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  1. Article: History of the liver-heart relationship.

    Lee, Samuel S / Zhang, Jing / Chen, Annie Yan / Liu, Hongqun

    Clinical liver disease

    2024  Volume 23, Issue 1, Page(s) e0151

    Language English
    Publishing date 2024-04-26
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2657644-2
    ISSN 2046-2484
    ISSN 2046-2484
    DOI 10.1097/CLD.0000000000000151
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Dysregulated Calcium Handling in Cirrhotic Cardiomyopathy.

    Hwang, Sang Youn / Liu, Hongqun / Lee, Samuel S

    Biomedicines

    2023  Volume 11, Issue 7

    Abstract: Cirrhotic cardiomyopathy is a syndrome of blunted cardiac systolic and diastolic function in patients with cirrhosis. However, the mechanisms remain incompletely known. Since contractility and relaxation depend on cardiomyocyte calcium transients, any ... ...

    Abstract Cirrhotic cardiomyopathy is a syndrome of blunted cardiac systolic and diastolic function in patients with cirrhosis. However, the mechanisms remain incompletely known. Since contractility and relaxation depend on cardiomyocyte calcium transients, any factors that impact cardiac contractile and relaxation functions act eventually through calcium transients. In addition, calcium transients play an important role in cardiac arrhythmias. The present review summarizes the calcium handling system and its role in cardiac function in cirrhotic cardiomyopathy and its mechanisms. The calcium handling system includes calcium channels on the sarcolemmal plasma membrane of cardiomyocytes, the intracellular calcium-regulatory apparatus, and pertinent proteins in the cytosol. L-type calcium channels, the main calcium channel in the plasma membrane of cardiomyocytes, are decreased in the cirrhotic heart, and the calcium current is decreased during the action potential both at baseline and under stimulation of beta-adrenergic receptors, which reduces the signal to calcium-induced calcium release. The study of sarcomere length fluctuations and calcium transients demonstrated that calcium leakage exists in cirrhotic cardiomyocytes, which decreases the amount of calcium storage in the sarcoplasmic reticulum (SR). The decreased storage of calcium in the SR underlies the reduced calcium released from the SR, which results in decreased cardiac contractility. Based on studies of heart failure with non-cirrhotic cardiomyopathy, it is believed that the calcium leakage is due to the destabilization of interdomain interactions (dispersion) of ryanodine receptors (RyRs). A similar dispersion of RyRs may also play an important role in reduced contractility. Multiple defects in calcium handling thus contribute to the pathogenesis of cirrhotic cardiomyopathy.
    Language English
    Publishing date 2023-07-04
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2720867-9
    ISSN 2227-9059
    ISSN 2227-9059
    DOI 10.3390/biomedicines11071895
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Role of Galectin in Cardiovascular Conditions including Cirrhotic Cardiomyopathy.

    Liu, Hongqun / Hwang, Sang-Youn / Lee, Samuel S

    Pharmaceuticals (Basel, Switzerland)

    2023  Volume 16, Issue 7

    Abstract: Abnormal cardiac function in the setting of cirrhosis and in the absence of a primary cardiac disease is known as cirrhotic cardiomyopathy. The pathogenesis of cirrhotic cardiomyopathy is multifactorial but broadly is comprised of two pathways. The first ...

    Abstract Abnormal cardiac function in the setting of cirrhosis and in the absence of a primary cardiac disease is known as cirrhotic cardiomyopathy. The pathogenesis of cirrhotic cardiomyopathy is multifactorial but broadly is comprised of two pathways. The first is due to cirrhosis and synthetic liver failure with abnormal structure and function of many substances, including proteins, lipids, hormones, and carbohydrates such as lectins. The second is due to portal hypertension which invariably accompanies cirrhosis. Portal hypertension leads to a leaky, congested gut with resultant endotoxemia and systemic inflammation. This inflammatory phenotype comprises oxidative stress, cellular apoptosis, and inflammatory cell infiltration. Galectins exert all these pro-inflammatory mechanisms across many different tissues and organs, including the heart. Effective therapies for improving cardiac function in patients with cirrhosis are not available. Conventional strategies for other noncirrhotic heart diseases, including vasodilators, are not feasible because of the significant baseline vasodilation in cirrhotic patients. Therefore, exploring new treatment modalities for cirrhotic cardiomyopathy is of great importance. Galectin-3 inhibitors such as modified citrus pectin, N-acetyllactosamine, TD139 and GB0139 exert anti-apoptotic, anti-oxidative and anti-inflammatory effects and thus have potential therapeutic interest. This review briefly summarizes the physiological and pathophysiological role of galectin and specifically examines its role in cardiac disease processes. We present a more detailed discussion of galectin in cardiovascular complications of cirrhosis, particularly cirrhotic cardiomyopathy. Finally, therapeutic studies of galectin-3 inhibitors in cirrhotic cardiomyopathy are reviewed.
    Language English
    Publishing date 2023-07-07
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2193542-7
    ISSN 1424-8247
    ISSN 1424-8247
    DOI 10.3390/ph16070978
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Diagnostic Criteria of Cirrhotic Cardiomyopathy: Out With the Old, in With the New?

