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J Thorac Cardiovasc Surg 1998;116:139-147
© 1998 Mosby, Inc.

Cardiopulmonary Support And Physiology

Effects of amrinone, a phosphodiesterase inhibitor, on right ventricular/arterial coupling immediately after cardiac operations

From the Department of Cardiovascular Surgery, Faculty of Medicine, Kyushu University, Fukuoka, Japan.

Presented in part at the Sixty-ninth Scientific Sessions of the American Heart Association, New Orleans, La., November 10-13, 1996, and published in abstract form (Circulation 1996;94(Suppl):I379).

Received for publication Sept. 7, 1997. Revisions requested Oct. 31, 1997. Revisions received Dec. 16, 1997. Accepted for publication Jan. 30, 1998. Address for reprints: Shigeki Morita, MD, Department of Cardiovascular Surgery, Faculty of Medicine, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-82, Japan.

Objective: Amrinone, a selective phosphodiesterase III inhibitor, is reported to have a potent inotropic effect on the left ventricle, but the effects of this drug on right ventricular contractility in the clinical setting are unknown. The concept of ventricular/arterial coupling was applied to investigate the effects of amrinone on right ventricular contractility and afterload with transesophageal echocardiography.
Methods and Results: The study was performed in the intensive care unit with 11 patients who had undergone cardiac operations. Right ventricular cross-sectional area was measured with transesophageal echocardiography equipped with a capability of automated border detection as a surrogate for right ventricular volume. Multiple pressure-area loops were obtained by reducing preload to measure end-systolic elastance and effective arterial elastance. External work and pressure-volume area were also measured to calculate the efficiency of energy transfer from pressure-volume area to external work. Nitroprusside (0.3 to 0.5 µg · kg ^–1 · min^–1) and amrinone (1 mg · kg ^–1 intravenously followed by 10 µg · kg ^–1 · min^–1) were administered. With nitroprusside infusion, end-systolic elastance and effective arterial elastance remained unchanged (end-systolic elastance, 4.73 ± 2.18 mm Hg/cm² to 4.65 ± 2.09 mm Hg/cm²; effective arterial elastance, 8.05 ± 3.84 mm Hg/cm² to 7.70 ± 3.64 mm Hg/cm²). In contrast, amrinone reduced afterload (effective arterial elastance, 8.82 ± 3.99 mm Hg/cm² to 7.05 ± 4.01 mm Hg/cm², p = 0.004) and enhanced contractility (end-systolic elastance, 4.47 ± 1.79 mm Hg/cm² to 6.56 ± 2.22 mm Hg/cm², p = 0.007). Consequently, amrinone decreased the ventricular/arterial coupling ratio (effective arterial elastance/end-systolic elastance, 2.40 ± 1.45 to 1.16 ± 0.63, p = 0.009) and improved the efficiency of energy transfer (external work/pressure-volume area, 0.44 ± 0.15 to 0.54 ± 0.15, p = 0.013).
Conclusions: Right ventricular pressure-area relations obtained with transesophageal echocardiography could successfully separate the simultaneous change in right ventricular systolic mechanics and afterload caused by amrinone. Amrinone caused enhancement of right ventricular contractility and afterload reduction. (J Thorac Cardiovasc Surg 1998;116:139-47)

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