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. 2022 Apr 1;7(4):427-434.
doi: 10.1001/jamacardio.2022.0043.

Characteristics and Outcomes of Type 2 Myocardial Infarction

Tania Coscia  1   2 , Thomas Nestelberger  1   2   3 , Jasper Boeddinghaus  1   2 , Pedro Lopez-Ayala  1   2 , Luca Koechlin  1   2   4 , Òscar Miró  2   5 , Dagmar I Keller  6 , Ivo Strebel  1   2 , Ana Yufera Sanchez  1   2 , Bernhard Okamura  1   2 , Desiree Wussler  1   2 , Samyut Shrestha  1   2 , Katharina Hausknecht  1   2 , F Javier Martín-Sánchez  2   7 , Michael Christ  8 , Damian Kawecki  9 , Raphael Twerenbold  1   10 , Karin Wildi  1   11 , Maria Rubini Gimenez  1   2   12 , Christian Mueller  1   2 ; APACE Investigators
Collaborators, Affiliations

Characteristics and Outcomes of Type 2 Myocardial Infarction

Tania Coscia et al. JAMA Cardiol. .

Abstract

Importance: In contrast to type 1 myocardial infarction (T1MI) caused by atherothrombosis, characteristics and outcomes of type 2 myocardial infarction (T2MI) caused by supply-demand mismatch are incompletely understood.

Objective: To explore the characteristics and outcomes of patients with T2MI compared with those with T1MI.

Design, Setting, and Participants: In a prospective, international, multicenter cohort study including 12 emergency departments (EDs) in 5 European countries, unselected patients presenting with acute chest discomfort were enrolled from April 2006 to April 2018. Follow-up was done by telephone or in written form 3, 12, and 24 months after hospital discharge. Data were analyzed from April 2006 to April 2020.

Interventions: The final diagnoses of T2MI and T1MI were centrally adjudicated according to the Fourth Universal Definition of Myocardial Infarction by 2 independent cardiologists, including the pathophysiological trigger of T2MI.

Main Outcomes and Measures: Patient characteristics and outcomes, including 2-year all-cause and cardiovascular mortality and future T2MI and T1MI events.

Results: Of 6253 included patients, 2078 (33.2%) were women, and the median (IQR) age was 61 (48-74) years. Among 6253 patients with acute chest discomfort, the final adjudicated diagnosis was T2MI in 251 patients (4.0%), with tachyarrhythmia and hypertension responsible for two-thirds of cases, and T1MI in 1027 patients (16.4%). All-cause and cardiovascular mortality were comparable at 2 years (T2MI: adjusted hazard ratio, 1.0; 95% CI, 0.7-1.5; T1MI: adjusted hazard ratio, 0.7; 95% CI, 0.4-1.1). Patients with tachyarrhythmia or hypertension as their underlying trigger of T2MI had a lower mortality compared with patients with hypotension, hypoxemia, or anemia. Future T2MI was more likely among patients with index T2MI compared with patients with index T1MI (hazard ratio, 3.2; 95% CI, 1.4-7.5). Similarly, future T1MI was more likely to occur among patients with index T1MI (hazard ratio, 3.0; 95% CI, 1.2-7.4).

Conclusions and Relevance: Among patients with T2MI, tachyarrhythmia and hypertension were responsible for more than two-thirds of T2MI cases. While T2MI and T1MI had comparable all-cause and cardiovascular mortality at 2 years, patients with tachyarrhythmia or hypertension as their underlying trigger of T2MI had a lower mortality compared with patients with hypotension, hypoxemia, or anemia. Future T2MI occurred 3-fold more frequently among patients with T2MI vs T1MI as the index event. Improved understanding of the specifics of patients with T2MI should help improve management strategies.