    Liu, Hongqun / Lee, Samuel S

    Hepatology (Baltimore, Md.)

    2021  Volume 74, Issue 6, Page(s) 3523–3525

    MeSH term(s) Cardiomyopathies ; Humans ; Liver Cirrhosis
    Language English
    Publishing date 2021-08-22
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 604603-4
    ISSN 1527-3350 ; 0270-9139
    ISSN (online) 1527-3350
    ISSN 0270-9139
    DOI 10.1002/hep.32021
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Phytochemistry and Pharmacology of Sesquiterpenoids from

    Qu, Zhengyi / Liu, Hongqun / Zhang, Zhenghai / Zheng, Peihe / Zhao, Shuting / Hou, Wei

    Molecules (Basel, Switzerland)

    2024  Volume 29, Issue 6

    Abstract: The rhizomes of the ... ...

    Abstract The rhizomes of the genus
    MeSH term(s) Atractylodes/chemistry ; Rhizome/chemistry ; Sesquiterpenes/chemistry ; Sesquiterpenes, Eudesmane/chemistry ; Phytochemicals/pharmacology ; Phytochemicals/analysis ; Ethnopharmacology ; Plant Extracts/pharmacology ; Plant Extracts/analysis ; Phytotherapy
    Chemical Substances Sesquiterpenes ; Sesquiterpenes, Eudesmane ; Phytochemicals ; Plant Extracts
    Language English
    Publishing date 2024-03-20
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 1413402-0
    ISSN 1420-3049 ; 1431-5165 ; 1420-3049
    ISSN (online) 1420-3049
    ISSN 1431-5165 ; 1420-3049
    DOI 10.3390/molecules29061379
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Oxidative Mechanisms and Cardiovascular Abnormalities of Cirrhosis and Portal Hypertension.

    Liu, Hongqun / Nguyen, Henry H / Hwang, Sang Youn / Lee, Samuel S

    International journal of molecular sciences

    2023  Volume 24, Issue 23

    Abstract: In patients with portal hypertension, there are many complications including cardiovascular abnormalities, hepatorenal syndrome, ascites, variceal bleeding, and hepatic encephalopathy. The underlying mechanisms are not yet completely clarified. It is ... ...

    Abstract In patients with portal hypertension, there are many complications including cardiovascular abnormalities, hepatorenal syndrome, ascites, variceal bleeding, and hepatic encephalopathy. The underlying mechanisms are not yet completely clarified. It is well known that portal hypertension causes mesenteric congestion which produces reactive oxygen species (ROS). ROS has been associated with intestinal mucosal injury, increased intestinal permeability, enhanced gut bacterial overgrowth, and translocation; all these changes result in increased endotoxin and inflammation. Portal hypertension also results in the development of collateral circulation and reduces liver mass resulting in an overall increase in endotoxin/bacteria bypassing detoxication and immune clearance in the liver. Endotoxemia can in turn aggravate oxidative stress and inflammation, leading to a cycle of gut barrier dysfunction → endotoxemia → organ injury. The phenotype of cardiovascular abnormalities includes hyperdynamic circulation and cirrhotic cardiomyopathy. Oxidative stress is often accompanied by inflammation; thus, blocking oxidative stress can minimize the systemic inflammatory response and alleviate the severity of cardiovascular diseases. The present review aims to elucidate the role of oxidative stress in cirrhosis-associated cardiovascular abnormalities and discusses possible therapeutic effects of antioxidants on cardiovascular complications of cirrhosis including hyperdynamic circulation, cirrhotic cardiomyopathy, and hepatorenal syndrome.
    MeSH term(s) Humans ; Esophageal and Gastric Varices/complications ; Hepatorenal Syndrome/complications ; Reactive Oxygen Species/pharmacology ; Endotoxemia/complications ; Gastrointestinal Hemorrhage ; Liver Cirrhosis/therapy ; Hypertension, Portal/complications ; Oxidative Stress ; Inflammation/complications ; Cardiomyopathies/complications ; Cardiovascular Abnormalities/complications ; Endotoxins/pharmacology
    Chemical Substances Reactive Oxygen Species ; Endotoxins
    Language English
    Publishing date 2023-11-27
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms242316805
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Cardiomyopathy in cirrhosis: From pathophysiology to clinical care.

