The aim of this study is to assess the relationship between autoimmunity and endothelial activation/damage (ICAM-1 and vWF serum levels) and the degree of prothrombotic activity (thrombin-antithrombin complexes-TAT serum levels) in SLE. In 60 clinically stable SLE patients, levels of the following parameters were estimated in their serum: lupus anticoagulant (LA), anticardiolipin antibodies in both IgG and IgM classes (aCL-IgG and aCL-IgM, respectively), antiβ2GPI antibodies in both IgG and IgM classes (antiβ2GPI-IgG and antiβ2GPI-IgM, respectively), ICAM, von Willebrand factor (vWF), TAT, CRP, C3c, C4, and IL-6. ICAM-1 values exceeded the upper reference limit in 9 (15%) patients. vWF levels were increased in 21 (35%) patients. In all patients with elevated ICAM-1 values, vWF were also increased. TAT concentrations were elevated in 12 (20%) people. ICAM-1 were significantly higher in patients with elevated aCL-IgM (> 30 MPL vs ≤ 30 MPL; p < 0.05). Similarly, ICAM-1 were significantly higher in patients with elevated antiβ2-GPI-IgM (> 20 SMU vs ≤ 20 SMU; p < 0.05). There was no significant difference in ICAM-1 levels in relation to LA-positivity. vWF were not significantly different in relation to antiphospholipid antibodies nor the inflammation marker levels. TAT were significantly higher in patients with elevated aCL-IgM (> 30 MPL vs ≤ 30 MPL; p < 0.05). In one third of young patients with stable SLE, signs of endothelial activation/damage were found, as shown by elevated plasma ICAM-1 or vWF. Increased prothrombotic tendency manifested by elevated TAT was found in one fifth of the patients. Elevated anticardiolipin (IgM) and anti-β2-glycoprotein I (IgM) antibodies influence endothelial dysfunction and enhance prothrombotic state.
Introduction: Antiphospholipid antibodies (aPL) affect atherogenesis and may cause thromboembolism in systemic lupus erythematosus (SLE) and coronary artery disease (CAD). Intensive treatment with statins may reduce inflammation and decrease the number of thrombotic events. That may explain the beneficial effect of statin therapy in SLE and CAD. This study was established to investigate the influence of statin treatment on aPL antibody levels and selected endothelial dysfunction markers in CAD and SLE patients. Material and methods: Fifty-eight patients-40 after coronary revascularization (age 38.9 [27-46), 35 males) and 18 with clinically stable SLE (age 38.8 [18-62], 1 male)-were enrolled in the study. In both groups intensive atorvastatin treatment was administered. At baseline and after one year of follow-up serology tests were performed: anticardiolipin antibodies (aCL), anti-β2 glycoprotein I (aβ2GPI), lupus anticoagulant (LA), C-reactive protein (CRP), soluble form of intracellular adhesion molecule-1 (sICAM-1), vWF:Ag. Results: Coronary artery disease patients in one year follow-up revealed a decrease of aβ2GPI IgG and CRP. There was a significant increase in aCL IgG, sICAM-1 and vWF:Ag. In SLE patients aPL levels showed no significant reduction after treatment. Conclusions: In clinically stable patients IgM and IgG class aβ2GPI levels are higher in CAD than in SLE, whereas IgG class aCL levels are lower. Statin treatment decreases the CRP level in both SLE and CAD patients, while decreasing the aβ2GPI IgG level only in CAD patients.
