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Eur J Cardiothorac Surg 2000;18:83-89
© 2000 Elsevier Science NL

Myocardial efficiency in stunned myocardium. Comparison of Ca²⁺-sensitization and PDE III-inhibition on energy consumption

^a Department of Thoracic and Cardiovascular Surgery, Heinrich-Heine University, Moorenstrasse 5, 40225 Düsseldorf, Germany
^b Research Group of Experimental Surgery, Heinrich-Heine University, 40225 Düsseldorf, Germany

Received 7 September 1999; received in revised form 14 February 2000; accepted 21 February 2000.

Corresponding author. Tel.: +49-211-811-8331; fax: +49-211-811-8333
e-mail: usunderdiek{at}aol.com

Objective: In stunned myocardium oxygen consumption is relatively high compared with the reduced ventricular function. On the other hand, inotropic stimulation is frequently required to improve postischemic ventricular dysfunction. However, inotropic agents which act via intracellular increased calcium result in a higher oxygen demand. Therefore Ca²⁺-sensitization might be a favorable alternative. Methods: The effects of a novel Ca²⁺-sensitizer (EMD 60263, 10 µM, group 1) were compared with a phosphodiesterase (PDE) III-inhibitor (enoximon, 20 µM, group 2) on 14 isolated, blood-perfused rabbit hearts during reperfusion after a global ischemia of 20 min. Ventricular function, the pressure–volume area (PVA, a measure of total mechanical work), and total myocardial oxygen consumption (MVO₂) were assessed. Contractile efficiency (EF_cont), derived from the reciprocal of the slope of the MVO₂–PVA relation, and external efficiency (EF_ex, stroke work/MVO₂), were calculated. Results: At matched heart rate (group 1: 141±10 min^-1 group 2: 151±28 min^-1) and end-diastolic volume (1.3±0.2 ml) systolic variables were significantly decreased in stunned myocardium: LVP_max to 57±13% of control value in group 1 and to 76±7% in group 2, aortic flow to 20±4 vs. 25±8%. PVA was decreased to 57±13 and 67±11%, MVO₂ was non-significantly decreased to 73±22 and 88±14%. After administration of either inotropic agent LVP_max was significantly improved to 96±12 vs. 90±8% compared with preischemic levels, aortic flow to 103±24 vs. 88±9%, and PVA 99±11 vs. 89±16%, respectively. EMD 60263 increased MVO₂ to control levels (107±9%), and enoximon raised MVO₂ even more significantly above control (139±13%). Both myocardial efficiency indices were significantly diminished during reperfusion: EF_ex to 14±9 vs. 23±7% and EF_cont to 71±7 vs. 65±9% compared with preischemic levels. EF_ex (109±21%) was significantly, but EF_cont only slightly (84±11%) increased after administration of EMD 60263, whereas EF_ex (57±13%) and EF_cont (71±12%) remained depressed after enoximon. Conclusions: In stunned myocardium, the decreased efficiency indices show that energy utilization is disturbed. Both agents recruited an inotropic reserve, whereas Ca²⁺-sensitization seemed to be more favorable in terms of myocardial efficiency indices. These results indicate that alteration of myocardial calcium sensitivity contributes a major part to postischemic dysfunction. Therefore, Ca²⁺-sensitization may potentially be a superior method for inotropic support in the postischemic heart.

Key Words: Myocardial stunning • Efficiency, Ca²⁺-sensitivity • Inotropic stimulation • Thiadiazinone derivative • Isolated heart