Myocardial infarction with non-obstructive coronary arteries (MINOCA) defines a heterogeneous group of atherosclerotic and non-atherosclerotic conditions, causing myocardial injury in the absence of obstructive coronary artery disease. Unveiling the mechanisms subtended to the acute event is often challenging; a multimodality imaging approach is helpful to aid the diagnosis. Invasive coronary imaging with intravascular ultrasound or optical coherence tomography should be used, when available, during index angiography to detect plaque disruption or spontaneous coronary artery dissection. Cardiovascular magnetic resonance has instead a key role among the non-invasive modalities, allowing the differentiation between MINOCA and its non-ischaemic mimics and providing prognostic information. This educational paper will provide a comprehensive review of the strengths and limitations of each imaging modality in the evaluation of patients with a working diagnosis of MINOCA.

Advances in cancer therapies have led to a global improvement in patient survival rates. Nevertheless, the price to pay is a concomitant increase in cardiovascular (CV) morbidity and mortality in this population. Increased inflammation and disturbances of the immune system are shared by both cancer and CV diseases. Immunological effects of anti-cancer treatments occur with both conventional chemotherapy and, to a greater extent, with novel biological therapies such as immunotherapy. For these reasons, there is growing interest in the immune system and its potential role at the molecular level in determining cardiotoxicity. Early recognition of these detrimental effects could help in identifying patients at risk and improve their oncological management. Non-invasive imaging already plays a key role in evaluating baseline CV risk and in detecting even subclinical cardiac dysfunction during surveillance. The aim of this review is to highlight the role of advanced cardiovascular imaging techniques in the detection and management of cardiovascular complications related to cancer treatment.

Stress cardiac magnetic resonance (CMR) perfusion imaging is recommended in international guidelines as a class I indication in patients with known or suspected coronary artery disease,¹ and it is a promising non-invasive technique for the detection of cardiac allograft vasculopathy (CAV) in heart transplant (HT) recipients.^2,3 However, there are concerns regarding the use of adenosine as a vasodilator stress agent after heart transplantation due to increased susceptibility of the atrioventricular node of the denervated heart to exogenous adenosine.^4–6 Regadenoson (a selective A_2A adenosine receptor agonist) has proved safe in stress CMR after HT⁷ but there are sparse safety data on the use of adenosine CMR in this setting. Accordingly, we aimed to assess the safety and feasibility of adenosine stress CMR perfusion in orthotopic HT recipients with suspected CAV. This retrospective study received the approval of our local institutional review board. We analysed the incidence of adverse effects of adenosine stress CMR, systematically documented in our workflow, among orthotopic HT recipients undergoing clinically indicated stress perfusion CMR for suspected CAV between 2015 and 2023 at Harefield Hospital in the UK. Baseline CAV was assessed on either invasive or computed tomography coronary angiography based on the 2010 standardized nomenclature of the International Society for Heart and Lung Transplantation⁸ and accordingly classified based on the presence of moderate–severe (CAV_2–3) vs. non-significant or mild (CAV_0–1) vasculopathy. For each CMR study, changes in heart rate and blood pressure at baseline, stress, and rest were noted, along with any symptoms and the presence and extent of inducible myocardial ischaemia both on first-pass perfusion and perfusion mapping (quantitative perfusion). Stress adequacy was assessed based on patient symptoms and haemodynamic response. Indices of rest myocardial blood flow (MBF) and myocardial perfusion reserve (MPR) were derived by standardization of absolute parameters to the rate-pressure product (resting heart rate [bpm] · systolic blood pressure at baseline [mmHg]/1000), to account for variability in haemodynamic conditions.⁹