146 B-type natriuretic peptide and coronary atherosclerosis: an association dependent on central pulse pressure. (16th May 2012)

• Record Type: Journal Article
• Authors: Kotecha, D; New, G; Collins, P; Krum, H; Pepper, J; Flather, M D
• Is Part Of: Heart. Volume 98(2012)Supplement 1
• Page Start: A81
• Page End: A81
• Publication Date: 2012-05-16
• Subjects: B-type natriuretic peptide -- coronary artery disease -- pulse wave analysis; Heart -- Diseases -- Treatment -- Periodicals; Cardiology -- Periodicals; 616.12
• DOI: 10.1136/heartjnl-2012-301877b.146
• Languages: English
• ISSNs: 1355-6037

Abstract

Abstract : Background: B-type natriuretic peptide (BNP) is traditionally used as a marker of left-ventricular (LV) dysfunction. Prior studies have also identified BNP as a risk marker of coronary atherosclerosis, even in those with normal LV function. We sought to determine the clinical benefit of using BNP in an unselected population undergoing diagnostic angiography and identify any possible mechanisms for this association [the Alternative Risk Markers in Coronary Artery Disease (ARM-CAD) study]. Methods: 468 participants without prior coronary bypass surgery were assessed according to the presence/severity of angiographic CAD using a stenosis score weighted for the impact on usual coronary blood flow. Blood samples, risk factor data and radial artery pulse wave analysis (to derive central blood pressures [BP]) were obtained prior to angiography. Results: Mean age±SD was 64±11, BP 144/80±21/10, 65% were male, 21% had diabetes, 44% had prior angina or myocardial infarction and 16% had impaired LV. There was a linear increase in BNP with the severity of CAD (p for trend<0.0001). However, patients with minor coronary stenoses (30%–50%) had elevated BNP levels compared to those with normal coronaries or single vessel CAD (p<0.03), perhaps relating to coronary plaque stability. Multivariate regression, adjusted for risk factors, LV impairment and medications, determined that BNP was an independent marker of the presence of CAD; the OR for any degree of angiographic CAD was 1.33 per log-unit increase in BNP (95% CI 1.03 to 1.71; p=0.03). BNP was associated with disease in the left coronary arteries but not in the right coronary artery (see Abstract 146 figure 1A ). Further, the relationship between BNP and CAD was only present in patients with central pulse pressure above the median value of 50 mm Hg (see Abstract 146 figure 1B ), suggesting that central BP may be part of the mechanism for the BNP increase seen in patients with CAD. Conclusions: BNP is associated with the presence and severity of angiographic disease, irrespective of LV impairment. Our data suggest that in patients with coronary atherosclerosis, BNP may be a marker of ventricular wall tension and neurohormonal activation secondary to changes in central BP.