Liver and the Heart By Dr' Farook Redwan

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Liver and the HeartBy Dr. Farook Redwan

• Prof. of cardiology Internal medicine
• Mansoura Faculty of Medicine

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As you cant live without your heart you cant
live without your liver
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Heart in liver Disease
Classification

• Heart involvement in liver diseases
• This will include heart affection in the
  following conditions
• A) Viral hepatitis
• i- Acute .
• Ii- chronic
• (B) Schistosomal hepatic fibrosis
• i- Schistosomal corpulmonale .
• ii- Endomyocardial fibrosis ( EMF) and
  restrictive cardiomyopathy
• iii- direct Schistosomal affection of the heart .
• (C) Liver cirrhosis
• i- cirrhotic ardio-myopathy and myocardial
  dysfunction
• ii- pulmonary hypertension
• iii- Hepatopulmonary syndrome.
• IV-Endocarditis and pericarditis .
• V-diseases incidence of hypertension
  ,atherosclerosis and coronare artery disease.

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Disorders that involve both liver and heart -

• (D) Metabolic disorders
• (i)- Haemoochromatosis
• (ii)-Glycogen storage disease (type II,III,IV).
• (iii)- Diabetes mellitus
• (iv)- Mucopolysacharidosis .
• (E) Toxic disorders -
• i- Alcohol.
• (F) Collagen diseases -
• i- Rheumatiod arthritis
• ii- systemic lupus erythematosis .
• iii- Antiphospholipid antibody syndrome.
• Iv- systemic vasculitis .

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Disorders that involve both liver and heart -

• (G) Infective disorders-
• (1) Syphiylis
• (2) Tuberculosis
• (3) Hydatid diseas
• (4) Trypanosomiasis
• (5) Cystocercosis
• (6) Fungal infections
• (H) Haematologic disorders
• (1) Anaemias especially hemolytic
• (2) Leukemias and lymphomas.
• (3) Disseminated itravascular coagulation .
• (I) Others -
• (1) Amyloidosis
• (2) Sacoidosis .
• (3) Hereditary haemorrhagic telangiectasia

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• (J) Cardiovascular effects of some hepatic
  diagnostic and therapeutic interventions
• 1- Endoscopy and injection sclerotherapy or band
  ligaion
• 2- portosystemic shunt surgery and transjugular
  intrahepatic porto-systemic shunts and stents (
  TIPS).
• 3- paracentesis abdominals .
• 4- hepatic transplantation
• (K) Miscellaneous
• 1- congenital heart disease with
• Congenital hepatic fibrosis
• (L)Direct pericardial involvement in
• Liver absess
• Liver maligancy

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Heart The Liver
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Ischemic Hepatitis ( Hypoxic Hepatitis or Acute
Hepatic Infraction)
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Constrictive Percarditis
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THE LIVER IN CONGESTIVE HEART FAILURE
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LIVER HEART
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Viral Hepatitis
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• i-Acute Hepatitis
• Palpitation dyspnea , chestpain ,hypotension and
  sinus bradycaerdia ).Dehan et al ., (1946) Adler
  Lyen ( 1947)
• Fulminant hepatitis and acute hepatic failure
  were associated with many cardiac complications ,
  prolonged hypotension , pulmonary oedema adult
  respiratory distress syndrome (ARDS) arrhythmias
  (AF,ventricuelar premature contraction) ECG
  abnormalities even sudden cardiac death
  (Bell,1971,Gorden. 1989).
• Pericarditis with effusion was also reported
  after HBV infection (Adler et al ,1978).
• Impairment of systolic L.V functions was observed
  in patients with acute HBV infection by use of
  STIS ,The degree of impairment was more in
  patients with anaemia or high serum bilirubin
  .Prolonged QTc interval QRS duration in the ECG
  was also observed in these patients
  (Maatti,1990).
• ii-Chronic Hepatitis -
• Cardiac involvement in HBV associated vasculitis
  was reported by McMahon et al (1989) in 4 cases
  over 4 year follow up 2 with congestive heart
  failure 2 with pericarditis .

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• The association of chronic HCV hepatitis with
  polyarteries nodosa (PAN) has been suggested
  (cacoub et al ,1992, Deny et al., 1992 )(Carsonet
  al. , 1993).
• High frequencey of HCV infection was found in
  patients with dilated cardiomyopathy(16.9) by
  Matsumori et al. ,1996).
• Also high seropositivity for anti-HCV was
  detected in patients with hypertrophic
  cardiomyopathy (6of35 cases (17.6) HCV-RNA was
  detected in the myocardium in 3 patients (
  Matsumori et al. ,1995).

