LEFT MAIN CORONARY-ARTERY STENOSIS AFTER AORTIC-VALVE REPLACEMENT - GENETIC DISPOSITION FOR ACCELERATED ARTERIOSCLEROSIS AFTER INJURY OF THE INTACT HUMAN CORONARY-ARTERY

Background: Left main coronary artery stenosis is a rare but life-threatening complication after aortic valve replacement because of coronary perfusion-related trauma to the vessel wall with cannulation of the coronary ostia. We investigated whether this complication still occurs in the 1990s despite the use of more advanced catheter materials and modern surgical preservation techniques. Methods: Four years after identification of the first two cases in 1987, five further patients had developed left main coronary artery stenosis after aortic valve replacement (incidence, 0.9%) at the cardiothroacic clinic of the J.W. Goethe University and were studied for contributing factors. Results: Severe coronary ostial stenosis developed within 1 to 6 months after aortic valve replacement. In one such case, intimal proliferation was seen in a biopsy specimen that was comparable to the restenosis induced by coronary angioplasty. The clinical characteristics of the patients developing the complication, the surgical technique, and the intraoperative course did not differ from the other patients. However, five of the seven patients (71%) had a common genetic trait concerning their apolipoprotein E genotype (the epsilon4 allele) that is normally present in only 10% to 15% of patients screened (P < 0.01). Conclusions: These lesions seem to result from a uniform response of the vessel wall to injury. Their incidence is probably related in part to the degree of injury after trauma to the coronary ostia during cannulation for myocardial protection. Patients with the epsilon4 allele might be genetically predisposed for a pathologically increased response of proliferative repair mechanisms after arterial injury. The complication can be avoided by not instrumenting the coronary ostia for direct antegrade cardioplegia but using retrograde delivery as an alternative method of myocardial protection.