Добавил:

Sekretar kiopkiopkiop18@yandex.ru t.me/Prokururor I Вовсе не секретарь, но почту проверяю Опубликованный материал нарушает ваши авторские права? Сообщите нам.

Вуз:

Ростовский Государственный Медицинский Университет

Предмет:

Медицина общая

Файл:

Книга_51_библиотеки_им_акад_М_И_Перельмана

.pdf

Скачиваний:

Добавлен:

10.10.2026

Размер:

9 Мб

Скачать

☆

<<< < Предыдущая 12 13 14 15 16 17 18 19 20 21 22 2324 / 3824 25 26 27 28 29 30 31 32 33 34 35 36 > Следующая >>>

[15] Goulis J, Armonis A, Patch D, Sabin C, Greenslade L, Burroughs AK. Bacterial infection is independently associated with failure to con-

trol bleeding in cirrhotic patients with gastrointestinal hemorrhage. Hepatology. 1998;27(5):120712.

[16] Schrier RW, Arroyo V, Bernardi M, Epstein M, Henriksen JH, Rodes J. Peripheral arterial vasodilation hypothesis: a proposal for the initi-

ation of renal sodium and water retention in cirrhosis. Hepatology. 1988;8(5):11517.

[17] Guturu P, Shah V. New insights into the pathobiology of portal hypertension. Hepatol Res. 2009;39:101619.

[18] Rasaratnam B, Connelly N, Chin-Dusting J. Nitric oxide and the hyperdynamic circulation in cirrhosis: is there a role for selective intesti-

nal decontamination? Clin Sci (Lond). 2004;107(5):42534.

[19] Dampney RAL. Central neural control of the cardiovascular system: current perspectives. Adv Physiol Educ. 2016;40(3):28396.

[20]

Vallance P, Moncada S. Hyperdynamic circulation in cirrhosis: a role for nitric oxide? Lancet. 1991;337(8744):7768.

[21] Li Y, Liu H, Gaskari SA, Tyberg JV, Lee SS. Altered mesenteric venous capacitance and volume pooling in cirrhotic rats are mediated by

nitric oxide. Am J Physiol Gastrointest Liver Physiol. 2008;295(2):G2529.

[22] Gonzalez-Abraldes J, Garcia-Pagan JC, Bosch J. Nitric oxide and portal hypertension. Metab Brain Dis. 2002;17(4):31124.

[23] Wiest R, Groszmann RJ. The paradox of nitric oxide in cirrhosis and portal hypertension: too much, not enough. Hepatology. 2002;35(2):47891.

[24] Chu CJ, Lee FY, Wang SS, Lu RH, Tsai YT, Lin HC, et al. Hyperdynamic circulation of cirrhotic rats with ascites: role of endotoxin,

tumour necrosis factor-alpha and nitric oxide. Clin Sci. 1997;93(3):21925.

[25] Sarela AI, Mihaimeed FM, Batten JJ, Davidson BR, Mathie RT. Hepatic and splanchnic nitric oxide activity in patients with cirrhosis.

Gut. 1999;44(5):74953.

[26] Niederberger M, Martin PY, Gines P, Morris K, Tsai P, Xu DL, et al. Normalization of nitric oxide production corrects arterial vasodila-

tion and hyperdynamic circulation in cirrhotic rats. Gastroenterology. 1995;109(5):162430.

[27] Martin PY, Ohara M, Gines P, Xu DL, St John J, Niederberger M, et al. Nitric oxide synthase (NOS) inhibition for one week improves

renal sodium and water excretion in cirrhotic rats with ascites. J Clin Invest. 1998;101(1):23542.

[28] La Villa G, Barletta G, Pantaleo P, Del Bene R, Vizzutti F, Vecchiarino S, et al. Hemodynamic, renal, and endocrine effects of acute inhibi-

tion of nitric oxide synthase in compensated cirrhosis. Hepatology. 2001;34(1):1927.

[29] Lee FY, Wang SS, Tsai YT, Lin HJ, Lin HC, Chu CJ, et al. Aminoguanidine corrects hyperdynamic circulation without ameliorating portal

hypertension and portal hypertensive gastropathy in anesthetized portal hypertensive rats. J Hepatol. 1997;26(3):68793.

[30] Weigert AL, Martin PY, Niederberger M, Higa EM, McMurtry IF, Gines P, et al. Endothelium-dependent vascular hyporesponsiveness

without detection of nitric oxide synthase induction in aortas of cirrhotic rats. Hepatology. 1995;22(6):185662.

[31] Liu H, Song D, Lee SS. Increased nitric oxide synthase expression in aorta of cirrhotic rats. Life Sci. 1999;64(19):17539.

[32] Shah V, Cao S, Hendrickson H, Yao J, Katusic ZS. Regulation of hepatic eNOS by caveolin and calmodulin after bile duct ligation in rats.

Am J Physiol Gastrointest Liver Physiol. 2001;280(6):G120916.

[33] Wiest R, Das S, Cadelina G, Garcia-Tsao G, Milstien S, Groszmann RJ. Bacterial translocation in cirrhotic rats stimulates eNOS-derived

NO production and impairs mesenteric vascular contractility. J Clin Invest. 1999;104(9):122333.

[34] Garcia-Tsao G, Wiest R. Gut microflora in the pathogenesis of the complications of cirrhosis. Best Pract Res Clin Gastroenterol. 2004;18(2):35372.

[35] Longcope C, Pratt JH, Schneider S, Fineberg E. Estrogen and androgen dynamics in liver disease. J Endocrinol Invest. 1984;7(6):62934.

[36] Weiner CP, Lizasoain I, Baylis SA, Knowles RG, Charles IG, Moncada S. Induction of calcium-dependent nitric oxide synthases by sex

hormones. Proc Natl Acad Sci USA. 1994;91(11):521216.

