RESUMEN
To understand the mechanism underlying coronary artery abnormal dilatation (CAAD), the present study identified and compared the expression of circulating microRNAs (miRNAs) in three groups of patients. Group 1 included 20 patients with CAAD, Group 2 included 20 patients with angiographically confirmed coronary artery disease (CAD), and Group 3 included 20 patients with normal coronary arteries (control). miRNAs were isolated from plasma samples and were profiled using PCR arrays and miRCURY LNA Serum/Plasma Focus PCR Panels. The present study demonstrated that the plasma miRNA levels were significantly different in Group 1 compared with in Group 2 and Group 3 (fold change >2 and P<0.05). The comparison of Group 1 with Group 3 identified 21 significantly upregulated and two downregulated miRNAs in patients with CAAD compared with in the control group. Moreover, six upregulated and two downregulated miRNAs were identified in patients with CAD compared with in the controls. The third comparison revealed four upregulated and three downregulated miRNAs in Group 1, when compared with patients with CAD. In conclusion, the present study identified a specific signature of plasma miRNAs, which were upregulated and downregulated in patients with CAAD compared with in patients with CAD and control individuals.
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We aimed to evaluate the clinical course and impact of the SARS-CoV-2 pandemic on the rate of diagnosis and therapy in the complete Polish population of patients (pts) with pulmonary arterial hypertension (PAH-1134) and CTEPH (570 pts) treated within the National Health Fund program and reported in the national BNP-PL database. Updated records of 1704 BNP-PL pts collected between March and December 2020 were analyzed with regard to incidence, clinical course and mortality associated with COVID-19. Clinical characteristics of the infected pts and COVID-19 decedents were analyzed. The rates of new diagnoses and treatment intensification in this period were studied and collated to the proper intervals of the previous year. The incidence of COVID-19 was 3.8% (n = 65) (PAH, 4.1%; CTEPH, 3.2%). COVID-19-related mortality was 28% (18/65 pts). Those who died were substantially older and had a more advanced functional WHO class and more cardiovascular comorbidities (comorbidity score, 4.0 ± 2.1 vs. 2.7 ± 1.8; p = 0.01). During the pandemic, annualized new diagnoses of PH diminished by 25-30% as compared to 2019. A relevant increase in total mortality was also observed among the PH pts (9.7% vs. 5.9% pre-pandemic, p = 0.006), whereas escalation of specific PAH/CTEPH therapies occurred less frequently (14.7% vs. 21.6% pre-pandemic). The COVID-19 pandemic has affected the diagnosis and treatment of PH by decreasing the number of new diagnoses, escalating therapy and enhancing overall mortality. Pulmonary hypertension is a risk factor for worsened course of COVID-19 and elevated mortality.
Asunto(s)
COVID-19 , Hipertensión Pulmonar , COVID-19/epidemiología , Comorbilidad , Humanos , Hipertensión Pulmonar/epidemiología , Pandemias , SARS-CoV-2RESUMEN
The present study aimed to evaluate the plasma concentration of pro and antiangiogenic factors and their role in the pathogenesis of coronary artery abnormal dilation (CAAD). We measured the plasma concentration of matrix metalloproteinase-8 (MMP-8), transforming growth factor beta 1 (TGF-ß1), Angiopoietin-2, vascular endothelial growth factor (VEGF), and fibroblast growth factor (FGF) using a sandwich ELISA technique in the plasma of patients with coronary artery abnormal dilation (CAAD, Group 1), coronary artery disease (CAD, Group 2), and normal coronary arteries (NCA, Group 3). Patients suffering from CAAD showed significantly higher plasma concentrations of VEGF (p = 0.002) than those from the control group. Both pathological angiogenesis and inflammation appear to be crucial in the pathogenesis of aneurysmal dilatation of the coronary arteries.
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INTRODUCTION: Inflammation and angiogenesis disturbances are considered as factors contributing to the development of coronary artery ectasias (CAE). Endocan (endothelial cell-specific molecule-1 - ESM-1) regulates both inflammatory and angiogenetic processes. However, there are no data about the correlation between endocan level and the severity of CAE measured with total volume of coronary artery dilation. AIM: To assess whether the severity of the inflammatory process measured as endocan concentration correlates with the total volume of CAE. MATERIAL AND METHODS: We selected prospectively a total of 43 consecutive patients with coronary artery ectasia from 2240 patients who underwent coronary angiography in our center. Determination of endocan was performed by using the Human Endothelial cell-specific Molecule 1 (ECSM1/ENDOCAN) ELISA Kit. 3D QCA (three-dimensional quantitative coronary angiography) was used for coronary lesion and aneurysm quantification. The total volume of dilation was defined as the volume of all aneurysms and ectasias of coronary arteries in 1 patient. RESULTS: The mean volume of all aneurysms in 1 patient was 677 ±878.7 mm3. The total aneurysm volume was positively strongly correlated with endocan concentration (Pearson correlation coefficient: 0.811; 2-tailed p < 0.001). CONCLUSIONS: Endocan is a potential marker of vascular wall damage mainly as a result of inflammation in the course of atherosclerosis, but also vascular remodeling as a result of a disturbance of pro- and anti-angiogenic processes. Endocan level reflects the intensity of the above processes and therefore correlates with the severity of CAE, measured as the total volume of dilation.