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BACKGROUND: Premature ventricular contractions (PVCs) are common arrhythmias with diverse clinical implications. This retrospective study aimed to evaluate the efficacy of medical treatments using various clinical, imaging, and electrocardiographic parameters in patients with idiopathic PVCs. METHODS: A total of 1051 patients with idiopathic PVCs were retrospectively analyzed. Patients were categorized into three groups based on treatment response: beta-blocker (BB) responders (479 patients), calcium-channel blocker (CCB) responders (335 patients), and class 1c antiarrhythmic (AA) responders (237 patients). Clinical, imaging, and electrocardiographic data were collected and analyzed to assess the factors influencing treatment response. RESULTS: Age, left ventricular ejection fraction (LVEF), PVC QRS duration, CI variability, and multiple PVC morphologies were identified as significant factors affecting treatment response. Older age and lower LVEF were associated with better response to BB treatment, whereas CCB responders showed narrower QRS complexes. BB responders also exhibited higher CI variability, possibly linked to automaticity mechanisms. Moreover, the BB responder group had a higher frequency of multiple PVC morphologies. CONCLUSION: These findings emphasize the importance of tailored treatment approaches based on individual patient characteristics.
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Study objectives: Patients with carpal tunnel syndrome (CTS) show manifestations of arterial abnormalities, including carotid intimal thickening and increased vascular stiffness. As carpal tunnel syndrome is associated with amyloidosis, we hypothesized that previously observed abnormalities can largely be related with concomitant amyloidosis rather than CTS itself. Design: Prospective observational study. Setting: Medeniyet University Goztepe Hospital. Participants: 61 patients with CTS (of whom 32 had biopsy-proven amyloidosis) and 36 healthy controls. Interventions: Subjects underwent ultrasound examinations for the measurement of coronary flow velocity reserve (CFVR), flow-mediated vasodilatation (FMD) and carotid intimal-media thickness (CIMT). Main outcome measures: Comparison of CFVR, FMD and CIMT in CTS patients with or without amyloidosis. Results: Patients with either CTS or CTS with concomitant amyloidosis (CTS-A) had significantly lower FMD (9.7 % ± 4.0 % in CTS and 10.3 % ± 4.6 % in CTS-A groups, p < 0.05 for both) and CFVR (2.4 (2.1-2.8) in CTS and 1.8 (1.6-2.1) in CTS-A groups, p < 0.001 for both) as compared to controls, while CIMT was only increased in CTS-A group (0.70 (0.60-0.80), p < 0.001). The reduction in CFVR was solely related to an increased basal flow velocity in CTS patients while there was also a reduced hyperemic flow velocity in patients with CTS-A. Conclusion: Most arterial phenomena in CTS patients could be attributable to concomitant amyloidosis, although endothelial dysfunction was present even in patients with CTS without amyloidosis.
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Resumo Fundamento O receptor fraco indutor de apoptose semelhante a fator de necrose tumoral solúvel (sTWEAK) é um membro da superfamília de TNF que tem um papel crítico na proliferação e inflamação na circulação arterial. Objetivos Este estudo prospectivo tem o objetivo de mostrar a relação entre os níveis de sTWEAK e calcificação da artéria coronária (CAC) em pacientes com doença renal crônica (DRC). Métodos Este estudo prospectivo incluiu 139 pacientes consecutivos que passaram por angiografia coronariana por tomografia computadorizada, por qualquer motivo, para síndromes coronarianas agudas, de agosto de 2020 a fevereiro de 2021. Um total de 12 pacientes foi excluído do estudo devido aos critérios de exclusão. Os pacientes foram divididos em dois grupos com base em terem um escore CAC menor que 400 (n=84) ou um escore de 400 ou mais (n=43). A significância foi presumida em p-valor bilateral <0,05. Resultados À medida que o escore CAC aumentou, os níveis de sTWEAK diminuíram de forma estatisticamente significativa e detectou-se uma relação forte entre níveis de sTWEAK e escore CAC (r: -0,779, p<0,001). A análise ROC revelou que o nível de corte ideal de sTWEAK para prever o escore CAC de 400 era 761 pg/mL com uma sensibilidade de 71% e especificidade de 73% (AUC: 0,78; IC 95%: 0,70-0,85; p <0,001). Conclusões Embora os estudos em larga escala tenham demonstrado uma correlação positiva entre os níveis de TFGe e sTWEAK, alguns estudos detectaram que o aumento nos níveis de sTWEAK estão associados a mortalidade e gravidade do sistema da artéria coronária em pacientes com DRC. Nossos resultados comprovam nossa hipótese de que os níveis de sTWEAK mostram calcificação coronária em vez de outros tipos de placas ateroscleróticas.
