Measurement of portal pressure and its clinical application

Reynolds, Telfer B.; Ito, Sosuke; Iwatsuki, Shunzaburo

doi:10.1016/s0002-9343(70)80131-0

Cited by 157 publications

(44 citation statements)

References 31 publications

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“…It was suggested [14] that in some patients with nonalcoholic cir rhosis, PHG may be different from portal pressure measured using a thin needle ad vanced into the portal system through the liv er, but other authors [15,16] did not report any differences between PHG and direct por tal pressure measurement in similar condi tions. Although the measurement of EHBF using ICG constant infusion is not completely free from criticism because of some inaccura cies [17,18], it remains the reference tech nique and was used in other studies on the hemodynamic effects of SRIF [3,4,7], In our series, SRIF decreased EHBF, but did not modify the levels of portal hyperten sion.…”

Section: Discussionmentioning

confidence: 99%

Effect of Somatostatin on Splanchnic Hemodynamics in Patients with Liver Cirrhosis and Portal Hypertension

et al. 1985

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The effect of somatostatin on splanchnic hemodynamics in patients with liver cirrhosis is not clearly defined, as some authors report a decrease in portal pressure and in liver blood flow during intravenous administration of this hormone, while others do not. In 19 subjects with liver cirrhosis and portal hypertension the following parameters were measured before and during intravenous administration of somatostatin (7.5 μg/min): porto-hepatic gradient, estimated hepatic blood flow, specific splenic blood flow, cardiac index. Estimated hepatic blood flow decreased significantly during somatostatin infusion (p < 0.05), averaging a 13% decrease; porto-hepatic gradient, splenic specific blood flow and cardiac index did not vary significantly. These data indicate that somatostatin infused at a dose of 7.5 μg/min induces a slight decrease in liver blood flow without affecting portal hypertension.

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Section: Discussionmentioning

confidence: 99%

Effect of Somatostatin on Splanchnic Hemodynamics in Patients with Liver Cirrhosis and Portal Hypertension

et al. 1985

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“…Adequacy of occlusion was always checked by distal injection of a small amount of radiographic contrast medium. HVPG, expression of portal pressure in sinusoidal and postsinusoidal outflow block, as it occurs in cirrhosis, [10][11][12][13] was calculated as the difference between occluded and free HVPG. At least 3 measurements were always performed, electronic means were obtained during one minute recordings, and results were given as arithmetic means of these 3 measurements.…”

Section: Methodsmentioning

confidence: 99%

The Hemodynamic Response to Medical Treatment of Portal Hypertension As A Predictor of Clinical Effectiveness in the Primary Prophylaxis of Variceal Bleeding in Cirrhosis

et al. 2000

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In the prevention of variceal rebleeding, it is already established that hemodynamic response to drug treatment (decrease in hepatic venous pressure gradient [HVPG] to 12 mm Hg or by >20%) is predictive of clinical effectiveness. In primary prophylaxis very few clinical data are available. We assessed the role of the hemodynamic response to beta-blockers or beta-blockers plus nitrates in predicting clinical efficacy of prophylaxis. A total of 49 cirrhotic patients with varices at risk of bleeding, without prior variceal bleeding, were investigated by hepatic vein catheterization before and after 1 to 3 months of chronic treatment with nadolol or nadolol plus isosorbide mononitrate, and were followed during treatment for up to 5 years. A total of 30 patients (61%) were good hemodynamic responders, and among them in 12 (24%) HVPG was <12 mm Hg during treatment. During treatment 9 patients had variceal bleeding: 7 were poor responders and 2 were good responders. The probability of bleeding at 3 years of follow-up was significantly higher in poor responders (41%) than in good responders (7%; P ‫؍‬ .0008). No patient reaching an HVPG of 12 mm Hg or less during treatment had variceal bleeding during follow-up. Cox's regression analysis showed that poor hemodynamic response was the main factor predicting bleeding (␤ ‫؍‬ 1.91; SE(␤) ‫؍‬ 0.80; P ‫؍‬ .01). During follow-up 11 patients died of hepatic causes. Survival was related to Child-Pugh class and to initial value of HVPG, according to Cox's analysis. In conclusion, the assessment of hemodynamic response to drugs in terms of HVPG is the best predictor of efficacy of prophylaxis of variceal bleeding in patients treated with beta-blockers or beta-blockers plus nitrates. (HEPATOLOGY 2000;32:930-934.)It is clearly established that prophylaxis with beta-blockers decreases the risk of first variceal bleeding in cirrhotic patients with portal hypertension and esophageal varices at risk of bleeding. 1 Recently, it was also shown that the efficacy of beta-blockers may be enhanced by the addition of long-acting nitrates. 2 These treatments, however, do not abolish the risk of bleeding but decrease it by half or by three quarters, respectively. For these reasons, it may be useful to know factors predicting clinical response or nonresponse to treatment to allow treatment of nonresponders with alternative methodologies.In patients treated with beta-blockers 3-5 or beta-blockers plus nitrates 6 for prevention of rebleeding, it was observed that a decrease in portal pressure under chronic treatment, expressed as a decrease in hepatic venous pressure gradient (HVPG), is a strong predictor of clinical effectiveness. Indeed, decreases of HVPG to 12 mm Hg or less, or decreases by at least 20% from baseline values were associated with a negligible risk of rebleeding, whereas risk of rebleeding was confined to patients not meeting these hemodynamic end points. A single report was unable to confirm the clinical value of these hemodynamic end points. 7 In the clinical setting of prophylaxi...

