The Hyperdynamic Circulation of Chronic Liver Diseases: From the Patient to the Molecule

Iwakiri, Yasuko; Groszmann, Roberto J.

doi:10.1002/hep.20993

Cited by 540 publications

(473 citation statements)

References 128 publications

(145 reference statements)

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“…Usually, the HVPG ranges from 1 to 5 mmHg, becoming clinically significant when it reaches 10 mmHg [6]. In clinical practice, an increase in HPVG values of at least 12 mmHg is usually associated with the presence of esophageal varices [2,6]. Progressing through the stages of cirrhosis, there is a wide development of a network of collateral vessels, which bypassing the liver, creates communication between the portal vein and the systemic circulation.…”

Section: Hemodynamic Changes Contributing To Hyperdynamic Syndromementioning

confidence: 99%

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Clinical implications of the hyperdynamic syndrome in cirrhosis

Licata

Mazzola

Ingrassia

et al. 2014

European Journal of Internal Medicine

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The hyperdynamic syndrome is a late consequence of portal hypertension in cirrhosis. The principal hemodynamic manifestations of the hyperdynamic syndrome are high cardiac output, and increased heart rate and total blood volume, accompanied by reduced total systemic vascular resistance. Pathophysiology involves a complex of humoral and neural mechanisms that can determine hemodynamic changes, and lead to hyperdynamic circulation. In this review we focus our attention on the manifestations of the hyperdynamic syndrome. Some of these are well described and directly related to portal hypertension (varices, ascites, hepatic encephalopathy, and hepatorenal syndrome), while others, such as hepatopulmonary syndrome, portopulmonary hypertension, and cirrhotic cardiomyopathy, are less known as clinical manifestations related to cirrhosis and, therefore, merit further investigation.

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Section: Hemodynamic Changes Contributing To Hyperdynamic Syndromementioning

confidence: 99%

“…The hyperdynamic syndrome (HS) is a consequence of cirrhosis of varying etiologies [1,2]. This syndrome has been defined by high cardiac output, increased heart rate and total blood volume, reduced total systemic vascular resistance, and low, normal or decreased arterial pressure [1][2][3].…”

Section: Introductionmentioning

confidence: 99%

Clinical implications of the hyperdynamic syndrome in cirrhosis

Licata

Mazzola

Ingrassia

et al. 2014

European Journal of Internal Medicine

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“…Nitric oxide (NO), tumor necrosis factoralfa (TNF-α), endocannabinoids, adrenomedullin, calcitonin gene-related peptide (CGRP), and carbon monoxide (CO) are the most important mediators in this field [13,14]. On the contrary, a concomitant activation of the sympathetic nervous system and the renin-angiotensin aldosterone system (RAAS) (noradrenaline, neuropeptide-Y, endothelin-1, angiotensin II, and vasopressin) has been observed [15,16] (Fig. 1).…”

