Coronary optical coherence tomography and cardiac magnetic resonance imaging to determine underlying causes of MINOCA in women

Selected in Circulation by N. Ryan

The Women’s Heart Attack Research Programme was a prospective multicentre observational study using a combined imaging strategy to determine the underlying aetiology of MINOCA.

Reviewer

Nicola Ryan

@NicolaRyanI1

Interventional cardiologist / Cardiologist

Aberdeen, United Kingdom

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My Comment

Why this study? – the rationale/objective

The Women’s Heart Attack Research Programme was a prospective multicentre observational study using a combined imaging strategy to determine the underlying aetiology of MINOCA.

Myocardial infarction with non-obstructive coronary artery disease (MINOCA) is a relatively common finding, particularly in women. The underlying pathophysiology includes plaque rupture, thrombosis, vasospasm, embolism and dissection as well as non-vascular aetiology such as myocarditis, non-ischaemic cardiomyopathy and Takotsubo’s cardiomyopathy, MINOCA is not a benign diagnosis with significant morbidity and mortality associated with the diagnosis. The most appropriate therapeutic strategy post MINOCA remains uncertain, with recent guidelines recommending determination of the underlying aetiology in order to best tailor therapy to the individual. This study aimed to implement a comprehensive combined imaging protocol to identify the underlying causes of MINOCA and guide future practice/trials. 

How was it executed? – the methodology

The Women’s Heart Attack Research Programme was a prospective multicentre observational study in women undergoing coronary angiography for clinically diagnosed MI. Patients with no evidence of obstructive CAD (<50% stenosis) were then eligible to undergo OCT in all three main coronary arteries, aiming to include at least the proximal 60mm of each artery, at the time of angiography and CMR within one week of presentation.

• The primary objective was to determine the prevalence of vascular causes of MINOCA detected by OCT and the prevalence of myocardial abnormalities, ischaemic or non-ischaemic, seen on CMR in MINOCA. 
• The secondary objective was to determine the proportion of patients in whom the aetiology of the MI could be defined using combined OCT and CMR results.
• OCT and CMR images were evaluated by independent core laboratories, with OCT culprit lesions classified as plaque rupture, thrombus without plaque rupture, intra-plaque cavity, layered plaque, plaque erosion, spontaneous dissection or intimal bumping, CMR abnormalities were characterised as ischaemic or non-ischaemic. 
• If a culprit lesion was identified on OCT a diagnosis of MI was made if the CMR identified infarction or regional injury in a territory attributed to the culprit lesion or was normal.
• If there was Ischaemic LGE with associated myocardial oedema, if OCT demonstrated plaque rupture or thrombus without plaque rupture or if OCT demonstrated intra-plaque cavity without thrombus, layered plaque or intimal bumping and CMR identified regional injury in a coronary territory subtended by the OCT culprit MI was considered definite.

What is the main result?

The study enrolled 301 women of whom 170 had a diagnosis of MINOCA; 145 had interpretable OCT imaging, of these 116 had an interpretable CMR. The majority presented with a working diagnosis of NSTEMI (97%) with ECG abnormalities in almost two thirds (66%) and of those undergoing ECHO a regional wall motion abnormality was seen in 44% (49/111). 

• OCT was obtained in three arteries in 59.3% (86), two arteries in 32.4% (47) and one artery in 8.3% (12). 
• 46.2% of patients (67/145) had a definite or possible culprit identified on OCT with atherosclerotic plaque disruption, plaque rupture, intra-plaque cavity and layered plaque, most common (57/145). The remaining culprits were thrombus without plaque rupture (5) intimal bumping (3) and SCAD (1). 
• Patients with culprit lesions on OCT were older [66.05 (57.14, 72.61) vs. 55.96 (48.55, 64.36, p<0.001], more commonly diabetic (26.9% vs. 6.4%, p=0.002) and dislipidaemic 49.3% vs. 23.1%, p=0.002) compared to those without. 
• On CMR 32.8% had an ischaemic pattern of LGE (infarction) and 20.7% regional injury, myocarditis was seen in 14.7%, Takotsubo’s cardiomyopathy in 3.4% and 2.6% had a non-ischaemic cardiomyopathy. The remainder of CMRs were normal (25.9%). 
• Abnormal CMR was associated with higher peak TnI levels (1.79ng/ml (IQR 0.66-6.53) vs. 0.52 (IQR 0.19-0.92), P<0.001] but not with the presence of a culprit lesion on OCT.
• Combining OCT and CMR the prevalence of abnormalities indication an underlying aetiology was 84.5% (95% CI 76.3-90.3%), higher than OCT (44%, 95%CI 34.9-53.5%, p<0.001) or CMR (74.1%, 95%CI 65.0-81.6%, p=0.001) alone. 
• A final diagnosis of MI (vascular mechanism) was confirmed in 63.8%, in 15.5% of cases no mechanism was identified with the remainder diagnosed as myocarditis (14.7%), Takotsubo’s cardiomyopathy (3.4%) or non-ischaemic cardiomyopathy (2.6%).

Critical reading and the relevance for clinical practice

The results of this study show that an underlying aetiology for MINOCA can be identified in a significant percentage (84.5%) of patients using a combined imaging strategy. Almost two-thirds had an ischaemic aetiology suggesting they may benefit from secondary prevention however the exact therapeutic strategy requires clarification in large RCT’s. In one fifth of cases an alternative diagnosis to MI was identified allowing appropriate risk stratification and treatment. There was no association between angiographic severity and likelihood of identifying a culprit lesion, in women with more vessels images a culprit lesion was more likely to be identified suggesting that multivessel rather than targeted OCT may be more useful in defining the underlying aetiology.

A note of caution when interpreting the results, one must bear in mind that this was a relatively small study with almost three quarters of the screen eligible patients not enrolled, the majority of which were STEMI or occurred out of hours. Operators should be facile in using intracoronary imaging both in and out of hours in order to determine the underlying diagnosis in this group of patients. The protocol does not systematically carry out ECHO or LV grams which may have helped identify the underlying aetiology particularly in patients who are unable or unwilling to undergo CMR.

Furthermore, provocation testing was not carried out due to concerns with regard to its safety in the acute setting, coronary spasm has been shown to be an important cause of MINOCA, therefore, should be considered in the diagnostic algorithm. Given that approximately half of the patients with CMR evidence of infarction or regional injury did not have a culprit on OCT, provocation test may have helped differentiate spasm from thromboembolism as potential aetiologies. 

In summary, this study provides prospective observational data showing the feasibility of a combined imaging strategy (OCT and CMR) in defining the underlying aetiology of MINOCA. Imaging in MINOCA has been incorporated into clinical practice guidelines however larger multicentre trials and longer-term follow-up with help solidify its role in everyday clinical practice.