[Identification of the ischemic origin of dilated myocardiopathy using positron emission tomography]. / Identificación del origen isquémico de la miocardiopatía dilatada mediante tomografía por emisión de positrones.

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.

Spontaneous coronary artery dissection.

Spontaneous coronary artery dissection is a rarely identified entity whose exact incidence, etiology, pathogenesis, medium-term evolution, and optimal treatment have not yet been firmly established. This article describes five new cases with additional specific characteristics. Five of 2,241 coronary arteriograms taken between September 1989 and November 1992 showed angiographic signs of coronary dissection. Three of the patients were treated pharmacologically, and two were operated on. All were evaluated angiographically 10-18 months after diagnosis and followed up clinically for > or = 20 months. Three patients exhibited acute myocardial infarction, one showed effort angina and the fifth unstable angina. In four cases, coronary dissection was associated with coronary atherosclerosis, but in the fifth the coronary tree was apparently healthy except for the dissection. Dissection affected the right coronary artery in three cases and the left in two. Angiographic evolution varied among the five and was uncorrelated with treatment. Dissection disappeared in three; it persisted, with total obstruction of the artery in the middle of the dissected segment in one case; and advanced to affect the whole left coronary tree in the fifth. After an 18-month follow-up, none of the five patients experienced symptoms. These cases provide a good illustration of the variability of spontaneous coronary dissection as regards etiology, clinical presentation, treatment, and evolution. Coronary dissection is always caused by hemorrhage in the media of the arterial wall; its variability in evolution and in optimal treatment may be derived from the cause of the hemorrage, which possibly was not the same in all cases.

Family history as an independent risk factor for ischaemic heart disease in a low incidence area (Galicia, Spain).

It has been suggested that a family history positive for coronary heart disease (CHD) increases the risk of CHD. We studied this association to determine the degree of risk, the independence of this association and the presence of interaction of a family history of CHD with the major known risk factors in a low incidence area. One hundred and six hospital cases (85 males and 21 females) of CHD and 106 hospital controls individually matched with each case for sex, age and place of residence (rural-urban) were studied. From every participant, information was collected on their personal and family history of cardiovascular disease and risk factors; height, weight, lipid profile and blood pressure were measured, and an electrocardiogram was recorded. Conditional logistic regression was used in the analysis. The observed odds ratio of patients suffering from CHD among those with, compared to those without, a positive family history of CHD was 4.95 (95% confidence interval = 1.27-19.28) after adjusting for the major known risk factors in each individual and their families (no interaction term remained in the model). The results support the hypothesis that a family history of CHD, acting through mechanisms other than known risk factors or their familial aggregation, is an independent risk factor for CHD even in a low incidence area. No interaction effect was observed between family history and the presence of the three major risk factors of CHD. This should help to identify individuals at greater risk of CHD.