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Background Polymicrobial pericarditis is an extremely rare and lethal form of pericarditis. Prompt initiation of appropriate antimicrobial treatment and pericardial drainage are crucial. Case summary A 57-year-old immunocompromised male patient presented to the emergency department due to dyspnoea, chest pain, and fever lasting for 7 days. Following clinical, laboratory, and imaging work-up, he was found to have pericardial effusion with signs of tamponade. After pericardiocentesis through subxiphoid and apical approaches, 800 mL of gross purulent fluid was obtained. Blood and pericardial fluid cultures confirmed the diagnosis of polymicrobial purulent pericarditis (Staphylococcus aureus and Bacteroides vulgatus). Further work-up revealed minor peritoneal effusion, and paracentesis fluid culture revealed the presence of S. aureus and, additionally, Candida albicans. After treatment initiation with intravenous antibiotics, pericardial, drainage and supportive measures, the patient's condition initially improved despite the development of constrictive pericarditis. However, he suddenly deteriorated after 37 days of hospitalization and passed away after 51 days of hospitalization. Discussion To the best of our knowledge, this is the first report of purulent pericarditis and purulent peritoneal effusion in the settings of S. aureus bacteraemia with an absent primary infection focus. Clinicians should be aware of treatment options for purulent pericarditis and consider intrapericardial fibrinolysis, especially in patients not suited for more invasive pericarditis treatment. [ABSTRACT FROM AUTHOR]

Background: We examined the role of rs1333049 polymorphism of the CDKN2B Antisense RNA 1 (CDKN2B-AS1) on the prevalence of myocardial infarction (MI) in Slovenian subjects with type 2 diabetes mellitus (T2DM). Methods: A total of 1071 subjects with T2DM were enrolled in this retrospective cross-sectional case-control study. Of the subjects, 334 had a history of recent MI, and 737 subjects in the control group had no clinical signs of coronary artery disease (CAD). With logistic regression, we performed a genetic analysis of rs1333049 polymorphism in all subjects. Results: The C allele of rs1333049 polymorphism was statistically more frequent in MI subjects (p = 0.05). Subjects with CC genotype had a higher prevalence of MI than the control group in the co-dominant (AOR 1.50, CI 1.02–2.21, p = 0.04) and recessive (AOR 1.38, CI 1.09–1.89, p = 0.04) genetic model. Conclusions: According to our study, the C allele and CC genotype of rs1333049 polymorphism of CDKN2B-AS1 are possible markers of MI in T2DM subjects in the Slovenian population. [ABSTRACT FROM AUTHOR]

On an annual basis, 13.2% of all deaths are attributable to coronary artery disease (CAD), which makes CAD - with 7.4 million deaths - the leading cause of death in the world. In this review, we discuss current knowledge in the pathophysiology of atherosclerosis with its progression to stable CAD and its destabilization and complication with thrombus formation - myocardial infarction (MI). Next, we describe mechanisms of myocardial cell death in MI, the ischemia-reperfusion injury, leftventricular remodeling and complications of MI. Furthermore, we add acute management strategies concentrating on medical therapy, a decision on the reperfusion strategy, timing and cardiac protection by ischemic preconditioning, post-conditioning and remote ischemic conditioning., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.)

The worldwide increasing prevalence of obesity and sedentary lifestyle is the main cause of the rising incidence of T2DM. Due to chronic macrovascular and microvascular complications, T2DM represent a huge socioeconomic burden in the world. Oxidative stress is a key pathogenic mechanism implicated in diabetic coronary artery disease (CAD). Polymorphisms of oxidative stress genes are known to influence oxidative stress levels and are therefore thought to impact CAD pathogenesis. Identifying higher risk groups would be rational, since it would allow better sample selection and thus better results in antioxidant trials. In this review, we summarize the evidence of oxidative stress gene polymorphisms related to the pathogenesis of CAD. Moreover, we provide a review of antioxidants tested in subjects with CAD.