ABSTRACT
INTRODUCTION: Left ventricular hypertrophy (LVH) is a significant risk factor for cardiovascular complications in hemodialysis (HD) patients. Hypervolemia has been accepted as an independent risk factor for progressive LVH in HD patients. Additionally, high FGF23 levels have been a significant predictor of cardiovascular mortality and morbidity in chronic kidney disease and HD patients. The aim of our study is to investigate the correlation among LVH, interdialytic volume increase and FGF-23 in the patients on a chronic hemodialysis program. DESIGN AND METHODS: A total of 97 chronic hemodialysis patients (64.43 ± 11.28 years old, M/F:47/50) were included in the study. Human FGF-23 ELISA kit was used for FGF-23 analysis of predialysis blood samples. Echocardiographic evaluation was performed in all of the patients after dialysis. Left Ventricular Mass Index (LVMI) was calculated by using the Devereux Formula. We collected the following data: LVMI, FGF-23 levels, interdialytic fluid gain, blood pressure changes, and the other biochemical and clinical parameters. RESULTS: Mean LVMI of the patients was 184.41 ± 48.62 g/m(2). LVMI of the patients with daily urine output > 250 mL was found significantly lower. Statistically significant positive correlation was found between predialysis systolic blood pressure, predialysis diastolic blood pressure, predialysis mean arterial blood pressure and LVMI measurements (p < 0.01). Mean interdialytic volume excess was correlated with LVMI measurements of the patients (r = 0.459; p < 0.01). Increased FGF-23 levels (159.79 ± 134.99 ng/L) predicted increased LVMI measurements of the patients (r = 0.322; p < 0.01). In addition, FGF-23 levels were also increased as the interdialytic fluid volume increased (r = 0.326; p < 0.05). A positive correlation was also found between FGF-23 levels and interventricular septum thickness (r = 0.238; p < 0.05). Predialysis mean arterial blood pressure, predialysis volume overload and presence of diabetes were determined to be independent risk factors on LVMI on multivariate regression analysis. CONCLUSION: Our study showed that interdialytic volume overload increased both LVMI and FGF-23 values. We can consider that interdialytic volume control exerts positive effects on increased FGF-23 levels which predict the negative cardiovascular outcomes.
Subject(s)
Fibroblast Growth Factors/blood , Hypertrophy, Left Ventricular/etiology , Hypertrophy, Left Ventricular/mortality , Kidney Failure, Chronic/therapy , Renal Dialysis/adverse effects , Water-Electrolyte Imbalance/complications , Adult , Aged , Biomarkers/blood , Cohort Studies , Disease Progression , Echocardiography, Doppler/methods , Female , Fibroblast Growth Factor-23 , Hemodialysis Units, Hospital , Humans , Hypertrophy, Left Ventricular/blood , Kidney Failure, Chronic/diagnosis , Kidney Failure, Chronic/mortality , Linear Models , Male , Middle Aged , Predictive Value of Tests , Prognosis , Prospective Studies , Renal Dialysis/methods , Risk Assessment , Survival Rate , Treatment Outcome , Turkey , Water-Electrolyte Imbalance/diagnosisABSTRACT
We report a 59-year old patient with a double J ureteral catheter displaced out of the ureter through the inferior vena cava and right ventricle. The catheter was removed successfully under cardiopulmonary bypass.
