly through an increase in myocardial oxygen demand. This study reports the effects of clonidine in patients with hypertension complicating acute myocardial infarction. Forty patients (37 men and three women, average age 53 years) with acute myocardial infarction, admitted to the coronary care unit not more than 24 h after the onset of symptoms, were studied. Thirty-four had anterior myocardial infarction and six had inferior myocardial infarction. All patients were in Forrester I [WP less than 18 mm Hg, cardiac index (CI) greater than 2.21 L/min/m2] or II (WP greater than 18 mm Hg, CI greater than 2.21 L/min/m2) hemodynamic subset. Blood pressure limits were systolic blood pressure greater than or equal to 150 mm Hg and diastolic blood pressure greater than or equal to 95 mm Hg. Clonidine was administered intravenously in a dose of 5 micrograms/kg over a 5-min period. Hemodynamic parameters (Swan-Ganz thermodilution catheter), systolic time intervals (Weissler), and calculated hemodynamic indexes were measured both before and 60 min after cessation of intravenous injection. Blood pressure fell from 161 +/- 20 to 126 +/- 19 mm Hg (systolic) and from 105 +/- 7.6 to 84.7 +/- 9 mm Hg diastolic. Overall, clonidine produced a decrease in total systemic resistance (-21%). Cardiac index did not change significantly (-3%). Left ventricular stroke work index was significantly reduced (-21%, p less than 0.001), as was the triple product, suggesting a favorable effect of clonidine on myocardial oxygen supply/demand ratio. This may result in a reduction in infarct size.(ABSTRACT TRUNCATED AT 250 WORDS)