Background: Myocardial infarction with non-obstructive coronary arteries (MINOCA) occurs in 6-15% of MI and disproportionately affects women. Scientific statements recommend multi-modality imaging in MINOCA to define the underlying cause. We performed coronary optical coherence tomography (OCT) and cardiac magnetic resonance imaging (CMR) to assess mechanisms of MINOCA. Methods: In this prospective, multicenter, international, observational study, we enrolled women with a clinical diagnosis of MI. If invasive coronary angiography revealed <50% stenosis in all major arteries, multi-vessel OCT was performed, followed by CMR (cine imaging, late gadolinium enhancement, and T2-weighted imaging and/or T1 mapping). Angiography, OCT, and CMR were evaluated at blinded, independent core laboratories. Culprit lesions identified by OCT were classified as definite or possible. The CMR core laboratory identified ischemia-related and non-ischemic myocardial injury. Imaging results were combined to determine the mechanism of MINOCA, when possible. Results: Among 301 women enrolled at 16 sites, 170 were diagnosed with MINOCA, of whom 145 had adequate OCT image quality for analysis; 116 of these underwent CMR. A definite or possible culprit lesion was identified by OCT in 46.2% (67/145) of participants, most commonly plaque rupture, intra-plaque cavity or layered plaque. CMR was abnormal in 74.1% (86/116) of participants. An ischemic pattern of CMR abnormalities (infarction or myocardial edema in a coronary territory) was present in 53.4% of participants undergoing CMR (62/116). A non-ischemic pattern of CMR abnormalities (myocarditis, takotsubo syndrome or non-ischemic cardiomyopathy) was present in 20.7% (24/116). A cause of MINOCA was identified in 84.5% of the women with multi-modality imaging (98/116), higher than with OCT alone (p<0.001) or CMR alone (p=0.001). An ischemic etiology was identified in 63.8% of women with MINOCA (74/116), a non-ischemic etiology was identified in 20.7% (24/116), and no mechanism was identified in 15.5% (18/116). Conclusions: Multi-modality imaging with coronary OCT and CMR identified potential mechanisms in 84.5% of women with a diagnosis of MINOCA, three-quarters of which were ischemic and one-quarter of which were non-ischemic, alternate diagnoses to MI. Identification of the etiology of MINOCA is feasible and has the potential to guide medical therapy for secondary prevention. Clinical Trial Registration: URL: https://clinicaltrials.gov Unique Identifier: NCT02905357
Heart failure (HF) continues to increase in prevalence, representing a significant burden to healthcare systems in the USA. Despite several established HF therapies, particularly for HF with reduced ejection fraction (HFrEF), rates of HF hospitalizations and cardiovascular (CV) mortality remain very high. Type 2 diabetes (T2D) is an important risk factor for HF, with the two conditions often occurring concurrently. Several CV outcomes trials have shown that the sodium–glucose cotransporter 2 inhibitor (SGLT2i) class of antihyperglycemic drugs reduces the risk of HF-related outcomes in patients with T2D and either established CV disease or multiple CV risk factors. Subsequently, there have been large clinical studies that have investigated the effects of SGLT2is in patients with HFrEF, with or without T2D, which have shown that both dapagliflozin and empagliflozin have significant reductions in hospitalization for HF and CV mortality. These data led to US Food and Drug Administration approval of dapagliflozin and empagliflozin as a novel treatment pathway for patients with HFrEF; empagliflozin has subsequently been approved for the treatment of HF regardless of ejection fraction. A clinical practice algorithm can assist cardiologists in identifying patients who may be eligible for SGLT2i treatment as well as the appropriate timeframe for initiating therapy and the parameters for patient monitoring. Given the evidence that SGLT2is are beneficial in the management of HF, specifically HFrEF, irrespective of underlying T2D, evidence-based recommendations and greater clinician familiarity can facilitate the integration of SGLT2is into general HF therapeutic management.
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