2017

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COPD Exacerbations in Those with CVD May Increase Heart Attack/Stroke Risk

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Embargoed until May 21, 9:15 a.m. ET

 

FOR MORE INFORMATION, CONTACT:
Dacia Morris
dmorris@thoracic.org
ATS Office 212-315-8620 (until May 17)
Cell Phone 917-561-6545

 

Session: A14: COPD: Systems Biology and Comorbidity
Abstract Presentation Time: Sunday, May 21, 10:45 a.m. ET
Location: Walter E. Washington Convention Center, Room 202A (South Bldg., Level 2)

 

ATS 2017, WASHINGTON, DC ─ After an acute exacerbation of chronic obstructive pulmonary disease, or COPD, people with a history of cardiovascular disease (CVD) or people at risk for CVD appear more likely to suffer a heart attack or stroke, according to new research presented at the ATS 2017 International Conference.  

The researchers found that within 30 days after an acute exacerbation, the odds of heart attack or stroke was nearly four-fold higher. Within 31 days to a year after the exacerbation, the odds were nearly double. A year after the exacerbation, the risk was not significantly different.

“Previous studies have shown that lower lung function, such as occurs with  COPD,  is a risk factor for cardiovascular disease,”  said Ken M. Kunisaki, MD, MS, lead study author and associate professor of medicine at the University of Minnesota and Minneapolis VA Health Care System.

 “One theory for why this happens is that COPD triggers inflammation and that, in turn, leads to CVD,” he added. “Because COPD exacerbations lead to particularly high levels of inflammation, we wondered if these exacerbations would be linked to higher rates of CVD events.”

The researchers analyzed data from the Study to Understand Mortality and MorbidiTY (SUMMIT) trial. SUMMIT enrolled current and former smokers between the ages of 40 and 80 who had CVD or multiple risk factors for CVD and whose forced expiratory volume in one second (FEV1) was 50-70 percent of predicted and whose FEV1/forced vital capacity (total volume of exhalation) was ≤ 70 percent.

Their findings have led the researchers to consider interventions they might study following a COPD exacerbation in patients with CVD.    

“One approach might be to study currently used cardiac medications, such as antiplatelet agents, statins and/or beta-blockers immediately following COPD exacerbations,” Dr. Kunisaki said. “Another approach might be to use experimental drugs that specifically reduce inflammation.”

Until effective interventions are identified, he added, patients who have recently experienced a COPD exacerbation “should pay attention to and seek immediate care” for symptoms of heart attack, such as chest pain and sudden worsening of shortness of breath, and stroke, including weakness of one limb, sudden changes in vision and the inability to speak clearly.

Care providers, he said, should be particularly aware of the risk of a CVD event in patients seeking acute medical care following a COPD exacerbation.

Study limitations include the fact that all patients in the study had a CVD history or multiple risk factors for CVD. It is not known if COPD exacerbations would pose the same risk of a CVD in patients with no or lower CVD risk.

Contact for Media: Ken M. Kunisaki, MD, MS, kunis001@umn.edu

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Abstract 5060

Acute Exacerbations of Chronic Obstructive Pulmonary Disease Increase Subsequent Cardiovascular Event Risk: A Secondary Analysis of Adjudicated SUMMIT Study Data

Authors: K.M. Kunisaki1, M. Dransfield2, J.A. Anderson3, R.D. Brook4, P.M.A. Calverley5, B.R. Celli6, C. Crim7,B.F. Hartley8, F.J. Martinez9, D.E. Newby10, A.A. Pragman1, J. Vestbo11, J. Yates7, D.E. Niewoehner1; 1Minneapolis VA Health Care System - Minneapolis, MN/US, 2University of Alabama - Birmingham, AL/US, 3GlaxoSmithKline - Stockley Park/GB, 4University of Michigan - Ann Arbor, MI/US, 5University of Liverpool - Liverpool/GB, 6Brigham and Women's Hospital - Boston, MA/US, 7GlaxoSmithKline - Research Triangle Park, NC/US, 8Veramed Ltd - Twickenham/GB, 9Weill Cornell Medical College of Cornell University - New York, NY/US, 10University of Edinburgh - Edinburgh/GB, 11University of Manchester - Manchester/GB; on behalf of the SUMMIT Investigators

Rationale: Ischemic heart disease, stroke, and chronic obstructive pulmonary disease (COPD) are the three leading causes of death globally. COPD and lower forced expiratory volume in 1 second (FEV1) are considered risk factors for cardiovascular disease (CVD). The mechanisms explaining this association are not clear, but COPD is often associated with increased concentrations of circulating inflammatory biomarkers, especially during acute exacerbations of COPD (AECOPD). We hypothesized that among patients with COPD, periods following AECOPD would be associated with higher risk for subsequent CVD events compared with time periods free of AECOPD. We tested this hypothesis in a large (n=16,485), international cohort that collected AECOPD data and adjudicated CVD events.

Methods: We analyzed data post hoc from participants in the Study to Understand Mortality and MorbidITy (SUMMIT) trial that enrolled current or former smokers, aged 40–80 years, with FEV1/forced vital capacity ≤0.70, FEV1 50%-70% of predicted, and with a history of CVD or with an increased risk of CVD. For this analysis, our primary interest was CVD events (cardiovascular death, myocardial infarction, stroke, unstable angina, and transient ischemic attack) as determined by a blinded adjudication committee. We used a Cox model with a time- dependent covariate for AECOPD events (defined as symptomatic deterioration requiring treatment with antibiotics or systemic corticosteroids). While controlling for other risk factors we analyzed the hazard of CVD events at 1-30 days, 31 days-1 year, and >1 year following AECOPD events. Our primary analysis included data from all four SUMMIT arms (placebo, fluticasone furoate, vilanterol, fluticasone furoate + vilanterol), but additional sensitivity analyses restricted the model to individual study arms.

Results: The hazard of CVD events following AECOPD was significantly increased, particularly in the first 30 days following AECOPD (HR 3.8; 95%CI: 2.7, 5.5), though it remained increased between 30 days to 1 year (HR 1.8; 95%CI: 1.5, 2.3), and was no longer significant beyond 1 year following AECOPD (HR 1.1; 95%CI: 0.8, 1.6) (Table). When analyses were restricted to the individual treatment arms in SUMMIT, we observed the same general pattern in each, with an increased risk for CVD events early after AECOPD and no significant increase >1 year after AECOPD.

Conclusions: AECOPD events confer an increased risk of CVD events, especially in the first 30 days following AECOPD. Clinicians should have heightened vigilance for CVD events following AECOPD. Our data also suggest the need for intervention studies to reduce the risk of post-AECOPD CVD events.