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HsTnT in Stable Coronary Artery Disease

Completed
Conditions
Coronary Artery Disease
Interventions
Other: Progress of CHD
Registration Number
NCT01954303
Lead Sponsor
University Hospital Heidelberg
Brief Summary

Coronary artery disease (CAD) is one of the leading causes of morbidity and mortality worldwide. Life threatening manifestations such as acute myocardial infarction (AMI) and sudden cardiac death are the most important causes of death in many countries. Cardiac troponin is a biomarker with a high specificity for cardiac necrosis and is recommended for diagnosis of acute myocardial infarction by the Universal definition of myocardial infarction. Since a new generation of high-sensitivity cardiac troponin assays has become commercially available a few years ago, myocardial infarction can be detected earlier and even small AMIs, that were classified as unstable angina pectoris (UAP) with the less sensitive assays, are detectable now. On the other side, more patients with acute or chronic myocardial damage not due to AMI are identified now. Thereby, the reason for elevated troponin levels should be sought actively, because high troponin levels were associated with adverse outcome - independent of the underlying pathomechanism. The reasons for troponin elevations in patients with stable CAD are not clear yet. Associations with extensive atherosclerosis, carotid lesions and complex coronary plaques in coronary CT scans were reported. Therefore, patients with elevated troponin levels represent a risk population and might profit from intensified secondary prevention. In this context, ticagrelor might be part of a prevention strategy as currently tested in the PEGASUS trial.

We plan to conduct a single-centre pilot study in a cohort with clinically stable patients of our outpatient clinic, because data regarding prevalence, causes and prognosis of elevated troponin values in unselected cohorts is sparse. Therefore, all patients (n=910) that presented to our outpatient clinic 12 months after introduction of the high-sensitivity troponin T assay (june 2009) and were free of complaints or presented with UAP are being enrolled. All patients are characterized by demographic, laboratory and clinical characteristics (including medication) and all available imaging data (exercise-ecg, echocardiography, stress-echocardiography, computed tomography, cardiac MRI and coronary angiography) in order to compare baseline characteristics of troponin positive and troponin negative patients. In addition, the Framingham- and PROCAM-Score representing established calculators of long-term risk prediction are calculated.

Prognostic endpoints are defined as severe cardiovascular events and progress of the initially diagnosed disease. Those endpoints are associated with the initial hs-cTnT value and serial changes.

Detailed Description

Not available

Recruitment & Eligibility

Status
COMPLETED
Sex
All
Target Recruitment
965
Inclusion Criteria
  • Patients of outpatient clinic presenting 12 months after introduction of the hs-TnT test in june 2009
Exclusion Criteria
  • none

Study & Design

Study Type
OBSERVATIONAL
Study Design
Not specified
Arm && Interventions
GroupInterventionDescription
Troponin statusProgress of CHDPatients are divided into "troponin positive" (if hsTnT on first presentation is \<14 ng/L) and "troponin negative" (if hsTnT on first presentation is \>=14 ng/l).
Primary Outcome Measures
NameTimeMethod
Cardiovascular death3 years
Secondary Outcome Measures
NameTimeMethod
Recurrent Myocardial Infarction3 years
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