Aortic Pulse Wave Velocity Predicts All-Cause Mortality in Chronic Obstructive Pulmonary Disease.

To the Editor:

We read with keen interest the results of the SUMMIT (Study to Understand Mortality and Morbidity in COPD) randomized controlled trial of fluticasone furoate/vilanterol in patients with moderate chronic obstructive pulmonary disease (COPD) with a history of cardiovascular disease or at increased cardiovascular risk (1). The trial evaluated both the value of aortic pulse wave velocity (aPWV) to predict all-cause mortality (ACM) in this population and the effect of inhaled therapy on aPWV. A secondary endpoint was the cardiovascular composite of myocardial infarction, unstable angina, stroke, transient ischemic attack, and cardiovascular death.

We congratulate the authors on conducting this large population-based trial to evaluate an important clinical question. Although inhaled therapy had no effect on aPWV, the finding that aPWV may be useful to predict ACM in patients with COPD merits further consideration. First, we are interested to know what specific adjustments were included in the analysis of aPWV predicting ACM. “Various ischemic and vascular indicators” are mentioned (1). In particular, were adjustments for blood pressure and heart rate included? aPWV is influenced by these factors, and published data from the SUMMIT trial already showed a U-shaped curve of blood pressure to predict both ACM and cardiovascular events, whereas there was a linear relationship with increased heart rate (2–4). Another important question is whether the analysis included adjustment for other established Framingham cardiovascular risk factors, such as diabetes, hypertension, cholesterol level, and diabetes (5).

A further point of interest is the lack of relationship between aPWV and the cardiovascular composite (which included cardiovascular death), despite elevated aPWV predicting ACM. This is striking and leads to the question, what did patients in the study die from? And was aPWV associated with any other cause of death? The authors point out previous studies’ findings of elevated aPWV in patients with COPD and speculate on mechanisms linking aPWV to cardiovascular disease in patients with COPD. However, the results of this study do not support an association between aPWV and cardiovascular events in patients with COPD.

Importantly, many of these surrogate markers of cardiovascular risk only add moderately to standard risk factors (6). The importance of routinely assessing cardiovascular risk in patients with COPD using validated risk scores such as Framingham or QRISK and mitigating such risk in individual patients is likely to remain the optimal clinical and cost-effective approach to reduce cardiovascular risk in patients with COPD.