Type 2 myocardial infarction due to supply–demand mismatch

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Abstract

The best-accepted definition of myocardial infarction (MI) is provided by statements from the Universal Definition of MI Global Task force. This article, now in its third iteration, defines MI as myocardial cell death due to prolonged myocardial ischemia. It further delineates an increasingly incident subclassification of MI known as type 2 MI (T2MI). T2MI identifies instances of myocardial necrosis in which an imbalance between myocardial oxygen supply and/or demand occurs for reasons other than atherosclerotic plaque disruption. While associated with considerable risk (comparable to that of type 1 MI, which has well-defined management strategies), the spectrum of potential etiologies for T2MI makes development of precise diagnostic criteria and therapeutic implications of the diagnosis challenging.

Section snippets

Definition

The Universal Definition defines MI based on a rise and/or fall of cardiac biomarkers, preferably cardiac troponin (cTn) I or T, above the 99% of a normal reference population in conjunction with evidence consistent with MI from symptoms, imaging, electrocardiogram, or angiography [1]. Further, diagnosis of T2MI requires a clinical history suggestive of myocardial necrosis caused by an identifiable cause of supply/demand mismatch (Table 2). While some have called for diagnostic criteria for

Epidemiology

Epidemiologic understanding of T2MI is limited by the relatively recent introduction of the classification scheme, areas of uncertainty in the Universal Definition diagnostic criteria, and largely retrospective nature of existing evidence.

In retrospective cohort studies of patients, a cohort first identified by biomarker elevation then adjudicated for the clinical diagnosis of MI, the proportion of T2MI (amongst all MIs) varies widely, ranging from 2% to 30% (Table 3) [2], [3], [4], [5], [6],

Pathophysiologic considerations

The pathophysiology of T2MI reflects myocardial ischemia with necrosis resulting from either increased myocardial oxygen demand and/or decreased myocardial oxygen delivery. Often, both processes are involved in varying proportions. Myocardial oxygen demand is determined by systolic wall tension, contractility, and heart rate, while myocardial oxygen supply is determined by coronary blood flow and its oxygen carrying capacity [18]. Conditions that increase oxygen demand include supraventricular

Diagnosis and clinical presentation

Although the clinical history and symptoms of patients presenting with type 1 or T2MI can be similar. A higher proportion of patients with, some differences are observed (Table 5) type 1 MI report chest pain compared with those presenting with T2MI (89% vs. 51%), while there are no significant differences between type 1 MI and T2MI patients presenting with shortness of breath [13]. T2MI patients typically have an alternative diagnosis leading to their presentation and serving as the cause of

Biomarkers of myocardial necrosis in T2MI

The Universal Definition depends on an elevation and a rise or fall of cardiac biomarkers, with cardiac troponin preferred over the myocardial band of creatine kinase isoenzyme (CK-MB). An elevated troponin that does not change significantly over time suggests chronic myocardial injury. Conventional assays for troponin measurement (with first-draw sensitivity of 70–80% for detecting MI) on presentation are being widely replaced by troponin assays with substantially greater sensitivity in Europe

Angiography to evaluate T2MI

When compared to type 1 MI, patients with T2MI are less likely to undergo coronary angiography [6], [9]. This may reflect a selection bias against angiography in patients with a clinical diagnosis of T2MI in addition to the unclear role for percutaneous intervention in the absence of acute plaque rupture. Given the older age and increased number of comorbidities in patients with T2MI, a concern for post-procedural complications may also influence the frequency of coronary angiography.

Coronary

Prognosis

Despite controversies in precise categorization, prognostic significance of T2MI is clear. In the CASABLANCA study, over a median follow-up of 3.4 years, 152 patients had at least one T2MI [11]. Patients with T2MI developed adverse events significantly more frequently compared with those without T2MI (per 100 person/years: major cardiovascular events, 53.7 vs. 21.1, p < 0.001; all-cause death, 23.3 vs. 3.3, p < 0.001; cardiovascular death, 17.5 vs. 2.6, p < 0.001; heart failure events, 22.4 vs.

