Cirrhotic cardiomyopathy

During the course of cirrhosis, there is a progressive deterioration of cardiac function manifested by the disappearance of the hyperdynamic circulation due to afailure in heart function with decreased cardiac output. This is due to a deterioration in inotropic and chronotropic function which takes place in parallel with a diastolic dysfunction and cardiac hypertrophy in the absence of other known cardiac disease. Other findings of this specific cardiomyopathy include impaired contractile responsiveness to stress stimuli and electrophysiological abnormalities with prolonged QT interval. The pathogenic mechanisms of cirrhotic cardiomyopathy include impairment of the b-adrenergic receptor signalling, abnormal cardiomyocyte membrane lipid composition and biophysical properties, ion channel defects and overactivity of humoral cardiodepressant factors. Cirrhotic cardiomyopathy may be difficult to determine due to the lack of a specific diagnosis test. However, an echocardiogram allows the detection of the diastolic dysfunction and the E/e′ ratio may be used in the followup progression of the illness. Cirrhotic cardiomyopathy plays an important role in the pathogenesis of the impairment of effective arterial blood volume and correlates with the degree of liver failure. A clinical consequence of cardiac dysfunction is an inadequate cardiac response in the setting of vascular stress that may result in renal hypoperfusion leading to renal failure. The prognosis is difficult to establish but the severity of diastolic dysfunction may be a marker of mortality risk. Treatment is non-specific and liver transplantation may normalize the cardiac function.     

Cirrhotic cardiomyopathy

Liver cirrhosis is associated with a wide range of cardiovascular abnormalities. These abnormalities include hyperdynamic circulation characterized by an increase in cardiac output and a decrease in peripheral vascular resistance. Despite the increased cardiac output, impaired ventricular contractility in response to both physiological and pharmacological stimuli has been described. Other cardiac abnormalities include structural changes including enlargement or hypertrophy of different cardiac chambers and electrophysiological changes such as QT prolongation. This constellation of cardiac abnormalities is termed cirrhotic cardiomyopathy. The pathogenic mechanisms of cirrhotic cardiomyopathy are multifactorial and include cardiomyocyte plasma membrane physico-chemical changes, attenuated stimulatory pathways, and enhanced activity of inhibitory systems. Accumulating evidence suggests that cirrhotic cardiomyopathy plays a major role in the pathogenesis of cardiac dysfunction following liver transplantation or transjugular intrahepatic portosystemic shunt placement. Recent research also strongly suggests that cirrhotic cardiomyopathy contributes to the pathogenesis of hepatorenal syndrome, especially following infections such as spontaneous bacterial peritonitis. Treatment of this syndrome remains largely empirical. Successful liver transplantation is thought to improve all the organ-related hemodynamic dysfunctions, including hepatopulmonary syndrome, cerebral hypoperfusion, hepatorenal syndrome, and cirrhotic cardiomyopathy. The prolonged QT interval normalizes following liver transplantation. Thus, liver transplantation appears to be the ultimate treatment for the cardiovascular complications of cirrhosis.     

Cirrhotic cardiomyopathy

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 β-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 β-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.     

肝性心肌病

肝硬化患者心肌收缩力减弱 ,在应激情况下尤为明显 ,这种现象称为肝性心肌病 ,主要表现为心脏的β 肾上腺素能受体及其信息传递功能减弱 ,另外可能的机制为心肌细胞膜的生化特性改变、体液因素的异常及高动力循环等。5 0年前已证实肝硬化伴心输出量增加 ,心血流量增加 ,外周血管阻力降低的高动力循环状态。到目前为止 ,外周血管扩张仍为研究焦点。最近的研究发现一氧化氮和内皮因子在外周血管中的扩张作用[1] 。对心脏本身的研究始于 30年前 ,最初的研究对象为酒精性肝病 ,显示心脏的输出量增加 ,但在生理及药理应激状态下心脏的收缩力减弱 …     

Cirrhotic cardiomyopathy

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.     

Cirrhotic cardiomyopathy: Indian scenario

BACKGROUND: Cirrhotic cardiomyopathy has been reported to be a major cause of morbidity and mortality in liver transplant recipients. However, there is scant data from Asia. With liver transplantation programs gradually being established in the region, Asian hepatologists are bound to face this entity. METHODS: Thirty patients with alcoholic cirrhosis and 30 with cirrhosis of nonalcoholic etiology were enrolled, after excluding those with recent bleeding, gross ascites, severe anemia and other conditions which could alter cardiovascular status. Thirty healthy subjects without cardiovascular risk factors were enrolled as controls. Hepatic function status was assessed by biochemical tests and prothrombin time. Cardiac structural and functional assessment was performed non-invasively using transthoracic echocardiography. RESULTS: Deceleration time was significantly (P < 0.05) prolonged in both the cirrhotic groups (235.03 +/- 44.23 ms and 255.87 +/- 46.16 ms) compared to controls (185.83 +/- 25.04 ms), indicative of diastolic dysfunction in cirrhotic patients. Other parameters, viz. ejection fraction, E : A ratio, left ventricular relative wall thickness, interventricular septal thickness and left ventricular systolic as well as diastolic chamber dimensions did not show statistically significant difference between any of the groups. Cardiac structural and functional parameters were not correlated with the severity of liver dysfunction. There was no statistically significant difference between the alcoholic and nonalcoholic groups. CONCLUSIONS: Asian patients with cirrhosis do have evidence of diastolic dysfunction. Cardiac structural and functional parameters did not correlate with the severity of liver dysfunction. Cardiac dysfunction seemed to be the consequence of cirrhosis itself, rather than of alcohol.     

