Reduced cardiovascular responsiveness to exercise-induced sympathoadrenergic stimulation in patients with cirrhosis

Bernardi, Mauro; Rubboli, Andrea; Trevisani, Franco; Cancellieri, C.; Ligabue, A.; Baraldini, M.; Gasbarrini, Giovanni

doi:10.1016/0168-8278(91)90940-d

Cited by 127 publications

(89 citation statements)

References 32 publications

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“…Defect in electromechanical coupling leads to the asynchrony between electrical and mechanical systoles. The previously mentioned study by Bernardi et al [7] evaluating cardiac function in cirrhosis under rest and after isometric exercise showed that there was prolongation of the pre-ejection period at rest, together with defective shortening after exercise, suggesting that it was a defect in electromechanical coupling that was responsible for the contractile dysfunction in these patients. Henriksen and colleagues [25] reported that the difference between the electrical and mechanical systolic times was substantially longer in cirrhotic patients with prolonged QT intervals than those with normal QT intervals.…”

Section: Electrophysiological Abnormalitiesmentioning

confidence: 88%

“…Decrease in cardiac contractile function is consistently associated with sympathetic activation, both in early and advanced cirrhosis [7]. Increased baroreceptor-and volume-receptor-mediated sympathetic firing with subsequent neuronal release of norepinephrine is a physiological response to increase cardiac contractility, thereby returning cardiac performance to an adequate level but at the cost of substantial encroachment on the FrankStarling reserve [81].…”

Section: Clinical Presentations and Consequences Of Cirrhotic Cardiommentioning

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%

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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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Section: Electrophysiological Abnormalitiesmentioning

confidence: 88%

Section: Clinical Presentations and Consequences Of Cirrhotic Cardiommentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Cirrhotic cardiomyopathy

2008

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“…This finding confirms a previous study, 7 and recalls that the alterations in cardiac function, as assessed by systolic time intervals, occurred regardless of the etiology of cirrhosis. 33 This does not necessarily rule out a pathogenetic role for alcohol abuse, but suggests that, in cirrhosis, the contribution of alcohol toxicity is overwhelmed by other factors.…”

Section: Discussionmentioning

confidence: 99%

Q-T interval prolongation in cirrhosis: Prevalence, relationship with severity, and etiology of the disease and possible pathogenetic factors

et al. 1998

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Prolonged Q-T interval predicts severe arrhythmias and sudden death, and has been shown to occur in alcoholic liver disease and cirrhotic patients who are candidates for liver transplantation. This study first evaluated the prevalence of prolonged Q-T interval in a large population of unselected patients with cirrhosis, and assessed the relationship between abnormal Q-T, etiology, and severity of liver disease and mortality of patients. Possible causes of Q-T abnormality were also explored. Ninety-four patients with cirrhosis without overt heart disease and 37 control subjects with mild chronic active hepatitis were enrolled. Rate-corrected Q-T interval (Q-T c ) was assessed along with routine liver tests, Child-Pugh score, serum bile salts, electrolytes and creatinine, plasma renin activity, aldosterone, norepinephrine, atrial natriuretic factor and, gonadal hormones. Q-T c was longer in patients with cirrhosis than in controls (440.3 ؎ 3.2 vs. 393.6 ؎ 3.7 ms; P F .001) and prolonged (G440 ms) in 44 patients (46.8%) and 2 controls (5.4%; P F .001). Q-T c length was not influenced by the etiology of cirrhosis and correlated with Child-Pugh score (r ‫؍‬ .53; P F .001), liver tests such as prothrombin activity, and serum concentrations of albumin and bilirubin, plasma bile salts, and plasma norepinephrine. Multivariate analysis showed that only Child-Pugh score and plasma norepinephrine were independently correlated with Q-T c duration. Over a median follow-up period of 19 months (range, 2-33 months), patients with Q-T c longer than 440 ms had a significantly lower survival rate than those with normal Q-T c . Q-T interval is frequently prolonged in patients with cirrhosis, regardless the etiology of the disease, worsens in parallel with the severity of the disease, and may have an important prognostic meaning. In addition to other undefined factors related to the severity of cirrhosis, sympathoadrenergic hyperactivity may play a pathogenetic role. (HEPA-TOLOGY 1998;27:28-34.)

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“…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%

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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Reduced cardiovascular responsiveness to exercise-induced sympathoadrenergic stimulation in patients with cirrhosis

Cited by 127 publications

References 32 publications

Cirrhotic cardiomyopathy

Cirrhotic cardiomyopathy

Q-T interval prolongation in cirrhosis: Prevalence, relationship with severity, and etiology of the disease and possible pathogenetic factors

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

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