**2. Myocardial infarction: What it entails**

In Cardiology, the etiology of congestive heart failure (CHF) is coronary artery disease in approximately two-thirds of cases. The majority of these patients have hearts with myocardial infarcted segments. This infarcted myocardial wall mitigates adequate contraction of the wall. So, the end-result of an infarcted left ventricle (LV) is poor intra-LV velocity distribution and pressure-gradient distribution, causing impaired outflow from the LV into the aorta.

In the infarcted myocardial segments, the myocardial infrastructure of actin and myosin filaments (and their cross – bridges) is disrupted, and hence there is no contraction within these infarcted myocardial segments. The below figure 1 illustrates a myocardial sarcomere segment's bioengineering model, composed of two symmetrical myocardial structural units (MSUs). In these MSU(s), the contractile elements represent the actin-myosin contractile components of the sarcomere segment. The disruptions of these contractile elements impair the contractile capability of that sarcomere segment. Hence, a LV with infarcted myocardial segments will have diminished contractility, inadequate and improper intra-LV flow, and poor ejection.