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Evidence for association between hepatitis C
virus seropositivty and coronary artery disease

• One of the most interesting developments in
  recent years has been the idea that infective
  agents may induce a pro-inflammatory effect and
  have a crucial role in atherothrombosis (Shah
  2001) .
• This theory proposed that a mutation or a viral
  agent may represent events able to transform a
  single smooth muscle cell into the progenitor of
  a proliferative clone ,introducing the concept
  that the plaque may be considered a monoclonal
  benign neoplasm.

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• In particular ,very few data on the relation
  between hepatitis C virus (HCV) infection and
  atherosclerosis are available .However ,very
  recent results indicate that seropositivity for
  HCV shows a positive association with carotid
  artery plaque and carotid intima-media thickening
  ,independent from other risk factors for
  atherosclerosis (Ishizaka et al.2003).

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• Vassalle et al (2004) suggesed that
  HCVserpoositivitiy might be considered in the
  clinical setting as one of the risk factors
  affecting the onset and development of CAD.
• Fyurther studies are needed at this point to
  verify the potential additive effect of HCV
  infection with respect to the presence of other
  pathogens .This study might be relevant for
  adding new predicative and prognostic factors to
  the CAD multifactorial entity .

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Hemochromatosis
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• According to the Iron Disorders Institute ,the
  group at highest risk for HHC include
• Males of Scotch-Irish,British ,Dutch ,German
  ,French,Spanish,Italian,( Norther western
  Eruopean ),or Mediterranean descent ,orwith a
  family history or premature death by heart attack
  ,liver disease ,diabetes ,arthritis ,importence
  ,neurological disorders or cancer .
• Women who no longer have a period due to
  menopause ,premature discontinuation of period or
  an hysterectomy and who have the same ancestry
  and family history listed above .
• Blood relative of this men and women .
• Anyone homozygous for HFE gene mutations.

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- Serum Iron- Serum transferrin- Serum ferritin
- Biopsy
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• There are two known important mutations in HFE ,
  named C282 Y and H63D.C282Y is the most important
  .

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Alcohlic CM and liver disease
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Cirrhotic Cardiomyopathy
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Definition -

• A Cardiac dysfunction characterized by increased
  cardiac output and altered diastolic relaxation
  at rest associated with insufficient ventricular
  contractility under strain .

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Baseline features

• High rest cardiac output .
• Abnormal diastolic relaxation as indicated by
  reduced E/A ratio and prolonged deceleration time
  at echocardiography .
• Mild enlargement of left ventricular chambers and
  mild increase of wall thickness.
• Prolonged Q-T interval .

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Features Occurring under strain

• Blunted increase of cardiac output with tilting
  or vasoconstriction (increased after-load )
• Blunted increase of left ventricular ejection
  fraction (LVEF) with exercise or reduced LVEF
  after standing .
• Blunted chronotropic response to isoproterenol .
• Reduced aerobic exercise capacity .

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• The pathophysiological basis
• The presence of a hyperdynamic circulation which
  overloads heart with an impaired cardiac
  contractility ( Moller et al ( 1995 ) and
  Bernardi et al ( 1995 )
• Structural cardiac changes
• Autonomic dysfunction
• Conductance abnormalities .
• Biochemical abnormalities
• Receptor/postreceptor defects
• Impaired beta adrenergic signal transduction ,
• abnormal plasma membrane fluidity ,
• altered ion channel function may be important (
  Ma et al ( 1996 ) and Zevecz et
  al ( 2000) .
• over production of nitric Oxide (NO), increased
  bile acid ,TNF- a , Endotoxius , endotheln.

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Investigation

• Biomarkers
• Elevated cardiac Tropnin I
• Increased BNP
• Increased palsma aldostesone
• Increased PRA
• ECG
• Q-T piolongation
• Echo
• Septal hypertrophy
• decreased E/A ratio
• Mild increase of LV chambers
• Mild increase of wall thickness
• Blunted increase of LVEF with exercise

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• Biopsy
• Both macroscopic and microscopis changes have
  been described in cirrhotic hearts , thus septal
  hypertrophy has been described in a considerable
  number of cirrhotic patioents . Histological
  patchy fibrosis interstitiel oedema.

