Isolated systolic hypertension and subclinical cardiovascular disease in the elderly. Initial findings from the Cardiovascular Health Study

Objectives: To evaluate whether late-life depression mediates the association of subclinical cardiovascular disease (CVD) with all-cause mortality. Method: Using data from 3,473 Cardiovascular Health Study participants, the Cox proportional hazards model was used to examine the direct and indirect (via late-life depression) effects of the association between baseline subclinical CVD and all-cause mortality with weights derived from multivariable logistic regression of late-life depression on subclinical CVD. Results: Subclinical CVD led to a higher risk of all-cause mortality (hazard ratio [HR] = 1.51, 95% confidence interval, [CI] = [1.42, 1.94]). Total effect of subclinical CVD on all-cause mortality was decomposed into direct (HR = 1.41, 95% CI = [1.37, 1.58]) and indirect (HR = 1.07, 95% CI = [1.01, 1.23]) effects; 16.3% of the total effect of subclinical CVD on all-cause mortality was mediated by late-life depression. Discussion: Late-life depression accounts for little, if any, of the association between subclinical CVD, a risk factor of all-cause mortality, and all-cause mortality.

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No Association of Plasma Prothrombin Concentration or the G20210A Mutation with Incident Cardiovascular Disease

Thrombosis and Haemostasis ◽

10.1055/s-0037-1613057 ◽

2002 ◽

Vol 87 (04) ◽

pp. 614-621 ◽

Cited By ~ 29

Author(s):

Adam Smiles ◽

Nancy Jenny ◽

Zhonghua Tang ◽

Alice Arnold ◽

Mary Cushman ◽

...

Keyword(s):

Cardiovascular Disease ◽

Cardiovascular Health ◽

Plasma Lipids ◽

The Elderly ◽

Health Study ◽

Cardiovascular Health Study ◽

Case Group ◽

Cvd Risk ◽

G20210a Mutation ◽

Subclinical Cvd

SummaryProthrombin is a key factor in blood clotting, a process intimately involved in thrombotic disease. We assessed prothrombin levels and G20210A genotype in a case-control study within the Cardiovascular Health Study. Cases included angina, myocardial infarction, stroke, and the presence of MRI-detectable infarcts (n ≈ 250 each). Populationbased controls free of clinical cardiovascular disease (CVD) (n ≈ 500) and a subset free of clinical and subclinical CVD (n ≈ 250) were used for comparison. The 20210 A allele, frequency 2.9%, was associated with higher mean prothrombin levels: 166.3 vs. 139.5 µg/ml (P <0.001). Significant correlates of prothrombin included gender, plasma lipids, other vitamin K-dependent proteins, and inflammatory markers, but not race, smoking, hypertension, diabetes, measures of subclinical CVD, or markers of procoagulant activity. Compared to controls, neither genotype nor prothrombin level was associated with any CVD case group. We conclude that, in the elderly, neither prothrombin level nor 20210 genotype were associated with either CVD risk factors or events. This is consistent with the lack of association of prothrombin levels with measures of underlying CVD or procoagulant markers.

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