Author + information
- Yvette R.B.M. van Gestel, MSc,
- Don D. Sin, MD, FCCP and
- Don Poldermans, MD, PhD⁎ ()
- ↵⁎Erasmus Medical Center Rotterdam, ‘s-Gravendijkwal 230, 3015 CE Rotterdam, the Netherlands
We read with great interest the recent article by Daniels et al. (1) in which the investigators reported that detectable cardiac troponin T and N-terminal pro-B-type natriuretic peptide (NT-proBNP) were both associated with increased all-cause and cardiovascular death in healthy older adults.
NT-proBNP was previously identified as a prognostic cardiac risk marker associated with increased mortality. NT-proBNP is released by cardiac myocytes in response to wall stress in conditions associated with volume overload as in heart failure and chronic kidney disease, pressure overload as in patients with heart valve abnormalities, and ischemia owing to coronary disease. In the present study, the association remained even after participants with baseline coronary heart disease were excluded, which was 30% of the subjects with elevated (≥450 pg/ml) NT-proBNP levels.
However, the authors might have overlooked the effect of chronic obstructive pulmonary disease (COPD) on NT-proBNP levels. COPD is associated with cardiovascular disease and is an independent risk factor for cardiovascular morbidity and mortality (2). We recently investigated the relationship between COPD, both the presence and severity, and NT-proBNP levels in 376 patients. To mitigate the influence of heart failure, chronic kidney disease, and myocardial ischemia, we adjusted for history of angina pectoris, myocardial infarction, heart failure, and renal function. In addition, all patients had resting left ventricular function of more than 40% using echocardiography. The severity of COPD was assessed using pulmonary function tests with the GOLD (Global Initiative for Chronic Obstructive Lung Disease) classification. We found COPD to be an independent risk factor for increased NT-proBNP levels, and the levels increased with the severity of COPD.
The underlying mechanism is likely to be pulmonary hypertension and right ventricular dysfunction caused by pulmonary arterial pressure overload (3). COPD may induce wall stretching, ventricular dilation, and/or increased vascular pressures, which may promote the secretion of the neurohormone NT-proBNP. Because COPD is common in the elderly population (affecting nearly 35% of this population) (4), the addition of spirometric data to the analysis by Daniels et al. (1) would have been very interesting and informative. The less severe forms of COPD are often asymptomatic and therefore frequently underestimated, especially in the elderly. Thus, the presence of underlying COPD might have contributed to the observed correlation between NT-proBNP and outcome in this elderly population.
- American College of Cardiology Foundation
- Daniels L.B.,
- Laughlin G.A.,
- Clopton P.,
- Maisel A.S.,
- Barrett-Connor E.
- Nagaya N.,
- Nishikimi T.,
- Okano Y.,
- et al.