Background: In sudden cardiac deaths (SCD), visceral adipose tissue has begun to manifest interest as a standalone cardiovascular risk factor. Studies have shown that epicardial adipose tissue can be seen as a viable marker of coronary atherosclerosis. This study aimed to evaluate, from a forensic perspective, the correlation between body mass index (BMI), heart weight, coronary and valvular atherosclerosis, left ventricular morphology, and the thickness of the epicardial adipose tissue (EAT) in sudden cardiac deaths, establishing an increased thickness of EAT as a novel risk factor. Methods: This is a retrospective case–control descriptive study that included 80 deaths that were autopsied, 40 sudden cardiac deaths, and 40 control cases who hanged themselves and had unknown pathologies prior to their death. In all the autopsies performed, the thickness of the epicardial adipose tissue was measured in two regions of the left coronary artery, and the left ventricular morphology, macro/microscopically quantified coronary and valvular atherosclerosis, and weight of the heart were evaluated. Results: This study revealed a higher age in the SCD group (58.82 ± 9.67 vs. 53.4 ± 13.00; p = 0.03), as well as a higher incidence in females (p = 0.03). In terms of heart and coronary artery characteristics, there were higher values of BMI (p = 0.0009), heart weight (p < 0.0001), EAT of the left circumflex artery (LCx) (p < 0.0001), and EAT of the left anterior descending artery (LAD) (p < 0.0001). In the multivariate analysis, a high baseline value of BMI (OR: 4.05; p = 0.004), heart weight (OR: 5.47; p < 0.001), EAT LCx (OR: 23.72; p < 0.001), and EAT LAD (OR: 21.07; p < 0.001) were strong independent predictors of SCD. Moreover, age over 55 years (OR: 2.53; p = 0.045), type Vb plaque (OR: 17.19; p < 0.001), mild valvular atherosclerosis (OR: 4.88; p = 0.002), and moderate left ventricle dilatation (OR: 16.71; p = 0.008) all act as predictors of SCD. Conclusions: The data of this research revealed that higher baseline values of BMI, heart weight, EAT LCx, and EAT LAD highly predict SCD. Furthermore, age above 55 years, type Vb plaque, mild valvular atherosclerosis, and left ventricle dilatation were all risk factors for SCD.

Acromegaly is mainly due to the somatotroph pituitary neuroendocrine tumors (PitNET)s. These have been subtyped into densely granulated (DG) and sparsely granulated (SG) tumors, which differ in clinical, histological and biological characteristics and in response to somatostatin analogs (SA)s. The variable remission rate after surgical resection, as first line treatment, has increased interest in identifying pathological markers to better predict the response to medical treatment. Several techniques have shown somatotroph tumors to express somatostatin receptors (SSTR)s, and mainly SSTR2 and SSTR5. The molecular methods appear to give contradictory results, are expansive and cannot be routinely performed. Immunohistochemistry, while being the most powerful technique, requires optimal fixation and the use of monoclonal antibodies against at least SSTR2 and SSTR5. Almost all somatotroph tumors express SSTR2 or SSTR5, and, in great majority, at a high level. More importantly, the type of SSTR, the level of expression, and the response to SA treatment appear well correlated. Indeed, a significantly higher expression of SSTR2 in DG compared to in SG tumors likely explains the better response of DG tumors to the normalization of growth hormone and insulin-like growth factor-1 under SA. However, a reproducible scoring and a cut-off from which the SA efficacy can be reliably predicted, remain to be found. In conclusion, the SSTR expression profile and morphological subtypes of the somatotroph tumor may help predict the response to medical treatment. Such pathological profiling could become a useful decision-making tool for clinicians in the context of a multidisciplinary approach, after surgery failure.

One of the hallmarks of Alzheimer’s disease (AD) is the deposition of amyloid-β (Aβ) within the extracellular spaces of the brain as plaques and along the blood vessels in the brain, a condition also known as cerebral amyloid angiopathy (CAA). Clusterin (CLU), or apolipoprotein J (APOJ), is a multifunctional glycoprotein that has a role in many physiological and neurological conditions, including AD. The apolipoprotein E (APOE) is a significant genetic factor in AD, and while the primary physiological role of APOE in the brain and peripheral tissues is to regulate lipid transport, it also participates in various other biological processes, having three basic human forms: APOE2, APOE3, and APOE4. Notably, the APOE4 allele substantially increases the risk of developing late-onset AD. The main purpose of this review is to examine the roles of CLU and APOE in AD pathogenesis in order to acquire a better understanding of AD pathogenesis from which to develop targeted therapeutic approaches.

