[Identification of the ischemic origin of dilated myocardiopathy using positron emission tomography].

INTRODUCTION AND OBJECTIVES

The aim of this study was to differentiate ischemic from nonischemic dilated cardiomyopathy with positron emission tomography. This differentiation is necessary to establish an adequate treatment, and it is often difficult with non-invasive diagnostic procedures.

METHODS

Ten patients with an echocardiographic diagnosis of dilated cardiomyopathy who had undergone coronary angiography were selected. The presence or absence of angiographic coronary lesions was used to define the ischemic (n = 6) and the nonischemic group (n = 4). The ejection fraction was depressed in both groups, with no significant differences found. A perfusion study with 13N-ammonium and a metabolic imaging with 18F-florodeoxyglucose were performed on each patient. The images were quantitatively and qualitatively analysed, defining three criteria: accumulation defect (areas with activity under 50% of the maximal radioactivity), degree of heterogeneity, and match of images with both tracers. To determinate the degree of heterogeneity, nine segments on the three standard tomographic planes were studied. Based on the following heterogeneity features: irregular borders, coexisting different degrees of accumulation, and patched accumulation, a score ranging from 0 to 3 points was assigned to these segments. To analyse the radioactivity defects and the matching of studies with both tracers, the accumulation defects or the accumulating surface were outlined on a midventricular level coronal plane.

RESULTS

The ischemic group has contrary to the nonischemic one, wider perfusion (0.26 +/- 0.21 vs 0.00) and metabolism defects (0.38 +/- 0.30 vs 0.06 +/- 0.09; p < 0.05). The degree of heterogeneity is significantly higher in the nonischemic group, either in perfusion (14.5 +/- 8.38 vs 2.5 +/- 1.04; p < 0.05) or in metabolism studies (15.5 +/- 3.31 vs 2.33 +/- 1.50; p < 0.005). Assigning wide defects and homogeneous accumulation to ischemic cardiomyopathy, and absence of defects and heterogeneous accumulation to nonischemic cardiomyopathy, the aetiology of the disease was identified in 9 of the 10 cases in the perfusion study and 100% of them with the metabolism imaging.

CONCLUSIONS

Positron emission tomography allows to identify the aetiology of dilated cardiomyopathy, either with coronary perfusion or with myocardial glucose metabolism studies. Thus, only one of both PET studies could be used. Ischemic cardiomyopathy is characterised by wide defects and homogeneous radioactivity, and the nonischemic one by the absence of defects and heterogeneous accumulation of the tracer.