From the Journals

High-sensitivity cardiac troponin levels linked to cardiovascular outcomes in COPD patients

 

Key clinical point: In patients with COPD and heightened cardiovascular risk, high levels of high-sensitivity cardiac troponin were strongly associated with risk of cardiovascular outcomes.

Major finding: Compared to those in the lowest quintile, patients in the highest quintile of baseline plasma cardiac troponin concentrations had an increased risk of a cardiovascular composite event (hazard ratio, 3.67; 95% CI, 1.33-10.13; P = 0.012).

Study details: Post-hoc analysis of 1,599 patients in the SUMMIT trial who had a baseline cardiac troponin I assessment and 1,258 who had a 3-month follow-up assessment.

Disclosures: The study was supported by GlaxoSmithKline and a Butler British Heart Foundation Senior Clinical Research Fellowship. Authors reported disclosures related to GlaxoSmithKline, Veramed Limited, Abbott Diagnostics, Roche, Singulex, AstraZeneca, Zambon, Bayer, Novartis, and others.

Source: Adamson PD et al. J Am Coll Cardiol. 2018 Sep 4;72(10):1126-37.

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‘Robust’ findings have implications for clinical practice

The current study data are “robust” and suggest a strong association between high-sensitivity cardiac troponin values and cardiovascular event risk in these COPD patients, according to authors of an editorial.

The study also showed that a change in high-sensitivity cardiac troponin at 3 months is associated with increased risk, noted editorial authors Allan S. Jaffe, MD, and H. Ari Jaffe, MD.

“Most of these events probably represent acceleration of atherosclerosis, given the effects of smoking on atherosclerotic disease and its progression,” the authors said in the Journal of the American College of Cardiology.

However, study authors could have more extensively addressed how to use that information to improve the care of COPD patients at elevated cardiovascular event risk, they added.

A “pilot algorithm” that could be used to apply this biomarker analysis in clinical practice was proposed in an editorial accompanying the research report.

They suggest repeating high-sensitivity cardiac troponin measurements to reduce variability, as well as repeating samples at 3 months to detect changes that could signal increased risk.

“In addition, one should avoid decisions based on small differences,” they wrote.

Allan S. Jaffe, MD, is with the department of cardiovascular medicine and the department of laboratory medicine and pathology at the Mayo Clinic in Rochester, Minn. He reported serving as a consultant for Beckman, Abbott, Siemens, ET Healthcare, Sphingotec, Becton Dickinson, Quindel, and Novartis. H. Ari Jaffe, MD, is with the department of medicine, pulmonary division at University of Illinois at Chicago, Jesse Brown VA Medicine Center, Chicago. He reported he has no relationships to disclose relevant to the contents of the editorial.


 

FROM THE JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY

In patients with COPD and heightened cardiovascular risk, high levels of high-sensitivity cardiac troponin are strongly associated with risk of poor cardiovascular outcomes, according to a post-hoc analysis of a clinical trial.

An increased risk of cardiovascular adverse events and cardiovascular death was seen in COPD patients in the highest quintile of plasma cardiac troponin concentrations at baseline, results of the analysis show.

The findings highlight the potential utility of high-sensitivity cardiac troponin in both clinical trials and clinical practice, according to researcher Nicholas L. Mills, MD, PhD, BHF/University Centre for Cardiovascular Science, The University of Edinburgh, Scotland, and co-investigators.

“Recognizing the risk associated with increased troponin concentrations might encourage clinicians to address cardiovascular risk due to lifestyle choices, and make patients more likely to engage with these recommendations,” Dr. Mills and co-authors wrote in the Journal of the American College of Cardiology.

Improved risk stratification may also help clinicians more appropriately target the use of preventive medications in COPD patients, they added in the report.

The analysis by Dr. Mills and colleagues was based on assessment of cardiac troponin I concentrations for patients in SUMMIT, a randomized trial assessing inhaled corticosteroids and long-acting beta agonists in COPD patients with ele-vated cardiovascular risk.

A total of 1,599 patients in the SUMMIT trial had a baseline cardiac troponin I assessment, and 1,258 had a follow-up assessment at 3 months following randomization.

Compared with those in the lowest quintile, patients in the highest quintile of baseline plasma cardiac troponin concentrations had an increased risk of a cardiovascular composite event, even after adjusting for confounding variables (hazard ratio, 3.67; 95% confidence interval, 1.33-10.13; P = .012)..

Increased risk of cardiovascular death was also seen in the highest quintile as compared with the lowest quintile (HR, 20.06; 95% CI, 2.44-165.15; P = .005), investigators said.

There was no difference in risk of COPD exacerbations between the highest and lowest quintiles, they added.

At 3 months, there were no differences in troponin concentrations related to COPD treatment, consistent with previous observations in the SUMMIT trial that treatment did not impact the cardiovascular composite endpoint, investigators said.

However, patients with a plasma troponin of 5 ng/L or greater recorded at either the baseline or 3-month assessment had an increased rate of the composite cardiovascular endpoint and a “markedly increased” risk of cardiovascular death, they wrote.

The research was supported by GlaxoSmithKline and a Butler British Heart Foundation Senior Clinical Research Fellowship received by Dr. Mills. Disclosures reported by Dr. Mills included consultancy, research grants, and speaker fees from Abbott Diagnostics, Roche, and Singulex. Study co-authors reported disclosures related to GlaxoSmithKline, Veramed Limited, AstraZeneca, Zambon, Bayer, Novartis, and others.

SOURCE: Adamson PD et al. J Am Coll Cardiol. 2018 Sep 4;72(10):1126-37.

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