Background: We sought to examine whether people with a diagnosis of cardiovascular disease (CVD) experienced a greater incidence of subsequent cognitive impairment (CI) compared to people without CVD, as suggested by prior studies, using a large longitudinal cohort. Methods: We employed Health and Retirement Study (HRS) data collected biennially from 1998 to 2014 in 1305 U.S. adults age ≥ 65 newly diagnosed with CVD vs. 2610 age- and gender-matched controls. Diagnosis of CVD was adjudicated with an established HRS methodology and included self-reported coronary heart disease, angina, heart failure, myocardial infarction, or other heart conditions. CI was defined as a score < 11 on the 27-point modified Telephone Interview for Cognitive Status. We examined incidence of CI over an 8-year period using a cumulative incidence function accounting for the competing risk of death. Results: Mean age at study entry was 73 years, 55% were female, and 13% were non-white. Cognitive impairment developed in 1029 participants over 8 years. The probability of death over the study period was greater in the CVD group (19.8% vs. 13.8%, absolute difference 6.0, 95% confidence interval 2.2 to 9.7%). The cumulative incidence analysis, which adjusted for the competing risk of death, showed no significant difference in likelihood of cognitive impairment between the CVD and control groups (29.7% vs. 30.6%, absolute difference − 0.9, 95% confidence interval − 5.6 to 3.7%). This finding did not change after adjusting for relevant demographic and clinical characteristics using a proportional subdistribution hazard regression model. Conclusions: Overall, we found no increased risk of subsequent CI among participants with CVD (compared with no CVD), despite previous studies indicating that incident CVD accelerates cognitive decline.

Patients with gout are at elevated risk of multiple vascular and metabolic comorbidities. Whether they are also at risk of sarcopenia, which is known to affect patients with other rheumatic diseases, has not been previously assessed. We examined whether patients with gout have decreased lumbar muscle quality and quantity, indicating an association between gout and sarcopenia. 50 gout subjects and 25 controls, ages 45-80, underwent computed tomography imaging of the lumbosacral spine. We measured muscle quantity (skeletal muscle area [SMA] and index [SMI]) and quality (skeletal muscle radiation attenuation [SMRA] and intermuscular adipose tissue [IMAT] area and index [IMATI]) of the psoas and erector spinae muscles at the L3 level. 70 subjects (45 gout and 25 controls) were included in the analysis. Gout subjects had higher BMI, more kidney disease and hypertension, lower exercise frequency, and higher mean serum urate and creatinine vs. controls. Lumbar SMRA was significantly lower in gout subjects vs. controls, indicating reduced muscle quality. Lumbar IMAT area was significantly higher in gout subjects vs. controls, as was lumbar IMATI, indicating increased muscle adiposity. These differences persisted after adjusting for potential confounders. In contrast, there was no significant difference between gout and control groups in lumbar SMA or lumbar SMI, suggesting that muscle quantity may not be routinely affected by the diagnosis of gout. Gout patients exhibit decreased lumbar muscle quality compared with controls, consistent with an association between gout and sarcopenia.

Prior research suggests a connection between osteoarthritis and gout at sites commonly affected by gouty attacks. Whether this connection exists at sites with known monosodium urate crystal deposition but less commonly affected by gouty attacks, such as the lumbosacral spine, has not been previously investigated. We assessed whether lumbosacral osteoarthritis is more prevalent and more severe in subjects with gout compared with controls, and whether lumbosacral osteoarthritis is associated with higher levels of spinal monosodium urate deposition. Fifty gout subjects and 25 controls underwent dual-energy computed tomography imaging of the lumbosacral spine. We assessed lumbosacral osteoarthritis using a modification of a validated computed tomography scoring system, incorporating grade of intervertebral disc narrowing and facet joint osteoarthritis, and presence of spondylolysis and spondylolisthesis. We quantified spinal monosodium urate deposition using the default post-processing algorithm, plus a maximally specific algorithm to exclude potential artefacts. Forty-six gout subjects and 25 controls, average age 62 years, were included in the final analysis. Both gout and control subjects exhibited high rates of facet joint osteoarthritis and degenerative disc disease, with no difference in prevalence or severity between groups. Gout subjects did not have differing prevalence of spondylolysis and spondylolisthesis vs. controls. Subjects with lumbosacral osteoarthritis did not have higher levels of spinal monosodium urate deposition. Overall, lumbosacral osteoarthritis was not more prevalent or more severe in gout patients compared with controls, and spinal monosodium urate crystal deposition did not differ between patients with and without lumbosacral osteoarthritis.

Background: We sought to examine whether people with a diagnosis of cardiovascular disease (CVD) experienced a greater incidence of subsequent cognitive impairment (CI) compared to people without CVD, as suggested by prior studies, using a large longitudinal cohort. Methods: We employed Health and Retirement Study (HRS) data collected biennially from 1998-2014 in 1,305 U.S. adults age ≥65 newly diagnosed with CVD vs. 2,610 age- and gender-matched controls. Diagnosis of CVD was adjudicated with an established HRS methodology and included self-reported coronary heart disease, angina, heart failure, myocardial infarction, or other heart conditions. CI was defined as a score <11 on the 27-point modified Telephone Interview for Cognitive Status. We examined incidence of CI over an 8-year period using a cumulative incidence function accounting for the competing risk of death.Results: Mean age at study entry was 73 years, 55% were female, and 13% were non-white. Cognitive impairment developed in 1,029 participants over 8 years. The probability of death over the study period was greater in the CVD group (19.8% vs. 13.8%, p <.001). The cumulative incidence analysis, which adjusted for the competing risk of death, showed no significant difference in likelihood of cognitive impairment between the CVD and control groups (29.7% vs. 30.6%, p = 0.64). This finding did not change after adjusting for relevant demographic and clinical characteristics using a proportional subdistribution hazard regression model.Conclusions: Overall, we found no increased risk of subsequent CI among participants with CVD (compared with no CVD), despite previous studies indicating that incident CVD accelerates cognitive decline.