Left ventricular systolic and diastolic dysfunction in the acute phases of myocardial ischaemia and infarction, and in the later phases of recovery. Function follows morphology.

Abstract

Myocardial ischaemia and infarction result in major changes in myocardial function, due to the metabolic and structural cause. The observed morphological changes may be macroscopic--as in clinical myocardial infarction, microscopic--as in severe, prolonged ischaemia, or ultramicroscopic--in regard to the collagen matrix. Recognition of the vulnerability of these structures to the metabolic and mechanical stresses associated with severe ischaemia or infarction allows an understanding of the processes of acute dilatation, late adverse remodelling and compensatory hypertrophy, which determine both systolic and diastolic dysfunction and define the principal clinical complications. Morphology--'Form'--is the primary determinant of function, while metabolic and other factors are secondary, variably dependent on the integrity of structure.