Treatment

Treatment of T2MI is complicated by the lack of prospective evidence and therefore established guidelines. Correction of the underlying cause of supply/demand mismatch remains the primary mainstay of management. Reflecting the difficulties in clinical discernment between type 1 and T2MI and the tendency to initiate type 1 MI guideline-supported therapy for T2MI, the use of intravenous and subcutaneous anticoagulants may not differ between type 1 and T2MI [6].

Although little prospective evidence

Conclusion

Since 2007 when the Universal Definition of Myocardial Infarction introduced the subclassification of T2MI, interest has focused on this increasingly incident and highly morbid form of MI. With global introduction of high-sensitivity troponin assays, the recognized incidence of T2MIs will likely increase. While associated with considerable risk (comparable to that of type 1 MI, which has well-defined management strategies), the spectrum of potential etiologies for T2MI makes development of

References (41)

  • J.S. Alpert et al.

    Diagnostic and therapeutic implications of type 2 myocardial infarction: review and commentary

    Am J Med

    (2014)
  • H.D. White

    Pathobiology of troponin elevations: do elevations occur with myocardial ischemia as well as necrosis?

    J Am Coll Cardiol

    (2011)
  • M. Maeder et al.

    Sepsis-associated myocardial dysfunction: diagnostic and prognostic impact of cardiac troponins and natriuretic peptides

    Chest

    (2006)
  • N. Pathan et al.

    Role of interleukin 6 in myocardial dysfunction of meningococcal septic shock

    Lancet

    (2004)
  • F.K. Korley et al.

    Preparing the United States for high-sensitivity cardiac troponin assays

    J Am Coll Cardiol

    (2013)
  • J.A. Ambrose et al.

    Angiographic correlates in type 1 and 2 MI by the universal definition

    JACC Cardiovasc Imaging

    (2012)
  • A.A. Mohammed et al.

    Patients with left main coronary artery vasospasm inadvertently undergoing coronary artery bypass grafting surgery

    J Am Coll Cardiol

    (2013)
  • Y. Sandoval et al.

    Cardiac troponin changes to distinguish type 1 and type 2 myocardial infarction and 180-day mortality risk

    Eur Heart J Acute Cardiovasc Care

    (2014)
  • T. Baron et al.

    Type 2 myocardial infarction in clinical practice

    Heart

    (2015)
  • D.A. Morrow et al.

    Effect of the novel thienopyridine prasugrel compared with clopidogrel on spontaneous and procedural myocardial infarction in the trial to assess improvement in therapeutic outcomes by optimizing platelet inhibition with prasugrel-thrombolysis in myocardial infarction 38: an application of the classification system from the universal definition of myocardial infarction

    Circulation

    (2009)
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    The authors have indicated there are no conflicts of interest.

    Funding: Dr. Gaggin is supported in part by the Clark Fund for Cardiac Research Innovation, Dr. Januzzi is supported in part by the Hutter Family Professorship.

    Relationship with industry: Dr. Januzzi reports the following disclosures: (1) Roche Diagnostics: research grants, consultancy; (2) Siemens Diagnostics: research grants; (3) Prevencio: research grants; (4) Singulex: research grants; (5) Critical Diagnostics: consultancy; (6) Philips: consultancy; (7) Novartis: clinical endpoints committee, consultancy; (8) Boehringer-Ingelheim: clinical endpoints committee, consultancy; and (9) Amgen: data monitoring committee.

    Dr. Gaggin reports the following disclosures: (1) Roche Diagnostics: research grant, consultancy; (2) Portola: research grant; (3) Amgen: consultancy; (4) American Regent: consultancy; (5) Boston Heart Diagnostics: consultancy; (6) Critical Diagnostics: consultancy; (7) EchoSense: clinical endpoint committee; (8) Radiometer: clinical endpoint committee; and (9) Ortho Clinical: consultancy.

    Dr. Mihatov does not have any disclosures.

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