To correlate extracellular volume (ECV) measurement at diagnosis with sudden cardiac death in patients with AL amyloidosis from South Asia. This ambispective study included 188 AL amyloidosis patients from January 2000 to October 2024 at Amrita Institute of Medical Sciences, Kochi. Patients had serum free light chain restriction (FLC-diff ≥ 18 mg/dL) and biopsy-proven amyloidosis and/or cardiac amyloidosis phenotype. ECV was calculated from T1 mapping in cardiac MRI. Normal ECV was defined as < 25%.Of 188 patients (median age 64.5 years, male: female 2:1), 43 underwent cardiac MRI with 22 having evaluable ECV. Five patients had normal ECV (< 25%) and 17 had abnormal ECV (≥ 25%). Patients with abnormal ECV showed significantly higher baseline lambda light chains (558 vs. 46 mg/dL) and NT-proBNP (5587 vs. 1254 pg/mL). All 10 deaths occurred in the abnormal ECV group versus none in the normal ECV group (p < 0.05). ECV values were significantly higher in patients with sudden cardiac death (p = 0.03). Abnormal ECV demonstrated perfect sensitivity (100%) but lower specificity (41.67%) for predicting mortality. Although limited by its sample size, ECV mapping can be a useful tool predicting survival in AL amyloidosis patients, with abnormal ECV predicting sudden cardiac death in this South Asian cohort.

Systemic sclerosis (SSc) is a rare systemic disease characterised by progressive fibrosis, vasculopathy, and immune dysregulation, resulting in multiorgan damage. Independently of pulmonary arterial hypertension, cardiac involvement, encompassing myocardial fibrosis, coronary microvascular dysfunction, arrhythmias, conduction disorders, pericardial and valvular disease, and heart failure, represents a frequently underestimated cause of morbidity and mortality. Clinically manifest cardiac disease is observed in 15 to 35% of patients, while subclinical dysfunction is detectable in approximately 70% when advanced screening tools are employed. The annual incidence of sudden cardiac death is estimated at between 1.0% and 3.3%, exceeding the general-population risk by more than tenfold. The pathophysiological framework rests on coronary microvascular dysfunction driven by endothelial injury, ischaemia-reperfusion cycles, and TGF-β-mediated replacement fibrosis, potentiated by autonomic nervous system imbalance and activation of the renin-angiotensin-aldosterone system. Electrocardiographic abnormalities, detectable in 25 to 85% of patients, are independent predictors of mortality, while diastolic dysfunction, present in 18 to 62% of cases, constitutes a robust prognostic marker. Cardiac magnetic resonance imaging has transformed subclinical detection, revealing late gadolinium enhancement fibrosis in the majority of screened patients without a prior cardiovascular diagnosis. Management requires a multidisciplinary approach, integrating SSc-specific adaptation of guideline-directed heart failure therapies, immunosuppression targeting inflammatory and fibrotic pathways, arrhythmia management with implantable devices, and EULAR-recommended cardiovascular risk reduction. This narrative review synthesises current evidence on the epidemiology, pathogenesis, diagnostic evaluation, and therapeutic strategies of cardiac involvement in SSc, highlighting the need for early, systematic, risk-stratified screening and the establishment of dedicated multidisciplinary cardiac teams.

Cardiac fibrosis is one of the main causes of mortality from cardiovascular disorders and may result in heart failure, irregular heartbeats, and sudden cardiac death. Multiple complex mechanisms involved in cardiac fibrosis are beyond the scope of current treatments. Inflammasomes are significant inflammatory modulators. Inflammasome impairment may exacerbate heart failure. The most specific inflammasome associated with inflammatory and cardiovascular disorders is Nucleotide-binding oligomerisation domain leucine-rich repeat and pyrin domain-containing protein 3 (NLRP3). Pathogen-associated molecular patterns and damage-associated patterns are recognised by the intracellular sensor NLRP3, which causes the NLRP3 inflammasome to assemble and become active. Thus, a greater awareness of the pathological function of the inflammasome in heart fibrosis may lead to new approaches to the disease's early detection and management. Understanding the inflammasome's regulatory functions in fibrosis of the heart in its entire form has been made possible by recent research on the subject. The most recent studies on the roles of the NLRP3 inflammasome in different cardiac conditions are included in this review. According to recent research, the NLRP3 inflammasome promotes a number of inflammatory reactions and is linked to myofibroblast development, mitochondrial modulation, and pyroptosis in cardiac fibrosis. These discoveries provide light on the critical function of the NLRP3 inflammasome in the aetiology of heart fibrosis, which may help establish novel paths for therapy and prevention.

