Strain echocardiography in cardiac surgery - studies on the effects of loading conditions and inotropic agents on myocardial contraction and relaxation

Sammanfattning: Background: Although reductions in myocardial contractility and relaxation are key compo-nents in heart failure (HF), assessment of them is difficult, as clinical measurements deal with a net effect of myocardial contractility, heart filling (preload), outflow impedance (afterload) and heart rate (HR). Echocardiographic (echo) deformation parameters, like strain (myocardial shortening) and strain rate (the speed of deformation, SR), have been proposed to more accu-rately measure myocardial function, but incongruent previous studies have raised concerns that they may be load-dependent. This load-dependency of echo measurements in general also explains the difficulties assessing right ventricular (RV) function whenever left ventricular (LV) failure is present. Lastly, the inodilators milrinone (MIL) and levosimendan (LEV), often used in treating severe HF, have never been compared head-to-head taking this load-dependency into account. Aims and methods: We wanted to evaluate whether strain and SR were dependent on preload, afterload and HR (paper I). While keeping cardiac loading and HR constant, we compared the myocardial effects of MIL vs. LEV in a randomized trial, combining echo (for strain and systolic (SR-S) and diastolic (SR-E) SR) with hemodynamic measurements from a pulmonary artery catheter (papers II–III). We included post-cardiac surgery aortic stenosis patients with normal LV function for papers I–III. In paper IV, we retrospectively compared echo indices of RV function with right heart catheterization data in patients with severe HF, creating three groups: A) right atrial pressure (RAP) <10 mmHg and stroke volume index (SVI) ≥35 ml/m2, B) RAP <10 mmHg and SVI <35 ml/m2, and C) RAP ≥10 mmHg. The RV echo indices were assessed for their ability to identify group B from C. Results: With increased preload by passive leg elevation, cardiac output (CO), strain, SR-S, and SR-E increased significantly, while increased HR by atrial pacing increased only CO, SR-S, and SR-E. Under constant loading and HR, MIL and LEV increased CO by 20%, RV and LV strain by almost 20%, and SR-S and SR-E by almost 30% in both ventricles, with no differences be-tween groups. In paper IV, echo indices of RV longitudinal function (such as TAPSE, S’, FAC and strain) failed to distinguish group B from C, while all RV dimensional measurements could. By combining six RV echo indices into a novel score, the RV failure (RVF) score, significant discrimination between group B and C was found. Conclusions: 1) Strain is preload- and HR-dependent while SR depends on HR. 2) MIL and LEVO have comparable effects on LV and RV systolic and diastolic function. 3) To assess RVF in LV disease, a single-parameter approach is inadequate and we propose a combination of six parameters into a novel RVF score.