Characteristics and Outcomes of Type 1 versus Type 2 Perioperative Myocardial Infarction After Noncardiac Surgery

Abstract Background The objective of this investigation was to determine the etiology of perioperative acute coronary syndrome with a particular emphasis on thrombosis versus demand ischemia. Methods In this retrospective cohort study, adult patients were identified who underwent coronary angiography for acute coronary syndrome within 30 days of noncardiac surgery at a major tertiary hospital between January 2008 and July 2015. Angiograms were independently reviewed by two interventional cardiologists who were blinded to clinical data and outcomes. Acute coronary syndrome was classified as ST–elevation myocardial infarction, non–ST–elevation myocardial infarction, or unstable angina; myocardial infarctions were adjudicated as type 1 (plaque rupture), type 2 (demand ischemia), or type 4b (stent thrombosis). Results Among 215,077 patients screened, 146 patients were identified who developed acute coronary syndrome: 117 were classified as non–ST–elevation myocardial infarction (80.1%); 21 (14.4%) were classified as ST–elevation myocardial infarction, and 8 (5.5%) were classified as unstable angina. After coronary angiography, most events were adjudicated as demand ischemia (type 2 myocardial infarction, n = 106, 72.6%) compared to acute coronary thrombosis (type 1 myocardial infarction, n = 37, 25.3%) and stent thrombosis (type 4B, n = 3, 2.1%). Absent or only mild, nonobstructive coronary artery disease was found in 39 patients (26.7%). In 14 patients (9.6%), acute coronary syndrome was likely due to stress-induced cardiomyopathy. Aggregate 30-day and 1-yr mortality rates were 7 and 14%, respectively. Conclusions The dominant mechanism of perioperative acute coronary syndrome in our cohort was demand ischemia. A subset of patients had no evidence of obstructive coronary artery disease, but findings were consistent with stress-induced cardiomyopathy.

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Faculty Opinions recommendation of Characteristics and short-term prognosis of perioperative myocardial infarction in patients undergoing noncardiac surgery: a cohort study.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.9963956.10696054 ◽

2011 ◽

Author(s):

Thomas Slaughter

Keyword(s):

Myocardial Infarction ◽

Cohort Study ◽

Noncardiac Surgery ◽

Perioperative Myocardial Infarction ◽

Short Term

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Type 2 Myocardial Infarction: When Is It Really Type 1?

Heart Lung and Circulation ◽

10.1016/j.hlc.2016.06.162 ◽

2016 ◽

Vol 25 ◽

pp. S70-S71

Author(s):

J. Hung ◽

J. Harrington ◽

F. Scott ◽

S. Verma

Keyword(s):

Myocardial Infarction

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The Incidence of Perioperative Myocardial Infarction in Men Undergoing Noncardiac Surgery

Annals of Internal Medicine ◽

10.7326/0003-4819-118-7-199304010-00004 ◽

1993 ◽

Vol 118 (7) ◽

pp. 504 ◽

Cited By ~ 217

Author(s):

Carol M. Ashton

Keyword(s):

Myocardial Infarction ◽

Noncardiac Surgery ◽

Perioperative Myocardial Infarction

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Cardiac troponins and mortality in type 1 and 2 myocardial infarction

Clinical Chemistry and Laboratory Medicine (CCLM) ◽

10.1515/cclm-2016-0324 ◽

2017 ◽

Vol 55 (2) ◽

Cited By ~ 3

Author(s):

Giuseppe Lippi ◽

Fabian Sanchis-Gomar ◽

Gianfranco Cervellin

Keyword(s):

