Late presentation in ST-segment elevation myocardial infarction (STEMI) remains common and clinically challenging, as the duration of myocardial ischemia has traditionally been considered the main determinant of infarct size. However, the conventional 12-hour cut-off, derived from fibrinolytic-era evidence, no longer fully reflects contemporary understanding of ischemia pathophysiology, advances in percutaneous coronary intervention (PCI), and the ability to assess residual myocardial viability. The optimal management of late-presenting STEMI therefore remains debated, as reflected by divergent international guideline recommendations and the heterogeneity of available randomized clinical trials. While early studies failed to demonstrate a clear benefit of late reperfusion, more recent observational and imaging-based data suggest that selected patients may still experience myocardial salvage and improved outcomes even when revascularization is performed beyond traditional temporal thresholds. Collectively, these observations indicate that time from symptom onset represents an imprecise surrogate of myocardial infarct evolution. Focusing exclusively on symptom duration oversimplifies a complex pathophysiological process and risks denying reperfusion to patients who may still derive meaningful benefit. This state-of-the-art review critically appraises current evidence on late-presenting STEMI and proposes a physiology- and imaging-guided framework that integrates clinical presentation, electrocardiographic dynamics, biomarker kinetics, and cardiac imaging to support biologically informed decision-making beyond rigid time-based cut-off.

Sudden cardiac death (SCD) causes 4 to 5 million deaths each year globally. Electrical vortices (tornadoes or rotors) are the origin of ventricular fibrillation (VF), which often causes SCD. Cardiac electrical vortices have complex dynamics and have been shown in many mammalian species. During VF, the heart fails to contract suitably and is unable to pump blood. Once VF is initiated, drug treatments are ineffective and even make things worse. The only effective treatment is electrical shock to the ventricles. Our current understanding of VF mechanisms is fragmentary, hindering the development of personalized therapies. Yet recent insights into the roles of the most critical sarcolemmal ion channels in VF in controlling the excitation-recovery process provide hope. Substantial evidence indicates that the molecular interplay between the main cardiac sodium channel (NaV1.5) and the strong inward-rectifier potassium current (Kir2.1) controls cardiac excitability, wave propagation velocity, and rotor formation, as well as rotor stability and frequency during VF. Studies at the cellular, molecular, and ion channel levels are helping us understand how rotors generate the turbulence that characterizes VF, providing insights into how to prevent their initiation and identifying new therapeutic targets to avert premature death.

Postoperative atrial fibrillation (POAF) is a common complication that can affect up to 20-44% of patients undergoing cardiac surgery. Evidence suggests that atrial fibrosis is a key factor in the development of POAF due to the disruption of the myocardial electric properties. This systematic review examines the correlation between pre-existing atrial fibrosis and the development of POAF after cardiac surgery. A systematic literature search was conducted in MEDLINE, Embase, and Google Scholar (2000 to March 2025) to identify studies that conducted comparative analysis of atrial fibrosis levels between those who did and did not develop POAF, using histological assessment methods. Extracted data, included study characteristics, histopathological staining methods and analysis findings, fibrosis quantification methods, and overall POAF incidence. Thirteen studies met the inclusion criteria, resulting in a total of 1222 patients, primarily undergoing coronary artery bypass surgery. The incidence of POAF ranged from 14%-42.4% (median 31.6%). In more than half of the studies (7/13), patients who developed POAF demonstrated statistically significant higher degrees of atrial fibrosis compared to those that remained in sinus rhythm postoperatively (four exhibited p < 0.001). Of the eight studies that conducted multivariate analyses, three identified atrial fibrosis as an independent POAF predictor. High heterogeneity precluded pooling of results into a meta-analysis. The current evidence examining the link between pre-existing atrial fibrosis and the development of POAF is restricted by methodological heterogeneity and inconsistent findings. Further efforts to standardize fibrosis quantification methods and POAF definitions are warranted before histopathological assessments can reliably inform POAF risk before cardiac surgery.

Pharmacological and electrical cardioversion of atrial fibrillation (AF) is associated with markedly increased (>10-fold) risk of thromboembolic events clustering within 7 days following sinus rhythm restoration. Current evidence indicates that post-cardioversion thrombus formation from atrial stunning, rather than preexisting thrombus, causes most thromboembolic complications. Risk factors include traditional CHA2DS2-VASc components (particularly heart failure), AF duration ≥12 h, mitral valve stenosis, cardiac amyloidosis and hypertrophic cardiomyopathy. While placebo-controlled randomized trials are lacking, there is overwhelming observational evidence that oral anticoagulation (OAC) reduces post-cardioversion thromboembolism by 60-80 % to a residual risk of approximately 0.5 %. This benefit seems independent of CHA2DS2-VASc and AF duration (including <48 h). Current guidelines recommend OAC for ≥3 weeks before and ≥4 weeks after cardioversion, or to rule out intracardiac thrombus by imaging, with OAC immediately before cardioversion and for ≥4 weeks. The safety of this strategy was validated in large prospective trials. However, alternative durations of pre-/post-cardioversion OAC have never been tested in randomized trials. The optimal duration of pre-cardioversion OAC remains unclear. Shorter pre-cardioversion delay is associated with increased success of cardioversion, reduced AF recurrence, reduced severity and duration of atrial stunning, and possibly reduced thromboembolic complications. Likewise, antiarrhythmic drug (AAD) pre-treatment improves cardioversion outcomes but is sometimes withheld by fear of early sinus rhythm restoration and associated thromboembolic risk. Randomized data from the ACUTE trial have shown that early AAD introduction was safe. Given the short-lived but dramatic increase in thromboembolic risk post-cardioversion, intensifying OAC immediately before cardioversion might further reduce risk, as suggested by observational studies.

Suicide left ventricle (SLV) is a rare but potentially catastrophic complication of surgical or transcatheter aortic valve replacement, characterized by acute hemodynamic collapse after relief of aortic stenosis. Abrupt reduction in left ventricular afterload unmasks dynamic intracavitary obstruction driven by adverse ventricular geometry, hypercontractility, and impaired filling, resulting in a low-cardiac output state. Although increasingly recognized, SLV remains a rare yet potentially fatal condition that continues to pose diagnostic and therapeutic challenges. This review synthesizes available evidence on the mechanistic basis of SLV presents an operational framework for recognition, highlighting key clinical and echocardiographic features associated with susceptibility to this complication. We discuss a practical, physiology-guided management approach, including pharmacologic modulation, pacing strategies, septal reduction approaches, and selective use of mechanical circulatory support. Improved awareness and coordinated multidisciplinary care may help mitigate morbidity and optimize outcomes for this severe condition.