Author + information
- Jefferson L. Vieira, MD∗ (, )
- Guilherme V. Guimarães, PhD and
- Edimar A. Bocchi, MD, PhD
- ↵∗Heart Failure Department, Heart Institute (InCor), University of São Paulo Medical School, Avenida Doutor Enéas de Carvalho, São Paulo 05403-900, Brazil
We thank Dr. RuDusky for taking an interest in our work. Our study was intended to address the role of a respiratory filter intervention during controlled pollution exposure in patients with heart failure (HF). In 2007, HF was associated with 39.4% of all hospitalizations due to cardiovascular diseases in Brazil, and it may be responsible for 6.3% of all causes of deaths in South America (1). Regarding hypertension, it is a leading risk factor for cardiovascular disease and a significant cause of morbidity and mortality as long as it remains uncontrolled (2). A large body of evidence indicates that patients with hypertension are characterized by endothelial dysfunction (3). We excluded volunteers with uncontrolled hypertension because it could play an important role as a confounder and selection bias, especially in a small sample of patients with HF. Blood pressure (BP) was recorded during the initial pre-study evaluation and history and also at the beginning of each session. Uncontrolled hypertension was defined as an average systolic BP ≥140 mm Hg or an average diastolic BP ≥90 mm Hg, among those with diagnosed hypertension and who are currently using BP-lowering medication. As outlined in the article, patients with HF were receiving optimal medical therapy, and 2 volunteers from the control group were receiving beta-blocker therapy.
Although our neutral findings of heart rate variability (HRV) could be explained by the optimal beta-blocker therapy in the HF group, it is noteworthy that diesel exhaust exposure (DE) also did not affect HRV in the control group. This suggests that the use of cardiovascular therapies might not be the primary explanation for the absence of an effect of air pollution on autonomic function. There are several methodological differences between the recent study by Lee et al. (4) and ours that can explain these contradictory findings. Lee et al. (4) assessed lagged nocturnal effects of fine particulate matter (PM2.5), whereas we conducted an experimental short-term study with controlled DE exposure that provided a precisely defined PM2.5 concentration in a regulated environment. We cannot state whether longer-term air pollution exposure could affect the HRV in optimally treated HF patients.
The epidemiologic association between air pollution exposure and exacerbation of cardiovascular disease is well established, yet the mechanisms underlying the increased risk of cardiovascular events are incompletely understood. Increasing concern relating to the health effects of air pollution has led many individuals to use facemasks to reduce personal exposure (5). There is, therefore, a need to consider approaches that can reduce effects of ambient air pollution exposure on both a societal and a personal level. Reduction of traffic emissions involves economic and political difficulties. The pioneering demonstration that a simple filter intervention can reduce the adverse effects of pollution in patients with HF could provide an inexpensive strategy for preventing HF decompensation. Given the worldwide prevalence of exposure to traffic-related air pollution, we speculate that patients with uncontrolled hypertension may benefit from the filter intervention as well.
Please note: The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- American College of Cardiology Foundation