[37] Theodorakis NG, Wang YN, Skill NJ, Metz MA, Cahill PA, Redmond EM, et al. The role of nitric oxide synthase isoforms in extrahepatic

portal hypertension: studies in gene-knockout mice. Gastroenterology. 2003;124(5):15008.

[38] Iwakiri Y, Cadelina G, Sessa WC, Groszmann RJ. Mice with targeted deletion of eNOS develop hyperdynamic circulation associated

with portal hypertension. Am J Physiol Gastrointest Liver Physiol. 2002;283(5):G107481.

[39] Biecker E, Neef M, Sagesser H, Shaw S, Koshy A, Reichen J. Nitric oxide synthase 1 is partly compensating for nitric oxide synthase 3

deficiency in nitric oxide synthase 3 knock-out mice and is elevated in murine and human cirrhosis. Liver Int. 2004;24(4):34553.

[40] Xu L, Carter EP, Ohara M, Martin PY, Rogachev B, Morris K, et al. Neuronal nitric oxide synthase and systemic vasodilation in rats with

cirrhosis. Am J Physiol Renal Physiol. 2000;279(6):F111015.

[41] Moezi L, Gaskari SA, Lee SS. Endocannabinoids and liver disease. V. endocannabinoids as mediators of vascular and cardiac abnormali-

ties in cirrhosis. Am J Physiol Gastrointest Liver Physiol. 2008;295(4):G64953.

[42] Moezi L, Gaskari SA, Liu H, Baik SK, Dehpour AR, Lee SS. Anandamide mediates hyperdynamic circulation in cirrhotic rats via CB(1)

and VR(1) receptors. Br J Pharmacol. 2006;149(7):898908.

[43] Batkai S, Jarai Z, Wagner JA, Goparaju SK, Varga K, Liu J, et al. Endocannabinoids acting at vascular CB1 receptors mediate the vasodi-

lated state in advanced liver cirrhosis. Nat Med. 2001;7(7):82732.

[44] Ros J, Claria J, To-Figueras J, Planaguma A, Cejudo-Martin P, Fernandez-Varo G, et al. Endogenous cannabinoids: a new system involved

in the homeostasis of arterial pressure in experimental cirrhosis in the rat. Gastroenterology. 2002;122(1):8593.

[45] Fernandez-Rodriguez CM, Romero J, Petros TJ, Bradshaw H, Gasalla JM, Gutierrez ML, et al. Circulating endogenous cannabinoid anan-

damide and portal, systemic and renal hemodynamics in cirrhosis. Liver Int. 2004;24(5):47783.

[46] Siegmund SV, Uchinami H, Osawa Y, Brenner DA, Schwabe RF. Anandamide induces necrosis in primary hepatic stellate cells.

Hepatology. 2005;41(5):108595.

[47] Varga K, Wagner JA, Bridgen DT, Kunos G. Platelet- and macrophage-derived endogenous cannabinoids are involved in endotoxin-

induced hypotension. FASEB J. 1998;12(11):103544.

[48] Caraceni P, Viola A, Piscitelli F, Giannone F, Berzigotti A, Cescon M, et al. Circulating and hepatic endocannabinoids and

endocannabinoid-related molecules in patients with cirrhosis. Liver Int. 2010;30(6):81625.

[49] Baldassarre M, Giannone FA, Napoli L, Tovoli A, Ricci CS, Tufoni M, et al. The endocannabinoid system in advanced liver cirrhosis:

pathophysiological implication and future perspectives. Liver Int. 2013;33(9):1298308.

[50] Yang YY, Lin HC. Alteration of intrahepatic microcirculation in cirrhotic livers. J Chin Med Assoc. 2015;78(8):4307.

[51] Domenicali M, Ros J, Fernandez-Varo G, Cejudo-Martin P, Crespo M, Morales-Ruiz M, et al. Increased anandamide induced relaxation

in mesenteric arteries of cirrhotic rats: role of cannabinoid and vanilloid receptors. Gut. 2005;54(4):5227.

214 14. Peripheral vasculature in portal hypertension

III. Cardiovascular system in liver failure

https://t.me/medicina_free

[52] Lin HC, Yang YY, Tsai TH, Huang CM, Huang YT, Lee FY, et al. The relationship between endotoxemia and hepatic endocannabinoids

in cirrhotic rats with portal hypertension. J Hepatol. 2011;54(6):114553.

[53] Fernandez M, Lambrecht RW, Bonkovsky HL. Increased heme oxygenase activity in splanchnic organs from portal hypertensive rats:

role in modulating mesenteric vascular reactivity. J Hepatol. 2001;34(6):81217.

[54] Moreau R. Heme oxygenase: protective enzyme or portal hypertensive molecule? J Hepatol. 2001;34(6):9369.

[55] Makino N, Suematsu M, Sugiura Y, Morikawa H, Shiomi S, Goda N, et al. Altered expression of heme oxygenase-1 in the livers of

patients with portal hypertensive diseases. Hepatology. 2001;33(1):3242.

[56] Matsumi M, Takahashi T, Fujii H, Ohashi I, Kaku R, Nakatsuka H, et al. Increased heme oxygenase-1 gene expression in the livers of

patients with portal hypertension due to severe hepatic cirrhosis. J Int Med Res. 2002;30(3):2828.

[57] Guevara M, Gines P, Jimenez W, Sort P, Fernandez-Esparrach G, Escorsell A, et al. Increased adrenomedullin levels in cirrhosis: relation-

ship with hemodynamic abnormalities and vasoconstrictor systems. Gastroenterology. 1998;114(2):33643.

[58] Lee FY, Lin HC, Tsai YT, Chang FY, Lu RH, Hou MC, et al. Plasma substance P levels in patients with liver cirrhosis: relationship to sys-

temic and portal hemodynamics. Am J Gastroenterol. 1997;92(11):20804.

[59] Pak JM, Lee SS. Vasoactive effects of bile salts in cirrhotic rats: in vivo and in vitro studies. Hepatology. 1993;18(5):117581.