Abstract Background The soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) is a member of the TNF superfamily that plays a critical role in proliferation and inflammation in the arterial circulation. Objectives This prospective study aimed to show the relationship between the sTWEAK levels and coronary artery calcification (CAC) in patients with chronic kidney disease (CKD). Methods This prospective study included 139 consecutive patients undergoing computed coronary angiography for any reason except for acute coronary syndromes from August 2020 to February 2021. A total of 12 patients were excluded from the study due to exclusion criteria. Patients were divided into two groups with regard to having a CAC score of less than 400 (n=84) and 400 or more (n=43). Significance was assumed at a 2-sided p<0.05. Results As the CAC score increased, sTWEAK levels presented a statistically significant decrease, and a strong relationship between sTWEAK levels and the CAC score (r: -0.779, p<0.001) was observed. The ROC analysis revealed that the optimal cut-off level of sTWEAK for predicting the CAC score of 400 was 761 pg/mL with a sensitivity of 71% and a specificity of 73% (AUC: 0.78; 95% CI:0.70-0.85; p < 0.001) Conclusions Even though the large-scale studies showed a positive correlation between eGFR and the sTWEAK levels, some studies found the increased sTWEAK levels to be associated with mortality and the severity of the coronary artery system in patients with CKD. Our results support our hypothesis that the sTWEAK level shows coronary calcification rather than other types of atherosclerotic plaques.
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BACKGROUND: Coronavirus disease 2019 (COVID-19) was first detected as a form of atypical pneumonia. COVID-19 is a highly contagious virus, and some patients may experience acute respiratory distress syndrome (ARDS) and acute respiratory failure leading to death. We aim to evaluate the clinical, imaging, and laboratory parameters according to survival time to predict mortality in fatal COVID-19 patients. METHODS: Fatal 350 and survived 150 COVID-19 patients were included in the study. Fatal patients were divided into three groups according to the median value of the survival days. Demographic characteristics and in-hospital complications were obtained from medical databases. RESULTS: Of the non-survived patients, 30% (104) died within three days, 32% (110) died within 4-10 days, and 39% (136) died within over ten days. Pneumonia on computational tomography (CT), symptom duration before hospital admission (SDBHA), intensive care unit (ICU), hypertension (HT), C-reactive protein (CRP), D-dimer, multi-organ dysfunction syndrome (MODS), cardiac and acute kidney injury, left ventricular ejection fraction (LVEF), right ventricular fractional area change (RV-FAC), and Tocilizumab/Steroid therapy were independent predictors of mortality within three days compared to between 4-10 days and over ten days mortality. A combined diagnosis model was evaluated for the age, CT score, SDBHA, hs-TnI, and D-dimer. The combined model had a higher area under the ROC curve (0.913). CONCLUSION: This study showed that age, pneumonia on CT, SDBHA, ICU, HT, CRP, d-dimer, cardiac injury, MODS, acute kidney injury, LVEF, and RV-FAC were independently associated with short-term mortality in non-surviving COVID-19 patients in the Turkish population. Moreover, Tocilizumab/Steroid therapy was a protective and independent predictor of mortality within three days.
Subject(s)
Acute Kidney Injury , COVID-19 , Respiratory Distress Syndrome , Humans , Intensive Care Units , Multiple Organ Failure , Prognosis , Stroke Volume , Ventricular Function, LeftABSTRACT
BACKGROUND: The soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) is a member of the TNF superfamily that plays a critical role in proliferation and inflammation in the arterial circulation. OBJECTIVES: This prospective study aimed to show the relationship between the sTWEAK levels and coronary artery calcification (CAC) in patients with chronic kidney disease (CKD). METHODS: This prospective study included 139 consecutive patients undergoing computed coronary angiography for any reason except for acute coronary syndromes from August 2020 to February 2021. A total of 12 patients were excluded from the study due to exclusion criteria. Patients were divided into two groups with regard to having a CAC score of less than 400 (n=84) and 400 or more (n=43). Significance was assumed at a 2-sided p<0.05. RESULTS: As the CAC score increased, sTWEAK levels presented a statistically significant decrease, and a strong relationship between sTWEAK levels and the CAC score (r: -0.779, p<0.001) was observed. The ROC analysis revealed that the optimal cut-off level of sTWEAK for predicting the CAC score of 400 was 761 pg/mL with a sensitivity of 71% and a specificity of 73% (AUC: 0.78; 95% CI:0.70-0.85; p < 0.001). CONCLUSIONS: Even though the large-scale studies showed a positive correlation between eGFR and the sTWEAK levels, some studies found the increased sTWEAK levels to be associated with mortality and the severity of the coronary artery system in patients with CKD. Our results support our hypothesis that the sTWEAK level shows coronary calcification rather than other types of atherosclerotic plaques.
