Background: Epicardial fat (EF) is the visceral fat of the heart deposited under the visceral layer of the pericardium and has the same origin as abdominal visceral fat, which is shown to be strongly related to the development of coronary artery disease (CAD). We measured the volume of EF (EFV) by 64-multidetector computed tomography (MDCT) and studied the relationship between EFV and the severity of CAD. Hypothesis: Epicardial fat volume increases steeply in patients with significant coronary artery stenosis and in those with severe coronary artery calcification. Methods: We studied 197 patients with suspected CAD who underwent 64-MDCT and coronary angiography. Cross-sectional tomographic cardiac slices (3.0 mm thick) from base to apex (30 to 40 slices per heart) were traced semiautomatically and EFV was measured by assigning Hounsfield units ranging from −30 to −250 to fat. Results: Epicardial fat volume was 99.4 ± 40.0 ml (range, 11.6 to 263.8 mL) and coronary artery calcium score (CACS) was 267.2 ± 605.1 (range, 0 to 3780). There was a significant relationship between EFV and CACS (r = 0.210, P = 0.003). Patients with EFV >100 had a CACS that was significantly higher than in those with EFV <100 (384.0 ± 782.0 vs 174.8 ± 395.6; P = 0.016). The incidence of significant CAD was significantly higher in patients with EFV >100 compared with those with EFV <100 (40.2% vs 22.7%; P = 0.008). The EFV was significantly higher in patients with severe coronary artery stenosis and in those with severe coronary artery calcification (CACS >400). Conclusions: Our results showed that EFV was associated with coronary atherosclerosis, and EFV increased steeply in patients with severe coronary artery stenosis and in those with severe coronary artery calcification.

Our results show that the prevalence of coronary plaques detectable by 64-slice CT in asymptomatic diabetic patients is very high.

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The distribution of coronary atherosclerosis has not been fully clarified. We measured coronary artery calcium score (CACS) in 624 consecutive patients for the right coronary artery (RCA), left main trunk (LMT), left anterior descending coronary artery (LAD), and left circumflex coronary artery (LCx), then calculated total CACS. Coronary artery calcium score was measured using the Agatston method. We divided these patients into four groups: CACS 1-100 (Group A, n = 267), CACS 101-400 (Group B, n = 160), CACS 401-1000 (Group C, n = 110), and CACS >1000 (Group D, n = 87). In Group A, B, and C, the CACS in LAD was significantly higher than in the other three arteries (P < 0.0001). In Group D, the CACS was not significantly different between LAD and RCA (P = 0.6930). In Groups A, B, and C, coronary artery calcium (CAC) was more frequently found in LAD compared with other arteries (P < 0.0001). However, in Group D the prevalence of CAC was not significantly different among the three arteries (P = 0.4435). Coronary artery calcium was found more frequently in LAD than in the other coronary arteries in patients with mild to high CAC, but not in those with very high CAC.

Two patients with left recurrent laryngeal nerve paralysis in association with pulmonary artery hypertension are described. One had primary pulmonary hypertension and the other had patent ductus arteriosus. The greatly dilated pulmonary artery in these patients resulted in compression of the left recurrent laryngeal nerve and produced a cardiovocal (Ortner's) syndrome. The pathogenesis of the vocal cord palsy was documented by cross-sectional computed tomography. In conclusion, computed tomography is of great help in differentiating this syndrome from other diseases such as mediastinal mass or lymphadenopathy whenever hoarseness is complicated by pulmonary hypertension.