Key result
Central pulsatile blood pressure offers no predictive advantage over peripheral pressure for major cardiovascular events.
Why the study?
Pulsatile blood pressure confers cardiovascular risk, but whether cardiovascular end point associations are tighter for central than peripheral systolic blood pressure or pulse pressure is uncertain.
Does central pulsatile blood pressure measurement improve the prediction of cardiovascular outcomes compared to peripheral blood pressure measurement in adults?
Cohort (n=5,608)
Yes
Does central pulsatile blood pressure measurement improve the prediction of cardiovascular outcomes compared to peripheral blood pressure measurement in adults?
Central blood pressure measurements do not refine cardiovascular risk stratification beyond carefully recorded peripheral blood pressure in adults.
Central BP does not improve CV risk prediction over peripheral measures; leaves open whether central assessment adds value in targeted subgroups.
Pulsatile blood pressure (BP) confers cardiovascular risk. Whether associations of cardiovascular end points are tighter for central systolic BP (cSBP) than peripheral systolic BP (pSBP) or central pulse pressure (cPP) than peripheral pulse pressure (pPP) is uncertain. Among 5608 participants (54.1% women; mean age, 54.2 years) enrolled in nine studies, median follow-up was 4.1 years. cSBP and cPP, estimated tonometrically from the radial waveform, averaged 123.7 and 42.5 mm Hg, and pSBP and pPP 134.1 and 53.9 mm Hg. The primary composite cardiovascular end point occurred in 255 participants (4.5%). Across fourths of the cPP distribution, rates increased exponentially (4.1, 5.0, 7.3, and 22.0 per 1000 person-years) with comparable estimates for cSBP, pSBP, and pPP. The multivariable-adjusted hazard ratios, expressing the risk per 1-SD increment in BP, were 1.50 (95% CI, 1.33–1.70) for cSBP, 1.36 (95% CI, 1.19–1.54) for cPP, 1.49 (95% CI, 1.33–1.67) for pSBP, and 1.34 (95% CI, 1.19–1.51) for pPP ( P <0.001). Further adjustment of cSBP and cPP, respectively, for pSBP and pPP, and vice versa, removed the significance of all hazard ratios. Adding cSBP, cPP, pSBP, pPP to a base model including covariables increased the model fit ( P <0.001) with generalized R 2 increments ranging from 0.37% to 0.74% but adding a second BP to a model including already one did not. Analyses of the secondary end points, including total mortality (204 deaths), coronary end points (109) and strokes (89), and various sensitivity analyses produced consistent results. In conclusion, associations of the primary and secondary end points with SBP and pulse pressure were not stronger if BP was measured centrally compared with peripherally.
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Huang et al. (2020) conducted a cohort in General cardiovascular risk (n=5,608). Central pulsatile blood pressure (central systolic BP and pulse pressure) vs. Peripheral pulsatile blood pressure (peripheral systolic BP and pulse pressure) was evaluated on Composite cardiovascular outcome consisting of cardiovascular mortality and nonfatal end points (myocardial infarction, heart failure, stroke, and coronary revascularization) (HR 1.50, 95% CI 1.33-1.70, p=<0.001). Central pulsatile blood pressure components were not more closely associated with the primary composite cardiovascular endpoint than peripheral blood pressure components (p=0.86 for difference).
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