1. Boden WE, De Caterina R, Kaski JC, et al. Myocardial ischaemic syndromes: a new nomenclature to harmonize evolving international clinical practice guidelines. Eur Hear J 2024; 45:3701–6https://doi. org/10.1093/eurheartj/ ehae278. The authors propose a new binary classification of ‘acute myocardial ischaemic syndromes’ and ‘non-acute myocardial ischaemic syndromes’, which comprises both obstructive epicardial and non-obstructive pathogenetic mechanisms, including microvascular dysfunction, vasospastic disorders, and non-coronary causes. Overall, such a more encompassing nomenclature better aligns, unifies, and harmonizes different pathophysiologic causes of myocardial ischaemia and should result in more refined diagnostic and therapeutic approaches targeted to the multiple pathobiological precipitants of angina pectoris, ischaemia and infarction. 2. Yndigegn T, Lindahl B, Mars K, et al. Beta-blockers after myocardial infarction and preserved ejection fraction. N Engl J Med 2024;390: 1372–81.  . Among patients with acute myocardial infarction who underwent early coronary angiography and had a preserved left ventricular ejection fraction (≥50%), longterm beta-blocker treatment did not lead to a lower risk of the composite primary end point of death from any cause or new myocardial infarction than no beta-blocker use. 3. Silvain J, Cayla G, Ferrari E, et al. Betablocker interruption or continuation after myocardial infarction. N Engl J Med2024; 391:1277–86. IIn patients with a history of myocardial infarction, interruption of long-term beta-blocker treatment was not found to be noninferior to a strategy of beta-blocker continuation. 4. Butler J, Jones WS, Udell JA, et al. Empagliflozin after acute myocardial infarction. N Engl J Med 2024;390: 1455–66. https://doi.org/10.1056/NEJMoa2314051. https://www.nejm.org/doi/10.1056/NEJMoa2314051?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmed . Among patients at increased risk for heart failure after acute myocardial infarction, treatment with empagliflozin did not lead to a significantly lower risk of a first hospitalization for heart failure or death from any cause than placebo. 5. Park S-J, Ahn J-M, Kang D-Y, et al. Preventive percutaneous coronary intervention versus optimal medical therapy alone for the treatment of vulnerable atherosclerotic coronary plaques (PREVENT): a multicentre, open-label, randomised controlled trial.  Lancet 2024;403:1753–65. https://doi.org/ 10.1016/S0140-6736(24)00413-6. In patients with non-flow-limiting vulnerable coronary plaques, preventive percutaneous coronary intervention reduced major adverse cardiac events arising from high-risk vulnerable plaques, compared with optimal medical therapy alone. Given that PREVENT is the first large trial to show the potential effect of the focal treatment for vulnerable plaques, these findings support consideration to expand indications for percutaneous coronary intervention to include non-flowlimiting, high-risk vulnerable plaques. 6. Foley MJ, Rajkumar CA, Ahmed-Jushuf F, et al. Coronary sinus reducer for the treatment of refractory angina (ORBITA-COSMIC): a randomised, placebo-controlled trial. Lancet 2024;403:1543–53. https://doi. org/10. 1016/S0140-6736(24)00256-3. ORBITA-COSMIC found no evidence that the CSR improved transmural myocardial perfusion, but the CSR did improve angina compared with placebo. These findings provide evidence for the use of CSR as a further antianginal option for patients with stable coronary artery disease.   7. Chan K, Wahome E, Tsiachristas A, et al. Inflammatory risk and cardiovascular events in patients without obstructive coronary artery disease: the ORFAN multicentre, longitudinal cohort study. Lancet 2024;403: 2606–18. The perivascular fat attenuation index (FAI) score captures inflammatory risk beyond the current clinical risk stratification and coronary CT angiography interpretation, particularly among patients without obstructive coronary artery disease (CAD). The previously trained artificial intelligence -Risk prognostic algorithm, which integrates FAI Score with traditional cardiovascular risk factors and coronary atherosclerotic plaque burden classified individuals into risk categories, with good alignment between predicted and observed events, leading to significant reclassification of risk, particularly among those without obstructive CAD on coronary CT angiography. 8. Nurmohamed NS, Min JK, Anthopolos R, et al. Atherosclerosis quantification and cardiovascular risk: the ISCHEMIA trial. Eur Hear J 2024;45:3735–47. Quantitative coronary CT angiography parameters of stenosis severity and atherosclerotic burden were independently associated with cardiovascular death and MI in a patient population with advanced coronary artery disease and moderate or severe myocardial ischaemia. However, these parameters offered only modest improvement in prognostic value beyond clinical risk characteristics. 9. Serruys PW, Kageyama S, Pompilio G, et al. Coronary bypass surgery guided by computed tomography in a low-risk population. Eur Hear J 2024;45:1804–15. The planning and execution of CABG with the sole knowledge of anatomy from coronary CT angiography and without any visual information from conventional coronary angiography, in patients referred for coronary artery bypass graft is feasible and deemed safe in a select population with chronic coronary syndrome and low surgical risk. Efficacy and confirmed safety will have to be demonstrated in randomized controlled studies. 10. Sinha A, Dutta U, Demir OM, et al. Rethinking false positive exercise electrocardiographic stress tests by assessing coronary microvascular function. J Am Coll Cardiol 2024;83:291–9. Using comprehensive coronary physiology as the reference standard, ischemic ECG changes during exercise were highly specific for coronary microvascular dysfunction in our patient cohort. This is an important finding that highlights the limitations of using obstructive coronary artery disease as a reference standard to assess the accuracy of noninvasive imaging modalities.