Esophageal Varices in the Absence of Cirrhosis: Incidence and Characteristics in Congestive Heart Failure and Neoplasm of the Liver

Luna, A. Munoz; Meister, H; Szanto, Paul B.

doi:10.1093/ajcp/49.5.710

Cited by 18 publications

(8 citation statements)

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“…Although false-negative transjugular liver biopsies must be considered, it appears that with newer methods of treatment of heart failure, cardiac hepatopathy rarely progresses to this severe stage, and/or patients die of their cardiac condition before the development of cirrhosis. 11,13 As noted previously, 30 esophagogastric varices are uncommon in this condition. Because varices represent collateral vessels from the high-pressure portal circulation to the low-pressure systemic venous bed, they are unlikely to form in cardiac hepatopathy in which pressures generally remain high along the entire path of venous return to the right atrium.…”

Section: Discussionmentioning

confidence: 68%

Cardiac hepatopathy: Clinical, hemodynamic, and histologic characteristics and correlations

Myers¹

2003

Hepatology

208

190

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Cardiac hepatopathy, hepatic injury caused by cardiac dysfunction, is a common entity but has been characterized incompletely, particularly the relationship between hemodynamics and histology. We aimed to describe the clinical, biochemical, hemodynamic, and histologic characteristics of this disorder. Eighty-three patients from 2 tertiary referral centers were studied. Patients were divided into 3 groups based on the duration of cardiac dysfunction: (1) acute (n ‫؍‬ 12); (2) chronic (n ‫؍‬ 53); and (3) acute on chronic (n ‫؍‬ 18). Results showed that serum aminotransferase levels were increased typically, particularly in the acute group (median aspartate aminotransferase level was 30. . The hepatic venous pressure gradient was normal in most (81%), correlated moderately with the aminotransferase levels (aspartate aminotransferase level: r ‫؍‬ .59; P < .0001), and associated with the presence of centrilobular necrosis and inflammation, periportal necrosis, and stainable hepatic iron (P < .05 for all comparisons), but not fibrosis. Sinusoidal dilatation was associated with higher right atrial (P ‫؍‬ .047) and free hepatic venous pressures (P ‫؍‬ .06). Although cirrhosis was rare (n ‫؍‬ 1), centrilobular fibrosis was common (74%) and not associated with any hemodynamic measurement. In conclusion, cardiac hepatopathy has diverse clinical, hemodynamic, and histologic manifestations that vary with the temporal course of cardiac dysfunction. Hepatic fibrosis is common, but does not correlate with systemic or hepatic hemodynamics. (HEPATOLOGY 2003;37:393-400.)

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Section: Discussionmentioning

confidence: 68%

Cardiac hepatopathy: Clinical, hemodynamic, and histologic characteristics and correlations

Myers¹

2003

Hepatology

208

190

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“…Hepatic decompensation was defined based on previously validated ICD-9 diagnoses of ascites, portal hypertension, spontaneous bacterial peritonitis, and/or esophageal variceal hemorrhage, (31) which are relevant features in congestive hepatopathy. (32,33) Regression models were run using multiple imputation techniques that generated five datasets with complete covariate values. (34) Relative risk estimates using imputed data were consistent with those from the missing category analyses.…”

Section: Discussionmentioning

confidence: 99%

“…This was done to further minimize reverse causality by congestive hepatopathy. Hepatic decompensation was defined based on previously validated ICD‐9 diagnoses of ascites, portal hypertension, spontaneous bacterial peritonitis, and/or esophageal variceal hemorrhage, which are relevant features in congestive hepatopathy …”

Section: Methodsmentioning

confidence: 99%

FIB‐4 stage of liver fibrosis predicts incident heart failure among HIV‐infected and uninfected patients

