Contrast-enhanced cardiovascular magnetic resonance in primary and ischemic dilated cardiomyopathy.

OBJECTIVES

Differentiation between primary dilated cardiomyopathy and ischemic cardiomyopathy has an important clinical significance. Contrast-enhanced cardiovascular magnetic resonance can play a role in this task, identifying myocardial scarring or fibrosis as presence of delayed enhancement. The aim of the present study was to evaluate the diagnostic potential of contrast-enhanced cardiovascular magnetic resonance in differentiating dilated cardiomyopathy from ischemic cardiomyopathy.

METHODS

Contrast-enhanced cardiovascular magnetic resonance was performed in 100 patients with left ventricular dilatation and reduced systolic function: 24 had normal coronary arteries (dilated cardiomyopathy group) and 76 had significant coronary artery disease (ischemic cardiomyopathy group), with or without previous myocardial infarction.

RESULTS

In the dilated cardiomyopathy group, only seven (29%) patients showed delayed enhancement and its pattern was characterized by mid-wall, patchy or diffuse location. All patients with ischemic cardiomyopathy and prior myocardial infarction (54 subjects) showed delayed enhancement with subendocardial (n = 4) or transmural (n = 50) extension. Among the 22 patients with ischemic cardiomyopathy but without previous myocardial infarction, 13 (59%) showed either subendocardial (n = 4) or transmural (n = 9) delayed enhancement.

CONCLUSIONS

Patterns of delayed enhancement are different in dilated cardiomyopathy and ischemic cardiomyopathy, reflecting the presence of scarring or various degrees of fibrosis in left ventricular myocardium. The presence of subendocardial or transmural delayed enhancement at contrast-enhanced cardiovascular magnetic resonance allowed distinction between dilated cardiomyopathy and ischemic cardiomyopathy with high sensitivity (88%) and specificity (100%). Integration of cardiovascular magnetic resonance results with angiographic information can be useful in the identification of pathogenic mechanisms underlying left ventricular dysfunction.