CARDIOHEPATIC

INTERACTION
ASEP HARIROHMAN
BUDI S. PIKIR
 INTRODUCTION

• Heart Heartfailure (HF) is a major public health

problem
• Frequent hospitalizations, impaired quality of life,
and shortened life expectancy.
• As HF advances  increasing inability to meet the
metabolic requirements of end organs. ( Liver,
Kidney, Brain,… etc )
• Cardiorenal interaction  Much attention
• Cardiohepatic interaction  Poorly described

Samsky et. al., 2013

• HF patients may present with liver-related symptoms
: abdominal distention, right hypochondrial
discomfort, nausea, early satiety, or anorexia

Kusmana, 2016
CARDIAC-HEPATIC INTERACTIONS
IN HEART FAILURE
 Acute
cardiogenic
liver injury
 ACUTE CARDIOGENIC LIVER INJURY

Acute cardiogenic liver injury (ACLI), historically called

“Ischemic hepatitis,”
• HF  critical cardiogenic shock
However,
• Recent literatures  Acute change in hepatic blood
flow is not the sole incident responsible for ACLI
• Low COP and hypotension alone doesn’t produce
permanent liver injury, it needs HF and hepatic
congestion as a prerequisite to do that.

Nikolaou et.al., 2013

IMPAIRED PERFUSION MUST BE LINKED-TO-HIGH
VENOUS HEPATIC CONGESTION

A-Histo-pathological Features
• necrosis surrounding the central vein where the
oxygenation is poor  Zone (3)
• Bio-chemical Features
• The typical pattern in ACLI consists of :
• Sharp and early rise of AST & ALT (10 to 20 times ) between
1-3 days after hemodynamic insult, and without evidence
of another etiology such as cholecystitis or viral hepatitis
• Early and rapid increase in serum LDH is characteristic
• Ratio of serum alanine aminotransferase (ALT) to LDH <1.5 is
characteristic of cardiogenic injury
• abnormal alkaline phosphatase was associated with
marked signs of congestion and elevated right

Witczak et. al., 2015

• With correction of hemodynamics, these levels will
return to normal within 7 to 10 days

• Although there are few data regarding LFT

alterations among patients with acute HF, a
recently published analysis of the SURVIVE (Survival
of Patients With Acute Heart Failure in Need of
Intravenous Inotropic Support) trial Support these
explanations.

Witczak et. al., 2015

CONGESTIVE
HEPATOPATHY
• Hepatopathy secondary to chronic
congestive HF is attributed to 3 main
processes :
• increased hepatic venous pressure,
• decreased hepatic blood flow, and
• decreased arterial oxygen saturation
• Elevated Rt. Sided pressure

Nikolaou et. al., 2013

• Elevated central venous pressures are transmitted
through the hepatic veins and into the small
hepatic venules  passive congestion  elevated
hepatic venous pressure  impair delivery of
oxygen and nutrients to hepatocytes  leading to
sinusoidal fenestrae enlargement
• Consequently, hepatocyte necrosis and leakage of
protein-rich fluid into the space of Disse occurs with
stretching of the liver capsule resulting in abdominal
discomfort.

Samsky et. al., 2013

• The Resultant is ….

….”Nutmeg Liver”…
A-Histo-pathological Features
• 50% of patients with severe HF had pathologic
changes consistent with chronic passive liver
congestion
• Atrophy, necrosis, or both were present and most
pronounced in the central third of the hepatic
lobule
• Generally, these findings were most prominent
immediately adjacent to the central vein, with
decreasing degeneration towards the lobule
periphery

NECROSIS IS CENTRILOBULAR

Samsky et. al., 2013

Bio-chemical Features
• As cardiac output decreased and intracardiac
filling pressures increased :
• Elevations in transaminases, LDH
• Increased total bilirubin
• Cholestasis
• Increased alkaline phosphatase
• Increased gamma-glutamyl transpeptidase[GGT]
• Increased total bilirubin, and …
• Finally, Hypoalbuminemia

Poelzl et. al., 2009

LIVER FUNCTION TESTS AS A PROGNOSTIC TESTS
FOR PATIENTS WITH HEART-FAILURE

• CHARM and other large Trials confirm sensitivity of :

• Total Billirubin
• GGT ‘gamma glutaryl transpeptidase’
• Alkaline Phosphatase
• Hypo-albuminemia
• N-terminal pro-B Natriureticpeptide

• As a Marker For…
• Worsening of heart failure
• Recurrent hospitalization
• Short & Intermediate outcome of LVAD
• Urgent need for cardiac transplantation
• Predictive capacity for transplant free survival
• Cardiovascular & All cause Mortality
Poelzl et. al., 2009
 CIRRHOTIC
CARDIOMYOPATHY
 DEFINITION

• A cardiac dysfunction in patients with cirrhosis

characterised by impaired contractile
responsiveness to stress and/or altered diastolic
relaxation with electrophysiological abnormalities in
the absence of other known cardiac disease
• The prevalence is 40 to 50% in patients with cirrhosis.
• The development of cirrhotic cardiomyopathy -
independent of the aetiology of liver disease.
• There is no specific therapy but cirrhotic
cardiomyopathy is almost completely reversible
after liver transplantation.

Poelzl et. al., 2014

PATOPHYSIOLOGY
 PATHOPHYSIOLOGY

1. Hemodynamic Changes
2. Alterations of Cardiomyocytes
3. β-Adrenergic Receptor Signaling Pathways
4. Alteration in Membrane Biophysical
Characteristics
5. Endocannabinoid System
6. Sympathetic and Parasympathetic Nervous
System

Pudil et. al., 2013

 FEATURES OF CIRRHOTIC
CARDIOMYOPATHY
• Structural changes
• LVH and LA dilatation in more than 1/3rd cases
• Due to combination of mechanical overload due to
hyperdynamic circulation and neurohormonal activation.

• Impaired cardiac response to exercise

• The presence of chronotropic incompetence during exercise in
cirrhotic patients with ascites, who reached 65% of their
maximal predicted heart rate.
• Inability to increase LVEF during exercise despite normal or
even higher LVEF at rest compared to normal controls.
• Overall, the increase of cardiac output during exercise was
severely impaired in these patients.
• Acute exacerbation of anaemia, sepsis, or creation of TIPS
are known to precipitate HF in patients with cirrhotic
cardiomyopathy

Figueiredo et. al., 2012

DIAGNOSIS

Figueiredo et. al., 2012

 MANAGEMENT

• Medical Treatment
• No specific treatment
• Orthotopic Liver Transplantation
 CONCLUSION

• Acute and chronic heart failure can be

complicated in liver damage which has significant
implications for cardiovascular disease
management
• Management follows recent recommendations for
the treatment of heart failure and liver disease
• Abnormalities of liver function tests  prognostic
relevance
• Subsequent studies should pay greater attention to
cardiohepatic relationships