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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Liver cirrhosis is associated with several cardiovascular disturbances. These disturbances include hyperdynamic systemic circulation, manifested by an increased cardiac output and decreased peripheral vascular resistance and arterial pressure. Despite the baseline increase in cardiac output, cardiac function in patients with cirrhosis is abnormal in several respects. Patients show attenuated systolic and diastolic contractile responses to stress stimuli, electrophysiological repolarization changes, including prolonged QT interval, and enlargement or hypertrophy of cardiac chambers. This constellation of cardiac abnormalities is termed cirrhotic cardiomyopathy. It has been suggested that cirrhotic cardiomyopathy has a role in the pathogenesis of cardiac dysfunction and even overt heart failure after transjugular intrahepatic portosystemic shunt placement, major surgery and liver transplantation. Cardiac dysfunction contributes to morbidity and mortality after liver transplantation, even in many patients who have no prior history of cardiac disease. Depressed cardiac contractility contributes to the pathogenesis of hepatorenal syndrome, especially in patients with spontaneous bacterial peritonitis. Pathogenic mechanisms underlying cirrhotic cardiomyopathy include cardiomyocyte-membrane biophysical changes, attenuation of the stimulatory beta-adrenergic system and overactivity of negative inotropic systems mediated via cyclic GMP. The clinical features, general diagnostic criteria, pathogenesis and treatment of cirrhotic cardiomyopathy are discussed in this review.
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PMID:Therapy insight: Cirrhotic cardiomyopathy. 1674 52

Most patients with liver cirrhosis have hyperdynamic circulatory alterations with increased cardiac output, and decreased systemic vascular resistance and arterial pressure. But, in spite of the increased resting cardiac output, ventricular contractile response to stressful stimuli is attenuated in cirrhotic patients which is termed as cirrhotic cardiomyopathy. The prevalence of cirrhotic cardiomyopathy remains unknown at present. Clinical features include structural, histological, electrophysiological, systolic and diastolic dysfunction. Multiple factors are considered as responsible, including impaired beta-adrenergic receptor signal transduction, abnormal membrane biophysical characteristics, and increased activity of cardiodepressant systems mediated by cGMP. Generally, cirrhotic cardiomyopathy with overt severe heart failure is rare. However, major stresses on the cardiovascular system such as liver transplantation, infections and insertion of transjugular intrahepatic portosystemic shunts (TIPS) can unmask the presence of cirrhotic cardiomyopathy and thereby convert latent to overt heart failure. Cirrhotic cardiomyopathy may also contribute to the pathogenesis of hepatorenal syndrome and circulatory failure in liver cirrhosis. Because of the marked paucity of treatment studies, current recommendations for management are empirical, nonspecific measures. Further studies for pathogenesis and new therapeutic strategies in this area are required.
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PMID:[Cirrhotic cardiomyopathy]. 1738 71

Cirrhotic cardiomyopathy is the term used to describe a constellation of features indicative of abnormal heart structure and function in patients with cirrhosis. These include systolic and diastolic dysfunction, electrophysiological changes, and macroscopic and microscopic structural changes. The prevalence of cirrhotic cardiomyopathy remains unknown at present, mostly because the disease is generally latent and shows itself when the patient is subjected to stress such as exercise, drugs, hemorrhage and surgery. The main clinical features of cirrhotic cardiomyopathy include baseline increased cardiac output, attenuated systolic contraction or diastolic relaxation in response to physiologic, pharmacologic and surgical stress, and electrical conductance abnormalities (prolonged QT interval). In the majority of cases, diastolic dysfunction precedes systolic dysfunction, which tends to manifest only under conditions of stress. Generally, cirrhotic cardiomyopathy with overt severe heart failure is rare. Major stresses on the cardiovascular system such as liver transplantation, infections and insertion of transjugular intrahepatic portosystemic stent-shunts (TIPS) can unmask the presence of cirrhotic cardiomyopathy and thereby convert latent to overt heart failure. Cirrhotic cardiomyopathy may also contribute to the pathogenesis of hepatorenal syndrome. Pathogenic mechanisms of cirrhotic cardiomyopathy are multiple and include abnormal membrane biophysical characteristics, impaired beta-adrenergic receptor signal transduction and increased activity of negative-inotropic pathways mediated by cGMP. Diagnosis and differential diagnosis require a careful assessment of patient history probing for excessive alcohol, physical examination for signs of hypertension such as retinal vascular changes, and appropriate diagnostic tests such as exercise stress electrocardiography, nuclear heart scans and coronary angiography. Current management recommendations include empirical, nonspecific and mainly supportive measures. The exact prognosis remains unclear. The extent of cirrhotic cardiomyopathy generally correlates to the degree of liver insufficiency. Reversibility is possible (either pharmacological or after liver transplantation), but further studies are needed.
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PMID:Cirrhotic cardiomyopathy. 1738 39

