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Health See other Health Articles Title: Abnormal Troponin T Points to CVD Risk in Diabetic Patients With Stable CAD BOSTON, MA — An elevation in cardiac troponin T—the biomarker used to identify patients with ACS who present to the emergency department with chest pain—is associated with an approximate doubling of the risk of cardiovascular mortality, MI, and stroke in patients with stable ischemic heart disease and type 2 diabetes, according to the results of a new analysis[1]. Despite the increased risk, patients with elevations in cardiac troponin T who underwent prompt coronary revascularization did not have a reduction in the risk of cardiovascular events when compared with patients who were managed with medical therapy, report investigators. Published in the August 13, 2015 issue of the New England Journal of Medicine, the findings are derived from an analysis of the Bypass Angioplasty Revascularization Investigation in Type 2 Diabetes (BARI-2D) trial. To heartwire from Medscape, lead investigator Dr Brendan Everett (Brigham and Women's Hospital, Boston, MA) said that while cardiac troponin T is used to identify MI in the emergency-department setting, there has been evidence from primary and secondary populations, in patients with and without preexisting cardiovascular disease, that the concentration of circulating troponin is associated with future cardiovascular events. So far, though, few studies have carefully assessed cardiac troponin T as a marker of risk in patients with both diabetes and stable coronary disease or looked at whether or not opening the coronary arteries would benefit those with an abnormal troponin, he said. In the BARI-2D analysis of 2285 patients with type 2 diabetes and stable ischemic heart disease, nearly 40% of patients had an abnormal troponin-T concentration (defined as >14 ng/L), something that caught the researchers by surprise. In terms of clinical outcomes, 27.1% of individuals with a cardiac troponin-T concentration >14 ng/L had a cardiovascular event—the primary composite end point was death from cardiovascular causes, MI, or stroke at 5 years—compared with 12.9% of individuals with a normal cardiac troponin-T concentration (P<0.001). At 5 years, the rate of death from any cause was 19.6% and 7.1% among patients with and without an elevation in cardiac troponin T (P<0.001). In a model adjusted for cardiovascular risk factors and clinical characteristics, the risk of cardiovascular mortality, MI, or stroke was 85% higher at 5 years among those with an elevation in troponin T compared with those who did not have an increased concentration (P<0.001). No Benefit From Surgery or Stenting Strikingly, the patients with elevations in cardiac troponin T who underwent coronary revascularization as part of the BARI-2D study did not have a significant reduction in cardiovascular events when compared with those randomized to medical therapy alone. "Neither bypass surgery or stenting improved the outcomes of patients with an abnormal troponin, nor did it actually lower the troponin concentrations," said Everett. While revascularization didn't benefit the patients, it is not known what an intervention strategy would entail, because unlike an ACS, where the increase in troponin is directly related to the blocked coronary artery, researchers don't know what is causing the abnormal levels in stable patients. At this point, the source of the troponin could be a combination of hypertension, hyperglycemia, and perhaps dyslipidemia—all cardiovascular or metabolic stressors on the heart—but this is purely speculation at this stage, said Everett. "This is a different kind of heart injury," he added. If researchers can identify the source of the troponin increase, a more aggressive treatment approach could benefit these patients. Until then, the routine assessment of troponin-T concentrations in the stable setting would not be beneficial. It should be noted that the assay used to measure cardiac troponin T in BARI-2D is available only in Europe at present and is not yet approved by the US Food and Drug Administration. "If we can identify a treatment strategy that would reduce the risk in patients seen with an abnormal troponin, I think it could be a valuable risk-stratification tool," said Everett. "Absent a clinical intervention to improve their outcome, though, I would be hesitant to recommend it. For the time being, I would not recommend that [high-sensitivity cardiac troponin-T testing in stable patients] be used widely until we identify some kind of intervention that would mitigate the risk we see." In an editorial[2], Drs Chiara Melloni and Matthew Roe (Duke Clinical Research Institute, Durham, NC) point out that the cutoff for determining an increase in troponin T—in this case, >14 ng/L—is derived from studies of ACS patients. It remains uncertain, they write, whether this threshold applies to patients with stable ischemic heart disease. "Further studies should thus explore the continuous relationship between troponin values and ischemic outcomes in this population to more precisely delineate the thresholds that demarcate the increased risk of subsequent ischemic outcomes," according to the editorialists. Looking for the Source of Cardiac Troponin T To heartwire , Everett noted these stable patients have the potential to pose problems for treating physicians, especially given the high prevalence of those with an abnormal troponin T. If such a stable patient were to show up in the emergency department with chest pain—pain that may or may not be related to their heart—a diagnosis of ACS is possible given the abnormal concentration of cardiac troponin T. "If they were walk into an emergency room with a chest syndrome, which or may not be related to heart disease, 40% of these patients would have a positive troponin on the first analysis," said Everett. "That causes a lot of appropriate handwringing. What do we do with this information?" In such a situation, a second troponin test, as well as a detailed patient history, would be needed to determine whether the chest pain is unstable angina and not an ongoing chest syndrome, an important step to determine if the patient needs to be referred for angiography. BARI-2D was funded by the National Institutes of Health and Roche Diagnostics. Everett reports grant support from Roche and Novartis and financial compensation from Genzyme for serving on a clinical-events committee. Disclosures for the coauthors are listed in on the journal webs Related Links Use of hs-cTnT in Secondary Prevention Subclinical Myocardial Necrosis in Diabetics Ups CV Risk Troponin T Predicts Death and Heart Failure Risk in Stable CHD Patients Poster Comment: In my most severe tachycardia episode Troponin heart repair enzyme reached 13, well above normal of <0.15ug/L. The enzyme shows up in blood tests 4 hours after the event. That was when my LDL cholesterol was twice HDL. With medication, diet and exercise I'm now below the maximum recommended LDL. Anyone familiar with Wallach's tachycardia "prescription" as promoted on C2C's Criticalhealthnews.com Post Comment Private Reply Ignore Thread
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