ABSTRACT
BACKGROUND: Chronic Hepatitis C virus (HCV) infection and liver cirrhosis may be associated with atherosclerosis and coronary artery disease (CAD). There are two phases to atherosclerosis, Subclinical and Clinical. Assessment of atherosclerosis may be started at its Subclinical phase by the evaluation of Epicardial Fat Thickness (EpFT) and Carotid Intima Thickness (CIMT). AIM OF THE STUDY: The aim of the study was to evaluate Clinical and Subclinical atherosclerosis in chronic HCV patients with and without liver cirrhosis by evaluating CIMT and EpFT and correlating the results with Child-Pugh functional scoring of cirrhosis as well as with ultrasound and laboratory parameters that define the severity of liver disease. PATIENTS AND METHODS: This study involved 64 chronic HCV patients that were divided into two groups: 24 patients without liver cirrhosis and 40 patients with liver cirrhosis in addition to 20 apparently healthy volunteers serving as control. All of the 84 subjects were subjected to the following: Clinical evaluation; Routine Laboratory Evaluation (CBC, Liver Function Tests, Renal Function Tests, Serum electrolytes, Cholesterol, Triglycerides, HBs antigen and HCV antibody); ECG; Abdominal ultrasound; Echocardiographic evaluation of segmental wall motion abnormalities and EpFT and B-Mode Carotid ultrasonography for evaluation of CIMT. RESULTS: In the cirrhotic HCV group, the CIMT and EpFT were both significantly increased [Compared to control group (p = 0.000), compared to the non-cirrhotic HCV group (p = 0.000)]. In the non-cirrhotic HCV group, the CIMT and EpFT were both significantly increased compared to the control group with a p-value of 0.003 for CIMT and 0.048 for EpFT. The CIMT and EpFT were also positively correlated with each other (r = 0.456, p = 0.001). There was a statistically significant increase in the EpFT and CIMT in Child class B patients compared to Child class A (p = 0.007 for CIMT and p = 0.028 for EpFT) and in Child class C patients compared to Child class B patients (p = 0.001 for CIMT and 0.005 for EpFT). CIMT and EpFT were correlated positively with AST (r = 0.385, p = 0.002 for CIMT, and r = 0.379, p = 0.003 for EpFT), Total Bilirubin (r = 0.378, p = 0.003 for CIMT, and r = 0.384, p = 0.002 for EpFT), INR% (r = 0.456, p = 0.001 for CIMT, and r = 0.384, p = 0.001 for EpFT), CRP (r = 0.378, p = 0.003 for CIMT, and r = 0.386, p = 0.002 for EpFT), spleen span (r = 0.417, p = 0.001 for CIMT, and r = 0.437, p = 0.001 for EpFT) and portal Vein Diameter (r = 0.372, p = 0.003 for CIMT, and r = 0.379, p = 0.003 for EpFT). CIMT and EpFT were correlated negatively with Albumin (r = -0.379, p = 0.003 for CIMT, and r = -0.370, p = 0.003 for EpFT), platelets count (r = -0.382, p = 0.002 for CIMT, and r = -0.378, p = 0.003 for EpFT) and Liver Span (r = -0.433, p = 0.001 for CIMT, and r = -0.424, p = 0.001 for EpFT). CONCLUSION: EpFT and CIMT significantly increased in chronic hepatitis C virus patients especially in those with cirrhosis and closely correlated with each other. Their thickness also correlated with the Child-Pugh functional scoring of cirrhosis as well as with ultrasound and laboratory parameters that define the severity of liver disease.The echocardiographic assessment of EpFT and the carotid Doppler assessment of CIMT may provide appropriate and simple screening markers for subclinical atherosclerosis and cardiovascular risk in chronic HCV patients with and without cirrhosis.
ABSTRACT
INTRODUCTION: Atherosclerotic cardiovascular disease remains the leading cause of increased morbidity and mortality observed in chronic kidney disease (CKD) patients. Endothelial dysfunction (ED) is thought to be a key initial event in the development of atherosclerosis. The aim of this study was to evaluate the potential role of hemostatic factors in atherosclerosis, thrombosis and cardiovascular complications in patients suffering from chronic renal disease. METHODS: The study was conducted on 50 renal patients divided into two groups of equal size. Group 1 consisted of 25 patients with end-stage renal disease (ESRD) on regular hemodialysis. Group 2 consisted of 25 chronic renal disease patients on conservative treatment. Twenty age- and sex-matched healthy subjects were included in the study to serve as a control group. Thrombomodulin (TM), von Willebrand factor (vWF), tissue plasminogen activator (t-PA), plasminogen activator inhibitor (PAI-1) and hsCRP were assessed. High-resolution B-mode ultrasonography of both the common and internal carotid arteries to measure carotid intima media thickness (CIMT) was performed on all subjects. RESULTS: There were highly significant increases in hsCRP, TM, vWF, tPA and PAI-1 in both patient groups compared to the control group (P<0.01 for all except for TM between group 2 and 3 P<0.05) with significant increase in group 1 compared to group 2 (P<0.01). In addition, there was a highly significant increase in CIMT in both patient groups compared to the control group (P<0.01) with a significant increase in group 1 compared to group 2 (P<0.05). The study revealed significant positive correlation of hemostatic factors (TM, vWf, PAI-1 & t-PA) with creatinine, urea, hsCRP & CIMT. CONCLUSION: CKD patients have increased risk of atherosclerosis as measured by CIMT, which is used as a surrogate marker of early atherosclerosis and has been shown to be a strong predictor of future myocardial infarction and stroke. They have high levels of TM, vWF, tPA, PAI-1 that correlate with kidney function, hsCRP and CIMT. Therefore, these abnormalities in hemostasis may account for the increased risk of atherothrombosis in these patients. The elevated hsCRP levels and their correlation to hemostatic factors and CIMT might provide an important clue to link a systemic marker of inflammation to atherosclerosis. Further research is required to better understand the procoagulant state in patients with CKD.
