الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Heart failure is a complex syndrome with multiple organ
manifestations. Extracardial organ damage (kidney, liver, lung, and skeletal
muscle) present typically in the advanced stages of chronic heart failure.
Liver disorders in chronic heart failure result from either congestion and/or
hypo perfusion. Regional or systemic neurohormonal activation may also
play a role in liver dysfunction in chronic or acute heart failure. Liver
damage in heart failure is manifested by hepatomegaly and subicterus,
especially in cases where right-heart failure is present. In patients with acute
heart failure and a low cardiac index, liver transaminases rise significantly as
a manifestation of ischemic hepatitis. There are unique changes of portal
vein flow in heart failure. The portal vein is interposed between the
capillary net- work of splanchnic circulation and hepatic sinusoids.The
portal vein is easily accessible for ultrasound examination and its flow can
be analyzed using Doppler. Liver congestion causes transmission of flow
waveforms portal vein. measurement of portal flow is a good tool for
detection and quantification of systemic congestion.
In our study we investigated the changes of the portal vein flow in
patients with an acute exacerbation of heart failure in relation to right atrial
pressure and biochemical indicators of liver lesion.we investigated 30
patients with chronic heart failure with exacerbation presented at heart
failure unit at National Heart Institute for evaluation of heart failure
condition. The diagnosis of heart failure was based on a combination of
physical examination, laboratory tests, and imaging.
summary
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In our study we found that in pure cardiac liver disease the
PV flow becomes pulsatile.
In our study We found that there was significant correlation
between pulsatility index (PI) and elevated level of serum total
bilirubin (p. value was 0.013).
In our study We found that although serum amino transferases (ALT ,
AST ) and alkaline phosphatase were elevated there was no significant
correlation between pulsatility index (PI) and elevated level of serum amino
transferases(p value= 0.283). and alkaline phosphatase . (p value= 0.308).
In our study We found that although serum albumin level was declined but
there was no significant correlation between pulsatility index (PI) and
In our study We found that although INR mildly elevated there was no
significant correlation between pulsatility index (PI) and elevated level of
INR. (p value= 0. 0.066).
In our study We found that there was significant
correlation between pulsatility index (PI) and right atrial pressure
(p. value was 0.01).
In our study We found that there was significant correlation
between pulsatility index (PI) and tricuspid regurge (p. value was 0.0.044).
In our study We found that there was significant correlation
between pulsatility index (PI) and severity of heart failure determined
by using NYHA classification (p. value was 0.021)