Myocardial function

Begins at the cellular level with coordinated contraction of cardiac myocytes.

Cellular depolarization causes the release of calcium ions into the muscle sarcoplasm, leading to the excititation-contraction coupling of actin and myosin in the sarcomere.

The interaction of actin and myosin results in the shortening of thousands of sarcomeres that compose the cardiac myocyte ultrastructure and manifest macroscopically as cardiac contraction.

The arrangement of myocardial fiber bundles in the ventricular myocardium is complex, with fibers arranged to maximize the efficiency of cardiac contraction.

Myocardial fibers are arranged in a helical and perpendicular orientation, with clockwise epicardial and counterclockwise sub endocardial fibers.

The fiber orientation causes opposing directions of rotation at the left ventricle base and apex resulting in a cardiac emptying effect during ventricular systole.

Myofibril orientation varies throughout the myocardial wall.

There is a close relationship between declining left ventricular function and poor prognosis.

After myocardial infarction LV systolic dysfunction is associated with a 2.4 fold increase in the relative risk of death.

Survival in patients with coronary artery disease with left ventricular ejection fraction abnormalities followed for 12 years revealed survival was 21% for patients with LVEF less than 35% and 54% for those with LVEF of 35% to 49%.

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