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

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.

In 6 pigs, vascular properties [characteristic impedance (R(1)), peripheral resistance (R(2)), compliance (C), inductance (L), arterial elastance (E(a))] were estimated with a windkessel model. LV function was assessed by the slope (E(es)) 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).

Coronary occlusion induced an ESPVR rightward shift, and decreased E(es) 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 R2 increased from 1.72 (0.30) to 2.38 (0.16) mmHg x s x ml(-1) (p<0.05) and C decreased from 0.78 (0.16) to 0.46 (0.08) ml/mmHg (p<0.05), R(1) and L were unchanged. Coronary occlusion decreased SW from 4056 (223) to 2580 (122) mmHg.ml (p<0.001), while PVA and SW/PVA decreased from 5575 (514) to 4813 (317) mmHg x ml (NS), and from 0.76 (0.04) to 0.57 (0.03) (p<0.001), respectively.

Acute myocardial ischemia severely altered left ventriculo-arterial coupling and LV 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 LV contractility.