Clinical, laboratory and instrumental evaluation of structural and functional changes of the liver in patients with heart failure

Heart failure is detected in 2% of the population. The leading causes of heart failure are coronary heart disease, arterial hypertension, and valvular heart disease. The number of patients with chronic heart failure continues to increase despite the new methods of diagnosis and treatment. A special contribution is made by damage to target organs in the development of cardiovascular pathology. Impaired liver function or congestive liver is common in heart failure and increases the risk of death and requires further study. The mechanism of liver damage in chronic heart failure is complex and multicomponent. The sensitivity and specificity of standard clinical, laboratory and instrumental methods for the diagnosis of congestive liver are insufficient. With the increase, severity and duration of venous congestion, structural changes in the architectonics occur, leading to the formation of liver fibrosis. The development of cardiac liver fibrosis leads to a complication of the course of chronic heart failure and an increase in mortality. Among the new diagnostic methods, the most important are serological markers of liver fibrosis, which have high diagnostic accuracy, as well as histological determination of fibrosis, as well as ultrasound examination of the liver in B-mode and determination of liver stiffness by elastography. Direct and indirect serological markers have a higher diagnostic value when using their combination in the composition of panels in the development of hepatopathy of different origins. An increase in the concentration of markers of fibrosis and liver stiffness during elastography correlates with the severity of heart failure and a long-term prognosis for mortality, including from extrahepatic diseases. Performing liver elastography in dynamics allows to monitor the course and treatment of heart failure. The optimal diagnostic method is a combination of direct and indirect markers of fibrosis, ultrasound diagnostics and elastography, in addition to clinical assessment of signs and direct assessment of hemodynamic parameters.

A Case Report of Hepatocellular Carcinoma Derived from Rastelli Procedure-Related Congestive Liver Disease

[Background] The prognosis of congenital heart disease in children has improved, but late complications in adulthood are becoming an important problem. One late complication after congenital heart surgery is congestive liver disease, leading to liver cirrhosis and hepatocellular carcinoma (HCC). The Rastelli procedure is one of the surgical methods for transposition of the great arteries, and patients are thought have a low post-surgical risk of congestive hepatopathy by receiving re-intervention for right ventricular outflow tract obstruction.[Case presentation] We present the first case of HCC derived from Rastelli procedure-related congestive liver disease in a 41-year-old male. The patient underwent the Rastelli operation at 2 years of age and right ventricular outflow tract reconstruction at 10 and 35 years of age due to right ventricular outflow tract obstruction. At 41 years of age, a hepatic tumor was detected by computed tomography. Abdominal enhancing computed tomography revealed a partially hypervascular tumor in segment 2 in early phase and wash-out in late phase. The patient was diagnosed with HCC and underwent left lateral segmentectomy of the liver, splenectomy, and partial gastrectomy. The patient was discharged on the 28th postoperative day without postoperative complications. The resected tumor pathologically revealed moderately differentiated HCC and F3 liver fibrosis.[Conclusions] In the management of patients after the Rastelli operation, surveillance for congestive liver disease and HCC development is important, even if the patients have undergone right ventricular outflow tract reconstruction.

Noninvasive diagnosis of liver fibrosis in the complex cardiac malformation survivors – a review of the literature

The aim of this review is to summarize the information on the pathogenesis and diagnosis of congestive liver disease sec-ondary to the Fontan and Glenn surgery for complex cardiac malformations, focusing on non-invasive diagnostic modalities. We performed an electronic database search (Pubmed, Web of Science) with the data range from 2001 to 2020. We selected the studies that addressed the pathogenesis of congestive liver disease secondary to cardiac malformations and articles regarding noninvasive methods of determining liver fibrosis in this group. We found that conventional imaging methods do not allow the detection of the initial stages of liver fibrosis. Elastography results are altered by congestion and cut-off values are not yet validated. More studies are required in order to provide evidence-based guidelines regarding the non-invasive diagnosis of hepatic fibrosis secondary to congenital heart disease. Patients with congenital cardiac malformations require close monitoring and early diagnosis of liver complications to allow prompt therapeutic intervention.

