Alteration of left ventriculo-arterial coupling and mechanical efficiency during acute myocardial ischemia

Aim. Myocardial revascularisation being frequently performed during acute myocardial ischemia, in a hostile hemodynamic environment, we evaluated left ventriculo-arterial (VA) coupling, left ventricular (LV) mechanical efficiency, and the mechanical properties of the systemic vasculature during acute myocardial ischemia. Methods. In 6 pigs, vascular properties [characteristic impedance (RI), peripheral resistance (R-2), compliance (C), inductance (L), arterial elastance (E-a)] were estimated with a windkessel model. IV function was assessed by the slope (Ees) of end-systolic pressure-volume relationship (ESPVR), and stroke work (SW) - end-diastolic volume (EDV) relation. Pressure-volume area (PVA) was referred to as myocardial oxygen consumption.. VA coupling was defined as E-es/E-a, and mechanical efficiency as SW/PVA. After baseline recordings, the left anterior descending coronary artery was ligated and hemodynamic measures obtained every 30 minutes for 3 hours. Data are expressed as mean (SEM). Results. Coronary occlusion induced an ESPVR rightward shift, and decreased Ees from 3.67 (0.33) to 1.92 (0.20) mmHg/ml and the slope of the SW - EDV relationship from 72.3 (3.4) to 40.4 (4.5) mmHg (p < 0.001), while E-a increased from 3.33 (0.56) to 4.65 (0.29) mmHg/ml (p < 0.005). This was responsible for a dramatic alteration of VA coupling from 1.22 (0.11) to 0.44 (0.07), (p < 0.001). While R-2 increased from 1.72 (0.30) to 2.38 (0.16) mmHg.s.ml(-1) (p < 0.05) and C decreased from 0.78 (0.16) to 0.46 (0.08) ml/mmHg (p < 0.05), R, and L were unchanged. Coronary occlusion decreased SW from 4 056 (223) to 2 580 (122) mmHg.ml (p < 0.001), while PVA and SW/PVA decreased from 5 575 (514) to 4 813 (317) mmHg.ml (NS), and from 0.76 (0.04) to 0.57 (0.03) (p < 0.001), respectively. Conclusion. Acute myocardial ischemia severely altered left ventriculo-arterial coupling and IV mechanical efficiency. Impaired left VA coupling was due to a combination of augmented arterial elastance, secondary to early vasoconstriction later associated with decreased arterial compliance, and decreased IV contractility.