Limited information exists on the longitudinal association between the left ventricular (LV) structure and function and future cognitive impairment and dementia in a large population without clinically recognized cardiovascular disease at baseline. The aim of the present study was to investigate the association between cardiac structure and function and risk of dementia and cognitive impairment in the MESA (Multi-Ethnic Study of Atherosclerosis) cohort. Measures of LV structure and function were determined using magnetic resonance imaging at baseline in 4999 participants free of clinically diagnosed cardiovascular disease and dementia. Probable incident clinical dementia was ascertained from hospitalization discharge records. Cognitive function was evaluated using tests addressing global cognitive function, processing speed, and memory. Associations of measures of LV structure and function with the incidence of clinically diagnosed dementia and cognitive performance were evaluated using Cox proportional hazard regression models adjusted for demographics, cardiovascular risk factors, and cardiovascular events. During a median follow-up of 12 years, 130 probable incident dementia cases were documented. Higher LV mass index (hazard ratio, 1.01; 95% confidence interval, 1.00-1.02) and LV mass-to-volume ratio (hazard ratio, 2.37; 95% confidence interval, 1.25-4.43) were independently associated with incident dementia and impaired cognitive function. Measures of LV function were not associated with risk of dementia or cognitive impairment. In conclusion, in a multiethnic cohort of participants without clinically detected cardiovascular disease and dementia at baseline, LV hypertrophy and concentric remodeling were independently associated with incident dementia and cognitive impairment.
BackgroundSpondyloarthritis (SpA) are the most common group of chronic inflammatory rheumatic diseases affecting about 1.5% of the adult Caucasian population. Low back pain is the most common symptom. The aetiopathogenesis of SpA is multifactorial, with well-known genetic and environmental contributions. Furthermore, muscle properties might also be involved in the pathophysiological process and these could be modulated by the genetic background. Alpha-actinin-3 (ACTN3) and Vitamin D receptor (VDR) genes are well-known genes related with muscle performance. Our aim was to analyze four SNPs of these genes and to evaluate their influence in axial SpA (axSpA) susceptibility, phenotype and muscle properties.MethodsWe performed a pilot study based on case-control approach involving 56 participants: 28 axSpA patients and 28 healthy controls matched by age, gender and levels of physical activity. Clinical, epidemiological and muscle characterization data—muscle physical properties (stiffness, tone, and elasticity), strength, mass, and performance, were collected. Two different muscles were considered for analysis, the Multifidus and Gastrocnemius. Four SNPs of ACTN3 (rs1815739) and VDR (rs2228570, rs731236, and rs7975232), were selected, analyzed and correlated with clinical, epidemiological and muscle characterization data.ResultsIn total, 51 individuals (27 axSpA patients and 24 matched controls) were eligible for further genetic analysis, 66.7% being male and with a mean age of 36 years. Muscle physical properties, muscle strength and muscle mass were similar in both groups; however, axSpA patients showed a decrease in muscle performance. None of the studied SNPs were associated with disease susceptibility/phenotype, muscle physical properties, muscle strength or muscle mass. However, ACTN3 rs1815739 and VDR rs2228570 were shown to be associated with muscle performance.ConclusionOur results suggest an association between ACTN3 and VDR polymorphisms and muscle performance in axSpA.
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