[60] Lee SS, Chilton EL, Pak JM. Adenosine receptor blockade reduces splanchnic hyperemia in cirrhotic rats. Hepatology. 1992;15(6):110711.

[61] Desai MS, Eblimit Z, Thevananther S, Kosters A, Moore DD, Penny DJ, et al. Cardiomyopathy reverses with recovery of liver injury, cho-

lestasis and cholanemia in mouse model of biliary fibrosis. Liver Int. 2015;35(4):146477.

[62] Desai MS, Mathur B, Eblimit Z, Vasquez H, Taegtmeyer H, Karpen SJ, et al. Bile acid excess induces cardiomyopathy and metabolic dys-

functions in the heart. Hepatology. 2017;65(1):189201.

[63] Sheng M, Greenberg ME. The regulation and function of c-fos and other immediate early genes in the nervous system. Neuron. 1990;4(4):47785.

[64] Breitman DR, Lee SS. Blunted responsiveness of the neuronal activation marker Fos in brainstem cardiovascular nuclei of cirrhotic rats.

Hepatology. 1997;26(6):13805.

[65] Song D, Liu H, Sharkey KA, Lee SS. Hyperdynamic circulation in portal-hypertensive rats is dependent on central c-fos gene expression.

Hepatology. 2002;35(1):15966.

[66] Song D, Sharkey KA, Breitman DR, Zhang Y, Lee SS. Disordered central cardiovascular regulation in portal hypertensive and cirrhotic

rats. Am J Physiol Gastrointest Liver Physiol. 2001;280(3):G42030.

[67] Li Y, Song D, Zhang Y, Lee SS. Effect of neonatal capsaicin treatment on haemodynamics and renal function in cirrhotic rats. Gut.

2003;52(2):2939.

[68] Fernandez B, Vatta M, Rodriguez-Fermepin M, Bianciotti L, Romay S, Eizayaga F, et al. Norepinephrine uptake modifications in circum-

ventricular organs, pons and myelencephalic areas and nuclei in prehepatic portal hypertensive rats. Neurochem Int. 1999;34(3):17781.

[69] Lee SS, Sharkey KA. Capsaicin treatment blocks development of hyperkinetic circulation in portal hypertensive and cirrhotic rats. Am J

Physiol. 1993;264(5 Pt 1):G86873.

[70] Liu H, Schuelert N, McDougall JJ, Lee SS. Central neural activation of hyperdynamic circulation in portal hypertensive rats depends on

vagal afferent nerves. Gut. 2008;57(7):96673.

[71] Henriksen JH. Volume adaptation in chronic liver disease: on the static and dynamic location of water, salt, protein and red cells in cir-

rhosis. Scand J Clin Lab Invest. 2004;64(6):52333.

[72] Li Y, Liu H, Gaskari SA, McCafferty DM, Lee SS. Hepatic venous dysregulation contributes to blood volume pooling in cirrhotic rats.

Gut. 2006;55(7):10305.

[73] Campbell PJ, Leung WM, Logan AG, Debowski TE, Blendis LM, Skorecki KL. Hyperresponsiveness to water immersion in sodium

retaining cirrhotics: the role of atrial natriuretic factor. Clin Invest Med. 1988;11(6):3925.

[74] Cereda JM, Roulot D, Braillon A, Moreau R, Koshy A, Lebrec D. Reduction of portal pressure by acute administration of furosemide in

patients with alcoholic cirrhosis. J Hepatol. 1989;9(2):24651.

[75] Moreau R, Lee SS, Soupison T, Roche-Sicot J, Sicot C. Abnormal tissue oxygenation in patients with cirrhosis and liver failure. J Hepatol.

1988;7(1):98105.

[76] Iwakiri Y. The molecules: mechanisms of arterial vasodilatation observed in the splanchnic and systemic circulation in portal hyperten-

sion. J Clin Gastroenterol. 2007;41(Suppl 3):S28894.

[77] Arroyo V, Colmenero J. Ascites and hepatorenal syndrome in cirrhosis: pathophysiological basis of therapy and current management.

J Hepatol. 2003;38(Suppl 1):S6989.

[78] Iwakiri Y, Kim MY. Nitric oxide in liver diseases. Trends Pharmacol Sci. 2015;36(8):52436.

[79] Kimer N, Goetze JP, Bendtsen F, Moller S. New vasoactive peptides in cirrhosis: organ extraction and relation to the vasodilatory state.

Eur J Clin Invest. 2014;44(5):44152.

[80] Tazi KA, Barriere E, Moreau R, Heller J, Sogni P, Pateron D, et al. Role of shear stress in aortic eNOS up-regulation in rats with biliary

cirrhosis. Gastroenterology. 2002;122(7):186977.

[81] Moller S, Hobolth L, Winkler C, Bendtsen F, Christensen E. Determinants of the hyperdynamic circulation and central hypovolaemia in

cirrhosis. Gut. 2011;60(9):12549.

[82] Bernardi M, Moreau R, Angeli P, Schnabl B, Arroyo V. Mechanisms of decompensation and organ failure in cirrhosis: From peripheral

arterial vasodilation to systemic inflammation hypothesis. J Hepatol. 2015;63(5):127284.

[83] Mookerjee RP, Stadlbauer V, Lidder S, Wright GA, Hodges SJ, Davies NA, et al. Neutrophil dysfunction in alcoholic hepatitis superim-

posed on cirrhosis is reversible and predicts the outcome. Hepatology. 2007;46(3):83140.

[84] Gronbaek H, Sandahl TD, Mortensen C, Vilstrup H, Moller HJ, Moller S. Soluble CD163, a marker of Kupffer cell activation, is related to

portal hypertension in patients with liver cirrhosis. Aliment Pharmacol Ther. 2012;36(2):17380.

[85] Fernandez J, Gustot T. Management of bacterial infections in cirrhosis. J Hepatol. 2012;56(Suppl 1):S112.