    Liu, Hongqun / Naser, Jwan A / Lin, Grace / Lee, Samuel S

    JHEP reports : innovation in hepatology

    2023  Volume 6, Issue 1, Page(s) 100911

    Abstract: Cirrhotic cardiomyopathy (CCM) is defined as systolic or diastolic dysfunction in the absence of prior heart disease or another identifiable cause in patients with cirrhosis, in whom it is an important determinant of outcome. Its underlying pathogenic/ ... ...

    Abstract Cirrhotic cardiomyopathy (CCM) is defined as systolic or diastolic dysfunction in the absence of prior heart disease or another identifiable cause in patients with cirrhosis, in whom it is an important determinant of outcome. Its underlying pathogenic/pathophysiological mechanisms are rooted in two distinct pathways: 1) factors associated with portal hypertension, hyperdynamic circulation, gut bacterial/endotoxin translocation and the resultant inflammatory phenotype; 2) hepatocellular insufficiency with altered synthesis or metabolism of substances such as proteins, lipids, carbohydrates, bile acids and hormones. Different criteria have been proposed to diagnose CCM; the first in 2005 by the World Congress of Gastroenterology, and more recently in 2019 by the Cirrhotic Cardiomyopathy Consortium. These criteria mainly utilised echocardiographic evaluation, with the latter refining the evaluation of diastolic function and integrating global longitudinal strain into the evaluation of systolic function, an important addition since the haemodynamic changes that occur in advanced cirrhosis may lead to overestimation of systolic function by left ventricular ejection fraction. Advances in cardiac imaging, such as cardiac magnetic resonance imaging and the incorporation of an exercise challenge, may help further refine the diagnosis of CCM. Over recent years, CCM has been shown to contribute to increased mortality and morbidity after major interventions, such as liver transplantation and transjugular intrahepatic portosystemic shunt insertion, and to play a pathophysiologic role in the genesis of hepatorenal syndrome. In this review, we discuss the pathogenesis/pathophysiology of CCM, its clinical implications, and the role of cardiac imaging modalities including MRI. We also compare diagnostic criteria and review the potential diagnostic role of electrocardiographic QT prolongation. At present, no definitive medical therapy exists, but some promising potential treatment strategies for CCM are reviewed.
    Language English
    Publishing date 2023-09-23
    Publishing country Netherlands
    Document type Journal Article ; Review
    ISSN 2589-5559
    ISSN (online) 2589-5559
    DOI 10.1016/j.jhepr.2023.100911
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article: A narrative review of postoperative bleeding in patients with gastric cancer treated with endoscopic submucosal dissection.

    Liu, Li / Liu, Hongqun / Feng, Zhijie

    Journal of gastrointestinal oncology

    2022  Volume 13, Issue 1, Page(s) 413–425

    Abstract: Endoscopic submucosal dissection (ESD) is now considered a standard treatment for selected patients with early gastric cancer. Compared with endoscopic mucosal resection (EMR), ESD provides a higher complete resection rate (R0), and therefore, a lower ... ...

    Abstract Endoscopic submucosal dissection (ESD) is now considered a standard treatment for selected patients with early gastric cancer. Compared with endoscopic mucosal resection (EMR), ESD provides a higher complete resection rate (R0), and therefore, a lower local recurrence rate. However, ESD is a more time-consuming procedure, creating a wider and deeper ulcer floor which may cause complications. Post-ESD bleeding is one of them. Although most post-ESD bleedings can be controlled by endoscopic hemostasis at the time of operation, some bleeding after ESD may result in serious conditions such as hemorrhagic shock. Even with preventive methods such as ulcer closure, the application of fibrin glue and polyglycolic acid shielding, acid secretion inhibitors and hemostasis on second-look endoscopy, our experiences told us that post-ESD bleeding cannot be entirely avoidable, especially for patients with big size ulcer bed, anticoagulants/antithrombosis and chronic kidney diseases. The present review first defined post-ESD bleeding, then the incidence, the risk factors, such as the location of operative lesion, the size and depth, chronic kidney diseases, the impacts of anticoagulant and antithrombotic agents. We finally reviewed the managements of post-ESD bleeding, including approaches of coagulating potential bleeding spots during the procedure, lesion closure, lesion shielding and the application of gastric acid secretion inhibitors.
    Language English
    Publishing date 2022-02-28
    Publishing country China
    Document type Journal Article ; Review
    ZDB-ID 2594644-4
    ISSN 2219-679X ; 2078-6891
    ISSN (online) 2219-679X
    ISSN 2078-6891
    DOI 10.21037/jgo-21-466
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  9. Article: Cardiovascular events after liver transplantation: MACE hurts.

    Altieri, Mario H / Liu, Hongqun / Lee, Samuel S

    Reviews in cardiovascular medicine

    2022  Volume 23, Issue 3, Page(s) 91

    Abstract: The curative therapy for patients with end-stage liver disease is liver transplantation. However, liver transplantation challenges the cardiovascular system, and is associated with major adverse cardiovascular events (MACE). Immediately after ... ...

