ABSTRACT
Background: Previous studies have shown that Alzheimer's disease (AD) can cause myocardial damage. However, whether there is a causal association between AD and non-ischemic cardiomyopathy (NICM) remains unclear. Using a comprehensive two-sample Mendelian randomization (MR) method, we aimed to determine whether AD and family history of AD (FHAD) affect left ventricular (LV) structure and function and lead to NICM, including hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM). Methods: The summary statistics for exposures [AD, paternal history of AD (PH-AD), and maternal history of AD (MH-AD)] and outcomes (NICM, HCM, DCM, and LV traits) were obtained from the large European genome-wide association studies. The causal effects were estimated using inverse variance weighted, MR-Egger, and weighted median methods. Sensitivity analyses were conducted, including Cochran's Q test, MR-Egger intercept test, MR pleiotropy residual sum and outlier, MR Steiger test, leave-one-out analysis, and the funnel plot. Results: Genetically predicted AD was associated with a lower risk of NICM [odds ratio (OR) 0.9306, 95% confidence interval (CI) 0.8825-0.9813, p = 0.0078], DCM (OR 0.8666, 95% CI 0.7752-0.9689, p = 0.0119), and LV remodeling index (OR 0.9969, 95% CI 0.9940-0.9998, p = 0.0337). Moreover, genetically predicted PH-AD was associated with a decreased risk of NICM (OR 0.8924, 95% CI 0.8332-0.9557, p = 0.0011). MH-AD was also strongly associated with a decreased risk of NICM (OR 0.8958, 95% CI 0.8449-0.9498, p = 0.0002). Different methods of sensitivity analysis demonstrated the robustness of the results. Conclusion: Our study revealed that AD and FHAD were associated with a decreased risk of NICM, providing a new genetic perspective on the pathogenesis of NICM.
ABSTRACT
OBJECTIVE: To report the authors' experience in treating complex congenital heart diseases with cryopreserved viable pedicled aortic homografts (CVAHs). METHODS: CVAHs were obtained within 3 h after death of donors younger than 35 years old due to non-cardiovascular and non-infectious diseases. After routine treatment, the homografts were cryopreserved in liquid nitrogen and thawed in 0.9% sodium chloride solution at 37 to 42 degrees celsius before use. A CVAH was used as a valved conduit to connect the pulmonary artery and right ventricle in one case of double-outlet right ventricle, pulmonary stenosis and coronary artery deformation. In another case of severe tetralogy of Fallot, a CVAH was used as a valved patch to enlarge the right ventricle outlet. RESULTS: The homografts were preserved satisfactorily. The surgical results of the 2 cases with congenital heart diseases were satisfactory in perioperative and follow-up periods. CONCLUSION: CVAH is a good substitute to rebuild right ventricle-pulmonary artery connection in treatment of complex congenital heart diseases.
