Coronary stent implantation has revolutionised percutaneous coronary intervention (PCI), preventing vessel closure and reducing restenosis. Nonetheless, the permanent presence of an intracoronary endoprosthesis introduces two intrinsic major limitations: restenosis and stent thrombosis (ST). Although ST incidence has declined with last-generation drug-eluting stents, improved implantation technique and antiplatelet regimens, it remains a catastrophic event, typically presenting as ST-elevation myocardial infarction or sudden cardiac death, with persistently high early and late mortality. Standardised definitions classify ST by diagnostic certainty and timing from implantation, reflecting distinct underlying mechanisms across intraprocedural, early, late and very late phases. Early ST is most often driven by correctable procedural and pharmacological determinants, including underexpansion and malapposition, high thrombotic burden in acute coronary syndromes and premature discontinuation or inadequate effect, of dual antiplatelet therapy (DAPT). Late and very late ST are frequently related to delayed healing with uncovered struts, late-acquired malapposition and intrastent neoatherosclerosis or may involve hypersensitivity to stent components or allergy to external factors (Kounis syndrome type III). Intravascular imaging, particularly optical coherence tomography, complemented by intravascular ultrasound, is pivotal to identify the dominant mechanism and guide targeted therapy. Acute management relies on rapid reperfusion with PCI, mechanical optimisation and potent antithrombotic strategies; drug-coated balloon angioplasty is emerging as a mechanistically attractive option in selected late presentations to avoid additional metal. Prevention relies on imaging-guided implantation, individualised DAPT and strict risk-factor control. This narrative review summarises current definitions, epidemiology, mechanisms, diagnostic pathways and contemporary therapeutic and preventive strategies, integrating recent consensus recommendations.

Magnetic resonance imaging (MRI) abnormalities have been reported in individuals who later die from sudden unexpected death in epilepsy (SUDEP), but their specificity and predictive value remain uncertain. Postmortem MRI (PM-MRI) offers a unique opportunity to distinguish structural features associated with SUDEP from changes related to epilepsy, comorbid illness, or the postmortem interval. We performed PM-MRI in nine individuals: five with suspected SUDEP, two with epilepsy who died from non-seizure-related causes, and two without epilepsy who died from sudden cardiac death. Hippocampal, amygdala, and subcortical volumes were quantified using validated segmentation methods and compared with 70 healthy in vivo controls. Compared with non-SUDEP cases, SUDEP cases showed significantly larger hippocampal (p = 0.014) and amygdala (p = 0.023) volumes, with most exceeding the healthy control mean, whereas non-SUDEP cases consistently demonstrated volume reductions. These findings parallel in vivo MRI observations in individuals at high risk of SUDEP and are consistent with transient peri- or postictal structural changes. In the context of recent large-scale studies showing few validated clinical SUDEP biomarkers beyond frequent generalized tonic-clonic seizures and sleeping alone, PM-MRI may provide an objective approach to positively identifying individuals who died from SUDEP. PLAIN LANGUAGE SUMMARY: We used magnetic resonance imaging (MRI) scans taken after death to study brain changes in people who died from sudden unexpected death in epilepsy (SUDEP). We found that certain brain areas involved in seizure control and automatic body functions, such as breathing and heart rate, were larger in people who died from SUDEP than in people who died from other causes. These changes were similar to those previously seen on brain scans of people with epilepsy who are known to be at higher risk of SUDEP while they were still alive. Our findings suggest that postmortem MRI may help identify brain changes linked to SUDEP.

PRKAG2 syndrome is a rare, autosomal dominant, glycogen storage disease of the heart characterized by a triad of ventricular hypertrophy, progressive conduction abnormalities, and pre-excitation. In severe cases, patients may present with neonatal onset of significant ventricular dysfunction with outflow obstruction resulting in sudden cardiac death or the need for transplantation. We present a unique case of an infant with non-diagnostic whole genome sequencing who developed progressive biventricular hypertrophy, ultimately requiring mechanical circulatory support and heart transplantation. Pathological evaluation of the explanted heart revealed excessive free glycogen accumulation within cardiomyocytes. Genetic testing identified a mosaic PRKAG2 pathogenic variant, confirming the diagnosis of PRKAG2 syndrome. This case suggests mosaicism should be considered in the diagnostic workup of early-onset cardiomyopathy.

Gastrointestinal tract fistulas are relatively uncommon and can be congenital or acquired. Acquired fistulas which communicate with the cardiovascular system are of particular concern, as they may be associated with significant morbidity and mortality. When found at autopsy, gastrointestinal fistulas should be thoroughly documented. Sudden and unexpected deaths with a history of gastrointestinal or cardiovascular surgery and a recent history of gastrointestinal bleeding or fever of an undetermined etiology should be approached with a high index of suspicion by medical examiners and signal a need for more careful dissection and documentation. This study reports on three deaths related to acquired, postsurgical fistula formation involving the gastrointestinal and cardiovascular systems.

