Stable angina, also is known as typical angina or angina pectoris, is a symptom of myocardial ischemia. Stable angina is characterized by chest discomfort or anginal equivalent that is provoked with exertion and alleviated at rest or with nitroglycerin. This is often one of the first manifestations or warning signs of underlying coronary disease. Angina affects 10 million people in the United States (US); given this, it is important to not only recognize the signs and symptoms but also appropriately risk stratify and manage these individuals.[1]

Diabetic populations are predisposed to atypical, or sometimes silent, responses to myocardial ischemia. This is often the result of chronic neuropathy involving the nociceptive sympathetic pathways of the heart that converge at the T1-T4/5 spinal columns. When these signals are blunted, ischemic pain signals may be delivered via the "Arnold's nerve," the auricular branch of the vagus that innervates the external auditory canal. A 70-year-old woman with a history of type 2 diabetes (diagnosed 14 years before presentation), hypertension, hyperlipidemia, and chronic obstructive pulmonary disease presented to the urgent care for a 24-hour history of left ear pain. Following a negative otoscopic exam, she was advised to apply warm compresses and use Tylenol. The subsequent day, she developed intractable nausea, vomiting, and generalized weakness. Emergency medical services were notified and en route identified an acute inferior ST-elevation myocardial infarction (STEMI) via 12-lead electrocardiogram. Emergent left heart catheterization revealed total right coronary artery occlusion, which resolved after deployment of two drug-eluting stents. Her symptoms of left ear pain and nausea resolved postintervention, and she was discharged the following day. This case thus underscores an exceedingly rare but critical anginal equivalent in diabetics, left otalgia.

Chest pain remains one of the most common and challenging presentations in cardiovascular medicine. Clinical evaluation-including structured history-taking, recognition of anginal equivalents, and focused physical examination-continues to anchor early risk estimation. Artificial intelligence (AI) may augment cardiovascular specialist care through refined pre-test risk stratification by integrating clinical information, high-sensitivity troponin, electrocardiogram (ECG) data, and multimodal imaging. Deep-learning algorithms applied to ECGs identify subtle ischaemic patterns and support rule-out strategies with a high negative predictive value. Artificial intelligence-enhanced coronary computed tomography and cardiac magnetic resonance expand diagnostic capability by characterizing plaque, perfusion, and alternative non-ischaemic aetiologies. Multimodal models leveraging electronic health records produce dynamic risk estimates, while AI tools increasingly support identification of non-coronary but clinically relevant causes of chest pain. The clinical value of AI will ultimately depend on rigorous validation, thoughtful implementation, and clinician governance. When appropriately integrated, AI has the potential to improve consistency, equity, and accuracy in the assessment of chest pain.

Angina with no obstructive coronary artery disease (ANOCA) affects millions and is frequently under-recognised because diagnostic pathways and risk tools predominantly target obstructive coronary artery disease (CAD). This protocol describes shared methods for two machine-learning (ML) studies: (1) differentiating ANOCA from stable angina with obstructive CAD and (2) predicting long-term mortality among patients with ANOCA and obstructive CAD.

Accurate identification of acute coronary syndrome (ACS) in the prehospital setting is important for timely treatments that reduce damage to the compromised myocardium. Current machine learning approaches lack sufficient performance to safely rule-in or rule-out ACS. Our goal is to identify a method that bridges this gap. To do so, we retrospectively evaluate two promising approaches, an ensemble of gradient boosted decision trees (GBDT) and selective classification (SC) on consecutive patients transported by ambulance to the ED with chest pain and/or anginal equivalents. On the task of ACS classification with 23 prehospital covariates, we found the fusion of the two (GBDT+SC) improves the best reported sensitivity and specificity by 8% and 23% respectively. Accordingly, GBDT+SC is safer than current machine learning approaches to rule-in and rule-out of ACS in the prehospital setting.

Coronary artery disease remains a significant global health challenge, driven by a multifactorial pathophysiology, including immunological activation. The identification and management of potential risk factors are crucial for improving prevention opportunities. In this study, the role of novel, innate immune system response markers, such as podoplanin 38, in atherosclerosis was investigated. A total of 150 consecutive patients (87 (58%) male; median age of 68 (61-76) years) with chronic coronary symptoms (anginal equivalent, e.g., exertional dyspnea) who underwent clinical evaluation and de novo coronary angiography for a prospective single-center analysis were included. Demographic and clinical data, combined with echocardiographic and coronary angiography results, were analyzed in conjunction with laboratory results from admission, including serum podoplanin (PDPN) concentrations. Serum PDPN concentrations were significantly lower in the coronary artery disease group (238 (174-360) pg/mL) compared to the control group (428 (207-1381) pg/mL, p = 0.002). A negative correlation was observed between PDPN and the number of involved coronary arteries in the atherosclerotic process (R = -0.27, p < 0.01). In diabetic populations, glycemic hemoglobin (Hb1Ac) is correlated with the podoplanin concentration (r = -0.51, p = 0.001). A correlation between PDPN and the left ventricular ejection fraction was noted in both the control (r = 0.33, p < 0.01) and CAD groups (r = 0.37, p < 0.001). Podoplanin (PDPN) can be considered a novel marker for coronary atherosclerosis. Low serum podoplanin concentrations characterized patients with coronary artery disease.

