Atrial cardiomyopathy (ACM) provides a useful framework for understanding structural, architectural, contractile, and electrophysiological disease of the atria. ACM and atrial fibrillation (AF) are closely linked but are not interchangeable: ACM favors arrhythmogenesis, whereas sustained AF can accelerate atrial injury. This review considers ACM from the pathologist's perspective, encompassing primary atrial disease and secondary remodeling associated with valvular disease and classical cardiomyopathies. The histologic spectrum includes cardiomyocyte hypertrophy and myocytolysis, interstitial and replacement fibrosis, endocardial fibroelastosis, adipose and inflammatory infiltration, vascular injury, and amyloid deposition. Structural remodeling is regionally heterogeneous, and appendage specimens may underrepresent abnormalities elsewhere in the atrium. Histologic interpretation requires attention to intrinsic regional architecture, associated lesions, previous interventions, and methods of quantification. At the molecular and cellular level, genetic susceptibility and acquired stressors converge on cardiomyocyte dysfunction, inflammation, fibroblast activation, and extracellular-matrix remodeling. Correlating these tissue changes with mapping, imaging, biomarkers, and clinical outcomes will be necessary to validate noninvasive phenotypes and identify clinically meaningful disease subsets. At present, ACM should prompt etiologic investigation and risk assessment but does not by itself constitute an indication for specific therapy.

Aortic aneurysms have traditionally been studied as a single pathological entity, with emphasis on valve morphology. While histopathological differences between bicuspid (BAV) and tricuspid (TAV) aortopathy are well documented, less is known about how these mechanisms interact with aneurysm location within the ascending aorta. This gap complicates risk assessment and surgical planning beyond diameter-based criteria. We aimed to evaluate histopathological features of ascending aortic aneurysms across three topographical subgroups-root, tubular, and combined involvement-and assess modification by valve cuspidity. Using systematic criteria from the Society for Cardiovascular Pathology and the Association for European Cardiovascular Pathology consensus statement, the analysis focused on medial degeneration, adventitial alterations and atherosclerosis in patients undergoing ascending aortic surgery at a Finnish tertiary care center. The cohort comprised 296 patients with aneurysms located in the sinus of Valsalva (n = 122), tubular part (n = 130), and both regions (n = 44). Medial degeneration was present in all samples and predominantly moderate, with comparable median severity score of 2 (range 1-3, P = 0.829) across groups. In the overall cohort, no statistically significant differences were observed between topographical groups. Among TAV patients, tubular aneurysms demonstrated significantly higher histopathological scores for medial degeneration, elastic fiber fragmentation and loss, elastic fiber disorganisation, smooth muscle cell disorganization and nuclei loss, laminar medial collapse, medial fibrosis, adventitial fibrosis and atherosclerosis (all P < 0.05). In BAV patients, no statistical differences were found. Tubular aneurysms are characterized by more extensive wall remodeling and adventitial changes compared to root aneurysms, particularly in TAV patients. Notably, female sex emerged as a strong independent predictor of advanced medial and adventitial pathology. These findings underscore the importance of considering anatomical location, valve morphology, and sex in risk stratification and may inform surgical decision-making beyond diameter-based criteria.

A bifid cardiac apex is a rare congenital anomaly resulting from the nonunion of the right and left ventricles at the cardiac apex, producing two distinct apical projections with a cleft between them. This article illustrates two cases with a bifid apex: the first with a deep cleft and the other with an apparently superficial indentation. Dissection of the heart confirmed separation of the myocardium of both ventricles at the apex. Both cases were free of other congenital anomalies, and the cause of death was unrelated to the bifid apex. We also present a case of a prominent apical notch that might simulate a bifid apex; however, dissection demonstrated myocardial continuity. In addition, we summarized ten autopsy cases of bifid apices reported in the literature. Five cases had other concomitant fatal congenital cardiac anomalies. In four cases, a bifid apex was the sole congenital anomaly, and the patients died from poisoning, sickle cell disease, road traffic accidents, and drowning. In one case, the death was attributed to myocarditis, which was also unrelated to the bifid apex. The incidental discovery of a bifid apex at autopsy indicates its benign nature. Therefore, forensic medicine professionals must not attribute death to a bifid apex and must determine the actual cause of death. Most importantly, the presence of a bifid apex mandates a search for potential associated congenital anomalies through comprehensive cardiac dissection.

Data suggests that COVID-19 is less frequent in children, with a milder course. However, multisystem inflammatory syndrome in children has been reported to occur after COVID-19 and can cause severe cardiac manifestations, including coronary dilation and aneurysms. We report on the first histologically proven arteritis with coronary dilatation and thrombosis following Multisystem Inflammatory Syndrome induced by COVID-19 in a 21-month-old male infant.