    Abstract The curative therapy for patients with end-stage liver disease is liver transplantation. However, liver transplantation challenges the cardiovascular system, and is associated with major adverse cardiovascular events (MACE). Immediately after implantation of the liver graft, changes in cardiac preload and afterload increase the cardiac workload. Longer-term postoperatively, a more sedentary lifestyle and enhanced appetite increase obesity and body mass index. Immunosuppressants may also affect the cardiovascular system. All these factors that liver recipients encounter impact the function of the cardiovascular system. Cardiac events are the third-leading cause of death in liver recipients. This review describes the pertinent factors that predispose to development of MACE after liver transplantation, and how to predict these cardiovascular events in the post-transplant period. We review the roles of metabolic syndrome, renal dysfunction, non-alcoholic fatty liver disease, diagnostic tests such as imaging and biomarkers, and parameters such as systolic and diastolic dysfunction, and QT interval prolongation in cardiovascular events. We summarize the current literature on scoring systems to predict cardiovascular events.
    MeSH term(s) Cardiomyopathies/diagnosis ; Cardiovascular Diseases/diagnosis ; Cardiovascular Diseases/epidemiology ; Cardiovascular Diseases/etiology ; End Stage Liver Disease/complications ; End Stage Liver Disease/surgery ; Heart ; Heart Failure/etiology ; Humans ; Liver Transplantation/adverse effects ; Risk Factors
    Language English
    Publishing date 2022-03-22
    Publishing country Singapore
    Document type Journal Article ; Review
    ZDB-ID 2108910-3
    ISSN 1530-6550
    ISSN 1530-6550
    DOI 10.31083/j.rcm2303091
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Oxidative stress triggers hyperdynamic circulation via central neural activation in portal hypertensive rats.

    Liu, Hongqun / Alhassan, Noura / Yoon, Ki Tae / Almutlaq, Lamees / Lee, Samuel S

    Hepatology international

    2023  Volume 17, Issue 3, Page(s) 689–697

    Abstract: Background: Hyperdynamic circulation in portal hypertension (PHT) depends on central neural activation. However, the initiating mechanism that signals PHT to the central neural cardiovascular-regulatory centers remains unclear. We aimed to test the ... ...

    Abstract Background: Hyperdynamic circulation in portal hypertension (PHT) depends on central neural activation. However, the initiating mechanism that signals PHT to the central neural cardiovascular-regulatory centers remains unclear. We aimed to test the hypothesis that oxidative stress in the gut initiates the signal that activates central cardiovascular nuclei in portal hypertensive rats.
    Methods: Two groups of rats were used. One had portal hypertension produced by partial portal vein ligation, while controls underwent sham operation. Hemodynamics including portal pressure, cardiac output, mean arterial pressure (MAP) and peripheral vascular resistance were measured. Activation of central cardiovascular nuclei was determined by immunohistochemical Fos expression in the paraventricular nucleus (PVN) of the hypothalamus. Myeloperoxidase activity, an oxidative stress marker, was measured in the jejunum. Hydrogen peroxide, the antioxidant N-acetyl-cysteine (NAC) or saline controls were administered for 12-14 days by gavage or osmotic minipumps placed in the peritoneal cavity.
    Results: Compared with controls, PHT rats showed increased cardiac output (54.2 ± 9.5 vs 33.6 ± 2.4 ml/min/100 g BW, p < 0.01), decreased MAP (96.2 ± 6.4 mmHg vs 103.2 ± 7.8, p < 0.01) and systemic vascular resistance (1.84 ± 0.28 vs 3.14 ± 0.19 mmHg/min/ml/100 g BW, p < 0.01). PHT rats had increased jejunal myeloperoxidase and PVN Fos expression. NAC treatment eliminated the hyperdynamic circulation, decreased jejunal myeloperoxidase and PVN Fos expression in PHT rats, but had no effect on sham controls. H
    Conclusion: These results indicate that in PHT, mesenteric oxidative stress is the initial signal that activates chemoreceptors and triggers hyperdynamic circulation by central neural cardiovascular-regulatory centers.
    MeSH term(s) Rats ; Animals ; Peroxidase/metabolism ; Peroxidase/pharmacology ; Rats, Sprague-Dawley ; Hydrogen Peroxide/pharmacology ; Hypertension, Portal ; Hemodynamics ; Portal Vein ; Oxidative Stress
    Chemical Substances Peroxidase (EC 1.11.1.7) ; Hydrogen Peroxide (BBX060AN9V)
    Language English
    Publishing date 2023-02-01
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2270316-0
    ISSN 1936-0541 ; 1936-0533
    ISSN (online) 1936-0541
    ISSN 1936-0533
    DOI 10.1007/s12072-023-10481-5
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