Cardiac function and haemodynamics in alcoholic cirrhosis and effects of the transjugular intrahepatic portosystemic stent shunt

Huonker, M.; Schumacher, Y. O.; Ochs, Andreas; Sorichter, Stephan; Keul, J.; Rössle, Martin

doi:10.1136/gut.44.5.743

Cited by 170 publications

(122 citation statements)

References 35 publications

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“…Indeed, cardiac complications have been reported following TIPS insertion [82,83]. Huonker and colleagues [84] reported almost doubling of pulmonary wedge pressure and total pulmonary vascular resistance 90 min after a successful TIPS insertion, Fig. 3 The different phases of the action potential.…”

Section: Clinical Presentations and Consequences Of Cirrhotic Cardiommentioning

confidence: 99%

Cirrhotic cardiomyopathy

2008

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Cirrhotic cardiomyopathy is a recently recognized condition in cirrhosis consisting of systolic incompetence under condition of stress, diastolic dysfunction related to altered diastolic relaxation, and electrophysiological abnormalities in the absence of any known cardiac disease. It can be diagnosed by using a combination of electrocardiograph, 2-dimensional echocardiography, and various serum markers such as brain natriuretic factor. The underlying pathogenetic mechanisms include abnormalities in the b-adrenergic signaling pathway, altered cardiomyocyte membrane fluidity, increased myocardial fibrosis, cardiomyocyte hypertrophy, and ion channel defects. Various compounds for which levels are elevated in cirrhosis such as nitric oxide and carbon monoxide can also exert a negative inotropic effect on the myocardium, whereas excess sodium and volume retention can lead to myocardial hypertrophy. Various toxins can also aggravate the ion channel defects, thereby widening the QRS complex causing prolonged QT intervals. Clinically, systolic incompetence is most evident when cirrhotic patients are placed under stress, whether physical or pharmacological, or when the extent of peripheral arterial vasodilatation demands an increased cardiac output as in the case of bacterial infections. Acute volume overload such as immediately after insertion of a transjugular intrahepatic portosystemic shunt or after liver transplantation can also tip these cirrhotic patients into cardiac failure. Treatment of cirrhotic cardiomyopathy is unsatisfactory. There is some evidence that b-blockade may help some cirrhotic patients with baseline prolonged QT interval. Long-term aldosterone antagonism may help reduce myocardial hypertrophy. Future studies should include further elucidation of pathogenetic mechanisms so as to develop effective treatment strategies.

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Section: Clinical Presentations and Consequences Of Cirrhotic Cardiommentioning

confidence: 99%

Cirrhotic cardiomyopathy

2008

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“…[42][43][44] It has largely replaced the use of surgically placed shunts. Insertion of a TIPS shunt leads to a marked increase of cardiac output, right atrial pressure, and pulmonary artery pressure, 45 with a secondary decrease of systemic vascular resistance and an increase in pulmonary vascular resistance and effective arterial blood volume. Sodium excretion and renal function improve over 4 weeks.…”

Section: Transjugular Intrahepatic Portosystemic Shunt (Tips)mentioning

confidence: 99%

“…The development of hepatic encephalopathy occurs in ϳ30% of patients post-TIPS, but the incidence is higher in those patients with pre-TIPS encephalopathy and in those greater than 60 years old. 48 TIPS increases the cardiac preload 45 and may precipitate cardiac failure in patients with cardiac disease. Liver function can also deteriorate significantly in the post-TIPS period, possibly secondary to shunting of blood away from the liver.…”

Section: Transjugular Intrahepatic Portosystemic Shunt (Tips)mentioning

confidence: 99%

The Management of Ascites in Cirrhosis: Report on the Consensus Conference of the International Ascites Club