FUNDAMENTO: O receptor fraco indutor de apoptose semelhante a fator de necrose tumoral solúvel (sTWEAK) é um membro da superfamília de TNF que tem um papel crítico na proliferação e inflamação na circulação arterial. OBJETIVOS: Este estudo prospectivo tem o objetivo de mostrar a relação entre os níveis de sTWEAK e calcificação da artéria coronária (CAC) em pacientes com doença renal crônica (DRC). MÉTODOS: Este estudo prospectivo incluiu 139 pacientes consecutivos que passaram por angiografia coronariana por tomografia computadorizada, por qualquer motivo, para síndromes coronarianas agudas, de agosto de 2020 a fevereiro de 2021. Um total de 12 pacientes foi excluído do estudo devido aos critérios de exclusão. Os pacientes foram divididos em dois grupos com base em terem um escore CAC menor que 400 (n=84) ou um escore de 400 ou mais (n=43). A significância foi presumida em p-valor bilateral <0,05. RESULTADOS: À medida que o escore CAC aumentou, os níveis de sTWEAK diminuíram de forma estatisticamente significativa e detectou-se uma relação forte entre níveis de sTWEAK e escore CAC (r: -0,779, p<0,001). A análise ROC revelou que o nível de corte ideal de sTWEAK para prever o escore CAC de 400 era 761 pg/mL com uma sensibilidade de 71% e especificidade de 73% (AUC: 0,78; IC 95%: 0,70-0,85; p <0,001). CONCLUSÕES: Embora os estudos em larga escala tenham demonstrado uma correlação positiva entre os níveis de TFGe e sTWEAK, alguns estudos detectaram que o aumento nos níveis de sTWEAK estão associados a mortalidade e gravidade do sistema da artéria coronária em pacientes com DRC. Nossos resultados comprovam nossa hipótese de que os níveis de sTWEAK mostram calcificação coronária em vez de outros tipos de placas ateroscleróticas.
Subject(s)
Coronary Artery Disease , Renal Insufficiency, Chronic , Biomarkers , Coronary Artery Disease/complications , Coronary Artery Disease/diagnostic imaging , Humans , Prospective Studies , Renal Insufficiency, Chronic/complications , Tumor Necrosis Factor-alphaABSTRACT
BACKGROUND: The tumor necrosis factor-like weak inducer of apoptosis (TWEAK) is one of the inflammatory mediators contributing to the atherosclerotic process. TWEAK has been studied in patients with chronic kidney disease (CKD), and it has demonstrated that its level declines as estimated glomerular filtration rate (eGFR) decreases. Most studies have found that the decreased TWEAK levels were seen in atherosclerosis and associated with plaque calcification. The objective of this prospective study was to clarify any relationship between coronary slow-flow (CSF) and TWEAK levels in patients with CKD under conservative treatment. METHODS: This prospective study included 93 consecutive patients with CKD (mean creatinine level was 1.8±0.4 mg/dL) undergoing invasive coronary angiography (ICA) for any reason except for acute coronary syndromes from May 2019 to March 2020. A total of 93 patients were divided into two groups concerning having CSF (n=35) or no-CSF (n=58). RESULTS: Patients with CSF had higher TWEAK levels than those without CSF (695.2± 225.2 vs. 465.8±157.6, p<0.001). As the number of coronary arteries with slow flow increased, TWEAK levels increased statistically significantly (r:0.635/ p<0.001). Receiver operating characteristic (ROC) analysis showed that TWEAK levels of 516 pg/mL could predict CSF in patients with CKD. CONCLUSIONS: Our study has shown that plasma TWEAK levels were an independent predictor for CSF in patients with CKD. In addition, our study has found that elevated TWEAK levels may not reflect the healthy arteries as it was hypothesized in the past.
