Cardiac hemodynamics in alcoholic patients with chronic liver disease and a presystolic gallop

Gould, Lawrence; Shariff, Mahmood; Zahir, Md. Hasan; Lieto, Mary Di

doi:10.1172/jci106044

Cited by 121 publications

(57 citation statements)

References 23 publications

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“…However, analysis of lipid classes revealed enhanced ["C]oleic acid incorporation in counts per minute per gram, into triglyceride but diminished phospholipid radioactivity in the ethanol group, significant for subendocardial layers (Table III). This was also reflected in greater isotopic activity of triglyceride as a percentage of total radioactivity in subendocardium, 18 ±2.6% in controls vs. 45.2±7.8% for the experimental group (P <0.01). Phospholipid activity was 60.3± 5.0% in controls and was reduced to 35.1±5.2% after chronic use (P < 0.01).…”

Section: Resultsmentioning

confidence: 87%

Myocardial Function and Lipid Metabolism in the Chronic Alcoholic Animal

Regan¹,

Khan²,

Ettinger³

et al. 1974

J. Clin. Invest.

104

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Section: Resultsmentioning

confidence: 87%

Myocardial Function and Lipid Metabolism in the Chronic Alcoholic Animal

Regan¹,

Khan²,

Ettinger³

et al. 1974

J. Clin. Invest.

104

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“…Systolic function in cirrhosis is often normal at rest, and in advanced cirrhosis, it is even supernormal, with tachycardia, high ejection fraction, and increased cardiac output, the so-called hyperdynamic circulation [76]. However, systolic dysfunction is often unmasked when these patients are placed under physical [6,77] or pharmacological stress [78].…”

Section: Clinical Presentations and Consequences Of Cirrhotic Cardiommentioning

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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“…It seems paradoxical to speak of a cardiomyopathy when baseline ventricular contractility is increased. However, Gould et al in 1969 demonstrated that cardiac contractile response to stimuli was depressed in patients with alcoholic cirrhosis, a phenomenon presumed by the investigators to reflect the presence of a mild or latent alcoholic cardiomyopathy. 3 Several studies over the next decade, all done in alcoholic patients, confirmed these findings.…”

mentioning

confidence: 98%

“…However, Gould et al in 1969 demonstrated that cardiac contractile response to stimuli was depressed in patients with alcoholic cirrhosis, a phenomenon presumed by the investigators to reflect the presence of a mild or latent alcoholic cardiomyopathy. 3 Several studies over the next decade, all done in alcoholic patients, confirmed these findings. Only in the mid-1980s did some studies suggest that the depressed cardiac function is the result of cirrhosis rather than alcohol.…”

mentioning

confidence: 98%

Cardiac Dysfunction in Spontaneous Bacterial Peritonitis: A Manifestation of Cirrhotic Cardiomyopathy?

Lee

2003

Hepatology

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Cardiac hemodynamics in alcoholic patients with chronic liver disease and a presystolic gallop

Cited by 121 publications

References 23 publications

Myocardial Function and Lipid Metabolism in the Chronic Alcoholic Animal

Myocardial Function and Lipid Metabolism in the Chronic Alcoholic Animal

Cirrhotic cardiomyopathy

Cardiac Dysfunction in Spontaneous Bacterial Peritonitis: A Manifestation of Cirrhotic Cardiomyopathy?

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