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(Circulation. 1995;91:3002-3009.)
© 1995 American Heart Association, Inc.

Articles

Effect of Cocaine on Left Ventricular Function

Relation to Increased Wall Stress and Persistence After Treatment

Prabodh M. Mehta, MD; Terry A. Grainger, MD; Robert M. Lust, PhD; Assad Movahed, MD; Jarrett Terry, BS; M.G.F. Gilliland, MD; Stanley R. Jolly, PhD

From East Carolina University, Greenville, NC.

Correspondence to Assad Movahed, MD, Professor of Medicine and Radiology, Cardiology Section/Department of Internal Medicine, East Carolina University School of Medicine, Greenville, NC 27858-4354.

Background To determine whether alterations in left ventricular (LV) function after a cocaine infusion are due to reduced myocardial contractility or changes in loading conditions, we examined LV function in 30 morphine-sedated, closed-chest dogs. We also wanted to determine the time course of the effects of cocaine on LV function after the infusion was stopped.

Methods and Results Two-dimensional echocardiography and hemodynamics provided LV fractional shortening and end-systolic wall stress data. Radionuclide ventriculography was also performed. Four groups of dogs received saline or cocaine infusions of 10, 30, or 100 µg · kg^-1 · min^-1. Cocaine was infused for 90 minutes with ECG and arterial pressure monitoring. Animals were monitored for an additional 120 minutes after the infusion ended. Arterial pressure rose over the course of the experiment in all four groups, but saline and cocaine 10 µg · kg^-1 · min^-1 did not significantly change ejection fraction. Cocaine 30 and 100 µg · kg^-1 · min^-1 acutely increased arterial pressure and heart rate but decreased ejection fraction from 0.64±0.06 to 0.45±0.08 and from 0.65±0.10 to 0.46±0.11, respectively. Additionally, cocaine 100 µg · kg^-1 · min^-1 decreased fractional shortening from 36±9% to 23±12%. However, cocaine 30 and 100 µg · kg^-1 · min^-1 also increased wall stress from 42±15 to 65±11 g/cm² and from 37±15 to 90±33 g/cm², respectively. These results were analyzed by use of the relation between wall stress and fractional shortening as an index of contractility. Fractional shortening after cocaine infusion was displaced downward as a result of increased wall stress rather than changes in contractility. In addition, alteration of afterload with phenylephrine (6 µg/kg) and sodium nitroprusside (10 µg/kg) before and during infusion of cocaine 100 µg · kg^-1 · min^-1 showed similar regression lines for wall stress to fractional shortening.

Conclusions Ejection-phase indexes of LV function were reduced by cocaine in this model of conscious, sedated dogs, but effects were attributable to increased wall stress rather than to reduced myocardial contractility. These effects persisted for at least 2 hours after the infusion was stopped.

Key Words: cocaine • contractility • myocardial contraction • wall stress

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