Subject(s)
Atherosclerosis , Coronary Artery Disease , No-Reflow Phenomenon , Renal Insufficiency, Chronic , Humans , Atherosclerosis/blood , Atherosclerosis/complications , Biomarkers/blood , Creatinine/blood , Inflammation Mediators/blood , Prospective Studies , Renal Insufficiency, Chronic/blood , Renal Insufficiency, Chronic/complications , Renal Insufficiency, Chronic/therapy , No-Reflow Phenomenon/blood , No-Reflow Phenomenon/etiology , Coronary Artery Disease/blood , Coronary Artery Disease/etiologyABSTRACT
Sarcoidosis is a multisystemic chronic inflammatory disease that the specific etiology is not known clearly. The aim of this study is, to investigate the presence of subclinical atherosclerosis and endothelial dysfunction by using carotid intima-media thickness and flow-mediated dilatation measurements, measuring the copeptin values, which is a stress marker, and interpreting the association of copeptin values with these two variables in sarcoidosis patients without conventional risk factors for coronary artery disease. Seventy-four patients (50 f, 24 m) with histopathological diagnosis of sarcoidosis and 60 healthy volunteers (35 f, 25 m) with similar sociodemographic characteristics were included in this study. CIMT, FMD, and serum copeptin levels of all participants were measured. The values of CIMT and Copeptin in sarcoidosis patients were significantly higher (p = 0.001, p < 0.001 respectively), and FMD was significantly lower (p = 0.01) than the control group. In sarcoidosis patients not significant correlation found among CIMT with copeptin (r: 0.16, p = 0.18) and FMD with copeptin (r: 0.01, p = 0.96). With the demonstration of the presence of subclinical atherosclerosis and endothelial dysfunction, we suggest; sarcoidosis patients may be followed more closely in terms of cardiovascular diseases. And new studies are needed to investigate the pathophysiology and the effects of high copeptin levels in sarcoidosis patients.
Subject(s)
Carotid Artery Diseases/complications , Sarcoidosis/complications , Adult , Biomarkers/blood , Carotid Artery Diseases/blood , Carotid Artery Diseases/diagnostic imaging , Carotid Artery Diseases/physiopathology , Carotid Intima-Media Thickness , Case-Control Studies , Female , Glycopeptides/blood , Humans , Male , Middle Aged , Predictive Value of Tests , Prognosis , Sarcoidosis/blood , Sarcoidosis/diagnosis , Up-Regulation , VasodilationABSTRACT
OBJECTIVE: This study aims to assess endocan levels in patients with acromegaly who have active disease or disease in remission and to investigate a relation between endocan levels and endothelial dysfunction in these patients. DESIGN: The study is a case-control study. Study was conducted at Istanbul Medeniyet University Goztepe Training and Research Hospital between 2013 and 2019. Patients who were older than 18 years with acromegaly diagnosis were recruited if they agreed to participate. Patients with uncontrolled diabetes (DM), hypertension (HT), hyperlipidemia, decompensated heart failure, immune or infectious diseases, moderate-severe valve disease and stage 3 or more advanced chronic kidney disease were excluded. There were 30 healthy control subjects who agreed to participate to the study. Patients with acromegaly were divided into two groups as: disease active patients and patients in remission. Serum endocan levels were measured with enzyme linked immunosorbent assay (ELISA) method endothelial function was assessed with flow mediated dilatation (FMD). RESULTS: There were 85 patients included to the study. Twenty-three patients had active disease, 31 were in remission and 31 were healthy controls. FMD was higher in controls compared to patients in active disease and patients in remission (p < 0.001). There was no difference between patients with active disease for FMD and patients in remission (p = 0.088). There was statistically significant correlation between FMD and endocan and insulin like growth hormone-1 (IGF-1) levels of patients with acromegaly. As FMD increased endocan and IGF-1 decreased. A moderate negative relation between FMD and endocan was identified (p < 0.001, r:-0.409) as well as FMD and IGF-1 levels (p:0.011, r:-0.377). Along with endocan and IGF-1, DM, HT, sex, body mass index, age and uric acid were associated with changes in FMD. CONCLUSIONS: Endocan levels and endothelial function measured with FMD have an inverse relationship. Endocan may prove to be a marker for endothelial dysfunction in acromegaly.
