Operative and Mid-Term Outcomes of Thoracic Aortic Operation in Octogenarians and Beyond.

OBJECTIVES: To study the short and mid-term outcomes of thoracic aortic operations in patients ≥80 years old. METHODS: This is a retrospective chart review of patients ≥80 years old who underwent thoracic aortic operation in our institution between 2006 and 2013. RESULTS: Ninety-eight patients were studied. Fifty-four patients underwent open repair; 41 underwent endovascular repair; and three underwent hybrid repair with aortic arch debranching and subsequent endovascular stent graft. Hospital mortality rate among the entire cohort was 11/98 (11%): 7/54 (13%) for open repair; 2/41 (5%) for endovascular repair; and 2/3 (66%) for hybrid repair. Major adverse events occurred in 23/98 (23%) in the entire cohort: 15/54 (28%) in open repair; 5/41 (12%) in endovascular repair; and 3/3 (100%) in hybrid repair. Mean follow-up was 31 ± 28 months (median 26 months). Two- and five-year survival rates were 57%, and 34% for the open approach and 71%, and 43% for the endovascular approach respectively. CONCLUSIONS: Both open and endovascular thoracic aortic repairs can be performed with favorable mortality and perioperative morbidity in appropriately selected octogenarian patients. doi: 10.1111/jocs.12722 (J Card Surg 2016;31:334-340).

Spinocerebellar Ataxia Type 3: A Case Report and Literature Review.

Spinocerebellar ataxia type 3 (SCA3), also known by the eponym Machado-Joseph disease, is an autosomal dominant CAG trinucleotide (polyglutamine) repeat disease that presents in young- to middle-aged adults. SCA3 was first described in Azorean individuals and has interesting epidemiological patterns. It is characterized clinically by progressive ataxia and neuropathologically by progressive degenerative changes in the spinal cord and cerebellum, along with degeneration of the cortex and basal ganglia. Here, we describe the clinical and neuropathologic features in a case of SCA3 with unique findings, including involvement of the inferior olivary nucleus and cerebellar Purkinje cell layer, which are classically spared in the disease. We also discuss research into the disease mechanisms of SCA3 and the potential for therapeutic intervention.