COVID-19 Vaccine-Related Thrombosis: A Systematic Review and Exploratory Analysis.

Introduction: The World Health Organization declared the coronavirus disease 2019 (COVID-19) pandemic on March 11, 2020. Two vaccine types were developed using two different technologies: viral vectors and mRNA. Thrombosis is one of the most severe and atypical adverse effects of vaccines. This study aimed to analyze published cases of thrombosis after COVID-19 vaccinations to identify patients' features, potential pathophysiological mechanisms, timing of appearance of the adverse events, and other critical issues. Materials and Methods: We performed a systematic electronic search of scientific articles regarding COVID-19 vaccine-related thrombosis and its complications on the PubMed (MEDLINE) database and through manual searches. We selected 10 out of 50 articles from February 1 to May 5, 2021 and performed a descriptive analysis of the adverse events caused by the mRNA-based Pfizer and Moderna vaccines and the adenovirus-based AstraZeneca vaccine. Results: In the articles on the Pfizer and Moderna vaccines, the sample consisted of three male patients with age heterogeneity. The time from vaccination to admission was ≤3 days in all cases; all patients presented signs of petechiae/purpura at admission, with a low platelet count. In the studies on the AstraZeneca vaccine, the sample consisted of 58 individuals with a high age heterogeneity and a high female prevalence. Symptoms appeared around the ninth day, and headache was the most common symptom. The platelet count was below the lower limit of the normal range. All patients except one were positive for PF4 antibodies. The cerebral venous sinus was the most affected site. Death was the most prevalent outcome in all studies, except for one study in which most of the patients remained alive. Discussion: Vaccine-induced thrombotic thrombocytopenia (VITT) is an unknown nosological phenomenon secondary to inoculation with the COVID-19 vaccine. Several hypotheses have been formulated regarding its physiopathological mechanism. Recent studies have assumed a mechanism that is assimilable to heparin-induced thrombocytopenia, with protagonist antibodies against the PF4-polyanion complex. Viral DNA has a negative charge and can bind to PF4, causing VITT. New experimental studies have assumed that thrombosis is related to a soluble adenoviral protein spike variant, originating from splicing events, which cause important endothelial inflammatory events, and binding to endothelial cells expressing ACE2. Conclusion: Further studies are needed to better identify VITT's pathophysiological mechanisms and genetic, demographic, or clinical predisposition of high-risk patients, to investigate the correlation of VITT with the different vaccine types, and to test the significance of the findings.

Cardiovascular Implantable Electronic Device Infection and New Insights About Correlation Between Pro-inflammatory Markers and Heart Failure: A Systematic Literature Review and Meta-Analysis.

Introduction: Surgical approaches to treat patients with abnormal pro-inflammatory parameters remain controversial, and the debate on the correlation between hematological parameter alteration in cardiac implantable electronic device (CIED) infection and the increase in mortality continues. Methods: We performed a systematic review using the PubMed, Scopus, and Cochrane Library databases. Twenty-two articles from May 2007 to April 2020 were selected and divided according to the following topics: prevalence of microbes in patients with CIED infection; characteristics of patients with CIED infection; comparison between patients who underwent and did not undergo replantation after device extraction; and correlation between alteration of hematological parameters and poor prognosis analysis. Results: Epidemiological analysis confirmed high prevalence of male sex, staphylococcal infection, and coagulase-negative staphylococci (CoNS). The most common comorbidity was heart failure. Complete removal of CIED and antimicrobial therapy combination are the gold standard. CIED replacement was associated with higher survival. High preoperative white blood cell count and C-reactive protein levels increased the risk of right ventricular failure (RVF) development. Increased red blood cell distribution width (RDW) value or decreased platelet count was correlated with poor prognosis. No correlation was noted between preoperative leukocytosis and CIED infection. Discussion: A relevant correlation between leukocytosis and RVF was observed. Heart failure may be related to high RDW values and decreased platelet count. Data on the correlation between hematological parameter alteration and poor prognosis are missing in many studies because of delayed implantation in patients showing signs of infection.