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Acromegaly/pathology , Endothelium, Vascular/pathology , Neoplasm Proteins/blood , Proteoglycans/blood , Acromegaly/complications , Aged , Cardiovascular Diseases/complications , Case-Control Studies , Female , Glucose Tolerance Test , Humans , Inflammation/complications , Insulin-Like Growth Factor I/biosynthesis , Linear Models , Male , Middle Aged , ROC CurveABSTRACT
BACKGROUND: Celiac disease (CD) is an enteropathy characterized with immune reaction to gliadin protein. AIM: In this study, we aimed to assess effect of CD on coronary microvascular circulation and the association between coronary flow velocity reserve (CFVR) and hs-CRP/Albumin ratio. MATERIAL AND METHODS: Study was conducted between March 2017 and November 2018 with CD at Umraniye Training and Research Hospital Gastroenterology Clinic. CFVR was defined as the ratio of hyperemic to baseline diastolic peak velocities. CFVR ≥ 2.0 was considered normal. C-reactive protein/albumin ratio (CAR) was calculated as hs-CRP/albumin. RESULTS: Serum albumin (4.27 ± 0.56 vs 4.50 ± 0.34; P value: .04) level was significantly lower in celiac group but higher Hs-CRP (2.44 ± 1.24 vs 1.82 ± 1.29; P value < .01), hs-CRP/albumin ratio (0.57 ± 0.30 vs 0.41 ± 0.31; P value: .03) were recorded in celiac group. Both hyperemic flow and CFVR substantially lower in the celiac group compared to controls. In univariate analysis; age, hs-CRP, and hs-CRP/albumin ratio were associated with low CFVR and hs-CRP/albumin level was an accurate predictor of low CFVR at the ROC curve. CONCLUSION: In this study, we found that in patients with CD, coronary flow reserve is impaired.
Subject(s)
Celiac Disease , Blood Flow Velocity , Celiac Disease/complications , Coronary Circulation , Coronary Vessels/diagnostic imaging , Diastole , Humans , MicrocirculationABSTRACT
OBJECTIVE: In this study, we aimed to investigate the presence of subclinical atherosclerosis by measuring epicardial fat thickness (EFT) and carotid intima-media thickness (cIMT), evaluate low-level inflammation with high-sensitivity C-reactive protein (hsCRP), and evaluate whether there is a relationship among lipid profile, atherogenic indices, and hsCRP with these subclinical atherosclerosis markers in patients with celiac disease (CD). METHODS: After exclusion and inclusion criteria were applied, 31 patients with CD (24 female, mean age: 39.4±12.3 years) and 32 healthy controls (21 female, mean age: 39.5±4.4 years), totally 63 cases, were recruited. Subclinical atherosclerosis was evaluated with EFT by transthoracic echocardiography and cIMT by ultrasonography. Inflammatory markers including erythrocyte sedimentation rate (ESR), hsCRP, and lipid profile were recorded. Also, atherogenic indices were calculated: Castelli risk index I and II (TG/HDL-c and LDL-c/HDL-c, respectively), atherogenic index of plasma (AIP; logarithm TG/HDL-c), non-HDL-c (TG-HDL-c), and atherogenic coefficient (AC; non-HDL-c/HDL-c). RESULTS: EFT was significantly higher in the CD group (0.49±0.10 vs. 0.49±0.09; p-value: 0.02). Although cIMT was higher in the patient group, it did not reach statistical significance (0.51±0.08, 0.47±0.08; p-value: 0.10). HDL cholesterol level was found to be significantly lower (42.0±8.8 vs. 50.0±13.7; p-value: 0.01), and the plasma atherogenic index was found to be significantly higher in the patient group (0.98±0.50 vs. 0.62±0.64; p-value: 0.02). hsCRP (3.51±3.18 vs. 1.92±1.40; p-value: 0.02) and ESR (17.2±12.8 with 9.7±3.1; p-value: 0.01) were found to be significantly higher in the CD group. Although there was a significant positive correlation between EFT and hsCRP (r: 0.453; p-value: 0.01), there was a significant negative correlation between cIMT and HDL-cholesterol (-0.339; p-value: 0.05), and a significant positive correlation with the other components of the atherogenic index was found. CONCLUSION: The risk of atherosclerosis has been increased in patients with CD. Chronic inflammation may be responsible for this increase along with atherogenic indices.