Cardiac troponins and mortality in type 1 and 2 myocardial infarction

Abstract

Background: 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.

Diagnostic features, management and prognosis of type 2 myocardial infarction compared to type 1 myocardial infarction: a systematic review and meta-analysis

“…32 In our analysis, non-cardiac surgery as a trigger was less frequent than reported by other investigators 26 whereby perioperative stressors including blood loss, anaesthesia-induced hypotension and wound infections cause imbalance in myocardial contractility, oxygen demand and blood flow. 53 Analysis of cTn levels showed uniformly higher values in T1MI than T2MI which accord with one review 5 reporting cTn values 30%-94% higher in patients with T1MI, and which other investigators regard as being highly specific diagnostic markers for T1MI. 53 Coronary angiography and revascularisation were both performed much less frequently in patients with T2MI than those with T1MI.…”

“…In the absence of randomised controlled trials that have evaluated different investigational and therapeutic interventions in patients with T2MI, uncertainty remains around the appropriate management of such patients, particularly those with known or suspected coronary artery disease. Past reviews have assessed one or more attributes of T2MI in comparison to T1MI [4][5][6][7][8] but, to our knowledge, none have undertaken a comprehensive analysis of symptoms, physical signs, investigation results, management regimens and clinical outcomes, both short and long term, of T2MI versus T1MI.…”

Dyslipidemia and Its Role in the Pathogenesis of Atherosclerotic Cardiovascular Disease: Implications for Evaluation and Targets for Treatment of Dyslipidemia Based on Recent Guidelines

“…The pathophysiology that differentiates stable angina from ACS is acute plaque rupture or erosion that results in the acute worsening of coronary artery flow, with subsequent symptomatic, electrocardiographic, and biochemical clinical findings ranging from moderate to severe chest pain all the way to acute cardiogenic shock and cardiac arrest [120,121]. Myocardial infarction (MI), both NSTEMI and STEMI, caused by acute atherothrombotic disease of an eroded or ruptured plaque, is classified as a type I MI [115,122]. It is distinguished from other etiologies of cardiomyocyte damage, troponin elevation, and EKG changes such as other acute stressors such as anemia, sepsis, or tachyarrhythmia that cause oxygen demandsupply mismatch (type 2 MI), sudden cardiac death with symptoms suggestive of MI but no blood specimen available for troponin analysis (type 3 MI), type 4 MI as a complication of percutaneous coronary intervention (PCI), and type 5 MI as a complication of coronary artery bypass grafting (CABG) [115,[122][123][124].…”

“…Myocardial infarction (MI), both NSTEMI and STEMI, caused by acute atherothrombotic disease of an eroded or ruptured plaque, is classified as a type I MI [115,122]. It is distinguished from other etiologies of cardiomyocyte damage, troponin elevation, and EKG changes such as other acute stressors such as anemia, sepsis, or tachyarrhythmia that cause oxygen demandsupply mismatch (type 2 MI), sudden cardiac death with symptoms suggestive of MI but no blood specimen available for troponin analysis (type 3 MI), type 4 MI as a complication of percutaneous coronary intervention (PCI), and type 5 MI as a complication of coronary artery bypass grafting (CABG) [115,[122][123][124]. The severity of clinical presentation, along with the acute and long-term risk after adequate management of ACS, has led to countless clinical trials and guideline recommendations on the acute management, involving antiplatelet and anticoagulation therapy, thrombolysis, PCI, and CABG [104-106, 125-127].…”

Type 2 myocardial infarction in general medical wards

“…Myocardial infarction (MI) is an acute ischemic event associated with cardiomyocyte injury and constitutes a major cause of death and disability. [1,2] The Universal Definition of MI Global Taskforce introduced a classification system in 2007 (and reaffirmed in 2012) that defined 5 types of MI. Type 1 MI is caused by an acute atherothromboembolic coronary event, while type 2 MI is defined as imbalance in oxygen supply and demand which is attributed to a condition other than a coronary atherosclerotic plaque rupture or recent coronary revascularization.…”