Extrinsic compression of the left anterior descending coronary artery by rib in a patient with progressive left ventricular remodeling.

A 78-year-old man with a history of dilated cardiomyopathy diagnosed 5 years previously was admitted to our clinic with accelerating chest pain and dyspnea. The initial ECG showed sinus tachycardia and left bundle-branch block. Laboratory tests revealed elevated levels of troponin T (0.409 ng/mL), creatinine kinase (218 U/L), and creatinine kinase-MB isoenzyme (9.8 g/L). The peak level of creatinine kinase-MB isoenzyme was 41.9 g/L. Transthoracic echocardiography revealed a more progressed left ventricular remodeling in comparison with an echocardiography conducted 2 years previously. Compared with the previous study, the end-diastolic dimension of the left ventricle (LV) was increased from 68 mm to 76 mm and the LV end-diastolic volume was increased from 199 mL to 331 mL. Previously, the LV showed global hypokinesia with decreased global LV systolic function (ejection fraction 30%). The present study showed worsened regional wall motion abnormality at the territories of the left anterior descending coronary artery (LAD) with aggravated LV dysfunction (ejection fraction 23%; online-only Data Supplement Movies I and II). Coronary angiography revealed an unusual obstruction of the distal LAD (Figure 1). In the course of distal LAD, a filling defect, evident as a seeming loss of contrast, abruptly began and ended with sharp edges. The proximal and distal reference segments appeared normal. Intravascular ultrasonography (IVUS) and optical coherence tomography revealed that the distal LAD was deformed to a slitlike appearance, suggesting an extrinsic compression (Figure 2). To evaluate the cause of extrinsic compression of the distal LAD, cardiac multidetector computed tomography was performed. Cardiac multidetector computed tomography showed no evidence of mediastinal or intrathoracic masses, which could cause the extrinsic compression of LAD. Because the severely dilated LV contacted with the chest wall, the distal LAD was trapped between dilated LV and costochondral cartilage and was narrowed because of extrinsic compression by the costochondral cartilage (Figures 3 and 4). A diagnosis was made of extrinsic compression of the distal LAD secondary to LV remodeling resulting from dilated cardiomyopathy.