[86] Wiest R, Cadelina G, Milstien S, McCuskey RS, Garcia-Tsao G, Groszmann RJ. Bacterial translocation up-regulates GTP-cyclohydrolase I

in mesenteric vasculature of cirrhotic rats. Hepatology. 2003;38(6):150815.

[87] Gustot T, Durand F, Lebrec D, Vincent JL, Moreau R. Severe sepsis in cirrhosis. Hepatology. 2009;50(6):202233.

215References

III. Cardiovascular system in liver failure

https://t.me/medicina_free

[88] Bajaj JS, O’Leary JG, Wong F, Reddy KR, Kamath PS. Bacterial infections in end-stage liver disease: current challenges and future direc-

tions. Gut. 2012;61(8):121925.

[89] Lunzer MR, Newman SP, Bernard AG, Manghani KK, Sherlock SP, Ginsburg J. Impaired cardiovascular responsiveness in liver disease.

Lancet. 1975;2(7931):3825.

[90] Barron HV, Alam I, Lesh MD, Strunk A, Bass NM. Autonomic nervous system tone measured by baroreflex sensitivity is depressed in

patients with end-stage liver disease. Am J Gastroenterol. 1999;94(4):9869.

[91] Trevisani F, Sica G, Mainqua P, Santese G, De Notariis S, Caraceni P, et al. Autonomic dysfunction and hyperdynamic circulation in cir-

rhosis with ascites. Hepatology. 1999;30(6):138792.

[92] Hendrickse MT, Thuluvath PJ, Triger DR. Natural history of autonomic neuropathy in chronic liver disease. Lancet. 1992;339

(8807):14624.

[93] Oliver MI, Miralles R, Rubies-Prat J, Navarro X, Espadaler JM, Sola R, et al. Autonomic dysfunction in patients with non-alcoholic

chronic liver disease. J Hepatol. 1997;26(6):12428.

[94] Bernardi M, Fornale L, Di Marco C, Trevisani F, Baraldini M, Gasbarrini A, et al. Hyperdynamic circulation of advanced cirrhosis: a re-

appraisal based on posture-induced changes in hemodynamics. J Hepatol. 1995;22(3):30918.

[95] Spahr L, Burkhard PR, Grotzsch H, Hadengue A. Clinical significance of basal ganglia alterations at brain MRI and 1H MRS in cirrhosis

and role in the pathogenesis of hepatic encephalopathy. Metab Brain Dis. 2002;17(4):399413.

[96] Strauss GI, Hansen BA, Herzog T, Larsen FS. Cerebral autoregulation in patients with end-stage liver disease. Eur J Gastroenterol

Hepatol. 2000;12(7):76771.

[97] Butterworth RF. Pathogenesis of hepatic encephalopathy: new insights from neuroimaging and molecular studies. J Hepatol. 2003;39

(2):27885.

[98] Reynaert H, Geerts A. Pharmacological rationale for the use of somatostatin and analogues in portal hypertension. Aliment Pharmacol

Ther. 2003;18(4):37586.

[99] Baik SK, Jeong PH, Ji SW, Yoo BS, Kim HS, Lee DK, et al. Acute hemodynamic effects of octreotide and terlipressin in patients with cir-

rhosis: a randomized comparison. Am J Gastroenterol. 2005;100(3):6315.

[100] D’Amico G, Pagliaro L, Bosch J. The treatment of portal hypertension: a meta-analytic review. Hepatology. 1995;22(1):33254.

[101] Drsquo;Amico G, Pagliaro L, Bosch J. Pharmacological treatment of portal hypertension: an evidence-based approach. Semin Liver Dis.

1999;19(4):475505.

[102] Thiesson HC, Skott O, Jespersen B, Schaffalitzky de Muckadell OB. Nitric oxide synthase inhibition does not improve renal function in

cirrhotic patients with ascites. Am J Gastroenterol. 2003;98(1):1806.

[103] Forrest EH, Jones AL, Dillon JF, Walker J, Hayes PC. The effect of nitric oxide synthase inhibition on portal pressure and azygos blood

flow in patients with cirrhosis. J Hepatol. 1995;23(3):2548.

[104] Yu Q, Shao R, Qian HS, George SE, Rockey DC. Gene transfer of the neuronal NO synthase isoform to cirrhotic rat liver ameliorates

portal hypertension. J Clin Invest. 2000;105(6):7418.

[105] Albillos A, de la Hera A, Gonzalez M, Moya JL, Calleja JL, Monserrat J, et al. Increased lipopolysaccharide binding protein in cirrhotic

patients with marked immune and hemodynamic derangement. Hepatology. 2003;37(1):20817.

[106] Rasaratnam B, Kaye D, Jennings G, Dudley F, Chin-Dusting J. The effect of selective intestinal decontamination on the hyperdynamic

circulatory state in cirrhosis. A randomized trial. Ann Intern Med. 2003;139(3):18693.

[107] Baruch Y, Assy N, Weisbruch F, Reisner SA, Rinkevich D, Enat R, et al. A pilot study on the hemodynamic effect of short-term urso-

deoxycholic acid therapy in patients with stable liver cirrhosis. Am J Gastroenterol. 1999;94(10):30004.

[108] Wong F, Bomzon A, Allard J, Liu P, Blendis L. Effects of ursodeoxycholic acid on systemic, renal and forearm haemodynamics and

sodium homoeostasis in cirrhotic patients with refractory ascites. Clin Sci. 1999;96(5):46774.

[109] Verbeke L, Farre R, Trebicka J, Komuta M, Roskams T, Klein S, et al. Obeticholic acid, a farnesoid X receptor agonist, improves portal

hypertension by two distinct pathways in cirrhotic rats. Hepatology 2014;59(6):228698.