Deportalization, Venous Congestion, Venous Deprivation: Serial Measurements of Volumes and Functions on Morphofunctional 99mTc-Mebrofenin SPECT-CT

The objective was to assess the changes in regional volumes and functions under venous-impaired vascular conditions following liver preparation. Twelve patients underwent right portal vein embolization (PVE) (n = 5) or extended liver venous deprivation (eLVD, i.e., portal and right and middle hepatic veins embolization) (n = 7). Volume and function measurements of deportalized liver, venous-deprived liver and congestive liver were performed before and after PVE/eLVD at days 7, 14 and 21 using 99mTc-mebrofenin hepatobiliary scintigraphy with single-photon emission computed tomography and computed tomography (99mTc-mebrofenin SPECT-CT). Volume and function progressed independently in the deportalized liver (p = 0.47) with an early decrease in function (median −18.2% (IQR, −19.4–−14.5) at day 7) followed by a decrease in volume (−19.3% (−22.6–−14.4) at day 21). Volume and function progressed independently in the venous deprived liver (p = 0.80) with a marked and early decrease in function (−41.1% (−52.0–−12.9) at day 7) but minimal changes in volume (−4.7% (−10.4–+3.9) at day 21). Volume and function progressed independently in the congestive liver (p = 0.21) with a gradual increase in volume (+43.2% (+38.3–+51.2) at day 21) that preceded a late and moderate increase in function at day 21 (+34.8% (−8.3–+46.6)), concomitantly to the disappearance of hypoattenuated congestive areas in segment IV (S4) on CT, initially observed in 6/7 patients after eLVD and represented 35.3% (22.2–46.4) of whole S4 volume. Liver volume and function progress independently whatever the vascular condition. Hepatic congestion from outflow obstruction drives volume increase but results in early impaired function.

Use of Idarucizumab to Revert the Anticoagulant Effect of Dabigatran in Heart Transplant Surgery: An Institutional Experience

Heart transplant is a surgical procedure with a high risk of perioperative bleeding in patients with a previous history of sternotomy, congestive liver disease, and/or use of oral anticoagulants. Anticoagulation is usually done with coumarin agents (warfarin, acenocoumarol), while on the waiting list, vitamin K is available allowing for partial reversal of the anticoagulant effect, although with variable INR and risk of uncontrolled bleeding. Direct oral anticoagulants have emerged as an alternative to the use of coumarins in patients with nonvalvular atrial fibrillation (NVAF). The main disadvantage of this group of drugs is that there was no specific reversal agent available that would allow an urgent reversal of the anticoagulant effect. The recent commercialization of idarucizumab (specific reversal agent) has allowed patients with NVAF on the waiting list for heart transplant to be treated with dabigatran. We present the case of a patient with advanced chronic heart failure and NVAF anticoagulated with dabigatran, who underwent urgent heart transplant after administration of idarucizumab, without complications derived from its use or from anticoagulation.

Hyperthyroidism with Biventricular Heart Failure and Cirrhotic Transformation of the Liver

Cardiovascular symptoms remain the most common presenting features and leading causes of death in hyperthyroidism. We report a young female with reported thyroid disease and medication noncompliance presenting with atrial fibrillation, severe atrioventricular regurgitation, severely dilated right heart with reduced function, and moderate pulmonary hypertension (PH), which was further complicated by congestive liver injury with ascites and pancytopenia. Thyroid work-up revealed suppressed TSH, elevated free T4 and T3 along with elevated anti-thyroglobulin antibodies, thyroid peroxidase antibodies, and thyroid-stimulating immunoglobulin, suggesting Graves’ thyrotoxicosis. Ultrasound of the abdomen was suggestive of liver cirrhosis and ascites, which was thought to be cardiac cirrhosis, after multiple negative work-ups for alternate causes of cirrhosis. Ascitic fluid analysis revealed portal hypertension as the cause. The patient was restarted on antithyroid medication with gradual improvement of thyroid function and in clinical and echocardiogram findings. In contrast to primary PH that carries a poor prognosis and has limited treatment options, PH due to Graves’ disease carries a good prognosis with prior reports of resolution after appropriate treatment, emphasizing the importance of early recognition. Also, unlike cirrhosis caused by alcohol or viral hepatitis, the effect of cardiac cirrhosis on overall prognosis has not been clearly established.

Differential diagnosis of ascites in internal medicine: clinical case

Ascites and hydrothorax may be the symptoms of congestive heart failure and do not always reflects presense of the decompensated liver cirrhosis. Clinical examination of patient with chronic hepatitis C which cyanosis of the lips, cervival veins pulsation, a triple heart rhythm indicated on pathology of the heart (constrictive pericarditis), which was confirmed by instrumental methods. Congestive heart failure has lead to the congestive liver in a young female patient. Regression of all the symptoms of heart failure occurred after surgical treatment (pericardectomy).