The long-term outcome of patients with coronary disease and atrial fibrillation undergoing the cox maze procedure

AbstractBackgroundA significant number of patients presenting for coronary revascularization have chronic atrial fibrillation. Although the Cox maze III procedure is the gold standard for the surgical treatment of this arrhythmia, few of these patients undergo atrial fibrillation operations at the time of their coronary bypass grafting. This study examined the long-term outcome of patients with ischemic heart disease who underwent the Cox maze procedure at our institution.MethodsFrom 1990 to 2002, 47 patients undergoing operations for ischemic heart disease underwent a concomitant Cox maze III procedure. All patients underwent coronary bypass grafting, and 7 (15%) patients underwent coronary bypass grafting plus a mitral valve repair. Follow-up was performed by means of mail and telephone questionnaires with both the patients and their cardiologists. All patients who had any history of arrhythmia or who were taking medications had their rhythm documented by electrocardiogram.ResultsThe mean age of these patients was 62 ± 8 years, with a marked male predominance (45 men and 2 women). Twenty-eight (60%) of the patients had paroxysmal atrial fibrillation, and the remainder had persistent arrhythmias. The mean duration of atrial fibrillation was 7.6 ± 6.5 years. The operative mortality in this series was 2%. Nine (19%) patients required postoperative pacemakers. At last follow-up (mean of 5.7 ± 3.3 years), 98% of patients were free of atrial fibrillation.ConclusionThe Cox maze III procedure has a low operative mortality and excellent long-term efficacy in patients with ischemic heart disease. These data suggest a more widespread use of this procedure in these patients

Research priorities in hypertrophic cardiomyopathy: report of a Working Group of the National Heart, Lung, and Blood Institute.

Hypertrophic cardiomyopathy (HCM) is a myocardial disorder characterized by left ventricular (LV) hypertrophy without dilatation and without apparent cause (ie, it occurs in the absence of severe hypertension, aortic stenosis, or other cardiac or systemic diseases that might cause LV hypertrophy). Numerous excellent reviews and consensus documents provide a wealth of additional background.1–8 HCM is the leading cause of sudden death in young people and leads to significant disability in survivors. It is caused by mutations in genes that encode components of the sarcomere. Cardiomyocyte and cardiac hypertrophy, myocyte disarray, interstitial and replacement fibrosis, and dysplastic intramyocardial arterioles characterize the pathology of HCM. Clinical manifestations include impaired diastolic function, heart failure, tachyarrhythmia (both atrial and ventricular), and sudden death. At present, there is a lack of understanding of how the mutations in genes encoding sarcomere proteins lead to the phenotypes described above. Current therapeutic approaches have focused on the prevention of sudden death, with implantable cardioverter defibrillator placement in high-risk patients. But medical therapies have largely focused on alleviating symptoms of the disease, not on altering its natural history. The present Working Group of the National Heart, Lung, and Blood Institute brought together clinical, translational, and basic scientists with the overarching goal of identifying novel strategies to prevent the phenotypic expression of disease. Herein, we identify research initiatives that we hope will lead to novel therapeutic approaches for patients with HCM