Myocardial Infarction ◽

Cardiac Troponin ◽

Troponin I ◽

Troponin T ◽

Post Discharge ◽

Assay Sensitivity ◽

Percentage Difference ◽

Cardiac Troponins

AbstractBackground:The pathogenesis of different types of myocardial infarction (MI) differs widely, so that accurate and timely differential diagnosis is essential for tailoring treatments according to the underlying causal mechanisms. As the measurement of cardiac troponins is a mainstay for diagnosis and management of MI, we performed a systematic literature analysis of published works which concomitantly measured cardiac troponins in type 1 and 2 MI.Methods:The electronic search was conducted in Medline, Scopus and Web of Science using the keywords “myocardial infarction” AND “type(-)2” OR “type II” AND “troponin” in “Title/Abstract/Keywords”, with no language restriction and date limited from 2007 to the present.Results:Overall, 103 documents were identified, but 95 were excluded as precise comparison of troponin values in patients with type 1 and 2 MI was unavailable. Therefore, eight studies were finally selected for our analysis. Two studies used high-sensitivity (HS) immunoassays for measuring cardiac troponin T (HS-TnT), one used a HS immunoassay for measuring cardiac troponin I (HS-TnI), whereas the remaining used conventional methods for measuring TnI. In all studies, regardless of type and assay sensitivity, troponin values were higher in type 1 than in type 2 MI. The weighted percentage difference between type 1 and 2 MI was 32% for TnT and 91% for TnI, respectively. Post-discharge mortality obtained from pooling individual data was instead three times higher in type 2 than in type 1 MI.Conclusions:The results of our analysis suggest that the value of cardiac troponins is consistently higher in type 1 than in type 2 MI.

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Abstract 13297: Short-Term Mortality in Patients With Myocardial Injury and Myocardial Infarction Type 1 and Type 2

Circulation ◽

10.1161/circ.132.suppl_3.13297 ◽

2015 ◽

Vol 132 (suppl_3) ◽

Author(s):

Laura Sarkisian ◽

Lotte Saaby ◽

Tina S Poulsen ◽

Oke Gerke ◽

Axel C Diederichsen ◽

...

Keyword(s):

Myocardial Infarction ◽

Myocardial Injury ◽

Troponin I ◽

Clinical Indication ◽

Short Term ◽

Cox Regression Analysis ◽

Short Term Mortality

Introduction: Troponin elevations occur in a myriad of clinical conditions other than myocardial infarction (MI) and imply a poor prognosis. So far, data comparing the short-term outcome in patients with myocardial injury vs. patients with type 1 or type 2 MI are not available. Methods: Over a 1-year period we prospectively studied hospitalized patients having cardiac troponin I (cTnI) measured on clinical indication. The diagnosis of type 1 and type 2 MI was according to the universal definition involving a rising and/or falling pattern of cTnI values above the decision limit of 30 ng/L. cTnI elevations above this limit in patients without overt myocardial ischemia were defined as myocardial injury. A 1-month follow-up was done with mortality as endpoint. Results: The study covered 1577 consecutive patients with cTnI values >30 ng/L, of whom 360 had a type 1 MI, 119 a type 2 MI and 1089 had myocardial injury. Type 1 MI patients were younger with a median age of 70 (IQR 61-81) yrs, whereas the median ages in type 2 MI and myocardial injury were higher but comparable : 78 (IQR 67-84) vs. 77 (IQR 67-85) yrs. Peak cTnI values, however, were highest in type 1 MI: 3820 (530-19030) ng/L, lower in type 2 MI: 850 (390-3270) ng/L, and smallest in patients with myocardial injury: 90 (50-270) ng/L (p=0.0001). At one-month follow-up 285 patients had died. Mortality in the different subgroups was: 9% (33/360) in type 1 MI, 24% (28/119) in type 2 MI, and 21% (224/1089) in patients with myocardial injury. The results are depicted in the figure (Kaplan-Meier curves, log-rank-test; p-value <0.0001). Multivariate COX regression analysis revealed a Hazard Ratio (95%) of 2.1 (1.2-3.7) for type 2 MI and 1.4 (0.9-2.1) for myocardial injury. Conclusion: The short-term mortality in patients with myocardial injury and type 2 MI is almost identical but higher than in patients with type 1 MI. These prognostic findings imply that the clinical distinction between myocardial injury and type 2 MI may be somewhat artificial.

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