Section: Role Of the Vascular Tone In The Genesis Of Cirrhotic Cardiomentioning

confidence: 99%

Pathophysiological and Clinical Approach to Cirrhotic Cardiomyopathy

Páll¹,

Czifra²,

Vitális³

et al. 2014

JGLD

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Hyperdynamic circulation, systolic and diastolic left ventricular dysfunction and certain electrophysiological abnormalities have been associated with cirrhosis and known for a long time. These clinical features have been introduced as cirrhotic cardiomyopathy (CCM), which is characterized by blunted myocardial contractile responsiveness to physical, physiological and pharmacological stress. Importantly, cardiac dysfunction can be reversible and can improve due to effective medical treatment and also after liver transplantation. Echocardiography and electrocardiography are essential tools for recognizing the characteristic changes in the myocardial function and also the alterations in the electrophysiological properties of the heart. Laboratory markers are auxiliary modalities further aiding the establishment of the correct diagnosis. In this review, we aimed to collect the pathophysiological background and clinical characteristics of CCM with the intention of summarizing the current possibilities for the diagnosis establishment and treatment of this cardio-hepatic disorder.Abbreviations: A: late diastolic transmitral peak flow velocity; ACE: angiotensin converting enzyme; ANP: atrial natriuretic peptide; ARB: angiotensin receptor blocker; BNP: brain natriuretic peptide; cAMP: cyclic adenosine monophosphate; CCM: cirrhotic cardiomyopathy; CGRP: calcitonin gene-related peptide; CO: carbon monoxide; DD: diastolic dysfunction; DT: deceleration time; E: early diastolic transmitral peak flow velocity; Ea: early diastolic velocity of the septal mitral annulus; EF: ejection fraction; MUGA: Multi Gated Acquisition Scan; NO: nitric oxide; NSBB: non-selective beta-blocker; pro-BNP: pro-brain natriuretic peptide; QTc: corrected QT interval; RAAS: renin-angiotensin aldosterone system; RALES: Randomized Aldactone Evaluation Study; suPAR: urokinase-type plasminogen activator receptor; TDI: Tissue Doppler Imaging; TIPS: transjugular intrahepatic portosystemic shunt; TNF-alpha: tumor necrosis factor-alpha.

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“…Hyperdynamic circulation stands out among the splanchnic and systemic alterations related to portal hypertension [1,[11][12][13][14][15]. It has been suggested that the splanchnic and systemic vasodilation is the initial step leading to the hyperdynamic syndrome or progressive vasodilatory syndrome [12,16]. Multiple organ failure in portal hypertensive chronic liver disease is in large part attributeable to this syndrome [14,16].…”

Section: The Ischemia-reperfusion Phenotype: the Hydroelectrolitic Chmentioning

confidence: 99%

“…nance of an inflammatory response. First, the pathological increase of the portal pressure that occurs in the hyperdynamic splanchnic circulation could favor a disturbed splanchnic venous flow with shear stress mediated by non-laminar flow [12]. The disturbed or non-laminar flow with associated reciprocating low shear stress has profound effects on the biology of the vascular wall, particularly the vascular endothelium, and could stimulate inflammation [17,18].…”

Section: The Ischemia-reperfusion Phenotype: the Hydroelectrolitic Chmentioning

confidence: 99%

Portal hypertension-related inflammatory phenotypes: From a vitelline and amniotic point of view

Aller¹,

Arias²,

Prieto³

et al. 2012

ABB

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Prehepatic portal hypertension induces a splanchnic low-grade inflammatory response that could switch to high-grade inflammation with the development of severe and life-threatening complications when associated with chronic liver disease. The extraembryonic origin of the portal system maybe determines the regression to an extraembryonic phenotype, i.e., vitellogenic and amniotic, during the evolution of both types of portal hypertension. Thus, prehepatic portal hypertension, or compensated hypertension by portal vein ligation in the rat, is associated with molecular mechanisms related to vitellogenesis, where hepatic steatosis and splanchnic angiogenesis stand out. In turn, extrahepatic cholestasis in the rat induces intrahepatic portal hypertension, or decompensated hypertension, with ascites and hepatorenal syndrome. The splanchnic interstitium, the mesenteric lymphatic system, and the peritoneal mesothelium seem to create an inflammatory pathway that could have a key pathophysiological relevance in the production of ascites. The hypothetical comparison between the ascitic and the amniotic fluid also allows for translational investtigation. The induced regression of the splanchnic system to extraembryonic functions by portal hypertension highlights the great relevance of the extraembryonic structures even during post-natal life.

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The Hyperdynamic Circulation of Chronic Liver Diseases: From the Patient to the Molecule

Cited by 540 publications

References 128 publications

Clinical implications of the hyperdynamic syndrome in cirrhosis

Clinical implications of the hyperdynamic syndrome in cirrhosis

Pathophysiological and Clinical Approach to Cirrhotic Cardiomyopathy

Portal hypertension-related inflammatory phenotypes: From a vitelline and amniotic point of view

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