**Cardiac Myocardial Disease States Cause Left Ventricular Remodeling with Decreased Contractility and Lead to Heart Failure; Interventions by Coronary Arterial Bypass Grafting and Surgical Ventricular Restoration Can Reverse LV Remodeling with Improved Contractility**

Dhanjoo N. Ghista1, Liang Zhong2, Leok Poh Chua3, Ghassan S. Kassab4, Yi Su5 and Ru San Tan2 *1Department of Graduate and Continuing Education, Framingham State University, Framingham, Massachusetts, 2Department of Cardiology, National Heart Centre, 3School of Mechanical and Aerospace Engineering, Nanyang Technological University, 4Departments of Biomedical Engineering, Surgery, Cellular and Integrative Physiology, Indiana University-Purdue University Indianapolis, Indianapolis, Indiana, 5Institute of High Performance Computing, Agency for Science, Technology and Research, 1,4USA* 

*2,3,5Singapore* 

### **1. Introduction**

### **1.1 Theme and scope**

In this chapter, we are studying the course (i) of cardiomyopathy diseased LVs (with myocardial infarcts) progressing to heart failure (HF) through LV remodelling and decreased LV contractility, and (ii) their recovery through surgical therapeutic interventions of CABG and Surgical Ventricular Restoration (SVR), by restoration of myocardial ischemic segments, reversal of LV remodeling and improvement in LV contractility.

For this purpose, we first provide the methodology for detecting myocardial infarcts. Then, we characterize LV remodeling of cardiomyopathy diseased LVs (with myocardial infarcts) in terms of reduced change in curvedness from end-diastole to end-systole. In these LVs, there is also reduced contractility; so we provide an index for cardiac contractility, in terms of maximal rate-of-change of normalized wall stress, *dσ\*/dtmax,* and its decrease in an infarcted LV progressing to heart failure. We provide clinical studies of remodeled cardiomyopathy diseased LVs, in terms of reduced values of their curvedness index and contractility index.

By way of therapeutic interventions, we have presented the hemodynamic flow simulation of the CABG (carried out to enhance myocardial perfusion in the region around the blocked coronary artery), and pointed out certain factors and sites of wall shear stresses that cause intimal damage of vessels and hyperplasia, as potential causes for decreased patency. We have shown that surgical ventricular restoration (SVR), in conjunction with CABG, is seen to benefit the ischemic-infarcted heart, by (i) restoration of cardiac remodeling index of 'enddiastolic to end-systolic curvedness change', (ii) reduction of regional wall stresses, and (iii) augmentation of the cardiac contractility index value.
