Markers of Atherosclerosis: Part 1 - Serological Markers.

Atherosclerosis is a major contributor to morbidity and mortality worldwide. With therapeutic consequences in mind, several risk scores are being used to differentiate individuals with low, intermediate or high cardiovascular (CV) event risk. The most appropriate management of intermediate risk individuals is still not known, therefore, novel biomarkers are being sought to help re-stratify them as low or high risk. This narrative review is presented in two parts. Here, in Part 1, we summarise current knowledge on serum (serological) biomarkers of atherosclerosis. Among novel biomarkers, high sensitivity C-reactive protein (hsCRP) has emerged as the most promising in chronic situations, others need further clinical studies. However, it seems that a combination of serum biomarkers offers more to risk stratification than either biomarker alone. In Part 2, we address genetic and imaging markers of atherosclerosis, as well as other developments relevant to risk prediction.

Markers of Atherosclerosis: Part 2 - Genetic and Imaging Markers.

This is Part 2 of a two-part review summarising current knowledge on biomarkers of atherosclerosis. Part 1 addressed serological biomarkers. Here, in part 2 we address genetic and imaging markers, and other developments in predicting risk. Further improvements in risk stratification are expected with the addition of genetic risk scores. In addition to single nucleotide polymorphisms (SNPs), recent advances in epigenetics offer DNA methylation profiles, histone chemical modifications, and micro-RNAs as other promising indicators of atherosclerosis. Imaging biomarkers are better studied and already have a higher degree of clinical applicability in cardiovascular (CV) event prediction and detection of preclinical atherosclerosis. With new methodologies, such as proteomics and metabolomics, discoveries of new clinically applicable biomarkers are expected.

Polymicrobial purulent pericarditis and peritoneal effusion in an immunocompromised patient with Staphylococcus aureus bacteraemia: a case report.

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.

Late-post-COVID-19 cerebral venous sinus thrombosis and stroke: a case report.

INTRODUCTION: Coronavirus disease 2019 (COVID-19) disease increases risk of venous thromboembolisms (VTE), primarily deep vein thrombosis and pulmonary embolism. Only a few cases of cerebral venous sinus thrombosis (CVST) in association with a COVID-19 infection have been reported and are limited to acute COVID-19 disease. Hypercoagulable conditions persist in postacute COVID-19 disease, which carries an increased risk of VTE. CASE PRESENTATION: We report a case of CVST and stroke 56 days post-COVID-19 infection presenting with an atypical clinical picture. DISCUSSION: To the best of our knowledge, this is one of the first observations of CVST in the postacute phase of COVID-19 disease. Clinicians should be aware of this potential late complication and should consider appropriate diagnostic imaging techniques in patients with COVID-19-infection history.

Association of Myocardial Infarction with CDKN2B Antisense RNA 1 (CDKN2B-AS1) rs1333049 Polymorphism in Slovenian Subjects with Type 2 Diabetes Mellitus.

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.

The C allele of the reactive oxygen species modulator 1 (ROMO1) polymorphism rs6060566 is a biomarker predicting coronary artery stenosis in Slovenian subjects with type 2 diabetes mellitus.

BACKGROUND: We aimed to examine the role of the rs6060566 polymorphism of the reactive oxygen species modulator 1 (ROMO1) gene in the development of myocardial infarction (MI) in Caucasians with type 2 diabetes (T2DM). METHODS: A total of 1072 subjects with T2DM were enrolled in this cross-sectional case-control study: 335 subjects with MI and 737 subjects without clinical signs of coronary artery disease (CAD). The genetic analysis of the rs6060566 polymorphism was performed in all subjects. To assess the degree of coronary artery obstruction, a subpopulation of 128 subjects with T2DM underwent coronary computed tomography angiography. Next, endarterectomy samples were obtained during myocardial revascularization from diffusely diseased coronary arteries in 40 cases, which were analysed for ROMO1 expression according to their genotype. RESULTS: There were no statistically significant associations between different genotypes or alleles of the rs6060566 polymorphism and MI in subjects with T2DM. The carriers of the C allele of the ROMO1 rs6060566 had a threefold increased likelihood of having 50-75% coronary artery stenosis (Adjusted OR = 3.27, 95% CI 1.16-9.20). Subjects with two affected coronary arteries had a 3.72 fold higher prevalence of MI (OR = 3.72, 95% CI 1.27-10.84). With CAD in LMCA or LAD, MI prevalence was about 3.5-fold higher (p = 0.07 for LMCA and p = 0.01 for LAD). Furthermore, the carriers of the rs6060566 C allele showed higher number of positive cells for ROMO1 expression in endarterectomy samples of coronary arteries. CONCLUSIONS: According to our study, the rs6060566 polymorphism of the ROMO1 gene is not a risk factor for MI in Caucasians with T2DM. However, we found that subjects carrying the C allele were at a 3.27-fold increased risk of developing severe CAD compared with those who had non-obstructive CAD. Moreover, C allele carriers showed a statistically higher number of cells positive for ROMO1 compared with T allele carriers in coronary endarterectomy samples.

Pathophysiology of Myocardial Infarction and Acute Management Strategies.

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.

Oxidative Stress Genes, Antioxidants and Coronary Artery Disease in Type 2 Diabetes Mellitus.

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.