Resistance to first-generation somatostatin receptor ligand (fgSRL) treatment in acromegaly is common, making the identification of biomarkers that predict fgSRL response a desired goal. We conducted a retrospective analysis on 21 patients with acromegaly who underwent surgery and subsequent pharmacological treatment. Through immunohistochemistry (IHC), we assessed the expression of the somatostatin receptor subtypes SSTR2 and SSTR5, E-Cadherin, and cytokeratin granulation pattern (sparsely or densely). Patients were divided into responders and non-responders based on their biochemical response to fgSRL and/or the newer agent, Pasireotide, or the GH-blocker, Pegvisomant. Patients resistant to fgSRL (n = 12) exhibited lower SSTR2 and E-Cadherin expressions. Sparsely granulated tumors were more frequent in the non-responder group. SSTR2 (p = 0.024, r = 0.49) and E-Cadherin (p = 0.009, r = 0.64) positively correlated with the Insulin-like Growth Factor 1 (IGF-1) decrease after fgSRL, while SSTR5 (p = 0.107, r = −0.37) showed a trend towards negative correlation. SSTR5 positivity seemed to be associated with Pasireotide response, albeit the number of treated patients was too low (n = 4). No IHC markers correlated with Pegvisomant response. Our findings suggest that densely granulated tumors, with positive SSTR2 and E-Cadherin seem to be associated with favorable fgSRL responses. The strongest predictive value of the studied markers was found for E-Cadherin, which seems to surpass even SSTR2.

Sudden cardiac death (SCD) is the leading cause of mortality globally (violent or non-violent), with few to no feasible remedies. The etiopathogenesis of SCD involves a complex and multilayered substrate in which dynamic factors interact with a preexistent cardiovascular pathology, which is often undiagnosed and untreated, leading to the rapid development of cardiac rhythm disorders and cardiac arrest. Cardiovascular disease is a rare but emerging factor in maternal mortality that can be justified by an upward trend in the mean age of pregnant individuals. Spontaneous coronary artery dissection (SCAD) is defined as a non-traumatic and non-iatrogenic separation of the coronary arterial wall by intramural hemorrhage with or without an intimal tear. The resulting intramural hematoma compresses the coronary arteries, reducing blood flow and causing myocardial ischemia. SCAD continues to be misdiagnosed, underdiagnosed, and managed as an atherosclerotic acute coronary syndrome, which may harm patients with SCAD. The latest research shows that individuals who have or have had coronavirus disease 2019 (COVID-19) may also present coagulation abnormalities, so infection with COVID-19 during pregnancy can increase this hypercoagulable condition, thus increasing the risk of SCAD and SCD. This present study reports two cases over 35 years, one being infected with SARS-COV2 one month before the event and the other being tested positive during admission, both asymptomatic, who were declared healthy on periodic clinical evaluations, with pregnancies over 35 weeks, with normal fetal development, which suddenly caused chest pain, dyspnea, and loss of consciousness, required emergency c-sections, and died suddenly after they were performed. In both cases, the cause of death was SCAD on the anterior-descending artery. In both cases, emergency percutaneous coronary intervention was performed. The second part of the study represents a literature overview of SCAD during COVID-19. In addition to pregnancy hormonal changes, other potential hormone-mediated SCAD triggers are still under discussion.

Background: Sudden cardiac death (SCD) is a significant global public health issue and the leading cause of death worldwide. Its etiopathogenesis is complex and multilayered, involving dynamic factors interacting with a preexistent cardiovascular pathology, frequently unknown, and resulting in cardiac rhythm disorders and cardiac arrest; Methods: This study conducted a retrospective descriptive analysis over a one-year period, identifying 321 autopsy cases of sudden deaths from the Institute of Legal Medicine in Mures County, Romania, in 2019. From the 321 sudden death cases, 189 autopsy reports were selected for analysis based on inclusion and exclusion; Results: The autopsies had a mean age of 61.16 years and included 140 males and 49 females. No significant differences were found between the silent myocardial infarction (SMI) and no-SMI groups regarding demographic data. The SMI group exhibited higher thickness of LV (left ventricle), IV (interventricular septum), EAT LCx (epicardial adipose tissue at left circumflex artery), EAT LAD (epicardial adipose tissue at left anterior descending artery), heart weight, and BMI (body mass index). The left coronary artery showed a higher incidence of type V plaques, while the right coronary artery showed higher incidences of type V and type VI plaque. The SMI group also exhibited a higher incidence of moderate and severe valvular atherosclerosis, severe left ventricle dilatation, and a lower incidence of mild left ventricle dilatation. In addition, the SMI group showed a higher presence of contraction band necrosis on histological examination. Multivariate analysis revealed that type V and type VI plaques for the right and left coronary arteries, moderate and severe valvular atherosclerosis, severe left ventricle dilatation, heart weight, EAT LCx, EAT LAD, LV thickness, IV thickness, BMI, and the presence of contraction band necrosis are all independent predictors of SMI; Conclusions: The findings suggest that SCD is a complex condition, and its etiopathogenesis involves dynamic factors interacting with pre-existing cardiovascular pathology. The risk factors of SCD are similar to those of ischemic heart disease. The findings of this study could guide clinicians in identifying patients at risk of SCD and implementing preventive measures.