216 14. Peripheral vasculature in portal hypertension

III. Cardiovascular system in liver failure

https://t.me/medicina_free

CHAPTER

Cirrhotic cardiomyopathy

Hongqun Liu

, Daljeet Chahal

, Vladimir Marquez

and Samuel S. Lee

Liver Unit, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada

University of British

Columbia, Vancouve r, BC, Canada

Introduction

More than six decades ago, investigators noticed the presence of cardiovascular abnormalities in cirrhosis. Kowalski

and Abelmann in 1953 found that patients with cirrhosis had an increased cardiac output while mean arterial pressure

(MAP) and systemic vascular resistance were decreased

[1], the so-called hyperdynamic circulation. Later on physicians

perceived that despite an increased baseline cardiac output, the contractile response of the heart to pharmacological and

physiological stress is attenuated in patients with cirrhosis

[24]. For more than two decades, it was taken for granted

that the blunted cardiac contractile response was due to alcoholic toxicity, so-called alcoholic cardiomyopathy. This

opinion prevailed until the mid-1980s when Lee and others

[5] found that a similar pattern of cardiac dysfunction was

also present in nonalcoholic cirrhosis in humans and in animal models

[5,6]. These studies demonstrated that cirrhosis

per se induces this specific pattern of high-output heart failure, a phenomenon now termed cirrhotic cardiomyopathy.

Cardiomyopathy appears to reverse with recovery of liver injury

[7]. This chapter reviews the diagnostic criteria, preva-

lence, pathogenic mechanisms, clinical relevance, and management strategies of cirrhotic cardiomyopathy.

Definition and diagnostic criteria

Patients with cirrhosis, despite the baseline increase in cardiac output, when challenged, show attenuated sys-

tolic and diastolic contractile responses to stress stimuli, electrophysiological repolarization changes, including

prolonged QT interval, and enlargement or hypertrophy of cardiac chambers. This constellation of cardiac abnor-

malities is termed cirrhotic cardiomyopathy. The first attempt to define criteria was formulated at the 2005

World Congress of Gastroenterology in Montreal.

Diagnostic criteria [8]:

1. Abnormal systolic contractile responses to stress.

2. Diastolic dysfunction at rest.

3. Absence of clinically significant cardiopulmonary disease.

Systolic dysfunction (at least one of the following):

1. Blunted increase in cardiac output with exercise, volume challenge, or pharmacological stimuli.

2. Resting LVEF , 55%

Diastolic dysfunction (at least one of the following):

1. E/A ratio (age corrected) ,1.0

2. Prolonged deceleration time ( . 200 Ms)

3. Prolonged isovolumic relaxation time ( . 80 Ms)

217

Cardio-Hepatology.

DOI:

https://t.me/medicina_free

Supportive criteria:

1. Electrophysiological abnormalities including the following:

• Abnormal chronotropic response to stress.

• Electromechanical uncoupling/dyssynchrony.

• Prolonged QTc interval.

2. Heart chamber alterations: enlarged LA, increased LVWT.

3. Increased pro-BNP and BNP.

4. Increased troponin I.

BNP, Brain natriuretic peptide; LVEF, left ventricular ejection fraction; LVWT, left ventricular wall thickness.

More than 15 years have been passed since the creation of those criteria. Advances in both echocardiographic

techniques and also in our understanding of heart failure with preserved ejection fraction (HFpEF), the subgroup

that cirrhotic cardiomyopathy falls into, have allowed refinement and redefinition of the criteria. Accordingly,

we recommend that the 2005 Montreal criteria be abandoned and future studies should use the new CCM

Consortium criteria. The Cirrhotic Cardiomyopathy Consortium, which included a multidisciplinary expert

group (hepatology, anesthesia, and cardiology), redefined the diagnostic criteria of cirrhotic cardiomyopathy in

2020. In brief, these proposed criteria were based on the cardiac abnormalities detected under advanced methods

such as echocardiographic strain analysis and tissue Doppler imaging, in patients with cirrhosis. The new pro-

posed criteria by the Cirrhotic Cardiomyopathy Consortium are as follows:

Systolic dysfunction Advanced diastolic dysfunction Areas for future research

Any of the following

• LV ejection fraction # 50%

• Absolute GLS , 18%

$ 3 of the following

• Septal e

velocity , 7cm/s

• E/e

ratio $ 15

• LAVI .34 mL/m

• TR velocity . 2.8 m/s

• Abnormal chronotropic or inotropic response section

• Electrocardiographic changes

• Electromechanical uncoupling

• Myocardial mass change

• Serum biomarkers

• Chamber enlargement

• CMRI

CMRI, Cardiac magnetic resonance imaging; e

, early diastolic mitral annular velocity; E/e

, ratio of mitral peak velocity of early filling to early

diastolic mitral annular velocity; GLS, global longitudinal strain; LV, left ventricle; TR, tricuspid regurgitation; LAVI, left atrium volume

index.

According to either the old or new criteria, the prevalence of CCM ranges from 18% to 70% (Table 15.1).

Distinction from other cardiomyopathies

The diagnosis of cirrhotic cardiomyopathy is based on abnormal systolic and diastolic function, detected by

advanced ultrasonographic methods, in the absence of preexisting heart disease. Since different types of cardio-

myopathies such as alcoholic and ischemic cardiomyopathy manifest similar echocardiographic abnormalities, it

may be difficult to differentiate CCM from these conditions based purely on ultrasonography. Thus, a history of

alcohol excess, along with features of ischemic heart disease such as angina pectoris, and risk factors for athero-

sclerosis will help differentiate these other conditions.

Although the diagnosis of alcoholic cardiomyopathy can be nonspecific

[31], typically, it manifests a dilated

cardiomyopathy characterized by moderately or severely depressed contractility and ventricular dilatation.

