Author + information
- John S. Gottdiener, MD∗ ()
- Division of Cardiology, Department of Medicine, University of Maryland Medical Center, Baltimore, Maryland
- ↵∗Address for correspondence:
Dr. John S. Gottdiener, Division of Cardiology, Department of Medicine, University of Maryland Medical Center, Echocardiography Laboratory, 22 South Greene Street, Baltimore, Maryland 21201.
Both asthma and cardiovascular disease (CVD) have had a worldwide increase over several decades. The incidence of asthma in children has almost doubled since 1980 (1); its estimated prevalence is nearly 1 of 10 children, and is only slightly lower (7%) in adults (2). The prevalence of CVD—particularly stroke and heart failure—in adults is also increasingly high, and shares with asthma a predilection for urban at-risk minority populations. Exposures to cigarette smoking, air pollution, stress, and obesity are common to both.
It has been suggested that asthma may have a causal relationship with CVD, although the evidence for this is not conclusive. Studies have differed as to whether both stroke and heart disease are associated with asthma, whether limited childhood exposure to asthma is sufficient to result in CVD later in life, or whether the relationship is limited to women with adult-onset asthma.
Nonetheless, there are strong pathophysiological homologies that support a causal relationship of asthma with CVD and stroke. In particular, inflammation is central to both diseases. Research has shown that cytokines are important mediators of bronchoconstriction in asthma (3) and that leukotrienes—strongly proinflammatory cytokines found in high concentrations in asthmatic bronchioles—are also active in atherosclerotic plaque (4). Population studies have long shown that inflammation is associated with CVD, and in a population study of older individuals, inflammation, left ventricular hypertrophy (LVH), as well as decreased lung function were independently associated with incident heart failure (5).
Another potential link between asthma in childhood and adult life and CVD is LVH. LVH has been firmly established as a predictor of heart failure, coronary heart disease, cardiovascular death, stroke, and sudden death. Moreover, several comorbidities and components of asthma may also contribute to LVH and possibly right ventricular hypertrophy, including obesity, hypertension, inflammation, decreased peripheral arterial distensibility, usage of inhaled beta agonists and corticosteroids, and lung hyperinflation.
In this issue of JACC: Heart Failure, Sun et al. (6) present data from the long-running Bogalusa Heart Study on association of childhood asthma with LVH in asymptomatic young adults. This well-powered biracial prospective cohort population study found that those with a history of childhood asthma had a small but significantly greater left ventricular (LV) mass index (g/m2.7)—about 8%—than did nonasthmatics. Although this difference would by itself confer a relatively small incremental risk of incident CVD (about 1.08-fold increase) based on Framingham Heart Study data (7), in large populations with major comorbidities, the public health implications could be substantial. An additional important finding was the interaction of blood pressure and asthma on LV mass. Consequently, targeting individuals with asthma and hypertension or pre-hypertension for intensified risk reduction could have important benefits.
However, the study leaves several questions unanswered. Importantly, because no baseline echocardiograms were available, all we know is the difference in LV mass between those who did and did not have a diagnosis of asthma years before echocardiography was performed. Subjects could have had increasing LV mass, which began prior to the onset of asthma, perhaps due to common risk factors such as obesity, hypertension, air pollution, and inflammation. The current data do not exclude the possibility that asthma is a comorbidity of CVD, and perhaps is a fellow traveler with CVD severity rather than being a cause of CVD. Although statistical adjustments were made for potential sources of LVH other than asthma—including obesity, sex, race, and hypertension—there could be residual confounding by risk factors common to CVD and asthma. Also, it remains unknown whether LV mass was associated with the severity of asthma and the frequency of use of corticosteroids and beta agonists, important information for selecting individuals who are at the highest risk. It is unclear whether the risk of asthma for increases in LV mass is linear or concentrated at specific distributions, especially those values of LV mass exceeding reference levels demarcating normal LV mass from pathological hypertrophy.
Most importantly, LV mass, and even hypertrophy, are surrogate endpoints for outcome and do not replace the importance of determining the relationship of childhood (and adult) onset of asthma to hard endpoints of cardiovascular health. We look forward to further studies from the Bogalusa Heart Study and elsewhere, which will accurately determine the association of asthma with death (total, cardiovascular, and sudden), heart failure, myocardial infarction, and stroke. Of particular value will be learning how severe and long the asthmatic exposure needs to be to pose significant risk. This together with determining potential pathophysiological mechanisms will help to intelligently design effective prevention interventions validated by randomized controlled trials.
↵∗ Editorials published in JACC: Heart Failure reflect the views of the authors and do not necessarily represent the views of JACC: Heart Failure or the American College of Cardiology.
Dr. Gottdiener has reported that he has no relationships relevant to the contents of this paper to disclose.
- 2017 American College of Cardiology Foundation
- ↵Centers for Disease Control and Prevention. Summary Health Statistics: National Health Interview Survey. Table A-2a. Age-adjusted percentages (with standard errors) of selected respiratory diseases among adults aged 18 and over, by selected characteristics. Vol. 3. 2014. Available at: https://ftp.cdc.gov/pub/Health_Statistics/NCHS/NHIS/SHS/2014_SHS_Table_A-2.pdf. Accessed June 2, 2017.
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