Severe traumatic brain injury (sTBI) is a silent epidemic, causing approximately 300,000 intensive care unit (ICU) admissions annually, with a 30% mortality rate. Despite worldwide efforts to optimize the management of patients and improve outcomes, the level of evidence for the treatment of these patients remains low. The concomitant occurrence of thromboembolic events, particularly pulmonary embolism (PE), remains a challenge for intensivists due to the risks of anticoagulation to the injured brain. We performed a literature review on sTBI and concomitant PE to identify and report the most recent advances on this topic. We searched PubMed and Scopus for papers published in the last five years that included the terms “pulmonary embolism” and “traumatic brain injury” in their title or Exclusion criteria were papers referring to children, non-sTBI populations, and post-acute care. Our search revealed 75 papers, of which 38 are included in this review. The main topics covered include the prevalence of and risk factors for pulmonary embolism, the challenges of timely diagnosis in the ICU, the timing of pharmacological prophylaxis, and the treatment of diagnosed PE.

Background/Objectives: Mitochondria are the main organelles for ATP synthesis able to produce energy for several different cellular activities. Cardiac cells require high amounts of energy and, thus, they contain a high number of mitochondria. Consequently, mitochondrial dysfunction in these cells is a crucial factor for the development of cardiovascular diseases. Mitochondria constitute central regulators of cellular metabolism and energy production, producing approximately 90% of the cells’ energy needs in the form of ATP via oxidative phosphorylation. The mitochondria have their own circular, double-stranded DNA encoding 37 genes. Any mitochondrial DNA sequence anomaly may result in defective oxidative phosphorylation and lead to cardiac dysfunction. Methods: In this study, we investigated the potential association between mitochondrial DNA mutation and cardiovascular disease. Cardiac tissue and serum samples were collected from seven patients undergoing coronary artery bypass grafting. Total DNA was extracted from cardiac muscle tissue specimens and serum and each sample was subjected to polymerase chain reaction (PCR) to amplify the NADH dehydrogenase 1 (ND1) gene, which is part of the mitochondrial complex I enzyme complex and was screened for mutations. Results: We identified one patient with a homoplasmic A to G substitution mutation in cardiac tissue DNA and two patients with heteroplasmic A3397G mutation in serum DNA. Specifically, amplicon sequence analysis revealed a homoplasmic A3397G substitution in the ND1 gene in a tissue sample of the patient with ID number 1 and a heteroplasmic mutation in A3397G in serum samples of patients with ID numbers 3 and 6, respectively. The A to G substitution changes the amino acid from methionine (ATA) to valine (GTA) at position 31 of the ND1 gene. Conclusions: The detection of this novel mutation in patients with coronary artery disease may contribute to our understanding of the association between mitochondrial dysfunction and the disease, implying that mitochondria may be key players in the pathogenesis of cardiovascular diseases.