Does the use of an in situ or Y-configuration for bilateral internal thoracic arteries influence long-term survival, patency or repeat revascularization in coronary bypass surgery?

A best evidence topic was constructed according to a structured protocol. The question addressed was whether the configuration of bilateral internal thoracic arteries (BITAs) influences survival, patency or repeat revascularization in patients undergoing coronary artery bypass grafting. Five hundred and seventy-one papers were found using the reported searches, of which 8 represented the best evidence to answer the clinical question. One systematic review, 4 randomized trials and 3 observational studies were selected. The authors, date, journal, study type, population, main outcome measures and results are tabulated. All 4 prospective randomized trials found no significant difference in graft patency or mortality when comparing Y-graft and in situ configurations. Three of the 4 randomized trials found no difference in major adverse cardiovascular and cerebrovascular events or repeat revascularization at follow-up. An exception was Glineur et al. (Bilateral internal thoracic artery configuration for coronary artery bypass surgery: a prospective randomized trial. Circ Cardiovasc Interv 2016;9:7), who found that the Y-configuration resulted in lower rates of major adverse cardiovascular and cerebrovascular events. All 3 observational studies reviewed found no alteration in survival, cardiac events or repeat revascularization between in situ and Y-graft BITA configurations. One systematic review found similar outcomes with respect to mortality, cardiac events and repeat revascularization with in situ and composite BITA. In summary, existing literature demonstrates no difference in clinical outcomes between composite and in situ graft configurations. Furthermore, the configuration of BITA does not affect mortality, graft patency or repeat revascularization.

Evidence of endothelial dysfunction in the development of Alzheimer's disease: Is Alzheimer's a vascular disorder?

The etiology of Alzheimer's disease (AD) remains unclear. The emerging view is that cerebrovascular dysfunction is a feature not only of cerebrovascular diseases, such as stroke, but also of neurodegenerative conditions, such as AD. In AD, there is impaired structure and function of cerebral blood vessels and cells in the neurovascular unit. These effects are mediated by vascular oxidative stress. Injury to the neurovascular unit alters cerebral blood flow regulation, depletes vascular reserves, disrupts the blood-brain barrier and reduces the brain's repair capacity. Such injury can exacerbate the cognitive dysfunction exerted by incident ischemia and coexisting neurodegeneration. This article summarises data regarding cardiovascular risk factors, vascular abnormalities and brain endothelial damage in AD. In view of accumulating evidence of vascular pathology in AD, we also review the literature (MEDLINE, EMBASE) for clinical evidence of impaired endothelial function in AD. A total of 15 articles investigating endothelial dysfunction in AD were identified. 10 of these articles showed impaired endothelial function in AD patients. The current literature suggests endothelial dysfunction may be involved in the pathogenesis of AD. This aspect of AD pathology is particularly interesting in view of its potential for therapeutic intervention. Future research on endothelial function in AD should concentrate on population-based analysis and combine multiple methods to evaluate endothelial function.