Why the study?
Do brachial pulse pressure and sialic acid independently predict the risk of first cardiovascular events in individuals aged 50 or older?
Do brachial pulse pressure and sialic acid independently predict the risk of first cardiovascular events in individuals aged 50 or older?
Sialic acid, an inflammatory marker, is an independent predictor of cardiovascular events over 40 years of follow-up, whereas the predictive value of pulse pressure is highly dependent on mean arterial pressure.
Answers are grounded in this paper and cite their sources.
Sialic acid may aid CVD risk assessment in adults ≥50; hypothesis-generating and requires prospective validation before changing practice.
OBJECTIVE: Pulse pressure (PP) is a risk marker for cardiovascular disease (CVD) in individuals 50 years and older. Inflammation is suggested to influence atherosclerosis, but could also increase PP. We aimed to examine the combined effects of PP and the inflammatory marker sialic acid, and their independent roles on CVD risk. METHODS: From a population-based study in Sweden between 1962 and 1965, 18,429 men and 19,414 women at the age of 50 or older were selected and followed for first CVD event until 2005. We investigated the biological interactions between sialic acid and PP. The associations of PP and sialic acid with risk of CVD were calculated by using Cox proportional hazards model. Adjustments were made for conventional risk factors, mean arterial pressure (MAP) and socioeconomic status. RESULTS: The mean age was 59.5 (SD 6.5) years and the number of incident CVD events in men and women were 3641 and 3227, respectively. No biological interaction was seen between PP and sialic acid. In men, the adjusted hazard ratio for PP was 0.92 [95% confidence interval (CI) 0.88-0.96, P < 0.0001) for 1 SD of PP, and 1.09 (95% CI 1.05-1.13, P < 0.0001) for 1 SD of sialic acid. In women, the corresponding figures were 1.02 (95% CI 0.97-1.07, P = 0.48) and 1.09 (95% CI 1.05-1.13, P < 0.0001). CONCLUSIONS: Sialic acid but not PP was an independent risk factor for CVD. The risk induced by PP is highly affected by MAP. This suggests that both estimated arterial stiffness and inflammation contribute through different pathways to risk of CVD.
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Khalili et al. (2012) studied this question.
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