Subject(s)
Foreign-Body Migration/etiology , Heart Ventricles/surgery , Stents/adverse effects , Ureteral Calculi/therapy , Urinary Catheters/adverse effects , Vena Cava, Inferior/surgery , Cardiac Surgical Procedures , Device Removal , Female , Foreign-Body Migration/diagnosis , Foreign-Body Migration/surgery , Heart Ventricles/diagnostic imaging , Humans , Middle Aged , Phlebography , Tomography, X-Ray Computed , Treatment Outcome , Ureteral Calculi/diagnosis , Vena Cava, Inferior/diagnostic imagingABSTRACT
OBJECTIVE: Brain natriuretic peptide (BNP) is secreted predominantly from the ventricles in response to increased wall stress, which is known to be one of the major forces driving left ventricular (LV) remodeling. In this prospective study, we evaluated value of BNP levels in acute myocardial infarction (MI) patients for the prediction of heart failure during one year of follow-up. METHODS: Seventy-four patients with a first ST-elevation MI were examined prospectively after 5 days and 1 month with echocardiography and blood samples for BNP were obtained. Clinical events were recorded during 12 months of follow-up. Multivariate linear regression analysis was used to analyze the value of different baseline characteristics as independent predictors of LV ejection fraction (LVEF) = 40% and clinical heart failure. Diagnostic ability of BNP to detect LVEF = 40% and heart failure was evaluated with receiver operating characteristic (ROC) curves. RESULTS: Brain natriuretic peptide levels were higher in patients developing symptomatic heart failure during follow up irrespective of presence of LVEF =40% (68.9+/-52.5 vs 21.4+/-18.4, p=0.003, for baseline BNP and 79.3+/-35.8 pg/ml vs. 22.9+/-15.8 pg/ml for one month BNP, p<0.001). Regression analysis including pain duration, peak creatine kinase-MB levels, MI localization, baseline BNP levels and baseline LV volumes yielded that baseline BNP was the most powerful predictor of one-year LVEF =40% (Beta: 0.376, p=0.004). Multivariate analyses, testing for independent predictive information of pain duration, peak creatine kinase-MB, MI localization, thrombolytic therapy or primary percutaneous intervention, fifth day and one month LV volumes, LVEF and BNP levels, for development of clinical heart failure, showed that one month BNP was the single significant predictor (Beta: 0.675, p<0.001). There was a negative correlation between BNP levels and LVEF (r=-0.599, p<0.001, for baseline BNP level). Higher BNP levels were associated with greater increase in LV end-systolic (r= 0.531, p< 0.001) and end-diastolic volumes (r= 0.385, p= 0.001) during one year of follow-up. A baseline BNP level of >39 pg/ml identified LVEF = 40% at one year with a sensitivity of 72.7% and specificity of 91.9% (OR=30.4, 95% CI, 6.1-152.3, p<0.001, AUC=0.852). A BNP level <39 pg/ml also increased the risk of clinical heart failure (for baseline BNP sensitivity: 60.0%, specificity 89.1%, OR=12.2; 95% CI, 2.7-54.1, p=0.001 and for one month BNP sensitivity: 80.0%, specificity 85.9%, OR=24.4; 95% CI, 4.5-134.1, p<0.001). CONCLUSIONS: High level of BNP is a powerful marker of LV systolic dysfunction and poor prognosis after MI. Increased BNP levels are associated with progressive ventricular dilatation and development of clinical heart failure.
Subject(s)
Heart Failure/diagnosis , Myocardial Infarction/complications , Natriuretic Peptide, Brain/blood , Ventricular Dysfunction, Left/diagnosis , Case-Control Studies , Echocardiography , Female , Follow-Up Studies , Heart Failure/blood , Heart Failure/etiology , Humans , Male , Middle Aged , Myocardial Infarction/blood , Myocardial Infarction/diagnostic imaging , Predictive Value of Tests , Prognosis , Prospective Studies , ROC Curve , Sensitivity and Specificity , Ventricular Dysfunction, Left/blood , Ventricular Dysfunction, Left/etiologyABSTRACT
AIMS: The aim of our study was to evaluate the factors leading to embolization in patients with left atrial thrombi (LAT). With this purpose, we retrospectively analyzed clinical, transthoracic, transesophageal echocardiographic data of patients with LAT in the transesophageal echocardiographic evaluation. METHODS AND RESULTS: One hundred ninety-two patients with LAT not on anticoagulant therapy were divided into two groups according to the presence of prior ischemic stroke. The group with ischemic stroke included more patients with sinus rhythm and less patients with mitral stenosis. They had smaller left atrial diameter, more left atrial appendage spontaneous echo-contrast, higher appendage ejection fraction, and emptying velocity. CONCLUSION: Once the thrombus has been formed, cerebral embolization seems to be higher in patients with relatively preserved appendage ejection fraction and emptying velocity. Presence of atrial appendage spontaneous echo-contrast also favor embolization. Factors leading to embolization seem to differ in some respects from the causes of thrombus formation.