الفهرس 
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Abstract
The human liver is the largest single organ in the body and consists of parenchymal cells, which metabolize, detoxify, synthesize, and store nutrients.
Cirrhosis of the liver is a consequence of chronic liver disease characterized by irreversible replacement of a liver tissue by a fibrotic scar tissue as well as regenerative nodules, leading to progressive loss of liver function.
The term ”cirrhosis” was first used by René Laënnec (1781–1826) to describe the abnormal liver color of individuals with alcohol-induced liver disease.
Cirrhosis and chronic liver disease were the 10th leading cause of death for men and the 12th for women.
The exact prevalence of cirrhosis is unknown, but it has been estimated, through autopsies, to be between 5 and 10 percent.
The pathological hallmark of cirrhosis is the development of scar tissue that replaces normal parenchyma, blocking the portal flow of blood through the organ and disturbing normal function.
Prognosis is often unpredictable. It depends on factors such as etiology, severity, presence of complications, co morbid conditions, host factors, and effectiveness of therapy.
Generally, liver damage from cirrhosis cannot be reversed, but treatment could stop or delay further progression and reduce complications.
Hepatocellular carcinoma is Common cancer worldwide, and the third leading cause of cancer-related deaths about three-quarters of HCCs are attributed to chronic HBV and HCV infections. Tumor grade is important as high-grade tumors will have a poor prognosis, while low-grade tumors may go unnoticed for many years.
The usual outcome is poor, because only 10 - 20% of Hepatocellular carcinomas can be removed completely using surgery.
The main risk factors for hepatocellular carcinoma are Hepatitis B, Hepatitis C, Alcoholism, Aflatoxin, Cirrhosis of the liver and Wilsons disease. Although hepatocellular carcinoma most commonly affects adults, children who are affected with biliary atresia, infantile cholestasis, glycogen-storage diseases.
In particular, chronic infections of hepatitis B and/or C can aid the development of hepatocellular carcinoma by repeatedly causing the body’s own immune system to attack the liver cells, While this constant cycle of damage followed by repair can lead to mistakes during repair which in turn lead to carcinogenesis.
In patients with a higher suspicion of HCC (such as rising alpha-fetoprotein and des-gamma carboxy prothrombin levels), the best method of diagnosis involves a CT scan of the abdomen using intravenous contrast agent and three-phase scanning. An alternative to a CT imaging study would be the MRI.
The main line of management is liver transplantation with a cadaveric liver or a living donor graft.
Cardiovascular complication of liver cirrhosis is a hyperdynamic syndrome which comprises an increased heart rate, cardiac output, plasma volume and a reduced systemic vascular resistance and arterial blood pressure.
Cardiovascular complications of liver cirrhosis include cardiac dysfunction and abnormalities in the central-, splanchnic, - and peripheral circulation. Being often clinical latent, cirrhotic cardiomyopathy can be unmasked by physical and pharmacological strain.
Systemic Circulation in Cirrhosis: The mechanisms that may raise the cardiac output in cirrhosis are increased sympathetic nervous activity, vasodilatation, increased blood volume, and the presence of arterio venous communication.
Patients with advanced cirrhosis often develop a hyperdynamic circulation with central hypovolaemia. The events that initiate the systemic hemodynamic abnormalities and the coupling of these factors to splanchnic hemodynamic are still unclear.
Hypothesis of Prepheral Arterial Vasodilatation in Cirrhotic Patient: Peripheral arterial vasodilatation is one of the earliest observations in the cirrhotic patient. The Peripheral Arterial Vasodilatation Hypothesis also explains the continuum from compensated to decompensated cirrhosis to the hepatorenal syndrome.
Peripheral arterial vasodilatation in cirrhosis may be brought about either by:
1. Overproduction of circulating vasodilators.
2. Or vasodilators of intestinal or systemic origin.
3. Vasodilators that escape degradation in the diseased liver or bypass the liver through portosystemic collaterals.
There are anther Hypothesis which explain that the Hyperdynamic Circulation in Liver Cirrhosis: not peripheral vasodilatation but ‘Splanchnic Steal’
Cardiac Complication of Liver Cirrhosis:
The heart in patient with liver cirrhosis has the following character:
1. Change in heart mass and volumes.
2. Change in heart hemodynamic and pressures.
3. Ventricular dysfunction.
4. Electromechanical abnormalties.
Other Cardiac Manifestations of Cirrhosis:
Fibrinous pericarditis in cirrhotic patients has been described.
The incidence of pericardial effusions in patients with cirrhosis appears to correlate with the degree of liver failure. Also incidence of infective endocarditis in cirrhotic patients (0.34%) vs. non cirrhotic patients (0.1%).
Cirrhotic cardiomyopathy (CCM) is a chronic cardiac dysfunction in patients with cirrhosis, characterized by blunted contractile responsiveness to stress and/ or altered diastolic relaxation with electro-physiological abnormalities, in the absence of any known cardiac disease.
The exact prevalence of cirrhotic cardiomyopathy remains unknown as the prevalence of liver cirrhosis is also difficult to estimate.
Currently, the clinical features of cirrhotic cardiomyopathy can be characterized as follows:
1) Baseline increased cardiac output.
2) Attenuated systolic contractile and diastolic relaxant responsiveness to virtually all inotropic and chronotropic stimuli including drugs, exercise, volume expansion and contraction, and surgical stress.
3) Absence of florid ventricular failure.
4) Relatively modest morphological changes such as mild chamber dilatation.
Although patients may complain of dyspnea, reduced exercise capacity, peripheral fluid retention (dependent edema) and ascites.
There is no direct genetic predisposition to cirrhotic cardiomyopathy.
Evidence supporting the presence of cardiomyopathy in cirrhosis:
1) Systolic dysfunction: the decreased cardiac contractile response observed in cirrhosis.
2) Diastolic dysfunction: when present, is characterized by an abnormal pattern of transmitral flow and increased atrial contribution to the late ventricular filling.
3) Serum markers: Brain natriuretic peptide, a sensitive and useful marker for early stage heart disease, had been found to be elevated in most of ascitic cirrhotic patients
The exact prognosis of cirrhotic cardiomyopathy remains unclear. In other words, the extent of cirrhotic cardiomyopathy generally correlates to the degree of liver insufficiency.
To prevent cardiac complication of liver cirrhosis is to prevent liver cirrhosis itself.
As most cases of cirrhotic cardiomyopathy are subclinical, and symptoms become overt only when cardiac function is stressed, there has been very little interest in treating cirrhotic cardiomyopathy, especially at the asymptomatic stage.
Recently demonstrated that the use of an aldosterone antagonist, k-canrenoate, for 6 months can reduce the parietal wall thickness of the left ventricle even in patients at an early stage of cirrhosis.
Liver transplantation can completely reverse the changes of cirrhotic cardiomyopathy and therefore can potentially be one of the treatment options for this condition.
Future strategies will include formulation of anther treatment options such as the development of antagonists to TNF-α and NF-κB as treatments of systolic dysfunction, or the use of the combination of β-blockade with aldosterone antagonist, or the use of Ang II receptor antagonist as treatment of diastolic dysfunction. The removal of “cardiotoxins” using albumin is also a possibility.