Differential effects of brachial and central blood pressures on circulating levels of high-sensitivity cardiac troponin I in the general population.

BACKGROUND AND AIMS

Severe cardiac load increases circulating concentrations of high-sensitivity cardiac troponin I (hs-cTnI) through non-ischemic mechanisms. The present study was designed to investigate the effect of central blood pressure (BP), which reflects cardiac load rather than peripheral BP, on serum concentrations of hs-cTnI in subjects with or without increased arterial stiffness.

METHODS

We enrolled 1210 participants taking part in a yearly health checkup program. Laboratory measurements included serum concentrations of hs-cTnI and derivative reactive oxygen metabolites (d-ROM), as well as plasma concentrations of B-type natriuretic peptide (BNP). Central BP and the radial augmentation index (rAI) were evaluated non-invasively using an automated device.

RESULTS

Univariate and multivariable regression analysis showed that both brachial and central BP were significantly associated with hs-cTnI. When subjects were divided into two groups according to the mean rAI value, those with higher rAI had higher hs-cTnI concentrations than those with lower rAI. In subgroup analyses, in those with lower rAI, brachial but not central systolic BP was independently associated with hs-cTnI, whereas in those with higher rAI, central but not brachial systolic BP was independently associated with hs-cTnI. These associations remained significant after further adjustment for BNP and/or d-ROM concentrations.

CONCLUSIONS

Circulating levels of hs-cTnI increase with increasing brachial and central BP, but the effect of central BP was greater in subjects with higher rAI. This indicates that central BP may have a strong effect on silent myocardial damage, assessed as increased circulating hs-cTnI, particularly in subjects with increased arterial stiffness.