Introduction: Systemic lupus erythematosus (SLE) is characterized by early atherothrombosis. Pulse wave velocity (PWV) is a promising tool for the diagnosis of early vascular remodelling and initial atherosclerotic plaque formation. Our objective was to evaluate PWV and its relationship with coronary atherosclerosis and thrombotic biomarkers in patients with SLE. Material and methods: In 26 patients with SLE with stable clinical conditions, mean age of 39.1 ±11.7 years and without a history of coronary artery disease, multidetector computed tomography (MDCT)-based coronary calcium scoring (CACS) was performed and PWV measured. Laboratory evaluation included serum levels of anticardiolipin and anti-β2-glycoprotein antibodies (anti-β2-GPI), lupus anticoagulant (LA), D-dimers, thrombin-antithrombin complexes (TAT), and von Willebrand factor (vWF). Results: Multidetector computed tomography revealed coronary calcifications in 8 (30.8%) patients and the median CACS was 52.4 HU (range 2-843.2). The mean PWV was 9.0 ±3.2 m/s and was higher in patients aged > 50 years (+33.7% vs. < 50 years), those with positive LA (+28.2% vs. LA negative), TAT ≥ 10 µg/l (+18.1% vs. < 10 µg/l), vWF ≥ 200 IU/dl (+51.8% vs. < 200 IU/dl) and with coronary atherosclerosis (CACS > 0; +21.4% vs. CACS = 0). In contrast, the duration of the disease, D-dimers, anticardiolipin, and anti-β2-GPI antibodies did not influence PWV. In the group without atherosclerosis (CACS = 0, n =18), patients with vWF ≥ 200 IU/dl had a 19.3% higher PWV compared to the rest. Conclusions: In patients with SLE, PWV was associated with the presence of coronary atherosclerotic lesions in MDCT. Furthermore, arterial stiffness was higher in patients with markers of endothelial dysfunction and a prothrombotic state, suggesting their contribution to the early stages of arterial remodelling in SLE.
Based on the results of our study, we were unable to identify factors determining remission of AF coexisting with AFL in patients after percutaneous CTI ablation. These findings may indicate the need for complex ablation procedure (involving both CTI and pulmonary venous ostia ablation) in patients in whom these two arrhythmias coexist.
Purpose: Acute decompensated heart failure (ADHF) treatment leads to significant hemodynamic changes. The aim of our study was to quantitatively analyze the dynamics of mitral regurgitation (MR) severity (evaluated by transthoracic echocardiography) which occur during the treatment of ADHF and to correlate these changes with the clinical condition of patients as well as heart failure biochemical markers. Methods: The study included 27 consecutive adult patients (40.7% females, mean age 71.19±11.2 years) who required hospitalization due to signs of acute HF. Echocardiographic assessment was performed upon admission and discharge together with clinical and laboratory evaluation. Results: Significant reduction in dyspnea intensity [0-100 scale] (81.48±9.07 vs. 45.00±11.04 pts, p<0.001), body weight (84.98±18.52 vs. 79.77±17.49 kg, p<0,001), and NT-proBNP level (7520.56±5288.62 vs. 4949.88±3687.86 pg/ml, p=0.001) was found. The severity of MR parameters decreased significantly (MR volume 44.92±22.83 vs. 30.88±18.77 ml, p<0.001; EROA 0.37±0.17 vs. 0.25±0.16 cm2, p<0.001; VC 6.21±1.48 vs. 5.26±1.61 mm, p<0.001). Left atrial area (35.86±9.11 vs. 32.47±9.37, p<0.001) and mitral annular diameter (42.33±6.63 vs. 39.72±5.05. p<0.001) also underwent statistically significant reductions. An increase in LVEF was observed (34.73±13.88 vs. 40.24±13.19 %, p<0.001). In 40.7% of patients, a change in MR severity class (transition from a higher class to a lower one) was observed: 6/8 (75%) patients transitioned from severe to moderate and 6/18 (33.3%) patients transitioned from moderate to mild class.Conclusions: Treatment of ADHF leads to a significant reduction in MR severity, together with significant reductions in left atrial and mitral annular dimensions. Quantitative measurement of MR dynamics offer valuable assistance for ADHF management.
