Cardiac & Non-cardiac Investigations

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Summary

Non-cardiac Investigations

Acute pulmonary embolism may mimic AMI, presenting with chest pain and the associated acute right heart strain producing ECG changes and an increase in troponin levels. Thus, a diagnosis of acute pulmonary embolism needs to be considered in MINOCA, but the merits of routinely screening for this diagnosis are less clear. Collste et al. performed routine computed tomography pulmonary angiography in 100 consecutive MINOCA patients and did not identify any cases of pulmonary embolism.²¹ Accordingly, although this diagnosis needs to be considered in MINOCA, pulmonary angiography is not justified as routine assessment tool and should be reserved for clinically suspicious cases. The use of routine D-dimer assessment in patients with MINOCA to exclude pulmonary embolism needs to be evaluated.

Renal impairment may be associated with elevated troponin levels due to reduced clearance.²² Thus, the diagnosis of AMI may be difficult in the presence of renal impairment, but should be distinguishable by serial measurements.

Cardiac Investigations

Troponin may be released (a) from dysfunctional myocardial cells in disorders associated with structural myocardial dysfunction, and/or (b) during ischaemic myocardial injury arising from coronary artery spasm, coronary microvascular dysfunction or coronary thrombosis associated with a thrombophilic disorder (Table 2). Delineating these aetiologies is important considering the different treatment approaches required for the specific diagnoses.

Cardiac Magnetic Resonance Imaging

Cardiac MRI (CMRI) should be the initial diagnostic investigation for evaluating the cardiac causes of MINOCA. Non-contrast CMRI provides useful assessment of structural myocardial dysfunction and readily identifies cardiomyopathies, including takotsubo cardiomyopathy. Furthermore, late gadolinium enhancement images provide evidence for the diagnosis of myocarditis and subendocardial MI. In this regard, CMRI has a spatial resolution to detect a myocardial infarct zone with a mass as small as 0.16 grams.

The use of this imaging modality in MINOCA is well illustrated by Leurent et al., who performed CMRI in 107 consecutive MINOCA patients at a mean delay of 6.9 days.²³ They reported the following findings with CMRI: myocarditis in 60 %, AMI in 16 %, takotsubo cardiomyopathy in 14 %, and normal findings in 10 %.

Of note, the diagnostic yield with CMRI is increased when imaging is undertaken within 7 days of presentation, as delayed imaging may result in some features no longer being evident. However, even with early imaging, 10–20 % of CMRI studies failed to identify any abnormalities despite the clinical presentation consistent with an AMI.^14,23–25 Whether small infarcts may have been missed by the gadolinium enhancement CMRI remains a possibility.

Provocative Spasm Testing

Provocative spasm testing may be considered in patients with MINOCA. Studies have demonstrated a variable prevalence of inducible spasm in such patients (15–95 %).^10,26 It appears to be particularly prevalent among Asian patients, with a reported frequency of 81 % in Japanese²⁷ and 61 % in Korean²⁸ patients with MINOCA.

Drug Screening

Drug screening for sympathomimetic agents may be indicated in some patients, as cocaine²⁹ and methamphetamines^30,31 have been associated with MINOCA. These agents may induce coronary artery spasm via their alpha-agonist properties. Thus, evaluating the history for the use of these agents and, where appropriate, urine drug screening should be considered.

Thrombophilia Disorder Screening

Thrombophilia disorder screening has been performed in several MINOCA studies with abnormalities detected in as many as 19 % of patients.¹¹ Hereditary thrombophilia disorders reported in patients with MINOCA include Factor V Leiden, prothrombin variant G20210A, Factor XII deficiency and protein C and S deficiencies. Important acquired hypercoagulable states that may predispose to MINOCA include collagen vascular disorders, systemic vasculitis, systemic lupus, antiphospholipid syndrome, polycythemia vera, thrombocythaemia, and the use of anabolic steroids or oestrogens/progestins.

Therapeutic Measures

Identifying treatable causes of MINOCA is fundamental to its clinical assessment as these may have prognostic implications and may impact on its guarded prognosis. For example, coronary artery spasm is effectively treated with nitrates and calcium channel blockers, with use of the latter shown to be a survival determinant in patients with MINOCA.³² In addition, identification of thrombophilia disorders may influence treatment and could impact on the patient’s offspring in the case of hereditary thrombophilia.

The management of MINOCA with no specific underlying aetiology identified requires further investigation. There are no prospectively conducted studies to evaluate if conventional treatments used for AMI patients with obstructive CAD are of benefit in MINOCA. Thus, whether aspirin, statins, beta-blockers and/or angiotensin-converting enzyme inhibitors should be routinely used in patients with MINOCA is open to speculation.