Postprandial Hyperlipidemia: Association with Inflammation and Subclinical Atherosclerosis in Patients with Rheumatoid Arthritis

Objective: To describe postprandial lipidemia in patients with rheumatoid arthritis (RA) and to analyze its association with subclinical atherosclerosis and inflammatory activity. Methods: Observational study of 80 cases of RA and 80 sex- and age-matched controls. We excluded individuals with dyslipidemia. Postprandial hyperlipidemia (PPHL) was defined as postprandial triglycerides >220 mg/dL and/or postprandial ApoB48 levels >75th percentile (>p75). Plasma lipids, cholesterol, triglycerides, ApoB48, and total ApoB were evaluated at baseline and after a meal. Other variables analyzed included subclinical atherosclerosis (defined as presence of carotid atheromatous plaque), inflammatory activity (disease activity score (DAS28-ESR)), cytokines, apolipoproteins, and physical activity. A multivariate analysis was performed to identify factors associated with PPHL in patients with RA. Results: A total of 75 patients with RA and 67 healthy controls fulfilled the inclusion criteria. PPHL was more frequent in patients with RA than controls (No. (%), 29 (38.70) vs. 15 (22.40); p = 0.036), as was subclinical atherosclerosis (No. (%), 22 (30.10) vs. 10 (14.90); p = 0.032). PPHL in patients with RA was associated with subclinical atherosclerosis (OR (95% CI) 4.69 (1.09–12.11); p = 0.037), TNF-α (OR (95% CI) 2.00 (1.00–3.98); p = 0.048), high-sensitivity C-reactive protein (OR (95% CI) 1.10 (1.01–1.19); p = 0.027), and baseline triglycerides (OR (95% CI) 1.02 (1.00–1.04); p = 0.049). Conclusion: PPHL was more frequent in patients with RA than in controls. PPHL in patients with RA was associated with inflammation and subclinical atherosclerosis.

Association between Carotid Intima-Media Thickness and the Use of Biological or Small Molecule Therapies in Patients with Rheumatoid Arthritis

Objective: The objective of this study was to assess the association of carotid intima-media thickness (CIMT), and also the presence of atheromatous plaque, with biological and targeted synthetic disease-modifying antirheumatic drugs, in an established cohort of patients with rheumatoid arthritis (RA). Patients and Methods: We conducted a cross-sectional observational study based on a cohort of patients with RA and a registry of healthy controls, in whom the CIMT and presence of atheromatous plaque were assessed by ultrasound. Data were collected on disease activity, lab results and treatments. Descriptive and bivariate analyses were performed and two multivariate linear regression models (with CIMT as the dependent variable) were constructed to identify variables independently associated with CIMT in our sample of patients with RA. Results: A total of 176 individuals (146 patients with RA and 30 controls) were included. A higher percentage of patients than controls had atheromatous plaque (33.8% vs. 12.5%, p = 0.036), but no differences were found in terms of CIMT (0.64 vs. 0.61, p = 0.444). Compared to values in patients on other therapies, the CIMT was smaller among patients on tumour necrosis factor alpha (TNFα) inhibitors (mean [SD]: 0.58 [0.10] vs. 0.65 [0.19]; p = 0.013) and among those on Janus kinase inhibitors (mean [SD]: 0.52 [0.02] vs. 0.64 [0.18]; p < 0.001), while no differences were found as a function of the use of the other therapies considered. The multivariate linear regression analysis to identify factors associated with CIMT in our patients, adjusting for traditional cardiovascular risk factors such as hypertension, high levels of low-density lipoproteins, diabetes mellitus and smoking, showed that male sex, older age and having a greater cumulative erythrocyte sedimentation rate were independently associated with a larger CIMT, while patients on TNFα inhibitors had a CIMT 0.075 mm smaller than those on other treatments. Conclusions: The use of TNFα inhibitors may protect against subclinical atherosclerosis in patients with RA, patients on this biologic having smaller CIMTs than patients on other disease-modifying antirheumatic drugs. Nonetheless, these results should be confirmed in prospective studies with larger sample sizes.

Is There a Link between COVID-19 Infection, Periodontal Disease and Acute Myocardial Infarction?