Acute decompensated heart failure (ADHF) treatment leads to significant hemodynamic changes. The aim of our study was to quantitatively analyze the dynamics of mitral regurgitation (MR) severity (evaluated by transthoracic echocardiography) which occur during the treatment of ADHF and to correlate these changes with the clinical condition of patients as well as heart failure biochemical markers. The study included 27 consecutive adult patients (40.7% females, mean age 71.19 ± 11.2 years) who required hospitalization due to signs of acute HF. Echocardiographic assessment was performed upon admission and discharge together with clinical and laboratory evaluation. Significant reduction in dyspnea intensity [0–100 scale] (81.48 ± 9.07 vs. 45.00 ± 11.04 pts, p < 0.001), body weight (84.98 ± 18.52 vs. 79.77 ± 17.49 kg, p < 0.001), and NT-proBNP level (7520.56 ± 5288.62 vs. 4949.88 ± 3687.86 pg/ml, p = 0.001) was found. The severity of MR parameters decreased significantly (MR volume 44.92 ± 22.83 vs. 30.88 ± 18.77 ml, p < 0.001; EROA 0.37 ± 0.17 vs. 0.25 ± 0.16 cm2, p < 0.001; VC 6.21 ± 1.48 vs. 5.26 ± 1.61 mm, p < 0.001). Left atrial area (35.86 ± 9.11 vs. 32.47 ± 9.37, p < 0.001) and mitral annular diameter (42.33 ± 6.63 vs. 39.72 ± 5.05. p < 0.001) also underwent statistically significant reductions. An increase in LVEF was observed (34.73 ± 13.88 vs. 40.24 ± 13.19%, p < 0.001). In 40.7% of patients, a change in MR severity class (transition from a higher class to a lower one) was observed: 6/8 (75%) patients transitioned from severe to moderate and 6/18 (33.3%) patients transitioned from moderate to mild class. Treatment of ADHF leads to a significant reduction in MR severity, together with significant reductions in left atrial and mitral annular dimensions. Quantitative measurement of MR dynamics offer valuable assistance for ADHF management.
It is still disputable whether the specific morphological properties of the patent foramen ovale (PFO) may contribute to the occurrence of stroke. Therefore, the aim of this study was to evaluate the differences in the morphometric and functional features of the PFO channel in cryptogenic stroke and non‐stroke patients. A total of 106 consecutive patients with cryptogenic stroke and 93 non‐stroke control patients with diagnosed PFO (by transesophageal echocardiography) were analyzed. Multivariate regression logistic analyses indicated PFO channel length change (OR: 2.50 [95%Cl:1.75–3.55], p<0.001), the PFO length/height ratio during the Valsalva maneuver (OR: 0.75 [95%Cl:0.60–0.95], p=0.015), septum primum thickness (OR: 0.34 [95%Cl:0.14–0.80], p=0.013), septum secundum height (OR: 0.91 [95%Cl:0.84–0.98], p=0.013), the presence of an atrial septal aneurysm (OR: 3.38 [95%Cl:1.27–8.97], p=0.014), and large shunt (OR: 2.49 [95%Cl:1.13–5.46], p=0.022) as PFO‐related risk factors for stroke. A MorPFO score was developed (AUC=0.816, SD=0.031), where six factors were included: PFO channel length reduction (≥ 23%) (3 pts), low length/height ratio during the Valsalva maneuver (≤ 2.1) (1 pt), thin septum primum (≤ 1.5mm) (1 pt), short septum secundum (< 5.6mm) (1 pt), presence of an atrial septal aneurysm (1 pt), and large right‐to‐left shunt (1 pt). Patients with scores of 0–2 pts had low‐risk PFO channels, 3–4 pts intermediate‐risk PFO channels, and 5–8 points high‐risk PFO channels. In conclusion transesophageal echocardiography can be used to determine the PFO‐related risk of stroke. MorPFO score may help to identify high‐stroke‐risk PFO channels.
Apical hypertrophic cardiomyopathy (AHC) is a less common type of hypertrophic cardiomyopathy (HCM). It is characterized by typical changes in ECG (deeply inverted T waves that can mimic acute coronary syndrome), echocardiography (hypertrophy of apical segments) and ventriculography (spade-like shaped left ventricular cavity). Magnetic resonance is considered as a reference method for AHC diagnosis. We present a long follow-up period of a patient with this form of HCM. The management of patients with HCM is directed at decreasing left ventricle outflow tract narrowing (if present), decreasing of intraventricular gradient (if present), heart failure treatment and prevention of sudden cardiac death. In general treatment adequate hydration is essential and diuretics should be used with caution to prevent the increase of intraventricular gradient.
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