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“…Wedged hepatic venous pressure has been found to closely correlate with the portal pressure. 72,73 A catheter is introduced through the jugular vein to the hepatic vein and is advanced until it can go no farther. The pressure measurements are then taken in the free and wedged positions.…”

Section: Assessment Of Hepatic Status In Hfmentioning

confidence: 99%

Gastrointestinal and Liver Issues in Heart Failure

2016

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Abstract-Heart failure affects ≈23 million people worldwide and continues to have a high mortality despite advancements in modern pharmacotherapy and device therapy. HF is a complex clinical syndrome that can result in the impairment of endocrine, hematologic, musculoskeletal, renal, respiratory, peripheral vascular, hepatic, and gastrointestinal systems. Although gastrointestinal involvement and hepatic involvement are common in HF and are associated with increased morbidity and mortality, their bidirectional association with HF progression remains poorly fathomed. The current understanding of multiple mechanisms, including proinflammatory cytokine milieu, hormonal imbalance, and anabolic/ catabolic imbalance, has been used to explain the relationship between the gut and HF and has been the basis for many novel therapeutic strategies. However, the failure of these novel therapies such as anti-tumor necrosis factor-α has resulted in further complexity. Key Words: gastrointestinal tract ◼ heart failure H eart failure (HF) is a systemic disorder caused by the inability of the heart to accommodate the venous return and to maintain sufficient cardiac output to meet the body's metabolic needs.1 These hemodynamic perturbations result in a state of systemic inflammation with well-described and well-studied consequences in a variety of other organ systems, including the renal, cerebral, musculoskeletal, and immune systems. In contrast, the gastrointestinal and hepatic systems have received less attention, although gastrointestinal symptoms are common. With increasing clinical efforts to resuscitate the advanced HF patient, a greater appreciation and a better understanding of the gastrointestinal and hepatic manifestations of HF are needed. 2,3With some notable exceptions, gastrointestinal and hepatic involvement in heart disease has historically received little attention from cardiologists. 4 Mechanisms of gastrointestinal and hepatic dysfunction remain poorly understood despite the common presence of gastrointestinal-related symptoms and the increased morbidity and mortality associated with their presence. The specific involvement of the gastrointestinal system in HF results in a bidirectional relationship that has been called the cardiointestinal syndrome.5 For example, the systemic volume overload characteristic of HF is generally accompanied by concomitant gut edema, which can lead to bacterial translocation into the systemic circulation. Consequent monocyte activation and excessive cytokine release result in systemic inflammation, increased symptoms, and disease progression. In this review, we describe the current state of understanding of the gastrointestinal and hepatic systems in HF. Although nutritional status is also relevant in this discussion, we refer the reader to other excellent reviews of nutritional aspects of chronic disease. 7,8The Gut in HF Gastrointestinal System as a Venous ReservoirStudies of implantable hemodynamic monitors to manage HF patients document that acute decompensated HF was not associ...

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Measurement of portal pressure and its clinical application

Cited by 157 publications

References 31 publications

Effect of Somatostatin on Splanchnic Hemodynamics in Patients with Liver Cirrhosis and Portal Hypertension

Effect of Somatostatin on Splanchnic Hemodynamics in Patients with Liver Cirrhosis and Portal Hypertension

The Hemodynamic Response to Medical Treatment of Portal Hypertension As A Predictor of Clinical Effectiveness in the Primary Prophylaxis of Variceal Bleeding in Cirrhosis

Gastrointestinal and Liver Issues in Heart Failure

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