Both periodontal disease and atherosclerosis are chronic disorders with an inflammatory substrate that leads to alteration of the host’s immune response. In PD, inflammation is responsible for bone tissue destruction, while in atherosclerosis, it leads to atheromatous plaque formation. These modifications result from the action of pro-inflammatory cytokines that are secreted both locally at gingival or coronary sites, and systemically. Recently, it was observed that in patients with PD or with cardiovascular disease, COVID-19 infection is prone to be more severe. While the association between PD, inflammation and cardiovascular disease is well-known, the impact of COVID-19-related inflammation on the systemic complications of these conditions has not been established yet. The purpose of this review is to bring light upon the latest advances in understanding the link between periodontal–cardiovascular diseases and COVID-19 infection.

Micro-RNA as a predictor of cardiovascular diseases

Сердечно-сосудистые заболевания, особенно ишемическая болезнь сердца (ИБС), являются наиболее распространенными заболеваниями во всем мире. Более 50% смертности приходится на данную патологию. В последние десятилетия существует тенденция к «омоложению» сердечно-сосудистых заболеваний – прежде всего гипертонической болезни и ИБС, что вызывает особую тревогу. Общепризнано, что основным этиологическим моментом развития ИБС является атеросклероз. ИБС включает в себя целый ряд клинических диагнозов (стенокардия, инфаркт миокарда и т. д.) и связана с атеросклерозом, распространенным дегенеративным заболеванием, при котором липиды и фиброзный матрикс откладываются в артериальной стенке с формированием атероматозной бляшки. Разрыв нестабильных бляшек в коронарных артериях приводит к высвобождению тромбогенного содержимого в просвет сосуда, приводя к тромбозу коронарных артерий, окклюзии и последующему инфаркту миокарда – критическому состоянию с высокой смертностью [5]. Несмотря на большое количество известных факторов риска, влияющих на развитие данного заболевания, существуют данные, подтвержденные крупными исследованиями, о наличии генетической предрасположенности к нему. Cardiovascular diseases, especially coronary heart disease (CHD), are the most common diseases worldwide. More than 50% of mortality occurs in this pathology. In recent decades, there is a tendency to «rejuvenate» cardiovascular diseases – primarily hypertension and СHD, which is of particular concern [6, 8]. It is generally recognized that atherosclerosis is the main etiological moment in the development of coronary heart disease. CHD includes a number of clinical diagnoses (angina pectoris, myocardial infarction, etc.) and is associated with atherosclerosis, a common degenerative disease in which lipids and the fibrous matrix are deposited in the arterial wall with the formation of an atheromatous plaque. Rupture of unstable plaques in the coronary arteries leads to the release of thrombogenic contents into the lumen of the vessel, leading to coronary artery thrombosis, occlusion and subsequent myocardial infarction, critical state with high mortality [5]. Despite the large number of known risk factors affecting the development of this disease, there is evidence, confirmed by large studies, about the presence of a genetic predisposition to this disease.

Study of Carotid doppler in Patients with ischemic stroke

Introduction: Stroke is one of the major causes of increased morbidity and death. Large-vessel atherosclerosis of intracranial and extra cranial carotid vessels is an important cause of ischemic stroke. This research was undertaken to study the carotid Doppler findings in patients with acute ischemic stroke. Methods: A hospital-based prospective cross-sectional study was conducted from January 2020 till December 2020 in the department of Radio diagnosis and Imaging at Manipal Teaching Hospital, Pokhara, Nepal. Neuro-imaging and carotid Doppler findings in patients with ischemic stroke were studied. Data analysis was done using SPSS 20. Results: The mean age of subjects with ischemic stroke was 64 ± 13.4 years with the majority of cases in the age group of 51-70 years of age with male predominance (M: F= 3: 2). Lacunar infarcts (34.2%) were the most common findings followed by MCA infarct (30%) and ACA infarct (10.8%). Carotid plaques were seen in 43.3% patients. Bilateral ICA atheromatous plaque was seen in 48.1% of patients. Carotid bulb was the common site for plaque formation. Type III plaque was the commonest type. Significant ICA stenosis > 50 % was observed in 24.2% patients. Age >50 years, male sex, smoking, hypertension, diabetes, and hyperlipidemia were important risk factors. Conclusion: Carotid artery Doppler demonstrated atherosclerotic plaques and significant stenosis in patients with ischemic stroke. Increasing age >50 years, male sex, smoking, hypertension, diabetes, and hyperlipidemia were associated with an increased rate of atherosclerosis, carotid stenosis and ischemic stroke.