The heart and brain are anatomically and functionally interconnected through nervous and humoral feedback mechanisms. Under physiological conditions, the heart-brain axis helps maintain cardiovascular and cerebral homeostasis. Pathology affecting one organ can profoundly impact the other, significantly worsening prognosis. The term stroke-heart syndrome refers to cardiovascular complications following acute ischemic stroke, including myocardial injury, infarction, ventricular dysfunction, arrhythmias (e.g., atrial fibrillation), heart failure, takotsubo syndrome, and sudden cardiac death. Brain damage-induced cardiac injury arises from a complex interplay of neuroinflammation, systemic immune activation, sympathetic-immune interactions, catecholamine toxicity, endothelial dysfunction, and gut-brain-heart axis involvement. Conversely, cardiac conditions, including myocardial ischemia, heart failure, and atrial fibrillation, are associated with an increased risk of stroke and cognitive decline. Myocardial ischemia can initiate systemic inflammation and neuroinflammation through sympathetic overdrive and platelet activation. Heart failure causes cerebral hypoperfusion and high thromboembolic risk, and atrial fibrillation promotes thrombus formation due to blood stasis. Atrial dysfunction and prothrombotic states may also occur independently of arrhythmia. This review summarises current evidence on the pathological interactions within the heart-brain axis, in the context of stroke, mental stress, ischemic heart disease, heart failure, and atrial fibrillation.

Recent preclinical and clinical data suggest that moderate physical activity may be safe and beneficial in patients with hypertrophic cardiomyopathy (HCM). Evidence regarding a safe dose of high-intensity exercise remains limited; however, the marked heterogeneity in the morphology and pathophysiology of HCM implies that some individuals are capable of performing even vigorous exercise, including competitive high-intensity sports. Current data indicate that participation in intense exercise and competitive athletics may be considered in a carefully selected subset of predominantly adult patients with a low-risk profile. Studies evaluating the impact of vigorous exercise or moderate-to-high intensity competitive sports on the natural history of HCM remain few and are underpowered to definitively resolve this issue. Nonetheless, emerging evidence now supports a more liberal approach whereby-after appropriate selection, expert clinical evaluation, and shared decision-making-individuals with a low-risk profile may engage in high-intensity physical activity and competitive sports, leading active and fulfilling lives while minimizing risk.

The widespread adoption of coronary computed tomography angiography (CCTA) has led to a growing detection of coronary artery anomalies in contemporary clinical practice, often as incidental findings during the evaluation of suspected or known coronary artery disease. Among these, anomalous aortic origin of a coronary artery (AAOCA) represents the most clinically debated entity, historically associated with myocardial ischaemia and sudden cardiac death, yet increasingly identified in asymptomatic or minimally symptomatic adults. Accumulating evidence indicates that most AAOCA diagnosed in adulthood are not associated with functionally relevant ischaemia and frequently follow a benign clinical course, highlighting the limitations of anatomy-based risk stratification alone. In this context, CCTA plays a pivotal role by accurately defining coronary origin and course, characterizing proximal vessel morphology, and assessing concomitant atherosclerotic disease, which often represents the predominant determinant of symptoms and prognosis in adult patients. Recent studies have demonstrated that quantitative CCTA-derived parameters can reliably exclude hemodynamically significant AAOCA and reduce unnecessary downstream testing. In selected cases, invasive functional assessment and intracoronary imaging provide incremental value by clarifying the presence and mechanisms of ischaemia but should be reserved for carefully selected patients. This review summarizes current evidence on coronary artery anomalies with a specific focus on AAOCA and proposes a pragmatic, stepwise approach integrating anatomical and functional assessment to guide clinical decision-making in daily practice.

Ischaemic ventricular tachycardia (VT) represents a major cause of morbidity and mortality in patients with ischaemic heart disease. Transcatheter ablation has emerged as a complementary therapeutic strategy to implantable cardioverter-defibrillators (ICDs) and antiarrhythmic drug therapy. The efficacy, safety, optimal timing, and cost-effectiveness of catheter ablation justify its current role in patients with ischaemic cardiomyopathy who undergo device-based interventions. Randomized clinical trials, including VANISH, VANISH2, and PARTITA, have demonstrated that early ablation significantly reduces VT recurrence and ICD shocks compared with antiarrhythmic drug therapy alone. First-line ablation in patients with preserved left ventricular systolic function (LVEF >35%) is associated with excellent long-term outcomes and low rates of sudden cardiac death. Recent advances in functional substrate mapping techniques have further improved procedural outcomes. Periprocedural mortality remains low (0.4-5%) and is mainly attributable to early VT recurrence rather than procedural complications. Current evidence supports a broader use of catheter ablation in ischaemic VT, which has historically been confined to high-volume centres, and particularly suggests its adoption as an early or first-line strategy in selected patients.

Mitral valve prolapse (MVP) is the most common valvular heart disease, with a reported prevalence of 2-3% in the general population, and represents the leading structural cause of mitral regurgitation in Western countries. MVP has long been considered predominantly a benign condition; however, it may be associated with adverse clinical events, including severe mitral regurgitation, atrial fibrillation, congestive heart failure, endocarditis, stroke, and ventricular arrhythmias, potentially leading to sudden cardiac death.