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Eur J Cardiothorac Surg 2001;20:770-776
© 2001 Elsevier Science NL

Left ventricular dysfunction and disturbed O₂-utilization in stunned myocardium: influence of ischemic preconditioning

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

Received 5 March 2001; received in revised form 15 June 2001; accepted 20 June 2001.

Corresponding author.
e-mail: usunderdiek{at}aol.com

Objective: Myocardial dysfunction during postischemic reperfusion is frequently reported only in terms of left ventricular (LV) systolic properties. We additionally assessed diastolic properties, the cardiovascular tone and in particular, the relation between ventricular function and myocardial oxygen consumption. Moreover, these measures are investigated after cardioprotection via ischemic preconditioning (IP). However, this phenomenon is not fully understood, and therefore cardioprotective methods like ischemic preconditioning might provide only insufficient protection. Methods: In a total of 17 isolated rabbit hearts, perfused with an erythrocyte suspension (Hct 30%), we investigated the effect of 20 min low-flow ischemia also on diastolic properties, coronary resistance and cardiac energetics (n=9). During control and 30 min after the onset of reperfusion, LV systolic function was assessed in terms of aortic flow, dP/dt_max and the end-systolic pressure-volume relation (ESPVR). Early relaxation was evaluated via dP/dt_min and diastolic properties were assessed via the end-diastolic pressure-volume relation (EDPVR), i.e. using the equation LVP_ed=c·exp(m·LVV_ed), where c equals the LVP_ed-axis intercept and m equals LV stiffness. In addition, coronary resistance (R_cor) and the pressure-volume area (PVA) were calculated. Total oxygen consumption (MVO₂) was calculated as well as the contractile efficiency (E = inverse slope of the MVO₂-PVA relation). In a second series (n=8) the effect of ischemic preconditioning (3 min no-flow and 8 min reperfusion before the 20 min low-flow ischemia) was tested. Results: In the first series, systolic function was impaired during reperfusion: aortic flow to 32% of control, dP/dt_max to 74% and the slope of ESPVR to 73%. Early relaxation in terms of dP/dt_min decreased to 76%. The slope of the EDPVR was steeper in stunned myocardium with an increase of the ventricular stiffness (m increased from 3.2 to 4.1) and with an upward shift of the EDPVR (c from 0.6 to 2.4 mmHg). Coronary resistance was increased (from 0.9 to 1.4 mmHg/ml per min) and PVA was significantly decreased to 68%, whereas MVO₂ was not, indicating also a decrease in contractile efficiency E from 28 to 14%. In the second series, recovery of systolic function was significantly improved by IP compared with the first series (aortic flow 56% of preischemic control, dP/dt_max to 91% and ESPVR to 78%). LV stiffness m was also slightly increased from 3.1 to 3.9 and again, c was elevated, indicating no beneficial effect for diastolic properties including dP/dt_min (77%). But IP improved R_cor significantly (from 0.9 to only 1.0 mmHg/ml per min) and efficiency E to 21% (from 27% during control). Conclusion: Brief episodes of ischemia not only induce systolic but also diastolic and vascular stunning at almost maintained MVO₂. The decreased contractile efficiency clearly indicates an impaired O₂-utilization of the contractile apparatus. Ischemic preconditioning did not improve diastolic function during reperfusion, but it provided protection with respect to vascular stunning and myocardial energetics.

Key Words: Ischemic preconditioning • Myocardial stunning • Ventricular function • Myocardial energetics