et al. 2003

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Ascites is a common complication of cirrhosis, and heralds a new phase of hepatic decompensation in the progression of the cirrhotic process. The development of ascites carries a significant worsening of the prognosis. It is important to diagnose noncirrhotic causes of ascites such as malignancy, tuberculosis, and pancreatic ascites since these occur with increased frequency in patients with liver disease. The International Ascites Club, representing the spectrum of clinical practice from North America to Europe, have developed guidelines by consensus in the management of cirrhotic ascites from the early ascitic stage to the stage of refractory ascites. Mild to moderate ascites should be managed by modest salt restriction and diuretic therapy with spironolactone or an equivalent in the first instance. Diuretics should be added in a stepwise fashion while maintaining sodium restriction. Gross ascites should be treated with therapeutic paracentesis followed by colloid volume expansion, and diuretic therapy. Refractory ascites is managed by repeated large volume paracentesis or insertion of a transjugular intrahepatic portosystemic stent shunt (TIPS). Successful placement of TIPS results in improved renal function, sodium excretion, and general well-being of the patient but without proven survival benefits. Clinicians caring for these patients should be aware of the potential complications of each treatment modality and be prepared to discontinue diuretics or not proceed with TIPS placement should complications or contraindications develop. Liver transplantation should be considered for all ascitic patients, and this should preferably be performed prior to the development of renal dysfunction to prevent further compromise of their prognosis. (HEPATOLOGY 2003;38:258-266.)

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“…2 In recent years, especially since the introduction of transjugular intrahepatic portosystemic shunt (TIPS), many reports have used right atrial pressure (RAP) as the internal zero reference to calculate the portal pressure gradient (hepatic atrial pressure gradient [HAPG]). [14][15][16][17][18][19][20][21] There are several reasons for this trend. Many radiologists find it difficult to measure the IVCP during a TIPS procedure, and the RAP may be a closer estimate of the outflow pressure of the esophageal varices than the FHVP, because the varices drain mainly through the azygos vein into the superior vena cava in the vicinity of the right atrium.…”

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confidence: 99%

Right Atrial Pressure Is Not Adequate to Calculate Portal Pressure Gradient in Cirrhosis: A Clinical-Hemodynamic Correlation Study

et al. 2010

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Hepatic venous pressure gradient (HVPG), the difference between wedge and free hepatic venous pressure, is the preferred method for estimating portal pressure. However, it has been suggested that hepatic atrial pressure gradient (HAPG)-the gradient between wedge hepatic venous pressure and right atrial pressure (RAP)-might better reflect variceal hemodynamics. The aim of this study was to (1) investigate whether HAPG with nonselective beta-blockers correlates with prognosis in cirrhotic patients with portal hypertension at baseline and during treatment; (2) compare the prognostic value of HAPG with that of HVPG; and (3) investigate the agreement between portoatrial gradient (PAG) and portocaval gradient (PCG) in patients with transjugular intrahepatic portosystemic shunt (TIPS). We included 154 cirrhotic patients with varices with a complete hemodynamic study at baseline and on chronic treatment for primary (n 5 71) or secondary (n 5 83) prophylaxis for bleeding and 99 patients with TIPS. All patients were followed for up to 2 years; portal hypertensive-related bleeding and bleeding-free survival were analyzed. HVPG was equal or lower than HAPG in all patients (23.2 mm Hg; P < 0.001). Agreement between HAPG and HVPG was modest, especially in patients with increased intra-abdominal pressure. One hundred two patients were HVPG nonresponders and 52 patients were HVPG responders to nonselective beta-blockers, whereas 101 patients were HAPG nonresponders and 53 patients were HAPG responders (k 5 0.610). HVPG response revealed an excellent predictive value for bleeding risk and bleeding-free survival; HAPG did not. In our TIPS patients, 20% had a PCG 12 mm Hg and a PAG >12 mm Hg, which may have induced unnecessary overdilation of the TIPS. Conclusion: The excellent prognostic information provided by HVPG response to drug therapy is lost if HAPG response is considered. RAP should not be used for the calculation of portal pressure gradient in patients with cirrhosis.

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Cardiac function and haemodynamics in alcoholic cirrhosis and effects of the transjugular intrahepatic portosystemic stent shunt

Cited by 170 publications

References 35 publications

Cirrhotic cardiomyopathy

Cirrhotic cardiomyopathy

The Management of Ascites in Cirrhosis: Report on the Consensus Conference of the International Ascites Club

Right Atrial Pressure Is Not Adequate to Calculate Portal Pressure Gradient in Cirrhosis: A Clinical-Hemodynamic Correlation Study

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