Cardiovascular Disease Hospitalizations in Relation to Exposure to the September 11, 2001 World Trade Center Disaster and Posttraumatic Stress Disorder

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Abstract

Background

A cohort study found that 9/11‐related environmental exposures and posttraumatic stress disorder increased self‐reported cardiovascular disease risk. We attempted to replicate these findings using objectively defined cardiovascular disease hospitalizations in the same cohort.

Methods and Results

Data for adult World Trade Center Health Registry enrollees residing in New York State on enrollment and no cardiovascular disease history (n=46 346) were linked to a New York State hospital discharge–reporting system. Follow‐up began at Registry enrollment (2003–2004) and ended at the first cerebrovascular or heart disease (HD) hospitalization, death, or December 31, 2010, whichever was earliest. We used proportional hazards models to estimate adjusted hazard ratios (AHRs) for HD (n=1151) and cerebrovascular disease (n=284) hospitalization during 302 742 person‐years of observation (mean follow‐up, 6.5 years per person), accounting for other factors including age, race/ethnicity, smoking, and diabetes. An elevated risk of HD hospitalization was observed among women (AHR 1.32, 95% CI 1.01 to 1.71) but not men (AHR 1.16, 95% CI 0.97 to 1.40) with posttraumatic stress disorder at enrollment. A high overall level of World Trade Center rescue and recovery–related exposure was associated with an elevated HD hospitalization risk in men (AHR 1.82, 95% CI 1.06 to 3.13; P for trend=0.05), but findings in women were inconclusive (AHR 3.29, 95% CI 0.85 to 12.69; P for trend=0.09). Similar associations were observed specifically with coronary artery disease hospitalization. Posttraumatic stress disorder increased the cerebrovascular disease hospitalization risk in men but not in women.

Conclusions

9/11‐related exposures and posttraumatic stress disorder appeared to increase the risk of subsequent hospitalization for HD and cerebrovascular disease. This is consistent with findings based on self‐reported outcomes.

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Most cited references 26

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Impact of Psychological Factors on the Pathogenesis of Cardiovascular Disease and Implications for Therapy

Alan Rozanski, James Blumenthal, Jay A. Kaplan (1999)

Recent studies provide clear and convincing evidence that psychosocial factors contribute significantly to the pathogenesis and expression of coronary artery disease (CAD). This evidence is composed largely of data relating CAD risk to 5 specific psychosocial domains: (1) depression, (2) anxiety, (3) personality factors and character traits, (4) social isolation, and (5) chronic life stress. Pathophysiological mechanisms underlying the relationship between these entities and CAD can be divided into behavioral mechanisms, whereby psychosocial conditions contribute to a higher frequency of adverse health behaviors, such as poor diet and smoking, and direct pathophysiological mechanisms, such as neuroendocrine and platelet activation. An extensive body of evidence from animal models (especially the cynomolgus monkey, Macaca fascicularis) reveals that chronic psychosocial stress can lead, probably via a mechanism involving excessive sympathetic nervous system activation, to exacerbation of coronary artery atherosclerosis as well as to transient endothelial dysfunction and even necrosis. Evidence from monkeys also indicates that psychosocial stress reliably induces ovarian dysfunction, hypercortisolemia, and excessive adrenergic activation in premenopausal females, leading to accelerated atherosclerosis. Also reviewed are data relating CAD to acute stress and individual differences in sympathetic nervous system responsivity. New technologies and research from animal models demonstrate that acute stress triggers myocardial ischemia, promotes arrhythmogenesis, stimulates platelet function, and increases blood viscosity through hemoconcentration. In the presence of underlying atherosclerosis (eg, in CAD patients), acute stress also causes coronary vasoconstriction. Recent data indicate that the foregoing effects result, at least in part, from the endothelial dysfunction and injury induced by acute stress. Hyperresponsivity of the sympathetic nervous system, manifested by exaggerated heart rate and blood pressure responses to psychological stimuli, is an intrinsic characteristic among some individuals. Current data link sympathetic nervous system hyperresponsivity to accelerated development of carotid atherosclerosis in human subjects and to exacerbated coronary and carotid atherosclerosis in monkeys. Thus far, intervention trials designed to reduce psychosocial stress have been limited in size and number. Specific suggestions to improve the assessment of behavioral interventions include more complete delineation of the physiological mechanisms by which such interventions might work; increased use of new, more convenient "alternative" end points for behavioral intervention trials; development of specifically targeted behavioral interventions (based on profiling of patient factors); and evaluation of previously developed models of predicting behavioral change. The importance of maximizing the efficacy of behavioral interventions is underscored by the recognition that psychosocial stresses tend to cluster together. When they do so, the resultant risk for cardiac events is often substantially elevated, equaling that associated with previously established risk factors for CAD, such as hypertension and hypercholesterolemia.

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A prospective study of PTSD and early-age heart disease mortality among Vietnam veterans: implications for surveillance and prevention.

