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Objective-Coronary plaque instability causes myocardial infarction (MI). Angiographic lesions with such instability are complex lesions. Complex carotid plaques were reported to be prevalent in unstable angina. We investigated associations between coronary plaque instability, such as MI and angiographic complex coronary lesions, and aortic plaques. Methods and Results-Aortic MRI was performed in 146 patients undergoing coronary angiography, of whom 108 had coronary artery disease (CAD) and 44 also had MI. Prevalence of plaques in thoracic and abdominal aortas was higher in patients with than without CAD (73% and 94% versus 32% and 79%), but it was similar in CAD patients with and without MI. Notably, complex plaques in abdominal aorta were more prevalent in CAD patients with than without MI (36% versus 14%; PϽ0.025). In multivariate analysis, abdominal complex plaques were associated with MI (odds ratio [OR], 4.5; 95% CI, 1.5 to 13.8). Among patients without MI, thoracic and abdominal complex plaques were more prevalent in patients with than without complex coronary lesions (22% and 33% versus 2% and 7%; PϽ0.05).Abdominal complex plaques were also associated with complex coronary lesions (OR, 9.8; 95% CI, 1.1 to 85.9). Key Words: aorta Ⅲ coronary artery disease Ⅲ myocardial infarction Ⅲ MRI P laque instability is a main cause of acute coronary syndrome, such as myocardial infarction (MI). 1 Angiographic features of coronary lesions associated with plaque instability are sharp overhanging edge, irregular border, and intraluminal lucency, so-called complex lesions. 2,3 Although angiographic complex coronary lesions are seen in 10% to 20% of patients with stable angina, 2 such lesions are known to be common in acute coronary syndrome and to be predictive of coronary events. 2,4,5 Recently, complex plaques in carotid arteries were reported to be more prevalent in patients with unstable angina than in those with stable angina, suggesting a link between coronary and carotid plaque instability. 6 Plaque instability in patients with coronary artery disease (CAD) may not be confined to coronary arteries, but it may also involve other arteries. Complex plaques in thoracic aorta, detected by transesophageal echocardiography (TEE), were reported to be associated with systemic embolic events. 7,8 However, the association between coronary plaque instability and complex aortic plaques has not yet been elucidated. Conclusion-ComplexRecently, MRI became a useful tool for noninvasively detecting plaques in both thoracic and abdominal aortas. 9,10 We 11,12 and others 13 showed the good correlations for plaque morphology and characterization in the aortas between in vivo and ex vivo MRI findings and histopathology in animal models. In humans, we reported that MRI evaluations of thoracic aorta closely correlated with TEE findings. 9 Using MRI, we previously reported the association between the severity of coronary stenosis and the extents of aortic plaques in 102 patients undergoing coronary angiography. 10 In the present study, we ...

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SUMMARYPulmonary veins are the most frequent origin of focal and paroxysmal atrial fibrillation. Although radiofrequency ablation has been attempted for the treatment of focal and paroxysmal atrial fibrillation, the anatomy of the pulmonary vein is still not fully understood. To investigate the dimensions and anatomical variation of the pulmonary vein in patients with paroxysmal atrial fibrillation, we performed breath-hold gadolinium enhanced magnetic resonance (MR) angiography using a 1.5 T cardiac MR imager (GE CV/i) in 32 patients with paroxysmal atrial fibrillation (61 ± 8 years old), 11 patients with chronic atrial fibrillation (64 ± 9 years old), and 26 patients with normal sinus rhythm (55 ± 15 years old). Three dimensional images of the pulmonary veins were thus obtained, and the diameters of the most proximal portion of the left or right superior pulmonary vein and left or right inferior pulmonary vein were measured. Pulmonary vein branching variations were determined by a visual qualitative analysis by two separate readers' agreements, who were blinded to any clinical information. We focused on the existence of a complex-branching pattern draining into the orifice of four pulmonary veins. Patients with either paroxysmal atrial fibrillation or chronic atrial fibrillation showed larger superior pulmonary veins than those with normal sinus rhythm (mean ± SD; in the left superior pulmonary vein, 20 ± 3 mm, 23 ± 3 mm vs 16 ± 3 mm, P <0.05; in right superior pulmonary vein, 19 ± 4 mm, 19 ± 2 mm vs 16 ± 2 mm, P < 0.05). Complex-branching pattern was frequently observed in inferior pulmonary veins in patients with either paroxysmal atrial fibrillation or chronic atrial fibrillation; 25/32 patients with paroxysmal atrial fibrillation, 11/11 patients with chronic atrial fibrillation, compared to 7/26 patients with normal sinus rhythm. Complex-branching patterns were not observed in superior pulmonary veins in any patients in this cohort. Conclusion; In patients with paroxysmal atrial fibrillation or chronic atrial fibrillation, significant pulmonary vein dilation occurred mainly in the superior pulmonary veins, while a complex-branching pattern was frequently observed in the inferior pulmonary veins. These MR angiographic findings might be useful when From the

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