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.

We report the autopsy case of a female 10-month-old infant who presented with cardiocirculatory arrest due to hypoxia secondary to compressive asphyxia due parental co-sleeping on the sofa. Despite advanced life support, vasoactive therapy, and rescue administration of methylene blue for refractory vasoplegic shock, no hemodynamic improvement was achieved, and death occurred following recurrent cardiac arrest. Autopsy revealed a bluish-green discoloration of the myocardium with no structural cardiac abnormalities. To our knowledge, this is the first pediatric case describing the autoptic findings following the use of methylene blue.

Benign stromal proliferations of pigmented melanocytes or blue nevi have been documented in several extracutaneous sites, such as uterine cervix, prostate, and lymph nodes. We report a 54-year-old male with melanocytic pigmentation of the adventitia of the ascending aorta. This would appear to be the first documentation of stromal melanocytosis (or "blue nevus") of the aorta.

A 26-year-old woman was referred for the assessment of a symptomatic pulmonary valve lesion clinically thought to represent a papillary fibroelastoma. After surgery, a lipomatous hamartoma of pulmonary valve was diagnosed. Microarray analysis was compatible with a clonal neoplastic proliferation, similar to that seen in a classical lipoma. Benign primary adipocytic tumors of the heart, such as lipomatous hamartomas of a valve, lipomatous hypertrophy of the atrial septum and lipoma, are distinct and very rare entities, with incomplete understanding of their pathogenesis. The results of this case suggest that the so called lipomatous hamartoma of the valves may actually be better classified as a neoplasm.

Cardiac transthyretin amyloidosis (ATTR-CA) is caused by myocardial deposition of misfolded transthyretin, leading to progressive heart failure. Disease pathology, however, extends beyond passive amyloid deposition and also involves active processes such as extracellular matrix (ECM) remodeling and immune activation. Mass spectrometry (MS) is the gold standard for amyloid typing in diagnostics. Here, we applied quantitative MS-driven proteomics on formalin-fixed paraffin-embedded whole cardiac tissue sections from six ATTR-CA cases, ten unaffected controls and four AL-CA controls to investigate protein expression changes. In addition to transthyretin, over 500 proteins were upregulated in ATTR-CA biopsies, including complement and coagulation factors as well as extracellular matrix (ECM) remodeling proteins. Among these, members of the A Disintegrin and Metalloproteinase with Thrombospondin Motifs (ADAMTS) family, metalloproteinases (MMPs), and Tissue Inhibitor of Metalloproteinase-3 (TIMP3) showed significant upregulation. These proteins are key regulators of ECM turnover and structural integrity. Immunohistochemistry confirmed ADAMTS4 enrichment in amyloid deposits, while TIMP3 showed strong expression in cardiomyocytes and weaker staining within amyloid deposits. Together, these findings indicate that ECM remodeling, alongside complement and coagulation activation, represents a reproducible feature of cardiac ATTR amyloidosis. Whole-tissue proteomics provides biological insights that extend beyond amyloid typing, with potential implications for biomarker discovery and therapeutic targeting in ATTR-CA.