Joseph Boscarino (2008)

To examine prospectively early-age heart disease (HD) among a national random sample of 4328 male Vietnam veterans, who did not have HD at baseline in 1985. Studies have suggested that posttraumatic stress disorder (PTSD) may result in cardiovascular disease. However, many past studies had important methodological limitations to their designs. Using Cox regressions, we assessed PTSD, age, race, intelligence, family history, obesity, smoking, alcohol abuse, antisocial personality, and depression in predicting HD mortality at follow-up in December 31, 2000. The men were <65 years old at follow-up. Using two PTSD measures, a Diagnostic and Statistical Manual of Mental Disorders, 3rd Edition (DSM-III) measure (D-PTSD) and one developed by Keane (K-PTSD), we found that among Vietnam theater and era veterans combined (era veterans had no Vietnam service), having PTSD was associated with HD mortality for D-PTSD (hazard ratio (HR) = 2.25, p = .045) and approached significance for K-PTSD (HR = 2.16, p = .066). However, having higher PTSD symptoms on either scale was associated with mortality, with a 5-point increase associated with approximately 20% increase in mortality risk (all p < .05). Controlling for lifetime depression only slightly altered the results. The effects for theater veterans alone were stronger (D-PTSD: HR = 2.58, p = .025; K-PTSD: HR = 2.73, p = .022). Among theater veterans, controlling for lifetime depression or combat exposure made little difference. PTSD was prospectively associated with HD mortality among veterans free of HD at baseline. This study suggests that early-age HD may be an outcome after military service among PTSD-positive veterans.

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Posttraumatic stress disorder and the incidence of nicotine, alcohol, and other drug disorders in persons who have experienced trauma.

Peter Davis, Kim L Schultz, Naomi Breslau (2003)

We examine whether exposure to traumatic events increases the risk for nicotine dependence or alcohol or other drug use disorders, independent of posttraumatic stress disorder (PTSD). Data come from a longitudinal epidemiologic study of young adults in southeast Michigan. Prospective data covering a 10-year period and retrospective lifetime data gathered at baseline were used to estimate the risk for onset of substance use disorders in persons with PTSD and in persons exposed to trauma without PTSD, compared with persons who have not been exposed to trauma. The National Institute of Mental Health Diagnostic Interview Schedule for DSM-III-R was used. Logistic regression was used to analyze the prospective data, and Cox proportional hazards survival analysis with time-dependent variables was applied to the lifetime data. The prospective and retrospective data show an increased risk for the onset of nicotine dependence and drug abuse or dependence in persons with PTSD, but no increased risk or a significantly (P =.004) lower risk (for nicotine dependence, in the prospective data) in persons exposed to trauma in the absence of PTSD, compared with unexposed persons. Exposure to trauma in either the presence or the absence of PTSD did not predict alcohol abuse or dependence. The findings do not support the hypothesis that exposure to traumatic events per se increases the risk for substance use disorders. A modestly elevated risk for nicotine dependence might be an exception. Posttraumatic stress disorder might be a causal risk factor for nicotine and drug use disorders or, alternatively, the co-occurrence of PTSD and these disorders might be influenced by shared risk factors other than traumatic exposure.

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Author and article information

Journal

Journal ID (nlm-ta): J Am Heart Assoc

Journal ID (iso-abbrev): J Am Heart Assoc

Journal ID (hwp): ahaoa

Journal ID (publisher-id): jah3

Title: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

Publisher: Blackwell Publishing Ltd

ISSN (Electronic): 2047-9980

Publication date Collection: October 2013

Publication date (Electronic): 25 October 2013

Volume: 2

Issue: 5

Electronic Location Identifier: e000431

Affiliations

[1 ]World Trade Center Health Registry, New York City Department of Health and Mental Hygiene, Queens, NY (H.T.J., S.D.S., S.A.M.A., R.M.B., J.E.C.)

[2 ]Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY (S.D.S., A.M.)

[3 ]Barry Commoner Center for the Biology of Natural Systems, Queens College, City University of New York, New York, NY (A.M., Z.L.)

[4 ]Office of Health Care Access and Improvement, New York City Department of Health and Mental Hygiene, Queens, NY (H.A.)

Author notes

Correspondence to: Hannah T. Jordan, MD, MPH, World Trade Center Health Registry, New York City Department of Health and Mental Hygiene, 42‐09 28th Street, 7th floor, Long Island City, NY 11101. E‐mail: hjordan1@ 123456health.nyc.gov

Accompanying Table S1 is available at http://jaha.ahajournals.org/content/2/5/e000431/suppl/DC1

Article

Publisher ID: jah3335

DOI: 10.1161/JAHA.113.000431

PMC ID: 3835258

PubMed ID: 24157650

SO-VID: 15d035f4-75d8-4ece-9efa-1cee62396666

License:

This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

Cardiovascular Disease Hospitalizations in Relation to Exposure to the September 11, 2001 World Trade Center Disaster and Posttraumatic Stress Disorder

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Abstract

Background

Methods and Results

Conclusions

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Cardiovascular Innovations and Applications

Most cited references 26

Impact of Psychological Factors on the Pathogenesis of Cardiovascular Disease and Implications for Therapy

A prospective study of PTSD and early-age heart disease mortality among Vietnam veterans: implications for surveillance and prevention.

Posttraumatic stress disorder and the incidence of nicotine, alcohol, and other drug disorders in persons who have experienced trauma.

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