So‐Armah

Lim

et al. 2017

Hepatology

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Liver fibrosis is common, particularly in human immunodeficiency virus infected (HIV+) people. HIV+ people have excess congestive heart failure (CHF) risk compared to uninfected people. It remains unknown if stage of liver fibrosis influences the CHF risk or if HIV or hepatitis C virus (HCV) infection modifies this association. Our objectives were to assess whether: 1) stage of liver fibrosis is independently associated with incident CHF; 2) the association between stage of liver fibrosis and incident CHF is modified by HIV/HCV status. Participants alive on or after 4/1/2003 in the Veterans Aging Cohort Study were included. Those without prevalent cardiovascular disease (CVD) were followed until their first CHF event, death, last follow-up date or 12/31/2011. Liver fibrosis was measured by FIB-4, calculated using age, aminotransferases and platelets. Outcome: incident CHF (ICD-9 codes). Cox proportional hazards regression models were adjusted for CVD risk factors. Among 96,373 participants over 6.9 years, 3,844 incident CHF events occurred. FIB-4 between 1.45–3.25 (moderate fibrosis) and FIB-4>3.25 (advanced fibrosis/cirrhosis) were associated with CHF (HR (95% CI)=1.17 (1.07–1.27); 1.65(1.43–1.92)). The association of advanced fibrosis/cirrhosis and incident CHF persisted regardless of HIV/HCV status. Conclusions Moderate and advanced liver fibrosis/cirrhosis are associated with an increased risk of CHF. The association for advanced fibrosis/cirrhosis persists even among participants without hepatitis C and/or HIV infection. Assessing liver health may be important for reducing the risk of future CHF events, particularly among HIV and hepatitis C infected people among whom CVD risk is elevated and liver disease is common.

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“…Samples were sliced to obtain cross‐ and longitudinal sections with a cryostat at a thickness of approximately 12 µm, adhered to Superfrost Plus microscopy slides, and used for staining. Sections were stained for general morphology observations with hematoxylin and H&E as previously described (Luna, ). For immunohistochemical analysis, frozen sections were fixed with ice‐cold methanol for 10 min and rinsed with Phosphate Buffered Saline (PBS).…”

Section: Methodsmentioning

confidence: 99%

“…and used for staining. Sections were stained for general morphology observations with hematoxylin and H&E as previously described (Luna, 1968). For immunohistochemical analysis, frozen sections were fixed with ice-cold methanol for 10 min and rinsed with Phosphate Buffered Saline (PBS).…”

Section: D Muscle Construct Contractility Testingmentioning

confidence: 99%

TGF-β1 enhances contractility in engineered skeletal muscle

Weist

Wellington

Bermudez

et al. 2012

J Tissue Eng Regen Med

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Scaffoldless engineered 3D skeletal muscle tissue created from satellite cells offers the potential to replace muscle tissue that is lost due to severe trauma or disease. Transforming growth factor-beta 1 (TGF-β1) plays a vital role in mediating migration and differentiation of satellite cells during the early stages of muscle development. Additionally, TGF-β1 promotes collagen type I synthesis in the extracellular matrix (ECM) of skeletal muscle, which provides a passive elastic substrate to support myofibres and facilitate the transmission of force. To determine the role of TGF-β1 in skeletal muscle construct formation and contractile function in vitro, we created tissue-engineered 3D skeletal muscle constructs with varying levels of recombinant TGF-β1 added to the cell culture medium. Prior to the addition of TGF-β1, the primary cell population was composed of 75% Pax7-positive cells. The peak force for twitch, tetanus and spontaneous force were significantly increased in the presence of 2.0 ng/ml TGF-β1 when compared to 0, 0.5 and 1.0 ng/ml TGF-β1. Visualization of the cellular structure with H&E and with immunofluorescence staining for sarcomeric myosin heavy chains and collagen type I showed denser regions of better organized myofibres in the presence of 2.0 ng/ml TGF-β1 versus 0, 0.5 and 1.0 ng/ml. The addition of 2.0 ng/ml TGF-β1 to the culture medium of engineered 3D skeletal muscle constructs enhanced contractility and extracellular matrix organization.

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Esophageal Varices in the Absence of Cirrhosis: Incidence and Characteristics in Congestive Heart Failure and Neoplasm of the Liver

Cited by 18 publications

References 0 publications

Cardiac hepatopathy: Clinical, hemodynamic, and histologic characteristics and correlations

Cardiac hepatopathy: Clinical, hemodynamic, and histologic characteristics and correlations

FIB‐4 stage of liver fibrosis predicts incident heart failure among HIV‐infected and uninfected patients

TGF-β1 enhances contractility in engineered skeletal muscle

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