ABSTRACT
INTRODUCTION: Hyponatremia is common in cirrhosis. The relationship between hyponatremia and severity of cirrhosis is evidenced by its close association with the occurrence of complications, the prevalence of hepatic encephalopathy, hepatorenal syndrome, spontaneous bacterial peritonitis, refectory ascites, and hepatic hydrothorax. The aim of this study was assess the impact of hyponatremia on the occurrence of both liver-related complications and the hemodynamic cardiovascular dysfunction. METHODS: This prospective study was conducted in 2015 on 74 patients with liver cirrhosis. The patients were from the Gastroenterology and Hepatology Department of Theodor Bilharz Research Institute in Giza, Egypt. The patients were divided into three groups according to their serum level of sodium. Group 1 included 30 patients with serum sodium >135 meq/L, group 2 included 24 patients with serum sodium between135 and 125 meq/L, and group 3 included 20 patients with serum sodium <125 meq/L. For each of the patients, we conducted aclinical examination, laboratory investigations, chest X-ray, ECG, abdominal sonar, and echocardiography. RESULTS: Hyponatremia was found in 59.46% of our cirrhotic patients, and they showed significantly increased Model for End-Stage Liver Disease (MELD) score, MELD-Na score, QTc interval, Pulmonary vascular resistance (PVR) and inferior vena cava (IVC) collapsibility, and decreased SVR and IVC diameter. Also hepatic encephalopathy, ascites, renal failure, infectious complications, and pleural effusion were significantly more common in hyponatremic cirrhotic patients. CONCLUSION: In cirrhosis, hyponatremia is more common in severe cardiovascular dysfunction and associated with increased risk of hepatic encephalopathy, ascites, illness severity scores, renal failure, infectious complications, and pleural effusion. We recommend selective oral administration of vasopressin V2-receptor antagonist, tolvaptan, which acts to increase the excretion of free water, thereby resolving hypervolemic hyponatremia and may have the potential to improve outcomes in these patients.
ABSTRACT
BACKGROUND: Functional renal failure and cardiovascular dysfunction are common complications of liver cirrhosis. This study aimed to evaluate cardiac performance, systemic vascular resistance (SVR) and fluid status in patients with decompensated liver cirrhosis either with or without functional renal failure. METHODS: Sixty patients diagnosed as having decompensated liver cirrhosis were divided into two groups. Group 1 included 30 patients with decompensated liver cirrhosis with ascites and with creatinine values ≤ 1.5 mg/dl. Group 2 included 30 azotemic decompensated cirrhotic patients with diagnostic criteria of hepatorenal syndrome (HRS). Also, 20 healthy subjects, of matched age and sex to the Group 1 and Group 2 patients, were included in the study as the control group. All patients and normal controls were subjected to clinical examination, laboratory evaluation, ECG, abdominal ultrasonography and echocardiographic studies. RESULTS: The echocardiographic and ECG data showed significant increase in LAD (P<0.01, P<0.01), AoD (P<0.05, P<0.01), interventricular septum thickness (IVST) (P<0.01, P<0.01), posterior wall thickness (PWT) (P<0.01, P<0.01), EDD (P<0.01, P<0.01), ESD (P<0.05, P<0.01), left ventricular (LV) mass (P<0.01, P<0.01), and Corrected QT (QTc) (P<0.01, P<0.01) interval with significant decrease in SVR (P<0.01, P<0.01). Additionally, there was significant decrease in IVC diameter in both patients groups compared to the control group (P<0.01, P<0.01). CONCLUSION: Patients with decompensated liver cirrhosis have low SVR, and Doppler echocardiography provides an easy noninvasive tool to assess this finding. Also, these patients demonstrate small inferior vena cava (IVC) diameter with normal collapsibility, which indicates low effective plasma volume. Measuring IVC diameter and collapsibility are of value in the prediction of intravascular fluid status in liver cirrhosis. This is especially true with renal dysfunction. Early addition of oral vasoconstrictors in decompensated patients may correct the SVR and circulatory dysfunction and hinder HRS occurrence.
