Background: Evidence regarding the effects of twisting hamstring tendons on graft properties in anterior cruciate ligament (ACL) reconstruction remains controversial. The objective of this study was to evaluate the influence of a 180° twist on the tensile properties of human hamstring tendon grafts (HTGs). Methods: Fourteen human cadavers were included, and hamstring tendons (semitendinosus [ST] and gracilis [GR]) were harvested bilaterally. Matched pairs of tendons were allocated to the ST and GR groups and further subdivided into control (ST-0, GR-0) and experimental (ST-180, GR-180) subgroups. Standard tripled single-tendon grafts were prepared in the control groups, while grafts in the experimental groups were twisted by 180°. All grafts were preconditioned and tested using a universal testing machine (Shimadzu AGS-X, Shimadzu Corporation, Japan) to determine tensile strength, stiffness, tensile modulus, and energy absorption capacity. Results: In the semitendinosus group, the maximum force was 648.72 (±287.71) N for ST-0 and 853.11 (±189.14) N for ST-180, with energy absorption capacities of 9.21 (±4.47) J and 13.48 (±4.95) J, respectively. Although the mean values of the investigated parameters were consistently higher in the ST-180 group, these differences did not reach statistical significance. In the gracilis group, no statistically significant differences were observed between the GR-0 and GR-180 subgroups for any parameter. Conclusions: Twisting hamstring tendons by 180° during graft preparation results in limited alterations of biomechanical properties, without statistically significant improvements. These findings call into question the clinical relevance of this technique in enhancing graft material properties for ACL reconstruction.

Ischemic heart disease is the main cause of death worldwide. Classic cardiac biomarkers, such as troponin, which are released due to myocyte necrosis, are widely used for diagnosis, but they provide limited information about the initial underlying cellular processes involved in myocardial infarction. Autophagy is now considered fundamental in the pathophysiology of cardiac ischemia and related reperfusion injury. This systematic review aims to identify and highlight candidate autophagy-related biomarkers in cardiac ischemia and infarction with potential benefits for early diagnosis, prognosis, and therapy. A comprehensive literature search was conducted up to 1 June 2025. We included studies that examined biomarkers involved in the autophagy process in cardiac ischemia/infarction, which involved humans and animal models. A total of 14 eligible articles were reviewed. Thirteen autophagy-related biomarkers were identified, including LC3-II/I, Beclin-1, ATG5, ATG7, p62, WIPI1, FGF21, CHRF, Rubicon, IL-1β, IL-18, and adiponectin. These biomarkers have a dynamic pattern, and they exhibited time-dependent changes during the different stages of myocardial infarction. Autophagy biomarkers present a promising understanding of the molecular mechanism of early myocardial ischemia and infarction. Integration of autophagy biomarkers with the classic markers should improve risk stratification, therapeutic decision-making, and prognosis in patients with ischemic heart disease.

Objectives: Sudden cardiac death (SCD) is a leading cause of mortality, accounting for approximately 50% of all cardiovascular deaths and 20% of all-natural deaths in Western countries. In individuals over 50 years of age, coronary artery disease (CAD) is responsible for more than 80% of cases, whereas in younger subjects SCD is more frequently associated with non-ischemic myocardial diseases, including hypertrophic cardiomyopathy (HCM), arrhythmogenic cardiomyopathy (ACM), dilated cardiomyopathy (DCM), and myocarditis. Additional causes in young adults include coronary artery anomalies and primary arrhythmic disorders related to channelopathies. This study evaluated the diagnostic performance of post-mortem cardiac magnetic resonance imaging (PM-CMR) in identifying morphological substrates underlying SCD in formalin-fixed explanted hearts, with particular attention to the concordance between PM-CMR findings and autopsy results in cases of sudden coronary death. Material and Methods: We retrospectively reviewed 110 PM-CMR examinations from the Regional Register of Sudden Cardiac Death of Friuli-Venezia Giulia, of which 101 were included in the final analysis. Results: PM-CMR detected pathological findings in 60 hearts (59%), including acute ischemic lesions in 39 cases and other conditions, such as hypertrophic cardiomyopathy, chronic fibrotic ischemic changes, and adipose metaplasia in 21 cases. A good agreement between PM-CMR and autopsy findings was observed (Cohen’s kappa = 0.8). Conclusions: Overall, PM-CMR proved effective in identifying relevant morphological and signal alterations, supporting conventional autopsy. Despite some limitations, particularly in hyperacute ischemic lesions, PM-CMR appears to play a promising role in the diagnostic work-up of SCD and in supporting family screening programs for primary prevention.

Sudden cardiac death (SCD) is a devastating event not only for determining the cause of death but also for the health of surviving relatives, as autopsy fi