Circulatory changes in chronic liver disease

Murray, John F.; Dawson, A. M.; Sherlock, Sheila

doi:10.1016/0002-9343(58)90322-x

Cited by 457 publications

(174 citation statements)

References 21 publications

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“…Indeed, the mean cardiac index was nearly 5 l/ min per square meter, being significantly higher compared to controls. Besides chronic anemia, the frequently coexistent hepatic involvement [20] as well as the recently described pseudoxanthoma-elasticum-like diffuse elastic tissue [21][22][23][24][25], which probably renders vessels more susceptible to dilatation by pulse pressure increase in the context of a hyperkinetic state, may both play a role [7,[20][21][22][23][24][25]. However, it has been shown that LV function copes quite well with chronically increased cardiac output [26] whereas there was no correlation between hemoglobin or cardiac output levels with LV ejection fraction or tissue Doppler systolic indices.…”

Section: Discussionmentioning

confidence: 99%

Cardiac involvement in sickle β-thalassemia

et al. 2008

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Cardiovascular involvement is a leading cause of mortality and morbidity in patients with inherited hemoglobinopathies, but it has not been adequately assessed in sickle β-thalassemia. We evaluated 115 sickle β-thalassemia patients, aged 34±14 years, along with 50 healthy controls, by resting echocardiography. Patients with systolic left ventricular (LV) dysfunction or severe pulmonary hypertension (PHT) also underwent left and right cardiac catheterization and cardiac magnetic resonance imaging (CMR). Left and right chamber dimensions, LV mass, and cardiac index were significantly higher in patients compared to controls (p<0.001 in most cases). Three patients (2.9%) had reduced LV ejection fraction (<55%); mean LV ejection fraction was significantly lower in patients (p< 0.001). Left and right ventricular systolic tissue Doppler indices and LV diastolic tissue Doppler indices were also impaired in patients. All three patients with systolic LV dysfunction had normal coronary arteries and mild myocardial iron load (CMR T2* values, 18-25 ms). Systolic pulmonary artery pressure was significantly higher in patients compared to controls (p=0.002); PHT was present in 28 patients (27%), while severe PHT in three (2.9%). In three patients with severe PHT, only one had impaired LV ejection fraction and increased pulmonary wedge pressure. Overall, three patients (2.9%) had a history of heart failure, two with systolic LV dysfunction, and one with severe PHT. Cardiac involvement in sickle β-thalassemia concerns biventricular dilatation and dysfunction along with PHT, leading to congestive heart failure.

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Section: Discussionmentioning

confidence: 99%

Cardiac involvement in sickle β-thalassemia

et al. 2008

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“…Although this hypothesis provides a rational and simple explanation to the hemodynamic changes that take place in cirrhosis and HRS, it has not been tested in human studies. However, the markedly reduced systemic vascular resistance despite elevated norepinephrine, renin, and aldosterone levels is well documented and is compatible with peripheral vasodilation (10,11). Studies by Fernandez-Seara and others (12,13) demonstrate that the degree of hepatic decompensation directly correlates with the degree of hyperdynamic circulation and inversely correlates with the arterial BP, with the most extreme hemodynamic changes noted in patients with HRS.…”

Section: Peripheral Arterial Vasodilationmentioning

confidence: 97%

Hepatorenal Syndrome

Wadei

Martin

Ahsan

et al. 2006

Clinical Journal of the American Society of Nephrology

226

194

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“…These pathophysiological events manifest clinically as increased cardiac output, reduced mean arterial pressure, and reduced systemic vascular resistance, a syndrome termed the hyperdynamic circulation. 82 Numerous studies have implicated an increase in NO production as a major factor in the pathogenesis of the hyperdynamic circulation. However, the determination of the NOS isoform and the cell type responsible for the increase in NO has not reached a consensus.…”

Section: Pathogenesis Of Portal Hypertensionmentioning

confidence: 99%