Myocardial and vascular injury secondary to SARS-CoV-2 infection and vaccination has emerged as a clinically relevant phenomenon, with distinct but overlapping mechanisms. Myocardial injury in COVID-19 results from a complex interplay between direct viral effects and immune-mediated inflammation, supported by histopathological studies revealing macrophage-rich infiltrates, microthrombosis, and supporting fibrosis in isolated areas. In contrast, vaccine-associated myocarditis—reported predominantly following mRNA vaccines—has a self-limiting clinical course, with mechanisms likely involving molecular mimicry, aberrant immune activation, or hypersensitivity reactions, although these pathways require further validation. Although mRNA vaccines have been associated with a small increase in myocarditis, particularly in young men, the risk is significantly lower than that associated with COVID-19 infection, and the cardiovascular benefits of vaccination far outweigh these rare adverse events in most populations. After the end of the pandemic, the number of patients with severe forms of COVID-19 has decreased significantly, but we consider that cardiac involvement remains an important issue for the acute and long-term prognosis of patients with SARS-CoV-2 infection. Our paper synthesizes the latest epidemiological and mechanistic evidence on the link between COVID-19, vaccination, and myocardial and/or vascular injuries, highlighting the clinical implications and providing practical recommendations for management, as well as future perspectives on risk assessment, targeted immunotherapy, advanced diagnostic tools, and long-term monitoring.

Cardiovascular involvement in SARS-CoV-2 infection and following vaccination has emerged as a clinically relevant phenomenon with distinct yet overlapping mechanisms. Myocardial injury in COVID-19 results from a complex interplay between direct viral ef-fects, immune-mediated inflammation, endothelial dysfunction, oxidative stress, and, in rare occasions, cytokine storm. The virus primarily binds to ACE2 receptors, which are highly expressed in endothelial cells and pericytes, leading to microvascular damage and a systemic prothrombotic state. Additional viral entry pathways, including CD147, Neu-ropilin-1, and CD26, further contribute to vascular and myocardial injury, which is a ra-ther immune-driven process rather than a direct cytopathic one. Histopathological studies that reveal macrophage-rich infiltrates, microthrombosis, and patchy fibrosis support the immune-driven process theory. In contrast, vaccine-associated myocarditis – predomi-nantly reported following mRNA vaccines – presents a self-limiting clinical course, with mechanisms probably involving molecular mimicry, aberrant immune activation, or hy-persensitivity reactions. Despite an increased incidence in young males after the second dose, the overall risk remains low compared to infection-related myocarditis. Under-standing the pathophysiological interplay between infection- and vaccine-related cardiac involvement is essential for accurate risk assessment, improved diagnostic strategies, and targeted therapeutic approaches. Future research should focus on elucidating immune pathways, refining biomarkers, and developing personalized management strategies in order to mitigate cardiovascular sequelae of both COVID-19 and vaccination.

Deep vein thrombosis (DVT) is one of the most serious cardiovascular disease in all age groups and implies an elevated risk for death, via pulmonary thromboembolism. Classically described as Virchow's triad, the main three factors implied are venous stasis, vascular wall lesion, and an increased coagulation vs. fibrinolytic mechanism. These pathophysiological conditions are fulfilled when various predisposing factors meet the environmental risk factors. The clinical judgment points that if, in certain situations, when the likelihood of an inherited propensity for thrombosis is very high, the search for a specific trait has to be done, and sometimes beyond the current guideline recommendations, because it could be related to future recurrences and could identify potential other relatives at increased risk for this serious pathology. In this article, we discuss a case involving a 45-year-old man who was admitted for sudden-onset dyspnea. The clinical presentation, along with a family history of thrombophilia, raised initial suspicion of pulmonary embolism, which was confirmed by a chest computed tomography (CT) scan with contrast enhancement. Both the patient and his family members underwent extensive tests for hypercoagulable disorders, which returned positive results. We review the current evidence and reassess the importance of thrombophilia testing in similar patients, highlighting the role of EPCR in venous thromboembolic disease.

Myocardial infarction remains a leading cause of heart failure because current reperfusion therapies cannot prevent adverse ventricular remodeling or restore lost cardiomyocytes. Regenerative strategies based on stem cells and extracellular vesicles (EVs) have emerged as promising approaches; however, their clinical efficacy is limited by poor retention, rapid clearance, and the hostile post-infarction microenvironment. This narrative review critically examines the role of biomaterial-assisted delivery systems in enhancing stem cell and EV-based cardiac regeneration, with particular emphasis on the distinction between biomimetic and bioactive biomaterials, mechanisms of action, preclinical and clinical evidence, translational barriers, and emerging regenerative technologies. Current evidence demonstrates that injectable hydrogels, extracellular matrix-derived scaffolds, cardiac patches, conductive biomaterials, and multifunctional delivery platforms improve therapeutic retention, prolong paracrine signaling, and actively modulate inflammation, angiogenesis, fibrosis, and extracellular matrix remodeling, resulting in superior functional recovery compared with conventional delivery approaches in preclinical models. Nevertheless, robust clinical evidence remains limited because few biomaterial-assisted strategies have advanced beyond early-phase studies. Future progress will depend on integrating smart biomaterials with engineered extracellular vesicles, gene editing, and personalized regenerative approaches, together with standardized manufacturing, harmonized regulatory frameworks, and adequately powered clinical trials.