Left Ventricular Diastolic Function in Liver Cirrhosis

Finucci, GF; Desideri, Alessandro; Sacerdoti, David; Bolognesi, Massimo; Merkel, Carlo; Angeli, Paolo; Gatta, Angelo

doi:10.3109/00365529609004879

Cited by 144 publications

(119 citation statements)

References 18 publications

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“…Actually, most previous studies have investigated patients with mixed etiologies of liver disease [13,14] introducing a bias in the interpretation of results according to the known potential interference of various exogenous factors and pathologic conditions on cardiovascular variables. Nevertheless diastolic dysfunction has been reported even in patients with idiopathic (non cirrhotic) portal hypertension [16], pointing to the role of hemodynamic derangement characterizing advanced cirrhosis [24,29] as the leading factor.…”

Section: Discussionmentioning

confidence: 99%

“…Hyperdinamic circulation [3], QTc prolongation [4,5], beta-receptors desensitization [6,7], reduced systolic competence under strains [8][9][10][11] and diastolic dysfunction [12][13][14][15][16][17] are the key features of cirrhotic cardiomyopathy. Diastolic dysfunction, characterized by an altered pattern of transmitral flow due to impaired diastolic relaxation of left ventricle, can be easily assessed by echocardiography and accordingly can be considered as a marker of this condition.…”

Section: Introductionmentioning

confidence: 99%

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Heart Function and Myocardial Tissue Characterization in Patients with HCV Related Cirrhosis: Diastolic Dysfunction and Cardiac Hypertrophy

Pozzi¹,

Pizzala²,

Ratti³

et al. 2007

TOGASJ

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Evidence of diastolic dysfunction in cirrhosis contributed to the definition of cirrhotic cardiomyopathy. In 109 patients with chronic HCV infection with or without cirrhosis E/A ratio, a Doppler marker of diastolic dysfunction, was decreased in cirrhotics (0.89 ± 0.03 vs controls 1.21 ± 0.07, p < 0.01) and to a lesser extent in patients with advanced liver fibrosis (1.17 ± 0.07, p < 0.01). Left ventricular parietal wall thickness was increased. The nature of this abnormality in human cirrhosis has not been clarified, animal studies reporting cardiac hypertrophy. To this aim we employed the echocardiographic integrated backscatter (IBS) technique to obtain an indirect estimate of tissue density (decreased when a higher percentage of muscle fibres is present and increased when fibrosis prevails) to provide myocardial tissue characterization in a subset of patients with compensated HCV cirrhosis. The average IBS signal was reduced in cirrhotics at the level of the posterior wall (21.72 ± 1.46 dB versus 30.85 ± 1.40 dB in controls, p < 0.01). Our results confirm diastolic dysfunction in postviral cirrhosis pointing to cardiac hypertrophy as the anatomopathological background in the compensated stage of disease.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Heart Function and Myocardial Tissue Characterization in Patients with HCV Related Cirrhosis: Diastolic Dysfunction and Cardiac Hypertrophy

Pozzi¹,

Pizzala²,

Ratti³

et al. 2007

TOGASJ

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“…Removal of the ascitic fluid by rapid total paracentesis reduces the A wave velocity and increases the E/A ratio to values similar to those of cirrhotic patients without ascites but still abnormal as compared with healthy controls. Finucci et al [11] reported increased stroke volume, left ventricular end-diastolic volume, left atrial volume, peak A velocity, deceleration time of E wave, and decreased E/A ratio (1.02 vs. 1.22) in 42 Child-Pugh class B and C cirrhotic patients, half of whom with alcoholic etiology. The prolonged deceleration time was unaffected by the presence of ascites.…”

Section: Diastolic Dysfunctionmentioning

confidence: 99%

“…Over the last 2 decades, there is accumulating evidence to suggest that the presence of cirrhosis per se is associated with significant cardiovascular abnormalities, irrespective of the cause of cirrhosis. These include resting increased cardiac output; decreased systemic vascular resistance [1]; reduced myocardial contractility or systolic incompetence, especially under conditions of stress, whether physiological [5], physical [6,7], or pharmacological [8]; increased thickness of the left ventricle [9][10][11], associated with diastolic dysfunction; and electrophysiological abnormalities [12][13][14]. This constellation of abnormalities has been termed cirrhotic cardiomyopathy [15].…”

Section: Introductionmentioning

confidence: 99%

Cirrhotic cardiomyopathy

2008

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Cirrhotic cardiomyopathy is a recently recognized condition in cirrhosis consisting of systolic incompetence under condition of stress, diastolic dysfunction related to altered diastolic relaxation, and electrophysiological abnormalities in the absence of any known cardiac disease. It can be diagnosed by using a combination of electrocardiograph, 2-dimensional echocardiography, and various serum markers such as brain natriuretic factor. The underlying pathogenetic mechanisms include abnormalities in the b-adrenergic signaling pathway, altered cardiomyocyte membrane fluidity, increased myocardial fibrosis, cardiomyocyte hypertrophy, and ion channel defects. Various compounds for which levels are elevated in cirrhosis such as nitric oxide and carbon monoxide can also exert a negative inotropic effect on the myocardium, whereas excess sodium and volume retention can lead to myocardial hypertrophy. Various toxins can also aggravate the ion channel defects, thereby widening the QRS complex causing prolonged QT intervals. Clinically, systolic incompetence is most evident when cirrhotic patients are placed under stress, whether physical or pharmacological, or when the extent of peripheral arterial vasodilatation demands an increased cardiac output as in the case of bacterial infections. Acute volume overload such as immediately after insertion of a transjugular intrahepatic portosystemic shunt or after liver transplantation can also tip these cirrhotic patients into cardiac failure. Treatment of cirrhotic cardiomyopathy is unsatisfactory. There is some evidence that b-blockade may help some cirrhotic patients with baseline prolonged QT interval. Long-term aldosterone antagonism may help reduce myocardial hypertrophy. Future studies should include further elucidation of pathogenetic mechanisms so as to develop effective treatment strategies.

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“…When both organs are performing well, they are seemingly oblivious of one another, but when one fails or is dysfunctional, the other is likely to suffer. Cirrhosis and portal hypertension dilate the vasculature, 10 cause the heart to beat harder and faster, 11 raise the pressure in the pulmonary vascular tree, 12 interfere with both systolic 13,14 and diastolic function, 15 and even meddle with ventricular depolarization by decreasing conductance of potassium channels to prolong the Q-T interval. 16 By way of reciprocation, when there is cardiac misbehavior the liver feels the brunt, irrespective of whether it is the left heart or the right heart that is at fault, or both.…”

mentioning

confidence: 99%