Between 25,000 and 75,000 new cases of angina refractory to maximal medical therapy and standard coronary revascularization procedures are diagnosed each year. In addition, heart failure also places an enormous burden on the U.S. health care system, with an estimated economic impact ranging from $20 billion to more than $50 billion per year. The technique of counterpulsation, studied for almost one-half century now, is considered a safe, highly beneficial, low-cost, noninvasive treatment for these angina patients, and now for heart failure patients as well. Recent evidence suggests that enhanced external counterpulsation (EECP) therapy may improve symptoms and decrease long-term morbidity via more than 1 mechanism, including improvement in endothelial function, promotion of collateralization, enhancement of ventricular function, improvement in oxygen consumption (VO2), regression of atherosclerosis, and peripheral training effects similar to exercise. Numerous clinical trials in the last 2 decades have shown EECP therapy to be safe and effective for patients with refractory angina with a clinical response rate averaging 70% to 80%, which is sustained up to 5 years. It is not only safe in patients with coexisting heart failure, but also is shown to improve quality of life and exercise capacity and to improve left ventricular function long-term. Interestingly, EECP therapy has been studied for various potential uses other than heart disease, such as restless leg syndrome, sudden deafness, hepatorenal syndrome, erectile dysfunction, and so on. This review summarizes the current evidence for its use in stable angina and heart failure and its future directions.
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PMID:Enhanced external counterpulsation and future directions: step beyond medical management for patients with angina and heart failure. 1793 50

Liver cirrhosis is associated with several cardiovascular abnormalities. Despite an increased baseline cardiac output, cirrhotic patients have a suboptimal ventricular response to stress. This phenomenon is called cirrhotic cardiomyopathy. The pathogenesis of this syndrome is multifactorial and includes diminished beta-adrenergic receptor signal transduction, cardiomyocyte cellular plasma membrane dysfunction, and increased activity or levels of cardiodepressant substances such as cytokines, endogenous cannabinoids, and nitric oxide. Although cirrhotic cardiomyopathy is usually clinically mild or silent, overt heart failure can be precipitated by stresses such as liver transplantation or transjugular intrahepatic portosystemic shunt insertion. Moreover, cirrhotic cardiomyopathy may play a role in the pathogenesis of hepatorenal syndrome. Treatment of this condition is mainly supportive. Orthotopic liver transplantation appears to improve or normalize the condition, generally after a period of several months.
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PMID:Cirrhotic cardiomyopathy. 1829 77

The development of edematous states is usually due to heart failure, renal failure, hepatic failure, or a combination of these conditions. Although the number of patients with edema and ascites due to hepatic cirrhosis or renal failure is less frequent than with congestive heart failure, the treatment of these conditions is often difficult. Although diuretic therapy is often employed, effective reduction in edema or ascites may be difficult to achieve and is associated with significant side effects including hyponatremia, hypotension, and a further decrease in renal function. Aggressive diuretic therapy of ascites may result in hepatic encephalopathy or hepatorenal syndrome. Each condition needs to be evaluated, and an optimum therapeutic approach needs to be devised. This article provides a review of the challenges and therapeutic approaches for the treatment of these conditions and provides a review of new therapies on the horizon that may be promising.
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PMID:Therapeutic approaches to the treatment of edema and ascites: the use of diuretics. 1914 58

