Yu Horiuchi1,2, Nicholas Wettersten1, Mitul P Patel1, Christian Mueller3, Sean-Xavier Neath1, Robert H Christenson4, Nils G Morgenthaler5, James McCord6, Richard M Nowak6, Gary M Vilke1, Lori B Daniels1, Judd E Hollander7, Fred S Apple8, Chad M Cannon9, John T Nagurney10, Donald Schreiber11, Christopher deFilippi4, Christopher Hogan12, Deborah B Diercks13, Gary Headden14, Alexander T Limkakeng15, Inder Anand16, Alan H B Wu17, Stefan Ebmeyer18, Allan S Jaffe19, W Frank Peacock1, Alan Maisel1. 1. University of California, San Diego, La Jolla (Y.H., N.W., M.P.P., S.-X.N., G.M.V., L.B.D., A.M.). 2. Mitsui Memorial Hospital, Tokyo, Japan (Y.H.). 3. University Hospital Basel, Switzerland (C.M.). 4. University of Maryland School of Medicine, Baltimore (R.H.C., C.d.F.). 5. Charite, Campus Virchow-Klinikum, Berlin, Germany (N.G.M.). 6. Henry Ford Health System, Detroit, MI (J.M., R.M.N.). 7. Sidney Kimmel Medical College of Thomas Jefferson University, Philadelphia, PA (J.E.H.). 8. Hennepin Healthcare/Hennepin County Medical Center and University of Minnesota, Minneapolis (F.S.A.). 9. University of Kansas Medical Center, Kansas City (C.M.C.). 10. Massachusetts General Hospital, Boston (J.T.N.). 11. Stanford University School of Medicine, Palo Alto, CA (D.S.). 12. Virginia Commonwealth University, Richmond (C.H.). 13. University of Texas Southwestern Medical Center, Dallas (D.B.D.). 14. Medical University of South Carolina, Charleston (G.H.). 15. Duke University Medical Center, Durham, NC (A.T.L.). 16. University of Minnesota and VA Medical Center, Minneapolis (I.A.). 17. University of California, San Francisco (A.H.B.W.). 18. Thermo Scientific Biomarkers, Thermo Fisher Scientific/BRAHMS GmbH, Hennigsdorf/Berlin, Germany (S.E.). 19. Mayo Clinic, Rochester, MN (A.S.J.).
Abstract
BACKGROUND: The observed incidence of type 2 myocardial infarction (T2MI) is expected to increase with the implementation of increasingly sensitive cTn assays. However, it remains to be determined how to diagnose, risk-stratify, and treat patients with T2MI. We aimed to discriminate and risk-stratify T2MI using biomarkers. METHODS: Patients presenting to the emergency department with chest pain, enrolled in the CHOPIN study (Copeptin Helps in the early detection Of Patients with acute myocardial INfarction), were retrospectively analyzed. Two cardiologists adjudicated type 1 MI (T1MI) and T2MI. The prognostic ability of several biomarkers alone or in combination to discriminate T2MI from T1MI was investigated using receiver operating characteristic curve analysis. The biomarkers analyzed were cTnI, copeptin, MR-proANP (midregional proatrial natriuretic peptide), CT-proET1 (C-terminal proendothelin-1), MR-proADM (midregional proadrenomedullin), and procalcitonin. The prognostic utility of these biomarkers for all-cause mortality and major adverse cardiovascular event (a composite of acute myocardial infarction, unstable angina pectoris, reinfarction, heart failure, and stroke) at 180-day follow-up was also investigated. RESULTS: Among the 2071 patients, T1MI and T2MI were adjudicated in 94 and 176 patients, respectively. Patients with T1MI had higher levels of baseline cTnI, whereas those with T2MI had higher baseline levels of MR-proANP, CT-proET1, MR-proADM, and procalcitonin. The area under the receiver operating characteristic curve for the diagnosis of T2MI was higher for CT-proET1, MR-proADM, and MR-proANP (0.765, 0.750, and 0.733, respectively) than for cTnI (0.631). Combining all biomarkers resulted in a similar accuracy to a model using clinical variables and cTnI (0.854 versus 0.884, P=0.294). Addition of biomarkers to the clinical model yielded the highest area under the receiver operating characteristic curve (0.917). Other biomarkers, but not cTnI, were associated with mortality and major adverse cardiovascular event at 180 days among all patients, with no interaction between the diagnosis of T1MI or T2MI. CONCLUSIONS: Assessment of biomarkers reflecting pathophysiologic processes occurring with T2MI might help differentiate it from T1MI. All biomarkers measured, except cTnI, were significant predictors of prognosis, regardless of the type of myocardial infarction.
BACKGROUND: The observed incidence of type 2 myocardial infarction (T2MI) is expected to increase with the implementation of increasingly sensitive cTn assays. However, it remains to be determined how to diagnose, risk-stratify, and treat patients with T2MI. We aimed to discriminate and risk-stratify T2MI using biomarkers. METHODS: Patients presenting to the emergency department with chest pain, enrolled in the CHOPIN study (Copeptin Helps in the early detection Of Patients with acute myocardial INfarction), were retrospectively analyzed. Two cardiologists adjudicated type 1 MI (T1MI) and T2MI. The prognostic ability of several biomarkers alone or in combination to discriminate T2MI from T1MI was investigated using receiver operating characteristic curve analysis. The biomarkers analyzed were cTnI, copeptin, MR-proANP (midregional proatrial natriuretic peptide), CT-proET1 (C-terminal proendothelin-1), MR-proADM (midregional proadrenomedullin), and procalcitonin. The prognostic utility of these biomarkers for all-cause mortality and major adverse cardiovascular event (a composite of acute myocardial infarction, unstable angina pectoris, reinfarction, heart failure, and stroke) at 180-day follow-up was also investigated. RESULTS: Among the 2071 patients, T1MI and T2MI were adjudicated in 94 and 176 patients, respectively. Patients with T1MI had higher levels of baseline cTnI, whereas those with T2MI had higher baseline levels of MR-proANP, CT-proET1, MR-proADM, and procalcitonin. The area under the receiver operating characteristic curve for the diagnosis of T2MI was higher for CT-proET1, MR-proADM, and MR-proANP (0.765, 0.750, and 0.733, respectively) than for cTnI (0.631). Combining all biomarkers resulted in a similar accuracy to a model using clinical variables and cTnI (0.854 versus 0.884, P=0.294). Addition of biomarkers to the clinical model yielded the highest area under the receiver operating characteristic curve (0.917). Other biomarkers, but not cTnI, were associated with mortality and major adverse cardiovascular event at 180 days among all patients, with no interaction between the diagnosis of T1MI or T2MI. CONCLUSIONS: Assessment of biomarkers reflecting pathophysiologic processes occurring with T2MI might help differentiate it from T1MI. All biomarkers measured, except cTnI, were significant predictors of prognosis, regardless of the type of myocardial infarction.
Authors: Matthew T H Lowry; Dimitrios Doudesis; Ryan Wereski; Dorien M Kimenai; Christopher Tuck; Amy V Ferry; Anda Bularga; Caelan Taggart; Kuan K Lee; Andrew R Chapman; Anoop S V Shah; David E Newby; Nicholas L Mills; Atul Anand Journal: Circulation Date: 2022-09-15 Impact factor: 39.918