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Clinical Problems Therapeutics
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• CCM as a sub -clinical from of HF with no symptom
  at rest is not considered to need any special
  treatment .
• Patients with non compensated liver cirrhosis are
  usually subjects with limited exercise capacity
  and are usually under -

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• (1) Salt restriction ( to prevent water and
  sodium retention ) leading to decreased LV
  preload .
• (2) Peripheral vasodilatation (in the context of
  LCF ) decreases LV after -load and cardiac energy
  demands
• (3) Pharmacological treatment usually received
  with non compensated liver cirrhosis includes
  drugs with a direct or indirect beneficial effect
  on the cardiovascular system

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• Frusemide contribits to decreased renal
  reabsoption of sodium and water , decreasing the
  total plasma volume .
• Spironoloctone is considered to cause both .
• (a) Inhibition of renin-angiotension
  axis
• (b) Improvement in LV remodeling .

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Wet Wise W W orDry Demented D D
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• - Beta Blockers
• The use of BB ( propranolol ) in cirrhotic
  patients with portal hypertension and
  oesophegeal varices seems to have beneficial
  effect on B-adrenergic receptor density which is
  supposed to be down-regulated in cirrhosis

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• Nitrates
• Combined with BB in portal hypertension have
  -
• Coronary VD effect .
• Venodilatory effect with preload reduction

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Cardiovascular effects of some hepatic diagnostic
and therapeutic interventions
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Hepatic Transplantion
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Liver Transplantation

• constitutes a great physical stress for the
  cardiovascular system ,during both
  trans-operative and the postoperative period .
• Fifty six ( 56 ) of patients in certain
  series exhibited acute pulm oedema during the
  early postoperative period
• 7-21 of postoperative deaths were attributed to
  heart failure .

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• Postoperatively after-load augmentation due to
• Progressive normdization of the hyperdynemic
  circulation
• Elevation of the peripheral resistance .
• Elevation of the arterial BP.
• Sampathkumar etal (1998) have described a
  reversible form of DCM during the early post
  transplanted period with clinical manifestations
  of prlm.och a Rosp.tale acute pulm-oedema
  respiratory failure..

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Cardiovascular system alteration during the post
transplant period
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• (1)Navasa etal (1993) maintained that most of the
  humoral and hemodynaemic alterations in terminal
  stage liver disease are restored during the post
  transplant period .
• (2) Henderson etal ( 1992) suggested a residuel
  state of hyperdynamic circulation in the
  transplanted patients.
• (3)QT intervel prolongation is reversed during
  the posttransplant period as considered by
  Mochammad etal( 1996) and Gonzaleyz etal (1999).

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Liver transplants as a treatment for
hyperlipidemia
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• Interferon
• Cardiotoxicity of interferon therapy in chronic
  HCV hepatitis had been reported in 3.2 of
  patients ( Teragawa et al., 1996) and include
  arrhythmias ,ischemic heart disease and
  cardiomyopathy .
• Also , Sartori et al. 1996 reported decrease in
  LV ejection fraction with interferon therapy in
  chronic HCV hepatitis that return to pretreatment
  level after 3 months of the end of therapy .
• Kadayifei et al.,(1997) found no significant
  cardiac adverse effect by clinical examination or
  cardiovascular test in patients with chronic
  active hepatitis treated with interferon and
  concluded that it can be used safely in chronic
  active hepatitis patients .

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Sclerotherapy and band ligation
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TIPS
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Abdominal paracentesis
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Cardiovascular Drugs The liver
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Conclusion
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• Myocardial dysfunction in patients with liver
  cirrhosis and serious hepatic failure is
  described by the term cirrhotic cardiomyopathy
• Because of its mild , subclinical course this
  entity remains under estimated , since these
  patients usually exhibit a variety of more
  serious complications related to hepatic failure
  and portal hypertension .
• Further research is needed to evaluate wheather
  this entity influences morbidity and mortality
  under certain circumstances that modify
  cardiovascular status , such as liver
  transplantation .
• In the meantime , evaluation of pre-transplant
  cardiovascular function is deemed to be necessary
  .

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Acknowledgement

• Dr. Ahmed Abdullah
• Dr. Essam Mahfouz
• Dr. Abdel-Hamid Rashaad and
• Dr. Mohammad Khashaba

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