Selective adenosine A1 receptor antagonists targeting renal microcirculation are novel pharmacologic agents that are currently under development for the treatment of acute heart failure as well as for chronic heart failure. Despite several studies showing improvement of renal function and/or increased diuresis with adenosine A1 antagonists, particularly in chronic heart failure, these findings were not confirmed in a large phase III trial in acute heart failure patients. However, lessons can be learned from these and other studies, and there might still be a potential role for the clinical use of adenosine A1 antagonists.We review the role of adenosine A1 receptors in the regulation of renal function, and emerging data regarding the safety and efficacy of A1 adenosine receptor antagonists based on all available completed and reported clinical trials using A1 adenosine receptor antagonists. The majority of trials were done in heart failure patients. However, there is clear clinical evidence for a role of this new class in hepatorenal syndrome, hypotension on dialysis, and radiocontrast media-induced nephropathy.
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PMID:Adenosine A1 receptor antagonists in clinical research and development. 2059 13

Cardiorenal syndromes were defined and classified recently, but the mechanism of chronic renocardiac syndrome remains disputed. Theories about chronic renocardiac syndrome cannot offer a convincing explanation for it. As a result, the current therapies of chronic renocardiac syndrome do not contribute to a satisfied prognosis. Epoxyeicosatrienoic acids, the products of arachidonic acid metabolized by cytochrome P450 enzymes, play an important role in the maintenance of renal hemodynamics, and regulation of renal, cardiac, and vascular function with antihypertensive and anti-inflammatory properties. It is well documented that down-regulation of epoxyeicosatrienoic acids might be involved in alterations in various pathophysiological states, including hypertension, uremia and hepatorenal syndrome. Likewise, epoxyeicosatrienoic acids were reduced in heart failure and renal dysfunction. This leads to the proposed hypothesis that epoxyeicosatrienoic acids down-regulation may be the novel mechanism of chronic renocardiac syndrome. These findings suggest that manipulation of epoxyeicosatrienoic acid levels could be a novel pharmacological therapy strategy for chronic renocardiac syndrome.
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PMID:Epoxyeicosatrienoic acids--novel mechanism and pharmacological therapy of chronic renocardiac syndrome. 2133 54

Cirrhosis is a frequent and severe condition, which is the late stage of numerous chronic liver diseases. It is associated with major hemodynamic alterations characteristic of hyperdynamic circulation and with a series of structural, functional, electrophysiological and biological heart abnormalities termed cirrhotic cardiomyopathy. The pathogenesis of this syndrome is multifactorial. It is usually clinically latent or mild, likely because the peripheral vasodilatation significantly reduces the left ventricle afterload. However, sudden changes of hemodynamic state (vascular filling, surgical or transjugular intrahepatic porto-systemic shunts, peritoneo-venous shunts and orthotopic liver transplantation) or myocardial contractility (introduction of beta-blocker therapy) can unmask its presence, and sometimes convert latent to overt heart failure. Cirrhotic cardiomyopathy may also contribute to the pathogenesis of hepatorenal syndrome. This entity has been described recently, and its diagnostic criteria are still under debate. To date, current management recommendations are empirical, nonspecific measures. Recognition of cirrhotic cardiomyopathy depends on a high level of awareness for the presence of this syndrome, particularly in patients with advanced cirrhosis who undergo significant surgical, pharmacological or physiological stresses.
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PMID:[Cirrhotic cardiomyopathy: a specific entity]. 2211 74

Unlike hemoglobin or myoglobin, bilirubin, a breakdown product of the catabolism of heme molecules, usually is not seen as a nephrotoxic protein. We report the case of an adult kidney recipient who developed jaundice 4 years after transplantation because of a malignant cholangiocarcinoma. He progressively lost transplant function, accompanied by a continuous increase in bilirubinemia. Kidney biopsy showed bile granules in the cytoplasm of tubular epithelial cells and bile thrombi in dilated tubules, but no interstitial inflammation. The tumor was unresectable and the patient died 2 months later. Because the patient had no jaundice-associated confounding factor that could explain his kidney failure, such as sepsis, heart failure, or liver failure with hepatorenal syndrome, this exceptional case suggests that bilirubin per se should be seen as a potential cause of acute tubular necrosis.
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PMID:Bilirubin-associated acute tubular necrosis in a kidney transplant recipient. 2346 56


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