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. 2012 Nov;46(8):648-53.
doi: 10.1177/1538574412462634. Epub 2012 Oct 8.

Aortic augmentation index is independently associated with N-terminal pro B-type natriuretic peptide in patients with peripheral arterial disease

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Aortic augmentation index is independently associated with N-terminal pro B-type natriuretic peptide in patients with peripheral arterial disease

Yousef Shahin et al. Vasc Endovascular Surg. 2012 Nov.

Abstract

Objectives: To investigate the relationship of aortic augmentation index (AIx) with N-terminal pro B-type natriuretic peptide (NTproBNP) plasma levels in patients with peripheral arterial disease (PAD) with normal left ventricular (LV) function.

Methods: Totally, 31 patients (23 males, mean age 65 ± 7.4) with a confirmed diagnosis of PAD of the lower limbs (ankle-brachial pressure index [ABPI] <0.90 in at least 1 leg) were enrolled in this study. All patients underwent pulse wave analysis by applanation tonometry of the radial artery using the SphygmoCor system and had a measurement of plasma NTproBNP levels.

Results: Patients had a mean resting ABPI of 0.62 ± 0.19 and a mean AIx 32.6% ± 6.9. Median (interquartile range) NTproBNP plasma level was 75 (44-210) pg/mL. In a univariate analysis which included age, brachial systolic blood pressure (BSBP), brachial diastolic blood pressure (BDBP), ejection duration index (ED%), heart rate (HR), and NTproBNP, aortic AIx was significantly associated (Spearman rho) with NTproBNP, HR, and ED% (r = .49, P = .006; r = -.72, P = .000, and r = -.42, P = .02, respectively). Multivariate linear regression analysis showed that AIx was associated with NTproBNP (β = 0.38, P = .02) independent of gender, HR, ED%, and use of β-blockers. N-terminal pro B-type natriuretic peptide explained 8% of the variance in aortic AIx, whereas HR explained 15% of the variance.

Conclusion: In patients with PAD with normal LV systolic function, AIx is independently associated with NTproBNP. Structural changes in the myocardium might occur due to increased LV afterload as a result of increased wave reflections and arterial stiffness due to atherosclerosis leading to an increase in NTproBNP plasma levels.

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