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Evidence-based therapy for myocardial infarction (MI) has substantially progressed over the past 50 years with cardioprotective therapies now well established and used as a measure of quality clinical performance.1 These therapies are based on the premise of atherothrombotic plaque disruption being central in the pathogenesis of MI (ie, type-1 MI) and relevant in the context of obstructive coronary artery disease (CAD; ie, coronary stenosis ≥50%). However, in patients with myocardial infarction with non-obstructive coronary arteries (MINOCA), the question arises as to whether an ischaemic MI has occurred or if the abnormal troponin values are attributable to non-ischaemic causes such as myocarditis, stress cardiomyopathy, chronic kidney disease or pulmonary embolism. Moreover, if there is an ischaemic basis, is it a type-1 acute MI mechanism (plaque disruption) or do type-2 MI mechanisms need to be considered (eg, coronary microvascular dysfunction, vasospasm, coronary thrombi/emboli and spontaneous coronary artery dissection)?2 Hence, while diagnostic and therapeutic algorithms are relatively well defined and guidelines are available for those with MI associated with obstructive CAD, strategies for management of MINOCA are not clearly defined; yet, this condition is not uncommon (especially in women), has a guarded prognosis, has multiple aetiologies and thus divergent potential therapies.
What has become increasingly evident is that while patients with MINOCA have a lower mortality compared with those with obstructive CAD, they do not carry a benign prognosis; an alarming all-cause 1-year mortality risk of 4.7% (95% CI 2.6% to 6.9%) is found despite the absence of flow-limiting stenosis.3 In the Variation In Recovery: Role of Gender on Outcomes of Young AMI Patients (VIRGO) study (ages 18–55 years old), 1-year all-cause mortality in MINOCA was double that expected for a 47-year-old woman in the USA.4 This disconcerting risk in the setting of no obstructive CAD has also been reported in the context of angina …
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