Acute coronary syndrome (ACS) is a leading cause of cardiac arrest, and although historically seen in an older patient population, recent decades have shown an increase in prevalence among younger individuals. Emergency reperfusion or percutaneous coronary intervention (PCI) has been the standard of care for patients with electrocardiograms (ECGs) that meet the criteria for ST-elevation myocardial infarction (STEMI). Several ECG STEMI equivalents have also been introduced and implemented in emergency cardiac care, including the presence of hyperacute T waves. This case describes a 45-year-old previously healthy male with a history of anabolic steroid and pre-workout supplementation use who presented with chest pain. Initial ECG showed hyperacute T waves, and the patient's clinical status rapidly deteriorated, leading to ventricular fibrillation and cardiac arrest. Post-return of spontaneous circulation, the patient's ECG met clear STEMI criteria. Emergency physicians must be familiar with standard STEMI criteria, as well as STEMI equivalents, in order to appropriately involve interventional cardiology consultants early for consideration of coronary reperfusion. Emergency physicians should also maintain a higher clinical suspicion for ACS in individuals with anabolic steroid or unregulated pre-workout supplements.

Post-percutaneous coronary intervention (PCI) fractional flow reserve (FFR) is associated with future major adverse cardiac events and may reflect residual ischaemia and suboptimal stent result (SSR). Post-PCI FFR should therefore be considered to identify patients at high risk. Whether abnormal post-PCI FFR and non-hyperaemic pressure ratios, including resting full-cycle ratio (RFR), represent SSR after PCI remains to be determined, especially after chronic total occlusion (CTO) PCI. In addition, little is known about the association between post-PCI intracoronary physiology and SSR with residual anginal complaints.

Improving the prompt recognition of acute coronary syndrome symptoms in the prehospital period may reduce total ischemic time and improve patient outcomes. This study aimed to evaluate the occurrence, severity, and changes in patient-reported symptoms between the prehospital period and the emergency department and determine whether symptoms predicted an acute coronary syndrome diagnosis and/or adverse patient outcomes (eg, death).

Wellens syndrome is a relatively common yet fatal presentation of acute coronary syndrome and is considered a ST-segment elevation myocardial infarction (STEMI) equivalent. It often indicates an obstructive lesion in the proximal left anterior descending (LAD) artery and warrants early coronary angiography and revascularisation. We report the case of an elderly female in her 60s who presented to a primary health care centre with an acute-onset shortness of breath. A provisional diagnosis of acute exacerbation of chronic obstructive pulmonary disease (COPD) was made, and the patient was nebulized with salbutamol and cortisone. However, her condition worsened over the next hour, and she was transferred to our hospital. On arrival at our hospital, the patient was hypotensive and extremely distressed. A 12-lead ECG showed STEMI with elevation in leads V1-V6, lead I, and aVL. A diagnosis of anterior wall MI (AWMI) was confirmed. Angiography revealed thrombotic occlusion of the proximal LAD artery. This was subsequently tackled by implanting a drug-eluting Stent. Our patient presented with dyspnoea (an uncommon anginal equivalent) and mild wheezing on auscultation, which initially led to an erroneous diagnosis of acute exacerbation of COPD, as the serum troponins were initially normal and the ECG seemed apparently normal. On retrospective analysis, the clinician had missed a subtle biphasic T wave in V1-V3 with preserved R waves, suggesting Wellens syndrome.

Ischaemic chest pain or its equivalents are acute-onset in acute coronary syndrome (ACS) and chronic, episodic, and transient in chronic coronary syndrome (CCS). A 56-year-old Caucasian male with a history of premature atherosclerotic coronary artery disease (CAD) presented to secondary care with recurrent presyncope and syncope. He reported a year-long history of persistent left-sided neck and shoulder dull ache/tightness, unrelated to exertion and fluctuating unpredictably. His primary care had diagnosed the pain as musculoskeletal, attributing it to prior physical trauma. However, the pain did not respond to treatment. During his admission for suspected cardiac syncope, he experienced transient chest discomfort, transient inferior ST-segment elevation on electrocardiogram (ECG), and elevated troponin levels, indicating a non-ST-elevation myocardial infarction (NSTEMI). Coronary angiography revealed obstructive atherosclerotic two-vessel disease, with severe proximal stenosis in the right coronary artery (RCA) and moderate-to-severe stenosis in the left anterior descending artery (LAD). His chronic neck and shoulder pain resolved after percutaneous coronary intervention (PCI) with drug-eluting stent (DES) placement in the RCA, confirming it was an anginal equivalent. Although the chronicity of this anginal equivalent may align it more with CCS than ACS, its unremitting nature is inconsistent with CCS. Our patient's history also showed that his ischaemic symptoms changed over time, from remote exertional dyspnoea to persistent neck and shoulder pain, and then to the chest discomfort that preceded his NSTEMI. Our case highlights the importance of heightened clinician awareness of atypical CAD presentations and symptom variability over time. Symptoms initially considered non-anginal should be reassessed for CAD, particularly when alternative treatments prove ineffective. Similar cases like ours, in the future, could prompt updates to CCS diagnostic guidelines to address atypical presentations with persistent pain.