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Conflict of interest statement

Conflict of Interest Disclosures: Dr Nestelberger has received research support from the Swiss National Science Foundation, the Prof Dr Max Cloëtta Foundation, the Margarete und Walter Lichtenstein-Stiftung, and the University Hospital Basel as well as personal fees from Beckman Coulter, Bayer, Ortho Clinical Diagnostics, and Orion Pharma outside the submitted work. Dr Boeddinghaus received research grants from the University of Basel, the University Hospital of Basel and the Division of Internal Medicine, the Swiss Academy of Medical Sciences, and the Gottfried and Julia Bangerter-Rhyner-Foundation and personal fees from Siemens, Roche Diagnostics, Ortho Clinical Diagnostics, and Quidel Corporation outside of the submitted work. Dr Lopez-Ayala has received research support from the Swiss Heart Foundation and personal fees from Quidel paid to his institution outside the submitted work. Dr Koechlin received a research grant from the University of Basel, the Swiss Academy of Medical Sciences and the Gottfried and Julia Bangerter-Rhyner Foundation as well as the Freiwillige Akademische Gesellschaft Basel. Dr Martín-Sánchez has received personal fees from Novartis, Merck Sharp & Dohme, Bristol Myers Squibb, Pfizer, The Medicines Company, Otsuka, Thermo Fisher, Cardiorentis, and Sanofi and research grants from the Spanish Ministry of Health and Fondo Europeo de Desarrollo Regional, Mapfre, Novartis, Bayer, Merck Sharp & Dohme, Abbott, and Orion Pharma outside the submitted work. Dr Twerenbold has received research support from the Swiss National Science Foundation, the Swiss Heart Foundation, the Swiss Society of Cardiology, the Cardiovascular Research Foundation Basel, the University of Basel and the University Hospital Basel and personl fees from Abbott, Amgen, AstraZeneca, Roche, Siemens, Singulex, and Thermo Scientific BRAHMS outside the submitted work. Dr Rubini Gimenez has received research grants from the Swiss Heart Foundation and Swiss National Science Foundation as well as personal fees from Abbott, Ortho Clinical Diagnostics, Roche, and Siemens outside the submitted work. Dr Wildi has received research funding from the Freiwillige Akademische Gesellschaft Basel, the Julia und Gottfried Bangerter-Rhyner-Stiftung, the Prince Charles Hospital Foundation, The Wesley Medical Research Foundation, and the CRE Action fund as well as a PhD scholarship from the University of Queensland. Dr Mueller has received research support from the Swiss National Science Foundation, the Swiss Heart Foundation, the Kommission für Technologie und Innovation (KTI), the European Union, the University of Basel, the University Hospital Basel, Abbott, Beckman Coulter, Idorsia, Ortho Cinical Diagnostics, Quidel, Roche, Siemens, Singulex, and Sphingotec as well as personal fees from Acon, Amgen, AstraZeneca, Boehringer Ingelheim, Bristol Myers Squibb, Idorsia, Novartis, Osler, Roche, and Sanofi outside of the submitted work. No other disclosures were reported.

Figures

Figure 1.
Figure 1.. Cumulative Incidence of Mortality at 730 Days and Future Myocardial Infarction After Index Type 2 Myocardial Infarction (T2MI) and Type 1 Myocardial Infarction (T1MI)
A and B, Two-year all-cause mortality and 2-year cardiovascular mortality. Adjusted rates of both were similar between patients with T2MI and T1MI. C and D, Future T2MI and T1MI. Patients who developed a future T2MI more often had an index T2MI than T1MI, whereas the reverse was seen for patients who developed a future T1MI.
Figure 2.
Figure 2.. Cumulative Incidence of All-Cause Mortality at 730 Days of Follow-up
The cumulative incidence is stratified by the underlying cause of type 2 myocardial infarction. Patients with bradyarrhythmia or the subgroup others had the best prognoses. The subgroups type 1 myocardial infarction (T1MI), hypertension, and tachyarrhythmia had more favorable prognoses than multiple triggers, including hypotension, hypoxemia, or anemia. Multiple triggers defined as more than 1 of the mentioned reasons; others included coronary artery spasm, coronary embolism, and coronary artery dissection.
See this image and copyright information in PMC

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