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The Two Congested Failing Giants: Heart and Liver

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The Two Congested Failing Giants: Heart and Liver Internal and Emergency Medicine (2019) 14:907–910 https://doi.org/10.1007/s11739-019-02103-6 IM - COMMENTARY The two congested failing giants: heart and liver Piero Portincasa1,2 Received: 8 April 2019 / Accepted: 2 May 2019 / Published online: 11 May 2019 © Società Italiana di Medicina Interna (SIMI) 2019 Liver disease related to the heart includes acute liver injury NYHA II–IV secondary to ischemic heart disease 31% due to the heart, i.e., myocardial infarction, sustained and non-ischemic dilated cardiomyopathy 69%). Inclusion arrhythmia resulting in passive congestion of the liver, criteria were broad and included hepatomegaly, pruritus, chronic passive liver congestion, and “cardiac cirrhosis” jaundice and ascites, ultrasonographic fndings of liver dis- [1]. Causes of congestive heart failure appear in Fig. 1 [1]. ease and portal hypertension, upper endoscopy positive for Congestive heart failure occurs when patients with advanced varices, and abnormally persistent liver function tests. heart failure experience persistent and severe symptoms The liver receives about one-forth of cardiac output, is interfering with daily life. Advanced congestive heart failure very prone to injury when conditions afect blood vessels, manifests with typical symptoms (Fig. 1) and, by defnition, and contribute to passive congestion or decreased perfusion manifestations occur despite maximum evidence-based med- [10]. Patients developing right-sided heart failure alone ical therapy of heart failure, and reversible causes addressed or associated with left-sided heart failure may evolve to [2, 3]. Advanced heart failure has major socio-economic hepatic congestion, i.e., congestive hepatopathy resulting in burden; patients experience recurrent hospitalization, and elevation of central venous pressure. Congestive hepatopa- the risk of mortality increases with the frequency of re-hos- thy is suggested by liver enzyme abnormalities and right- pitalization [4, 5]. We reported that addressing an intensive sided heart failure or other cause of elevated central pres- outpatient management program to patients with chronic sures. Three major pathogenetic mechanisms predispose to heart failure has benefcial long-term efects on clinical hepatic injury under conditions of congestion, i.e., decreased parameters, and decreases hospitalization [6]. hepatic blood fow, decreased arterial oxygen saturation, and Durante-Mangoni et al. [7] describe a retrospective increased hepatic venous pressures (Fig. 1) [10]. At gross study on clinical and histopathological features of liver examination, the congestive liver has a “nutmeg” appearance injury in consecutive patients with advanced heart failure, [11] with dark centrilobular zones (sinusoidal congestion), seen between 2008 and 2016. The authors acknowledge which alternate with pale (normal) or yellowish (fatty) peri- that cardiogenic liver disease is a common, but yet poorly portal zones [11, 12]. characterized complication of advanced congestive heart Durante-Mangoni et al. [7] found that patients had a stif failure. Despite previous studies [8, 9], information about enlarged hepatomegaly, and elevated bilirubin. They also the ultimate impact of advanced heart failure in the liver included 19 viral hepatitis patients (42%), often encountered shows a wide variability. The authors reviewed 228 inpa- in the “real-life” setting without an a priori exclusion crite- tients undergoing screening for heart transplant. Forty-fve rion for heart transplant. Included were also patients with patients underwent liver biopsy for suspected liver disease fatty liver, hemochromatosis, autoimmune liver disease, or and median duration of cardiac symptoms of 5 years (class alcohol intake > 40 g/day in men and 30 g/day in women. A complete cardiovascular functional assessment by echocar- diography and Doppler ultrasound was performed. * Piero Portincasa Histological changes in congestive hepatopathy include [email protected] sinusoidal dilatation and edema, hepatic cord atrophy, con- 1 Division of Internal Medicine “Augusto Murri”, Department gestion, fatty change, red blood cells showing extravasation of Biomedical Sciences and Human Oncology, University into the Disse space, especially with increasing hepatic of Bari “Aldo Moro’’, Bari, Italy venous pressure [13, 14]. Cholestasis can also occur and 2 Department of Biomedical Sciences and Human Oncology, bile thrombi appear in the canaliculi [15]. Hepatic and right Clinica Medica “Augusto Murri”, University of Bari Medical atrial pressures, and ischemia do show a correlation with School, Policlinico Hospital, Piazza Giulio Cesare 11, 70124 Bari, Italy the extent of infammatory changes, necrosis (especially Vol.:(0123456789)1 3 908 Internal and Emergency Medicine (2019) 14:907–910 CONGESTIVE HEART FAILURE Major causes HEPATIC INJURY BLOOD • Miocardiomyopathy hepac blood flow serum bilirubin • Constricve pericardis arterial oxygen saturaon Total bilirubin generally <3 mg/dL • Tricuspid regurgitaon hepac venous pressures Mainly unconjugated • Mitral stenosis •Hemolysis • Congenital heart defects •Hepatocellular dysfunction •Canalicular obstruction (secondary to • Cor pulmonale distended hepatic veins) Symptoms •Pulmonary infarction Intolerance to exercise • •Drugs • Fague and dyspnea •Superimposed sepsis • Unintenonal weight loss • Refractory volume overload • Hypotension, signs of inadequate perfusion serumalkaline phosphatase Mildly elevated serumaminotransferase Mildly increased (2-3x UNL) serumalbuminemia ≤3.4 g/dL, rarely less than 2.5 g/dL Right hypocondrium dull pain • liver synthesis, Stretching of liver capsule • degradation Jaundice • vascular permeability Differential diagnosis from •Renal and gastrointestinal loss (protein- obstructive conditions losing enteropathy) •Ongoing intestinal lymphatic pressure Abnormal prothrombintime hepatic synthesis of coagulation factors(II,V,VII,IX, and X) LIVER CIRRHOSIS •Hepatomegaly •Increased portal hypertension •Ascites Fig. 1 Major etio-pathological, clinical, and laboratory changes with [30, 31]. Few factors contribute to this fnding [32, 33]. Longstand- ongoing congestive heart failure and congestive hepatopathy. Causes ing right heart failure and elevated central venous pressure can also of congestive heart failure and symptoms appear in the left upper yel- evolve to liver cirrhosis [14], and symptoms include a dull pain in low box. Major causes of hepatic injury, symptoms (pain), sign (jaun- the right hypocondrium because of stretching of the liver capsule. dice), and blood abnormalities (ULN = upper normal limit) appear in Jaundice requires diferential diagnosis from obstructive conditions. the other boxes. In particular, hyperbilirubinemia [28] occurs in about Liver cirrhosis will be associated with increasing portal hyperten- 70% of the patients and correlates more with right atrial pressure than sion [34] and hepatomegaly, more evident signs of right-heart failure, cardiac output [11]. Several factors contribute to elevated bilirubin hepatojugular refux and peripheral edema. If tricuspid regurgitation [11], which is associated with increased risk of death in heart failure develops, the liver might become pulsatile, a sign which is loss with [28]. A subgroup of patients show increased serum aminotransferase ongoing liver fbrosis and cirrhosis [33]. With ascites, the diagnostic levels [17] from ongoing ischemic hepatitis due to defective cardiac paracentesis shows high total protein content ( > 2.5 g/dL, due to pre- output [29]. Hypoalbuminemia occurs in 30% to 50% of the patients served synthetic function of the liver [10]) (colour fgure online) with advanced heart failure, and is associated with worse prognosis in zone 3) [16] and dilatation [9]. Liver cirrhosis is sec- aetiology or severity. Median necroinfammatory index ondary to the ongoing process of perivenular fbrosis with was 3, median fbrosis was 1, and steatosis was absent. The accumulation of reticulin and collagen in zone 3, due to the picture is a minor burden of histologically-proven liver chronic congestive status. Tipically, the fbrous bands extend disease. Viral hepatitis was the only variable associated outward from the central veins. The fbrous tissue can link with a higher grade of necroinfammation and advanced with portal tracts (namely cardiac fbrosis) with a picture fbrosis/cirrhosis. A viral hepatitis infection was found in resembling the micronodular cirrhosis. The ongoing portal 64% of the subgroup of patients (N = 14) with advanced fbrosis during congestive hepatopathy relates to increased fbrosis/cirrhosis. Splenomegaly was signifcantly associ- right atrial pressure, as well as dilatation of the right atrium ated with fbrosis. In addition, levels of liver injury mark- and ventriculum [14]. ers, the histology activity index, fbrosis and steatosis were Durante-Mangoni et al. [7] looked at necroinfamma- similar in patients with ischemic and non-ischemic cardio- tory histological activity index, fbrosis by the Ishak scor- myopathy, and according cardiac functional parameters. ing system, and steatosis. Sinusoidal dilatation occurred The Model for End-Stage Liver Disease (MELD) score in 64% of the patients, irrespective of heart disease did not correlate with cardiac index. A poor correlation 1 3 Internal and Emergency Medicine (2019) 14:907–910 909 existed between histologic and ultrasonographic param- Despite potential bias due to sampling error [26, 27] liver eters. By ultrasonography, a coarse pattern had a 29% biopsy will accurately stage liver
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