Systolic dyskinesia develops in the absence of reperfusion. After successful thrombolysis or angioplasty, a variable amount of myocardium is salvaged, and the nonfunctional segment may become akinetic. Dramatic improvement in regional left ventricular systolic function is not common after thrombolytic therapy. In each instance there is loss of contraction of the anterior wall and septum, and the remote muscle dilates as an adaptive mechanism to maintain stroke volume. Progressive remodeling, however, may become pathogenic through its effect on the remote non-infarcted myocardium.
Dilation distorts the normal fiber angle, which adversely effects systolic torsion.
Further enlargement leads to altered ventricular shape and papillary muscle orientation that restricts mitral leaflet coaptation, producing regurgitation. Experimental models show that this may occur even in the absence of mitral annular enlargement. Ventricular dysfunction occurs as a consequence of this remodeling and may lead to clinical congestive heart failure, which may develop months or years following anterior infarction. Thus, ventricular dilation is closely linked to the risk of death after infarction. Traditional surgical approaches to the treatment of ventricular dysfunction following infarction include coronary bypass, combined with mitral valve procedures if regurgitation is significant.