PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 8833359

Left ventricular diastolic function in liver cirrhosis.

G Finucci·A Desideri·D Sacerdoti·M Bolognesi·C Merkel·P Angeli·A Gatta
View original source ↗Export metadata ↓

Abstract

BACKGROUND: Left ventricular systolic abnormalities have been reported in liver cirrhosis (LC). Diastolic function in cirrhotics, on the contrary, does not seem to have been studied so far. METHODS: Diastolic function was evaluated in 42 cirrhotic patients and in 16 controls by means of Doppler echocardiography. RESULTS: Compared with the controls, cirrhotics had increased left ventricular end-diastolic and left atrial volume, stroke volume, late diastolic flow velocity (peak A) (71 + or - 17 cm/sec versus 56 +/- 18; p <0.01), time from onset of mitral inflow to the early peak (time E) (86 + or - 11 msec versus 72 +/- 14; p < 0.003), and deceleration time (DT) (194 +/- 40 msec versus 159 +/- 27; p < 0.001) and decreased ratio of peak E to peak A filling velocities (1.02 +/ - 0.35 versus 1.22 +/- 0.25; p < 0.02). Patients with tense ascites had a higher E/A ratio (p < 0.03) and a shorter DT (p < 0.03) than patients with mild or no ascites. CONCLUSIONS: The impaired left ventricular relaxation in the presence of high stroke volume suggests a myocardial involvement in LC. The pseudo normalization of the E/A ratio and DT in patients with tense ascites could reflect loading conditions masking the relaxation abnormality.

Explore related subjects

AscitesBlood PressureCardiac OutputDiastoleEchocardiography, DopplerFemaleHeart RateHumansLiver CirrhosisMaleMiddle AgedStroke VolumeVentricular Dysfunction, LeftVentricular Function, LeftJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

G Finucci, A Desideri, D Sacerdoti, M Bolognesi, C Merkel, P Angeli, A Gatta. 1996. Left ventricular diastolic function in liver cirrhosis.. https://doi.org/10.3109/00365529609004879

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2007

Torsion of a giant omental cyst mimicking ascites.

We report a case of omental cyst in an 11-month-old infant. The cyst occupied nearly the whole abdomen and mimicked massive ascites on sonography. The correct preoperative diagnosis was achieved through the use of CT, and partial torsion of a huge omental cyst was found at surgery. The diagnostic role of sonography and CT in ascites of unknown etiology is emphasized.

Ascites↗
PubMed2007

Non-invasive diagnosis of cirrhosis and the natural history of its complications.

Several methods have been studied in the attempt to reach a diagnosis of cirrhosis by non-invasive means. Although abdominal ultrasound can detect the hepatic and extra-hepatic changes consistent with cirrhosis, its ability to distinguish chronic hepatitis from compensated cirrhosis is limited. Serum markers can rule in or rule out fibrosis in up to 35% of patients but, in individual patients, cannot differentiate the stages of fibrosis reliably. Transient elastography (Fibroscan) might be of value for the non-invasive diagnosis of cirrhosis; however, its reproducibility needs to be further validated. Cirrhosis can be divided into 4 stages: stage 1, no varices, no ascites; stage 2, varices without ascites and without bleeding; stage 3, ascites+/-varices; stage 4, bleeding+/-ascites. Yearly mortality ranges from 1% in stage 1 to 57% in stage 4. The yearly incidence of oesophageal varices is 5-7%; their rate of enlargement is 10-12% per year. The incidence of variceal bleeding is about 25% at 2 years. Bleeding stops spontaneously in about 50% of cases but early rebleeding occurs in 30-40% of patients. Bleeding-related mortality has declined over time and is now around 20% at 6 weeks.

Ascites↗
PubMed2007

Management of ascites and hepatic hydrothorax.

The natural course of patients with cirrhosis is frequently complicated by the accumulation of fluid in the peritoneal or pleural cavities and interstitial tissue. Functional renal abnormalities that occur as a consequence of decreased effective arterial blood volume are responsible for fluid accumulation in the form of ascites and hepatic hydrothorax. Ascites is the most common complication of cirrhosis and poses an increased risk for infections, renal failure and mortality. Patients have a poor prognosis and it is estimated that nearly half will die in approximately 2 years without liver transplantation. Hepatic hydrothorax is defined as a pleural effusion greater than 500 mL (mostly right-sided) in patients with cirrhosis without cardiopulmonary disease; the estimated prevalence is approximately 5-10%. Liver transplantation is the most definitive cure for both conditions in those patients that are suitable candidates. However, the mainstay of therapy for minimizing fluid accumulation in both conditions includes sodium restriction and administration of diuretics. This article reviews the most current concepts of pathogenesis, clinical findings, diagnosis, and treatment of these complications of cirrhosis.

Ascites↗