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Cardiac troponin T may predict CV events in diabetes, stable ischemic heart disease
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Abnormal cardiac troponin T concentrations independently predicted CV death, MI or stroke in patients with diabetes and stable ischemic heart disease, according to a new analysis of the BARI 2D study.
However, patients with abnormal troponin T concentrations who were randomly assigned to prompt revascularization did not have improved outcomes compared with those assigned medical therapy alone.
Brendan M. Everett
Brendan M. Everett, MD, MPH, from the divisions of cardiovascular medicine and preventive medicine at Brigham and Women’s Hospital and Harvard Medical School, and colleagues analyzed 2,277 patients from the BARI 2D study to determine whether there was an association between cardiac troponin T concentration and the composite endpoint of CV death, MI or stroke. They also investigated whether random assignment to prompt revascularization reduced the incidence of the composite endpoint in patients with troponin T concentrations of at least 14 ng/L, which was classified as abnormal, compared with troponin T concentrations less than 14 ng/L.
Everett and colleagues reported that 39.3% of the study cohort had abnormal troponin T concentrations at baseline. Compared with normal concentrations, those with abnormal concentrations were more likely to be older, male, and have a history of MI, prior congestive HF requiring treatment, chronic renal dysfunction and longer diabetes duration (P < .001 for all).
More events at abnormal concentrations
At 5 years, among patients with abnormal troponin T concentrations at baseline, the rate of the composite endpoint was 27.1% vs. 12.9% for those with normal baseline concentrations, according to the results. After adjustment for CV risk factors, diabetes severity, ECG abnormalities and coronary anatomy, patients with abnormal baseline troponin T concentrations were at elevated risk for the composite endpoint (HR = 1.85; 95% CI, 1.48-2.32).
When the researchers analyzed patients with abnormal baseline troponin T concentrations, they found that those assigned prompt revascularization did not have a reduction in the composite endpoint rate compared with patients assigned medical therapy alone (HR = 0.96; 95% CI, 0.74-1.25).
“The strength of the relationship between troponin T concentration and the subsequent risk of myocardial infarction, stroke, heart failure, death from cardiovascular causes and death from any cause suggests that high-sensitivity cardiac troponin T concentration is a powerful prognostic marker in patients who have both type 2 diabetes and stable ischemic heart disease,” the researchers concluded.
Clinical implications
“Elevated troponin levels should be evaluated in future trials of therapies for stable ischemic heart disease as a potential ‘enrichment’ factor (a factor that is used to specify inclusion criteria for clinical trials to enhance event rates in a randomized population) and should be compared with standard clinical enrichment factors such as older age, diabetes and a history of [CV] events,” Chiara Melloni, MD, MHS, and Matthew T. Roe, MD, MHS, wrote in a related editorial.
Matthew T. Roe
Melloni and Roe, both from Duke Clinical Research Institute, also noted that “pathophysiological mechanisms that may contribute to elevated troponin values in patients with stable ischemic heart disease need to be investigated with the use of [CV] imaging studies … as well as with the use of biomarkers that reflect platelet and coagulation system activity.”
They concluded that “accumulating data suggest that cardiac troponin values may become routinely used for risk stratification across the spectrum of ischemic heart disease.” – by Erik Swain
Disclosures: Everett reports receiving grant support from Roche and Novartis and fees for serving on a clinical events committee from Genzyme. Please see the full study for a list of the other researchers’ relevant financial disclosures. Melloni reports no relevant financial disclosures. Roe reports receiving grant support from Daiichi-Sankyo, the Familial Hypercholesterolemia Foundation, Ferring Pharmaceuticals, KAI Pharmaceuticals and Sanofi-Aventis; grant support and personal fees from Eli Lilly and Janssen Pharmaceuticals; and personal fees from Amgen, AstraZeneca, Boehringer Ingelheim, Bristol-Myers Squibb, Elsevier Publishers, Merck, PriMed and Regeneron.
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