Author + information
- Published online June 5, 2017.
- aCenter for Healthcare Advancement & Outcomes, Baptist Health South Florida, Miami, Florida
- bMiami Cardiac & Vascular Institute (MCVI), Baptist Health South Florida, Miami, Florida
- cDepartment of Medicine, Herbert Wertheim College of Medicine and Department of Epidemiology, Robert Stempel College of Public Health, Florida International University, Miami, Florida
- dJohns Hopkins Ciccarone Center for the Prevention of Heart Disease, Baltimore Maryland
- eDepartment of General Internal Medicine, VCU Medical Center, Richmond, Virginia
- ↵∗Address for correspondence:
Dr. Khurram Nasir, Center for Healthcare Advancement & Outcomes, Baptist Health South Florida, 1500 San Remo Avenue, Suite 340, Coral Gables, Florida 33139.
Exposure to secondhand smoke (SHS) remains a relevant public health problem. According to recent statistics from the Center for Disease Control and Prevention, nearly 25% (58 million) of nonsmokers in the United States are exposed to varying degrees of SHS (1). Concerns about passive tobacco exposure was initially raised in 1972 with the first Surgeon General’s Report, which was followed by a plethora of large-scale clinical and epidemiological evidence linking SHS to elevated heart disease risk in nonsmokers by up to 30% (2), and conservatively estimated to result in at least 35,000 deaths each year in the United States (3).
Association between SHS exposure and impaired endothelial function, enhanced inflammatory milieu, coronary vasoconstriction, and susceptibility to enhanced thrombogenicity has been well documented. One can attribute this susceptibility to a significant exposure of chemicals, including nicotine, carbon monoxide, polycyclic aromatic hydrocarbons, and tobacco glycoproteins. More recently, interest has shifted to explore whether subclinical atherosclerotic disease mediates a relationship between SHS and adverse CVD outcomes. Many investigators have attempted to update our understanding by demonstrating independent associations between the duration and severity of exposure with the presence of subclinical disease across various vascular beds, including increased carotid intimal thickness (4), abnormal ankle brachial index (5), and the presence of subclinical coronary artery calcification (6).
In this issue of iJACC, Yankelevitz et al. (7) add to the current literature by examining early atherosclerotic changes, assessed by coronary computed tomography angiography (CTA), across the spectrum of SHS severity, among relatively young, nonsmoking volunteers. Coronary CTA has tremendous potential due to its ability to define obstructive coronary artery disease (CAD), examine the burden of nonobstructive disease, and characterize plaque (likely as the current gold standard). Although the study sample size is modest; the initial insights are astounding. The results of this study demonstrated a powerful graded linear relationship between the severity of SHS exposure and the presence and severity of coronary artery plaque that overcomes any lingering doubt about the deleterious impact of SHS. In simpler terms, within this traditionally low-risk group (nonsmokers), upon further inquiry, those most severely exposed to SHS had a nearly 3-fold risk for the presence on any plaque, 2 times the risk of obstructive CAD, as well as involvement of at least 3 major arteries (Table 3 in Yankelevitz et al. ). It is difficult to conceive more concrete evidence on the potential harms of SHS, which appears to be stronger than previously expected.
The study findings have important implications that deserve further discussion. Apart from further strengthening support for the implementation of public and workplace smoke-free restriction laws, that have already yielded a significant reduction in rates of reported cardiac events (8), it is worth asking how these findings may impact our individual management practices?
First, despite the strength of existing and emerging evidence, as well as widespread belief among the practicing physician community of the harms of SHS, there are hardly any concrete process measures to address this specific issue in real-world practice. The lack of traction toward SHS in our medical community is not surprising, given the little attention in our existing guidelines, beyond assessing SHS exposure in the pediatric population. Given the fact that 1 in 4 nonsmokers is exposed to SHS, screening for it with currently applied primary smoke screening and counseling, and subsequent incorporation of established interventions, such as Clinical Effort Against Secondhand Smoke Exposure (CEASE), can be encouraged if tracked as part of core quality performance measures.
Second, apart from screening and guiding our patients on avoiding SHS, in lieu of historical exposure, how do we convey the potential elevated future risk of an atherosclerotic CVD event and available management options? To put things into perspective, among those with severe exposure to SHS, a feature noted in 25% of smokers, the risk for early atherosclerotic disease is seen in 3 of 4 individuals, and 1 of 10 will have significant obstructive CAD. Although verification from other well-controlled cohorts is needed, evidence from the current study suggests that the risk for the presence of any plaque is similar in magnitude with diabetes mellitus and hypercholesterolemia, 2 well-established risk factors impacting the current pooled cohort equation for atherosclerotic cardiovascular disease risk assessment and subsequent management decisions. On the basis of estimates from recent large epidemiological studies, the presence of any atherosclerotic disease may portend to 10-year risk for developing clinical atherosclerotic cardiovascular disease, where current guidelines suggest these individuals are high risk enough to be considered statin candidates (9). In scenarios of uncertainty around management options with average risk profiles, imaging for atherosclerotic disease can potentially inform preventive treatment decisions.
Although the current study does not specify guidance on the differential risk of hard outcomes with the presence and absence of early atherosclerotic disease among the disparate groups exposed to varying degree of SHS or the implication of how it can reclassify risk or warrant further imaging to guide management, the authors need to be applauded for further accumulating the epidemiological link of the heightened risk of coronary atherosclerosis as a likely major contributing factor. The timely report by Yankelevitz et al. (7) provides an opportunity to: 1) discuss SHS exposure, cautioning the public of the potentially fatal coronary effects inflicted by the fumes of a burning cigarette; 2) facilitate policymakers with more evidence to accelerate efforts to widely implement smoke-free laws and impede smoking in public places to protect the cardiovascular health of otherwise innocent bystanders; 3) stimulate discussions among stakeholders to incorporate universal screening for SHS into our primary care practices; and 4) incentivize large population-based studies to clearly assess the postulated probability uniting atherosclerotic disease with SHS, and how it can aid in reclassifying risk that can guide downstream management options in a meaningful manner. Though in our early stages of completely understanding the intricacies of SHS from a CVD risk perspective, we feel confident in responding to an earlier editorialist query whether it was all smoke and mirrors (8)? The smoke has cleared.
↵∗ Editorials published in JACC: Cardiovascular Imaging reflect the views of the authors and do not necessarily represent the views of JACC: Cardiovascular Imaging or the American College of Cardiology.
Dr. Nasir is on the advisory board for Quest Diagnostic; and is a consultant for Regeneron. Dr. Patel has reported that he has no relationships relevant to the contents of this paper to disclose.
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