Clinical InvestigationAcute Ischemic Heart DiseaseCardiac troponin I for prediction of clinical outcomes and cardiac function through 3-month follow-up after primary percutaneous coronary intervention for ST-segment elevation myocardial infarction
Section snippets
Study design and population
This was a post hoc analysis of data from patients receiving PCI in the PROTECTION AMI (http://clinicaltrials.gov, NCT00785954) trial. The rationale, design, and main results have been published previously.9, 10 Briefly, PROTECTION AMI was a prospective, international, multicenter, phase II, randomized placebo-controlled trial that included individuals with suspected STEMI presenting within 6 hours of pain onset in 114 hospitals in 18 different countries between December 2008 and June 2010.
Baseline characteristics
In the PROTECTION AMI trial, 1,176 patients were included; and the present analyses consisted of 1,066 individuals all receiving primary PCI within 6 hours. The most common reasons for exclusion were no significant atherosclerotic stenosis (49 patients), anatomy unsuitable for revascularization (18 patients), or referral for coronary bypass surgery (11 patients). Median age was 61 years, and approximately 80% were males. Median time from symptom onset to PCI was 190 (143-265) minutes (Table I).
Discussion
In the present study, we evaluated the relation of cTnI to clinical outcomes and cardiac function in a large, well-described population of STEMI patients followed up for 3 months after primary PCI. The main findings were strong associations of single-point, peak, and cumulative cTnI with clinical events, NT-proBNP, and LVEF after MI. When added to clinical risk factors in multivariable regression models, cTnI significantly improved model discrimination for prediction of these end points. Thus,
Conclusions
Cardiac troponin I measured after primary PCI for STEMI is associated with clinical outcomes and cardiac function through 3-month follow-up. These results suggest that cTnI may be a useful risk stratification tool in STEMI patients.
Conflict of interest disclosures
Dr Hallén is an employee of Pronova BioPharma, Norway, with the company not being involved in this study. Dr Krucoff has received research funding from Abbott Vascular Business and has consulted for or received honoraria from Abbott Vascular Business, Angel Medical Systems, Cappella, Ischemix, KAI Pharmaceuticals, Medtronic, Merck, OrbusNeich, Svelte Medical, St Jude Medical, and Terumo. Dr Roe has received research funding from Eli Lilly, Sanofi-Aventis, Daiichi-Sanko, American College of
Acknowledgements
We thank all investigators and staff involved in the PROTECTION AMI trial. We also thank the statistical department at Cleveland Clinic Coordinating Center for Clinical Research for their assistance throughout the study and Øystein H. Horgmo at the University of Oslo for graphic processing of figures.
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Diagnostic methods for the canine idiopathic dilated cardiomyopathy: A narrative evidence-based rapid review
2020, Research in Veterinary ScienceCitation Excerpt :Cardiac troponins are part of the myofibrillar system of the heart, it regulates the interactions between actin and myosin allowing contraction and relaxation of the muscle (Li and Hwang, 2015). In people, cardiac troponin I (cTnI) is critical to recognize acute myocardial infarction (Druey et al., 2015; Hall et al., 2015; Liebetrau et al., 2015; Shah et al., 2015). Nevertheless, high concentrations of cTnI in animals increases due to different diseases, such as leishmaniosis, parvoviruses, cancer, systemic inflammatory response syndrome, sepsis and even in highly invasive surgery postoperative-period (Kocaturk et al., 2012; Verbiest et al., 2013; Xenoulis et al., 2014; Hamacher et al., 2015).
Impact of Left Ventricular Hypertrophy on Peak Serum Troponin T Levels in Patients With Acute Myocardial Infarction
2019, American Journal of CardiologyHigh-sensitivity cardiac troponin T, left ventricular function, and outcome in non–ST elevation acute coronary syndrome
2018, American Heart JournalCitation Excerpt :The adjusted risks along with higher hs-cTnT levels were particularly pronounced regarding cardiovascular mortality and readmission for heart failure. This supports the notion that cTn is a marker not only of acute myocardial damage but also of progressive myocardial remodeling after the acute phase of NSTE-ACS.2-7 The likelihood of adverse remodeling is difficult to assess by the means of echocardiography when performed during the acute hospitalization.
Cardiovascular Mortality in Chest Pain Patients: Comparison of Natriuretic Peptides With Novel Biomarkers of Cardiovascular Stress
2016, Canadian Journal of CardiologyCitation Excerpt :In contrast to other studies in ACS patients, troponin I had no prognostic effect, which might be related to the fact that only admission levels were present and no serial blood results were available.30 Therefore, a certain portion of the group of patients with acute myocardial infarction had to undergo urgent revascularization with lower admission levels, which did not reflect the myocardial damage; thus, post-treatment troponin I was lacking, which was described to have strong prognostic information.31 However, for improving diagnosis and facilitating treatment of patients with suggested ACS, cardiac troponins are the standard of care and indispensable in the ED.12
Efficacy of Early Invasive Management After Fibrinolysis for ST-Segment Elevation Myocardial Infarction in Relation to Initial Troponin Status
2016, Canadian Journal of CardiologyCitation Excerpt :These patients had higher 30-day cardiovascular mortality after fibrinolysis, even after adjusting for time from symptom onset to fibrinolytic treatment. In a post hoc study of the Safety and Efficacy Study of KAI-9803 to Treat Subjects with ST Elevation Myocardial Infarction (PROTECTION AMI) randomized trial, at least 75% of the 1066 patients presenting within 6 hours of symptom onset and receiving primary PCI had abnormal admission troponin I levels.26 Admission troponin levels were independently associated with higher clinical event rates (hazard ratio, 1.45; 95% CI, 1.26-1.66; P < 0.001).
Deepak L. Bhatt, MD, MPH, served as guest editor for this article.