Objective: The aim was to analyse whether the association between carotid atherosclerosis (CA) and atrial fibrillation (AF), heart function, and renal function is mediated by traditional risk factors.
Methods: In the prospective, single centre, long term, population based Hamburg City Health Study citizens, between 45 and 74 years of age were studied by cross sectional analysis of the first cohort. Laboratory values, blood pressure, heart rhythm, and body mass index (BMI) were examined. Carotid intima media thickness (CIMT) and plaques were assessed by carotid ultrasound, and CA was defined as either CIMT ≥ 1 mm or presence of plaques or both. N-terminal pro-brain natriuretic peptide (NT-proBNP), and glomerular filtration rate (eGFR) were quantified as measures of heart and renal function. Association between CA and AF, NT-proBNP, and eGFR was analysed by multivariable linear and logistic regression.
Results: Of the first 10 000 participants, carotid ultrasound was available for 9 466 (95%). Of these, 2 937 (31%) had carotid plaques, 643 (7%) had CIMT ≥ 1 mm, and 412 (4%) presented with both, so that 3 168 (34%) had CA. Participants with CA had AF more frequently (9.6% vs. 4.3%; p < .001), higher levels of NT-proBNP (median 100 vs. 73 pg/mL; p < .001), and lower eGFR (82.8 vs. 87.1 mL/min; p < .001) than those without CA. Adjusted for age and sex, CA was associated with AF (p = .01; OR 1.29) and higher NT-proBNP levels (p < .001; β = 0.12), but not with eGFR. After further adjustment for vascular risk factors and history of cardiovascular diseases, CA remained associated with NT-proBNP (p < .001; β = 0.10), but additionally adjusted for NT-proBNP (p < .001; OR 2.80) not with AF.
Conclusion: CA is independently associated with higher levels of NT-proBNP, through common risk factors and NT-proBNP with AF, and not with renal function. CA's association with a marker of cardiac dysfunction beyond known common risk factors supports the value of carotid ultrasound in defining patients' cardiovascular risk profile. The measures of CA, i.e., CIMT and carotid plaque, had an equally directed and additive influence.
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