Thus, in addition to the alcohol history, patients with alcoholic cardiomyopathy show much more overt heart

failure compared to C CM. Ischemic cardiomyopathy is defined as left ventricular dysfunction in the presence

of severe coronary artery disease

[32]. Similar to alcoholi c cardiomyopathy, ischemic cardiomyopathy is more

overt and more severe than CCM. Besides the history of angina, another possible differentiating feature in

ischemic cardiomyopathy may be the presence of localized ventricular wall motion abnormality compared to

mild diffuse or no wall motion changes in CCM

[33]. In that respect, a peculiar subtype of ventricular dysfunc-

tion, known as Takotsubo syndrome

[34], characterized by lack of coronary arterio sclerosis and acute onset of

heart failure, shares some features of cirrhotic cardiomyopathy. In both conditions, sympathetic overactivation,

in particular due to catecholamine surges, appear to play a pathogenic role. However, t he transient nature,

chest pain, and localized ventricular wall motion abnormalities readily distinguish Takotsubo syndrome from

cirrhotic cardiomyopathy.

218 15. Cirrhotic cardiomyopathy

III. Cardiovascular system in liver failure

https://t.me/medicina_free

TABLE 15.1 Prevalence of CCM in studies assessing systolic or diastolic dysfunction using echocardiography.

First author, year,

country

Subjects Etiology Cirrhosis severity Cardiac assessment

CCM

prevalence

(%)

Total

sample size

Age (x ) Male/

Female

Alcohol/

viral/other Child A/B/C

MELD

score (x ) Systolic or diastolic; method of assessment

Cazzaniga et al.

[9]

Italy

33 61

21/11

11/14/7 4/19/9 10 DD;

Echo: E/A ratio , 1

56.3

Alexander et al.

[10]

India

60 43.25

48/12

30/25/5 2/39/19 NR DD;

Echo: Diastolic Deceleration Time .250 ms

45.0

Raedle-Hurst et al.

[11]

Germany

31 50.9

19/12

20/10/1 11/11/9 NR DD;

Echo: Tissue Doppler: E/A , 1, 11of(Decel. 240 Ms, IVRT . 90 Ms, Ea , 8cm/s)

80.6

Rabie et al.

[12]

Canada

101 57.5

73/28

49/22/30 5/68/28 12.5 DD;

Echo: E/A Ratio , 1

40.6

Kazankov et al.

[13]

Denmark

44 53

27/17

32/5/7 20/12/8 12.3 DD;

Echo: Tissue Doppler: DT . 240 Ms, E/A , 1 and E’/A’ , 1

54.5

Merli et al.

[14] Italy 74 58

44/30

NR 39/35/26 13 DD;

Echo: Tissue Doppler: LFEF , 50, E/A , 0.8, DT . 200 Ms, IVRT . 100 Ms,

annular E’ , 8 cm/s and E/E’ lateral , 8

63.5

Enache et al.

[15]

France

83 52.1

64/19

41/24/18 NR 24 SD and DD;

Echo: LV EF , 55 or E/A , 1 or Deceleration .200 Ms ( . 240 in LV if .50 years,

or .220 in RV if .50)

18.1

Karagiannakis et al.

[16] Greece

45 57.2

33/12

22/19/4 26/15/3 11.5 DD;

Echo: Tissue Doppler: E’septal , 8 cm/s and E’lateral , 10 cm/s

37.8

Salari et al.

[17] Iran 100 52.78

63/37

0/31/69 22/38/40 DD;

Echo: 1 of E/A ratio , 0.8, dec Time . 280 Ms, E/Ea , 8

51.0

Nazar et al. [18] Spain 100 56.2

70/30

45/40/15 26/39/37 15.7 DD;

Echo: E/A ratio , 0.8, dec Time . 200 Ms, IVRT .100 ms

58.0

Mao et al.

[19] China 50 53.16

38/12

7/36/7 15/20/15 DD;

Echo: E/A , 1

56.0

Sampaio et al. [20]

Portugal

109 54

86/23

73/27/9 37/27/45 14 DD;

Echo: E/A ratio , 1, Deceleration . 200 Ms, IVRT . 80 ms

40.4

Raevens et al.

[21]

Belgium

173 57

111/62

69/23/10 NR 17 DD;

Echo: E/A ratio , 1, Deceleration . 200 Ms, IVRT . 80 ms

43.9

Somani et al.

[22] India 60 49.8

48/12

30/22/8 NR 14.75 DD;

Echo: E/A ratio , 0.8, dec Time . 200 Ms, IVRT . 100 ms

30.0

Falletta et al.

[23] Italy 84 53

56/28

8/57/19 14/29/41 13.9 DD;

Echo: Tissue Doppler; E/e’ ratio . 13

26.2

Celtik et al. [24]

Turkey

40 7.8

20/20

0/2/38 23/7/10 10 (PELD) SD or DD;

Echo: LVEF , 55 or Deceleration . 200 Ms or IVRT .100 or ECG: QTc . 0.45 ms

25.0

Voiosu et al.

[25]

Romania

74 58

46/28

28/37/9 43/12/19 12.6 SD or DD;

Echo: LVEF , 55, E/A , 1, IVRT . 80, DT . 200 ms

40.5

(Continued)

https://t.me/medicina_free

TABLE 15.1 (Continued)

First author, year,

country

Subjects Etiology Cirrhosis severity Cardiac assessment

CCM

prevalence

(%)

Total

sample size

Age (x ) Male/

Female

Alcohol/

viral/other Child A/B/C

MELD

score (x ) Systolic or diastolic; method of assessment

Barbosa et al.

[26]

Portugal

26 54.6

22/4

20/3/3 17/8/1 8.7 SD or DD;

Echo: Tissue Toppler: LVEF , 50% or Septal e’ , 8 cm/s and lateral e’ , 10 cm/s

61.5

Merli et al.

[27] Italy 90 60.4

59/31

28/49/13 74(A 1 B)/16 11.9 DD;

Echo: 2 of (E/A ratio , 0.8, dec Time . 200 Ms, IVRT . 100 Ms)

28.9

Hammami et al.

[28]

Tunisia

80 55

42/38

0/42/38 24/36/20 14.2 SD or DD

Echo:Tissue Doppler: LVEF , 55, E/A , 0.8, E’Ea , 10, tricuspid regurg

velocity , 2.8 m/s

70.0

Wiese et al.

