150 ABSTRACTS

congestive heart failure (CHF) is unknown. In 9 patients with CHF, the effects of amrinone and nitroprusside on hemodynamic and radionuclide measurements were com- pared to determine whether reduced afterload accounts for the amrinone-induced decrease in left ventricular end- systolic volume. In each patient, the end-systolic pressure- volume relation was derived using nitroprusside. After termi- nating nitroprusside treatment, intravenous amrinone (3 mg/kg) caused end-systolic volume to decrease from 148 + 35 ml/m’ (mean + standard deviation) to 133 + 32 ml/m* (p < O.OS), causing an increase in cardiac index from 1.9 + 0.8 to 2.7 + 0.8 liters/min/m’ (p < 0.001). Arterial end- systolic pressure decreased in all patients during amrinone administration, from 96 + 22 to 84 + 19 mm Hg (p < 0.005), as did systemic vascular resistance. Nitroprusside doses needed to match the decrease in LV end-systolic volume induced by amrinone caused significantly greater decreases in arterial end-systolic pressure than did amrinone (p < 0.01). The amrinone-induced decrease in end-systolic volume exceeded that predicted for a pure vasodilator based on arterial end-systolic pressure and the nitroprusside-derived pressure-volume relation in 6 patients. In 3 patients, the decrease in end-systolic volume did not exceed that expected for a pure vasodilator. In conclusion, after amrinone treat- ment, afterload reduction occurs in all patients with severe CHF and is the sole effect in some. However, the overall amrinone-induced improvement in LV end-systolic volume and cardiac index exceeds that expected for a pure vasodila- tor, indicating an inotropic contribution to the hemodynamic response. (Reprinted with permission.)

Systemic and Coronary Effects of intravenous Milrinone and Dobutamine in Congestive Heart Failure. Grose R, Strain J, Greenberg iM, et al. J Am Co11 Cardiol 7: 1107, 1986.

The effects of dobutamine and intravenous milrinone on systemic hemodynamics, coronary blood flow and myocardial metabolism were studied in 11 patients with severe congestive heart failure. Although milrinone and dobutamine similarly increased cardiac index from 1.9 i 0.4 to 2.5 + 0.4 liters/min per mZ (p < 0.001) and from 1.9 + 0.4 to 2.8 k 0.8 liters/min per m* (p < O.OOl), respectively, milrinone decreased left ventricular end-diastolic pressure to a greater extent than dobutamine, that is, from 26 + 6 to 12 + 8 mm Hg (p < 0.001) versus 26 + 8 to 20 + 8 mm Hg (p < 0.001). In contrast to dobutamine, milrinone significantly reduced mean systemic arterial and right atria1 pressures. Dobutam- ine increased the first derivative of left ventricular pressure (dP/dt) from 1,013 + 309 to 1,360 + 538 mm Hg/s (p x 0.01) but milrinone did not. Similarly, blood flow and myo- cardial oxygen consumption were increased by dobutamine from 152 -c 87 to 187 -c 118 ml/min (p < 0.05) and from 17.7 + 10.9 to 21.5 t 14.9 ml O,/min (p i 0.05), respec- tively, but were unchanged by milrinone. Both drugs signifi- cantly decreased coronary vascular resistance and myocar- dial oxygen extraction but did not change myocardial lactate extraction.

Thus, dobutamine and milrinone produce similar improve- ment in cardiac index. However, dobutamine increases myo- cardial oxygen consumption, whereas milrinone does not. This difference can probably be explained by the substantial

vasodilating properties of milrinone. (Reprinted with permis- sion.)

A Cooperative Multicenter Study of Captopril in Congestive Heart Failure: Hemodynamic Effects and Long-term

Response. Captopril Multicenter Research Group I. Am Heart J 110:439, 1985.

The acute hemodynamic effects, long-term clinical effica- cy, and safety of the oral angiotensin-converting enzyme inhibitor, captopril, were assessed in a multicenter coopera- tive study of 124 patients with heart failure resistant to digitalis and diuretics. The cardiac status of most patients was deteriorating prior to the study. Favorable acute hemo- dynamic effects consistently occurred with captopril. Maxi- mal mean percentage increases in cardiac index, stroke index, and stroke work index were, respectively, 35%, 44%, and 34%. Systemic and pulmonary vascular resistances were each decreased by approximately 40%, as were the filling pres- sures of the right and left heart. Infusion of nitroprusside in some of the same patients to an end point of a pulmonary capillary wedge pressure of 12 to 18 mm Hg (equivalent to that after captopril) revealed no significant difference in the effect of either drug on the other hemodynamic parameters. Recatheterization after 8 weeks of captopril therapy revealed sustained hemodynamic changes. Significant and sustained improvements in clinical status were observed in most patients as measured by changes in New York Heart Asso- ciation (NYHA) functional classification and exercise toler- ance times. Seventy-nine percent of patients for whom there were adequate NYHA class data improved. Twenty percent remained unchanged and 1% deteriorated. Those patients who had both pretreatment and post-treatment exercise stress testing exhibited a highly significant mean increase in exercise tolerance times of 34% (317 + 32 seconds pretreat- ment to 425 + 34 seconds, final measurement). There was no evidence of tachyphylaxis over an 18-month period. Survival rates at 6, 12, 18, and 24 months were 79%, 63%, and 58%, respectively. Cardiothoracic ratios showed a significant decrease from a mean of 0.60 to 0.57 at 2 months. All patients with hypokalemia at entry and all but one with hyponatremia normalized rapidly on captopril therapy. Cap- topril was generally well tolerated, although hypotension caused withdrawal of the drug in 6% of patients. The results suggest a useful role for captopril in heart failure. (Reprinted with permission.)

Electrocardiographic Criteria for Tricyclic Antidepressant Cardiotoxicity. Niemann JT, Bessen HA, Rothstein RJ, et al. Am J Cardiol57:1154, 1986.

To determine if electrocardiographic findings characterize tricyclic antidepressant (TCA) overdose and cardiotoxicity, 25 patients suspected of taking an overdose of TCA were studied. Toxicologic assays for a TCA were positive in 11 patients (+TCA, n = 11). Toxicologic study results for a TCA were negative in 14 patients (-TCA, control subjects). Patients with positive TCA results (+TCA) had a signifi- cantly greater heart rate (117 i- 23 vs 100 + 22 beats/min, p K .05), QRS duration (103 + 15 vs 87 * 10 ms, p cc 0.005) and corrected QT interval (449 + 38 vs 418 i: 36 ms, p < 0.05) than control patients (-TCA) on admission. Patients with positive TCA results also had a more rightward terminal