Sudden unexpected death in epilepsy (SUDEP) and long QT syndrome (LQTS) are severe disorders causing sudden death in the neurological and cardiovascular systems, respectively, and have traditionally been viewed as distinct clinical entities. However, their overlapping clinical phenotypes and partially shared genetic backgrounds suggest that, in a subset of patients, overlapping molecular mechanisms may contribute to neurocardiac vulnerability. This review systematically elucidates and bridges the potential mechanistic intersections between these two conditions at the level of ion channel dysfunction. It focuses on key shared ion channel genes, such as KCNQ1, KCNH2, and SCN5A, and analyzes how their variants may simultaneously induce neuronal hyperexcitability and cardiomyocyte repolarization abnormalities, thereby suggesting a potential risk-modifying framework of "cardio-cerebral ion channelopathies" in specific clinical scenarios. Additionally, this article discusses the significant implications of this shared mechanism for clinical practice, particularly in evaluating the cardiac safety of anti-seizure medications (ASMs), integrating genetic risk stratification, and developing future therapeutic strategies. By synthesizing and integrating existing evidence, this review aims to provide a broader pathophysiological perspective on the intrinsic links between SUDEP and LQTS, offering novel insights for interdisciplinary precision medicine.

Reproductive failure is the major problem in modern pig production, significantly affecting economic productivity. This study investigated factors associated with reproductive failure in the hyper prolific pig farms, focusing on abortion, mummification, stillbirth and sudden increased sow death. Seven individual sows with reproductive failure clinical signs were surveyed to evaluate the infection rate with related pathogens. Results showed the highest frequency of Mycopl asma suis infections with reproductive problems along with blood samples being 100% positive, fetal mummification rate of 33.33% and stillbirth rate of 25.00%. Additionally, 28.57% of the total blood samples exhibited porcine circovirus type 3 infection, while other pathogens were not detected. The percentage of concurrent infections with M. suis and porcine circovirus type 3 in reproductive sow was 28.57%. The partial 16S rRNA Porcine Haemoplasma is a trivial name for haemotropic Mycoplasma spp., which can attach to the surface of red blood cells leading to deformity and anaemia in a wide range of mammalian animals including pigs. H aemoplasma sequences in this study was absolutely clustered into Haemominutum group. This study demonstrated the first case of acute reproductive disorder due to M. suis reported in imported hyper prolific sows.

As a part of the 21st INTERPOL International Forensic Science Managers Symposium, this work explores the latest scientific developments, methodologies, and trends in forensic biology and forensic DNA analysis of biological evidence during the years 2023 to 2025 and builds upon previous INTERPOL DNA reviews. Almost 2000 references covering the three-year time range of this review were located via various online searches including use of Scopus, Web of Science, and PubMed. The scientific articles, which originated from more than 300 different journals, were curated in a Zotero reference manager database (see Supplemental File 1) and sorted into 15 topics and 116 sub-topics (see Supplemental File 2) under sections focused on advances in current practices (Section 3) and emerging technologies and research studies (Section 4). This triennial review describes 24 books or major reports, 20 special issues of journals on aspects of forensic DNA, 292 articles from 2 International Society for Forensic Genetics (ISFG) conference proceedings, and 70 guidance documents from 17 different organizations to assist in quality DNA testing. Publications were evaluated and sorted into 10 topics around advances in current practices and 5 topics related to emerging technologies and research studies. These topics, which are further sub-divided in a compiled list (see Supplemental File 2) included rapid DNA analysis; law enforcement DNA databases and ethics; forensic investigative genetic genealogy (FIGG); forensic biology and body fluid identification; DNA processing; DNA typing with short tandem repeat (STR) markers; DNA interpretation at the source or sub-source level of the hierarchy of propositions along with mixture interpretation using probabilistic genotyping software (PGS); DNA interpretation at the activity level along with aspects of DNA transfer, persistence, prevalence, and recovery (TPPR); statistics and population genetic data; human identification and kinship analysis; next-generation sequencing (NGS) and technology developments; forensic DNA phenotyping (FDP) and methylation; lineage markers (Y-chromosome, mitochondrial DNA, X-chromosome analyses); new markers and approaches (microhaplotypes, insertion/deletion markers, proteomics, microbiome, single-cell analysis, using environmental DNA, and biomarkers for diagnosis of sudden death, molecular autopsy, or post-mortem interval); and non-human DNA testing and wildlife forensics. Artificial intelligence (AI) tools for summarizing references were explored and utilized in performing this review of over 1900 publications.

