Key result
A 5-year change in log-transformed NT-proBNP was independently associated with incident left ventricular systolic dysfunction in patients with stable coronary artery disease (OR 2.48 × 10; P=0.002).
Why the study?
Is a 5-year change in NT-proBNP associated with changes in left ventricular structure and function in patients with stable coronary artery disease?
Cohort (n=593)
Is a 5-year change in NT-proBNP associated with changes in left ventricular structure and function in patients with stable coronary artery disease?
A long-term rise in NT-proBNP levels in patients with stable coronary artery disease is independently associated with incident left ventricular systolic dysfunction, suggesting utility in monitoring for LVEF decline.
Serial NT-proBNP monitoring may flag LV systolic dysfunction risk in stable CAD; leaves open prospective validation before guiding practice.
AIMS: We sought to characterize the association between long-term changes in the N-terminal fragment of the prohormone brain-type natriuretic peptide (NT-proBNP) and changes in left ventricular (LV) structure and function in patients with stable coronary artery disease. METHODS: We included 593 participants without significant valvular disease enrolled in the Heart and Soul Study. We evaluated the association of 5-year change in NT-proBNP (ΔNT-proBNP) with changes in echocardiography-determined LV ejection fraction (LVEF), LV systolic dysfunction (LVSD; LVEF < 50%), LV mass index, incident LV hypertrophy (LVH) (LV mass index >102 g/m for men and >88 g/m for women), and LV diastolic dysfunction (LVDD) using linear and logistic regression. RESULTS: Over 5 years, the prevalence of LVH declined from 36 to 32% (P < 0.001), the prevalence of LVDD increased from 11 to 14% (P = 0.035), mean LVEF decreased from 63 ± 9% to 62 ± 10% (P = 0.07), and the prevalence of LVSD increased from 9 to 11% (P = 0.12). Compared with the lowest ΔNT-proBNP quartile (≥8 ng/l decrease) the highest quartile (>218 ng/l increase) had significantly more incident LVH and LVSD (P < 0.001 for both), with a trend toward increased incidence of LVDD. In logistic regression models adjusted for demographics, cardiac comorbidities, baseline LV structure and function, medication use, kidney function, and baseline NT-proBNP, log-transformed ΔNT-proBNP was associated only with incident LVSD (odds ratio 2.48 × 10, 95% confidence interval 224.53-2.73 × 10, P = 0.002). CONCLUSION: A ΔNT-proBNP is independently associated with incident LVSD in patients with stable coronary artery disease. This suggests that a long-term rise in NT-proBNP levels may warrant evaluation for incident LVEF less than 50%.
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Psotka et al. (2017) conducted a cohort in stable coronary artery disease (n=593). 5-year change in NT-proBNP (ΔNT-proBNP) vs. Lowest ΔNT-proBNP quartile (≥8 ng/l decrease) was evaluated on incident LV systolic dysfunction (LVSD; LVEF < 50%) (OR 2.48 × 10, 95% CI 224.53-2.73 × 10, p=0.002). A 5-year change in log-transformed NT-proBNP was independently associated with incident left ventricular systolic dysfunction in patients with stable coronary artery disease (OR 2.48 × 10; P=0.002).
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