Association of coronary artery calcium and congestive heart failure in the general population: Results of the Heinz Nixdorf Recall study

Abstract

Background: The main causes of congestive heart failure (CHF) are coronary artery disease (CAD) and arterial hypertension. Coronary artery calcification (CAC) evidencing coronary atherosclerosis may occur prior to clinical CAD. The aim of our study was to assess the association between CAC as a sign of subclinical CAD and CHF in a general unselected population.

Methods: Participants of the Heinz Nixdorf Recall Study without known CAD but with known CHF as defined by a physicians' diagnosis of CHF and dyspnea were identified. B-natriuretic peptide was measured and an exercise stress test was performed as possible. Cardiovascular risk factors and the EBCT-based CAC Agatston score were determined.

Results: Those 105/4,230 subjects (2.5%) with CHF (age 65 +/- 7 years, 44% males), had higher brain natriuretic peptide (BNP) levels (median BNP 36.8 [16.5-70.1] vs. 17.6 [9.5-31.7] pg/ml, p<0.01) and lower exercise capacity (108.7 +/- 39.4 vs. 130.0 +/- 40.7 W, p<0.01) than those without. CAC in subjects with CHF was significantly higher than in those without (median CAC 64.7 [8.5-312.3] vs. 11.6 [0-109.8], p<0.01). In univariate analysis, CAC-burden after logarithmic transformation according to log(2)(CAC + 1) showed a significant association with the presence of CHF (odds ratio (OR) (95% CI): 1.16 (1.1-1.23), p<0.0001). Adjustment for age and sex (OR 1.11 (1.04-1.18), p<0.001), additional Framingham risk score (OR 1.09 (1.02-1.16), p = 0.015), and additional cardiovascular medication (OR 1.07 (0.998-1.14), p = 0.058) attenuated this association. Age, systolic blood pressure, antihypertensive medication and increased body mass index also remained significantly associated with presence of CHF in the full multivariate model.

Conclusion: The observed association between CAC and CHF in persons without clinically overt CAD is partly determined by risk factors that are involved in the natural history of both CAC and CHF. Whether CAC has a role to identify subjects at risk of future CHF remains to be determined using follow-up analyses.