Cardiac sarcoidosis is a rare but life-threatening manifestation of systemic sarcoidosis, frequently presenting with ventricular arrhythmias, heart block, or sudden cardiac death. It remains underdiagnosed owing to its diverse clinical presentation and rarity and the limitations of conventional diagnostic modalities. We report a case of a 42-year-old man with no prior cardiac history who presented with a three-day history of recurrent palpitations and three to four syncopal episodes. Electrocardiography during syncope demonstrated self-terminating ventricular tachycardia (VT), with one episode lasting five hours, requiring pharmacological cardioversion. Coronary angiography revealed entirely normal coronary arteries. Cardiac magnetic resonance imaging (CMR) with late gadolinium enhancement (LGE) identified a non-ischemic, epicardial-to-mid-myocardial enhancement pattern involving the interventricular septum, inferior wall, and lateral wall, accompanied by mediastinal and hilar lymphadenopathy. Two-dimensional echocardiography revealed severe left ventricular (LV) dysfunction with an ejection fraction of 15%. Serum angiotensin-converting enzyme levels were markedly elevated at 90 U/L (reference: 12-66 U/L). The patient was commenced on systemic corticosteroids (prednisolone), antiarrhythmic therapy (amiodarone), anticoagulation, and guideline-directed heart failure therapy. This case underscores the diagnostic utility of CMR-LGE in identifying non-ischemic infiltrative cardiomyopathy and highlights the importance of considering cardiac sarcoidosis in patients presenting with unexplained VT and severely reduced LV function. Early immunosuppressive therapy and multidisciplinary management are pivotal in improving clinical outcomes.

An anomalous left circumflex artery (LCx) arising from the right coronary sinus typically follows a retroaortic course and is considered benign regarding sudden cardiac death. However, it remains susceptible to atherosclerosis, where its unique vessel geometry may significantly influence percutaneous coronary intervention (PCI) strategies.

Sudden death in horses, often attributed to lethal arrhythmias, poses significant welfare and economic risks, yet its prediction remains challenging. This study aimed to characterize ventricular micro-potentials using signal-averaged electrocardiography (SAECG) and evaluate their potential for assessing sudden death risk. High-resolution orthogonal X-, Y-, and Z-lead ECGs were recorded in 24 healthy Thoroughbreds (aged 2-31 years), one horse with bupivacaine-induced myocardial injury, and three horses with persistent pathological murmurs. SAECG parameters, including filtered QRS duration (fQRS), LAS40, RMS40, and RMS50, were analyzed from the vector magnitude waveform. In healthy horses, fQRS showed a significant positive correlation with age, with older horses exhibiting a significantly longer fQRS and LAS40 and lower RMS40 and RMS50 compared with younger horses, likely reflecting age-related myocardial fibrosis. The experimental myocardial injury model, characterized by histopathologically confirmed necrosis, resulted in a prolonged fQRS and LAS40 and decreased RMS40 and RMS50, consistent with the development of ventricular late potentials. Conversely, horses with persistent cardiac murmurs showed SAECG parameters within the range of healthy horses, indicating that valvular abnormalities alone do not significantly affect intraventricular conduction. These findings demonstrate that SAECG can effectively detect ventricular micro-potentials and reflect structural myocardial changes such as necrosis and fibrosis in horses. Consequently, SAECG analysis appears to be a promising non-invasive tool for screening the risk of lethal arrhythmias and sudden death in equine clinical practice, especially when combined with other diagnostic modalities.