[29]

Denmark

52 57

34/18

40/0/12 NR/37/NR 10 SD or DD;

Echo: Tissue Doppler E/A ratio , 0.75 and E/e

ratio , 8

38.5

Huang et al.

[30]

Taiwan

80 48.5

64/16

28/52/0 31/22/27 NR DD;

Echo: E/A ratio , 0.8, dec Time . 200 Ms, IVRT . 100 ms

27.5

NR, Not reported; SD, systolic dysfunction; DD, diastolic dysfunction; E/A, ratio of early/late diastolic mitral inflow velocity; LVEF, left ventricular ejection fraction; IVRT, isovolumic relaxation time; E/E’, ratio of early

transmitral diastolic inflow to early mitral annular velocity.

https://t.me/medicina_free

Clinical significance

Prevalence

CCM prevalence ranges from 23.4% to 80.6% (Fig. 15.1, Table 15.2) [35]. The variability may be due to different

patient selection criteria and variable methods of cardiac function evaluation. CCM development is based on cir-

rhosis per se, not on the underlying etiology of cirrhos is

[3638]. However, Salari et al. found a higher preva-

lence of CCM in Hepatitis C-induced cirrhosis and Karagiannakis et al. reported that nonalcoholic cirrhosis had a

higher frequency of CCM

[16,17]. However, these two studies are outliers as the vast majority of studies demon-

strated that prevalence is independent of the cause of cirrhosis.

Razpotnik and colleagues recently compared the prevalence of CCM according to three different diagnostic criteria.

They examined the 2005 Montreal criteria, the 2020 Cirrhotic Cardiomyopathy Consortium criteria

[48],andthe

American Society of Echocardiography (ASE)/European Association of Cardiovascular Imaging (EACVI) criteria

(ASE/EACVI). They found that the overall prevalence of CCM was similar for the Montreal criteria (67.2%) compared

to the CCM Consortium criteria (55.7%, P5 .9). The study also revealed that these criteria have poor agreement; only

15.6% patients met all three criteria, which means that all three systems basically selected different subsets of patients.

As no clear “gold standard” for the diagnosis of CCM exists, in order to determine which definition system to use will

depend on which one correlates best with meaningful outcomes such as mortality and adverse cardiac events includ-

ing overt heart failure, arrhythmias, and sudden cardiac death. Thus this will require long-term outcome studies.

Mechelinck et al.

[49] found that the incidence of major adverse cardiac events (MACE) in patients with low

GLS was 64%, and with high GLS was 43%, significantly higher than that with normal GLS (27%, P , .05).

However, normal GLS cannot rule out the presence of MACE in liver transplant candidates. It is clear that we still

need to establish universally accepted diagnostic criteria for CCM. Because the new CCM Consortium criteria are

FIGURE 15.1 Estimated prevalence of cirrhotic cardiomyopathy. Source: Reproduced with permission, from Chahal D, Liu H, Shamatutu C,

Sidhu H, Lee SS, Marquez D. Review article: Comprehensive analysis of cirrhotic cardiomyopathy Aliment Pharmacol Ther. 2021; 53:985998.

221Clinical significance

III. Cardiovascular system in liver failure

https://t.me/medicina_free

TABLE 15.2 Studies assessing QTc reversibility following liver transplantation.

First author, year, country

Total Sample

Size

Subjects

Age (x )

Male/Female Time post-transplant Results Pre LT Post LT P

Bal and Thuluvath

[39] United

States

162 52.3

86/76

6 months 1. Decreased QTc (x )

2. Normalized of prolonged QTc in

55%

3. Worse or new QTc prolongation

in 23%

QTc (x ): 450 ms QTc (x ): 429 Ms

QTc normalized: 55%

QTc worse: 14%

New QTc prolongation:

,.002

Torregrosa et al.

[40] Spain 40 56.5

23/17

9 months (x )

Range: 612 months

1. Normalization of QTc in 100% QTc normalized: 100%

Adigun et al.

[41] United States 38 43.9

25/13

9.5 months (median) 1. Decreased QTc (x )

2. Normalization of prolonged QTc

in 50%

QTc (x ): 436 ms QTc (x ): 421ms

QTc normalized: 50%

.02

Carey and Douglas [42] United

States

46 49.9

24/22

4 months 1. Decreased QTc(x )

2. Normalization of prolonged QTc

in 84%

3. Worse or new QTc prolongation

in 6.5%

QTc (x ): 451 ms QTc (x ): 418

QTc normalized: 84%

QTc worse: 2.2%

New QTc prolongation:

4.3%

,.001

Zurick et al.

[43] United States 269 50.9

169/100

Range: 112 months 1. Decreased QTc (x )

2. Normalization of prolonged QTc

in 70%

QTc (x ): 449 ms QTc (x ): 417 Ms

QTc normalized: 70%

,.001

Dowsley et al.

[44] United

States

107 55

73/34

2.6 months (x )

Range: 06 months

1. Decreased QTc (x ) QTc (x ): 415 ms QTc (x ): 371 ms ,.001

Zahmatkeshan et al.

[45] Iran 22 21.5

16/6

6 months 1. Decreased QTc (x ) QTc (x ): 420 ms QTc (x ):390 ms .04

Sonny et al.

[46] United States 243 55

175/68

5.2 years (x ) 1. Decreased QTc (x ) QTc (x ): 452 ms QTc (x ): 442 ms ,.001

Gajanana et al. [47] United

States

73 55

47/26

371 days (x ) 1. Decreased QTc (x ) QTc (x ): 465 QTc (x ): 439 ms .01

https://t.me/medicina_free

based on modest adaptations of the ASE/EACVI criteria, for patients with cirrhosis, we believe that at present, the

field of cirrhotic cardiomyopathy would best be served if studies proceed using the 2020 CCM Consortium criteria.