Early Detection of Post-Endarterectomy Complication by Point-of-Care Ultrasound

Endarterectomy is an effective intervention to remove the atheromatous plaque in the inner lining of the artery, aiming to revascularize the occluded/stenosed vessel in patients with peripheral arterial occlusive disease (PAOD). The most common wound-related complication is postoperative bleeding, followed by infection, hematoma, and seroma. However, hematoma complications with air surrounded have rarely been reported in clinical cases. Case presentation: A 90-year-old female patient visited our emergency department because of a rapidly growing hematoma with pulsatile bleeding over her right groin area. She had received bilateral percutaneous transluminal angioplasty with endarterectomy for PAOD one month prior. A point-of-care ultrasound revealed a large hypoechoic mass, with a dirty shadow on the right groin area. Computed tomography angiography showed a hematoma over her right femoral region, with free air surrounding the right femoral artery. Angiography revealed an irregular shaped lesion on the right femoral artery without contrast extravasation. The patient was diagnosed with right-femoral post-endarterectomy infection with infected hematoma, with the inclusion of air. She underwent urgent excision and repair of the right femoral artery infectious lesion, debridement of the infectious hematoma and stenting of the right external iliac artery, common femoral artery and superficial femoral artery.

Differentiating Carotid Free-Floating Thrombus From Atheromatous Plaque Using Intraluminal Filling Defect Length on CTA: A Validation Study

Objective:To validate a previously proposed filling defect length threshold of >3.8 mm on CT-angiography (CTA) to discriminate between free-floating thrombus (FFT) and plaque of atheroma.Methods:Prospective multicenter observational study of 100 participants presenting with TIA/stroke symptoms and a carotid intraluminal filling defect on initial CTA. Follow-up CTA was obtained within one week, and at weeks 2 and 4 if the intraluminal filling defect was unchanged in length. Resolution or decreased length was diagnostic of FFT, whereas its static appearance after 4 weeks was indicative of plaque. Diagnostic accuracy of FFT length was assessed by receiver operating characteristic analysis.Results:Ninety-five participants (mean age [standard deviation], 68 [13] years; 61 men; 83 participants with FFT; 12 participants with a plaque) were evaluated. The >3.8 mm threshold had a sensitivity of 88% (73/83) (95% confidence interval {CI}: 78%, 94%) and specificity of 83% (10/12) (95% CI, 51%, 97%) (area under the curve [AUC], 0.91, p<.001) for the diagnosis of FFT. The optimal length threshold was >3.64 mm with a sensitivity of 89%( 74/83) (95% CI, 80%, 95%) and specificity of 83% (10/12) (95% CI, 51%, 97%). Adjusted logistic regression showed that every 1 mm increase in intraluminal filling defect length is associated with an increase in odds of FFT of 4.6 ([95% CI] 1.9-11.1; p=.01).Conclusion:CTA enables accurate differentiation of FFT versus plaque using craniocaudal length thresholds.Trial Registration Information:Clinical trial identifier:www.clinicaltrials.govNCT02405845Classification of Evidence:This study provides Class I evidence that in patients with TIA/stroke symptoms, the presence of CTA-identified filling defects of length >3.8 mm accurately discriminates free-floating thrombus from atheromatous plaque.

PCSK9 gene participates in the development of primary dyslipidemias

Dyslipidemias are a group of diseases, which are characterized by abnormal blood concentrations of cholesterol, triglycerides and/or low-density lipoprotein-cholesterol (LDL-c). Dyslipidemia is a determinant condition for the progress of an atherosclerotic plaque formation. The resulting atherogenicity is due to at least two mechanisms: first, to the accumulation in the plasma of lipid particles that have the capacity to alter the function of the endothelium and deposit at the atheromatous plaque, and second, at an insufficient concentration of multifactorial type of high density lipoprotein-cholesterol (HDL-c), whose function is to protect against the development of atherosclerosis. Its highest prevalence is encountered among individuals with diabetes, hypertension or overweight. Hyperlipidemia is one of the main predisposing factors for the development of cardiovascular disease. Hyperlipidemia can be the result of a genetic condition, the secondary expression of a primary process or the consequence of exogenous factors (food, cultural, socio-economic, etc.), all of which lead to the elevation of plasma lipid levels. The objective of this study was to carry out an analysis of the genes involved in the development of dyslipidemias that lead to cardiovascular disease with special emphasis on the proprotein convertase subtilin/kexin type 9 (PCSK9) gene. The PCSK9 gene participates in the development of primary dyslipidemias, mainly familial hypercholesterolemia, currently the pharmacological treatment of choice to reduce LDL-c are statins, however, it has been observed that these have been insufficient to eliminate cardiovascular risk, especially in subjects with primary forms of hypercholesterolemia related to genetic mutations, or statin intolerance.