Masashi Kawamura

Patency rate of the internal thoracic artery to the left anterior descending artery bypass is reduced by competitive flow from the concomitant saphenous vein graft in the left coronary artery

OBJECTIVE In coronary artery bypass grafting (CABG), insufficient bypass flow can be a cause of occlusion or string sign of the internal thoracic artery (ITA) graft. A patent saphenous vein (SV) graft from the ascending aorta can reduce the blood flow through the ITA graft, and may affect its long-term patency. In the present study, we examined the impact of the patent SV graft to the left coronary artery on the long-term patency of the ITA to left anterior descending (LAD) artery bypass. METHODS We reviewed the coronary angiograms of 313 patients who had two bypasses to the left coronary artery including 1 in situ ITA to LAD graft between March 1986 and December 2006. Patients who had occlusion of either bypass grafts to the left coronary artery in the early angiography, were excluded. In 64 patients (20.4%), bilateral ITAs were individually anastomosed to the LAD and the second target branch in the left coronary artery (BITA group), while 249 patients (79.6%) had the ITA to LAD bypass and the SV graft to the second target branch in the left coronary artery (ITA/SV group). The mean follow-up period was 6.8+/-4.9 years. RESULTS The cumulative patency rate of ITA-LAD bypasses at 10 years was 100% in the BITA group and 81.4% in the ITA/SV group. The ITA to LAD bypass was occluded in 14 (5.6%) patients of the ITA/SV group. In the ITA/SV group, the cumulative graft patency rate of the ITA to LAD bypass in patients who had severe (> or =76%) native coronary stenosis between the two anastomotic sites was 98.6% at 5 years, and was significantly higher than that of 82.3% in patients without severe stenosis (p<0.0001). CONCLUSIONS Long-term patency of the ITA-LAD bypass was affected by the presence of the patent SV graft to the left coronary artery, particularly when the native coronary stenosis between the two anastomotic sites was not severe. Competitive flow from SV graft could play an important role in occlusion of the in-situ arterial graft.

Layered smooth muscle cell–endothelial progenitor cell sheets derived from the bone marrow augment postinfarction ventricular function

Objective: The angiogenic potential of endothelial progenitor cells (EPCs) may be limited by the absence of their natural biologic foundation, namely smooth muscle pericytes. We hypothesized that joint delivery of EPCs and smooth muscle cells (SMCs) in a novel, totally bone marrow–derived cell sheet will mimic the native architecture of a mature blood vessel and act as an angiogenic construct to limit post infarction ventricular remodeling. Methods: Primary EPCs and mesenchymal stem cells were isolated from bone marrow of Wistar rats. Mesenchymal stem cells were transdifferentiated into SMCs by culture on fibronectin‐coated culture dishes. Confluent SMCs topped with confluent EPCs were detached from an Upcell dish to create a SMC‐EPC bi‐level cell sheet. A rodent model of ischemic cardiomyopathy was then created by ligating the left anterior descending artery. Rats were randomized into 3 groups: cell sheet transplantation (n = 9), no treatment (n = 12), or sham surgery control (n = 7). Results: Four weeks postinfarction, mature vessel density tended to increase in cell sheet‐treated animals compared with controls. Cell sheet therapy significantly attenuated the extent of cardiac fibrosis compared with that of the untreated group (untreated vs cell sheet, 198 degrees [interquartile range (IQR), 151‐246 degrees] vs 103 degrees [IQR, 92‐113 degrees], P = .04). Furthermore, EPC‐SMC cell sheet transplantation attenuated myocardial dysfunction, as evidenced by an increase in left ventricular ejection fraction (untreated vs cell sheet vs sham, 33.5% [IQR, 27.8%‐35.7%] vs 45.9% [IQR, 43.6%‐48.4%] vs 59.3% [IQR, 58.8%‐63.5%], P = .001) and decreases in left ventricular dimensions. Conclusions: The bone marrow‐derived, spatially arranged SMC‐EPC bi‐level cell sheet is a novel, multilineage cellular therapy obtained from a translationally practical source. Interactions between SMCs and EPCs augment mature neovascularization, limit adverse remodeling, and improve ventricular function after myocardial infarction.

Multiple saccular aneurysms in a young woman

On medical examination, the chest radiograph of a 25-year-old healthy woman incidentally revealed an abnormal shadow. Enhanced computed tomography (CT) revealed three saccular aneurysms, and the patient was referred for surgical treatment. Physical examination did not yield any particular findings. Three-dimensional CT showed that two of the aneurysms were located at the proximal descending aorta (cover). The larger aneurysm was 45 mm in diameter, and the smaller was 35 mm in diameter. The third aneurysm was located at the proximal part of the left subclavian artery, and it was 12 mm in diameter (cover). Thinning of the aorta and artery was also observed (A), but no other complications in the cardiovascular system were detected. Surgical treatment was performed. The aneurysms were exposed by a left thoracotomy via the fourth intercostal space (B). Graft replacement of the proximal descending aorta with reconstruction of the left subclavian artery was performed under deep hypothermic circulatory arrest. The blood vessels were very fragile and difficult to anastomose. Postoperative recovery was uneventful. The histopathological specimens of the resected aneurysms indicated severe cystic medial necrosis (elastic van Gieson stain, 40; C). Marfan syndrome and Ehlers-Danlos syndrome type IV (the vascular type) are well-known disorders characterized by the occurrence of aortic aneurysm or dissection at an early age. Molecular analyses of these syndromes have recently advanced. Mutations in the genes encoding fibrillin-1 and transforming growth factor beta receptor 1 and 2 have been shown in Marfan syndrome, and mutations in the gene encoding type III procollagen have been identified in Ehlers-Danlos syndrome type IV. In our patient, genetic testing for these genes was carried out, but it yielded negative results. Other cardiovascular disorders are expected to occur in this patient, and therefore, careful and lifelong follow-up is required.