The correlation between the severity of liver disease and CCM is unclear. In other words, are the features or

extent of cirrhotic cardiomyopathy more pronounced as the degree of liver failure increases with advancing cir-

rhosis? Some studies have indeed demonstrated an association between CCM and Child-Pugh Score and/or

model of end-stage liver disease (MELD) Scores

[9,16,29,50]; others did not find these relationships

[14,15,23,25,26,28]. In children with biliary atresia waiting for transplant, the association between the pediatric

end-stage liver disease score and cardiac dysfunction is also inconsistent across studies

[51,52].

However, we believe that CCM does indeed correlate with the severity of liver failure. This is based on four observa-

tions. (1) Cardiac dysfunction normalizes after liver transplantation although this is somewhat controversial. (2) There is

a consensus that electrocardiographic QT prolongation is correlated with the degree of liver failure and improves after

transplant (

Table 15.2). (3) Rats with prehepatic portal hypertension due to portal vein ligation have equal extent of por-

tal hypertension and hyperdynamic circulation compared to cirrhotic rats, but normal liver function; however, these

rats also have normal cardiac function

[53]. (4) Finally, we believe that the discrepancies in the literature are mainly due

to major differences in how extent of CCM was measured, that is, lack of universally accepted CCM criteria/definitions.

Morbidity/mortality after cardiovascular challenges

Cirrhotic cardiomyopathy is less likely to be clinically recognized in the absence of stressful stimuli. This is

because of the reduced ventricular afterload in cirrhotics due to peripheral vasodilation, thus “auto-treating” the

patient and preventing the development of overt congestive heart failure. However, if there is significant stress

on the heart, signs of cardiac dysfunction may become more evident. Overt heart failure can be precipitated by

stresses such as liver transplantation or transjugular intrahepatic portosystemic shunt (TIPS) insertion. Moreover,

cirrhotic cardiomyopathy may play an important role in the pathogenesis of hepatorenal syndrome.

Transjugular intrahepatic portal systemic shunts

As mentioned above, diastolic relaxation is impaired in cirrhotic cardiomyopathy, primarily because of stiffen-

ing and/or hypertrophy of the left ventricle, leading to decreased compliance and higher diastolic pressures.

Finucci and colleagues

[54] in the mid-1990s demonstrated diastolic dysfunction in cirrhotic heart, reporting that

almost all of the diastolic indices, such as left ventricular end-diastolic and left atrial volume, stroke volume, late

diastolic flow velocity (peak A) time from onset of mitral inflow to the early peak (time E) and deceleration time

(DT) were significantly impaired. The E/A ratio is the echocardiographic measurement of the E (early) wave veloc-

ity of blood filling the ventricle during the initial part of diastole divided by the velocity of late diastolic filling

wave (called A wave as the “‘atrial kick”’ predominates during this stage). The E/A is a common parameter used

for estimation of diastolic function but has a number of limitations including age- and preload-dependence. They

found that E/A ratio was significantly decreased in cirrhotic heart compared with controls

[54].

TIPS reduces portal pressure in cirrhotic patients and is widely used as a nonsurgical therapy to treat portal

hypertension-related complications, such as refractory ascites, recurrent variceal hemorrhage, or hepatorenal syn-

drome. TIPS has a marked effect on systemic hemodynamics. In particular, it rapidly shifts a large volume of

blood from the splanchnic vascular bed to the heart, thus increasing the cardiac preload. This poses a challenge

to the cirrhotic heart. Despite exclusion of patients with cardiac dysfunction from receiving TIPS, cases of unex-

plained cardiac events such as severe heart failure or even cardiac deaths sometimes occur after TIPS insertion

[55,56]. This emphasizes that cardiac dysfunction needs to be carefully ruled out before TIPS insertion.

Wong and colleagues demonstrated that the insertion of TIPS increases cardiac preload; thus, the cardiac out-

put is increased by B50%

[57] and the right atrial and pulmonary artery pressures by B100% [58]. Therefore,

this stress is likely to bring forth any subt le cardiac abnormalities in these patients. Indeed, all the cardiac deaths

occurred in patients who had an E/A ratio # 1 during their pre-TIPS work-up, while all other standard cardiac

investigations were normal

[58].

To sort out the relationship of TIPS and cardiac complications, two studies

[12] prospectively evaluated car-

diac function and its effect on patients’ outcomes after TIPS insertion. Cazzaniga et al. prospectively examined

the prognostic utility of both liver and cardiac functions in cirrhotic patients who underwent TIPS

[9]. Their uni-

variate analysis indicated that liver function, represented by baseline MELD score, and diastolic function

223Morbidity/mortality after cardiovascular challenges

III. Cardiovascular system in liver failure

https://t.me/medicina_free

<<< < Предыдущая 12 13 14 15 16 17 18 19 20 21 22 2324 / 3824 25 26 27 28 29 30 31 32 33 34 35 36 > Следующая >>>

Соседние файлы в папке Библиотека им академика М.И. Перельмана

#
29.08.202694 Мб0Книга_504_Библиотеки_им_академика_М_И_Перельмана.pdf
#
29.08.202694 Мб0Книга_505_Библиотеки_им_академика_М_И_Перельмана.pdf
#
29.08.202693 Мб0Книга_506_Библиотеки_им_академика_М_И_Перельмана.pdf
#
29.08.202693 Мб0Книга_507_Библиотеки_им_академика_М_И_Перельмана.pdf
#
29.08.202692 Мб0Книга_508_Библиотеки_им_академика_М_И_Перельмана.pdf
#
10.10.20269 Мб0Книга_51_библиотеки_им_акад_М_И_Перельмана.pdf
#
29.08.202691 Мб0Книга_510_Библиотеки_им_академика_М_И_Перельмана.pdf
#
29.08.202691 Мб0Книга_511_Библиотеки_им_академика_М_И_Перельмана.pdf
#
29.08.202690 Мб0Книга_512_Библиотеки_им_академика_М_И_Перельмана.pdf
#
29.08.202690 Мб0Книга_513_Библиотеки_им_академика_М_И_Перельмана.pdf
#
29.08.202690 Мб0Книга_514_Библиотеки_им_академика_М_И_Перельмана.pdf