Therapy insight: Cirrhotic cardiomyopathy

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.     

Diabetic cardiomyopathy: a controversial entity

We read with interest the study by Konduracka et al., ¹ whichconcludes that patients with long-term type 1 diabetes mellitusunder intensive insulin treatment do not have echocardiographic,biochemical, or morphological signs of diabetic cardiomyopathy.However, as the authors admit, this is directly opposed to severalprevious studies     

Cirrhotic cardiomyopathy.

Decompensated liver cirrhosis is characterized by a peripheral vasodilation with a low-resistance hyperdynamic circulation. The sustained increase of cardiac work load associated with such a condition may result in an inconstant and often subclinical series of heart abnormalities, constituting a new clinical entity known as "cirrhotic cardiomyopathy". Cirrhotic cardiomyopathy is variably associated with baseline increase in cardiac output, defective myocardial contractility and lowered systo-diastolic response to inotropic and chronotropic stimuli, down-regulated beta-adrenergic function, slight histo-morphological changes, and impaired electric "recovery" ability of ventricular myocardium. Cirrhotic cardiomyopathy is usually clinically latent or mild, likely because the peripheral vasodilation significantly reduces the left ventricle after-load, thus actually "auto-treating" the patient and masking any severe manifestation of heart failure. In cirrhotic patients, the presence of cirrhotic cardiomyopathy may become unmasked and clinically evident by certain treatment interventions that increase the effective blood volume and cardiac pre-load, including surgical or transjugular intrahepatic porto-systemic shunts, peritoneo-venous shunts (LeVeen) and orthotopic liver transplantation. Under these circumstances, an often transient overt congestive heart failure may develop, with increased cardiac output as well as right atrial, pulmonary artery and capillary wedge pressures.     

Cirrhotic cardiomyopathy: causes and consequences

Abstract   Cirrhotic cardiomyopathy is generally defined as subnormal ventricular response to stress in the face of high resting cardiac output. Although this syndrome was first noticed more than three decades ago in cirrhotic patients, it was originally ascribed to latent alcoholic cardiomyopathy. During the 1980s−1990s, it became clear that blunted ventricular contractility to stress is also present in non-alcoholic patients and animal models of cirrhosis. Mechanistic studies in experimental animal models of cirrhosis indicate that multiple factors are responsible, including abnormal biophysical membrane characteristics, impaired β-adrenergic signal transduction and increased activity of cardiodepressant systems mediated by cGMP. Cirrhotic cardiomyopathy appears to be precipitated or worsened by liver transplantation, insertion of transjugular intrahepatic portosystemic stent-shunts and infections. It may play a role in the pathogenesis of hepatorenal syndrome. Current management recommendations are empiric, non-specific measures; further research in this area is needed.     

Diabetic cardiomyopathy: a controversial entity: reply

We are most grateful to Dr Karamitsos et al. for showing suchan avid interest in our paper.¹ Upon its submission, we wereacutely aware that we might well shake things up, as prior toconfronting the actual study results we also used to supportthe notion of diabetic     

Transient mid-ventricular ballooning cardiomyopathy: a new entity of Takotsubo cardiomyopathy

We present a case of a 64-year-old man with transient mid-ventricular ballooning cardiomyopathy. Left ventriculography showed morphological differences with ballooning around the whole mid-portion of the left ventricle, although precipitating factors and clinical courses were similar to Takotsubo cardiomyopathy. We suspect that transient mid-ventricular ballooning cardiomyopathy is a new pathological entity in Takotsubo cardiomyopathy.     

Cirrhotic cardiomyopathy: review of pathophysiology and treatment

Cirrhotic cardiomyopathy is a cardiac condition observed in patients with cirrhotic regardless of the etiologies. It is characterized by the impaired systolic response to physical stress, diastolic dysfunction, and electrophysiological abnormalities, especially QT interval prolongation. Its pathophysiology and clinical significance has been a focus of various researchers for the past decades. The impairment of β-adrenergic receptor, the increase in endogenous cannabinoids, the presence of cardiosuppressants such as nitric oxide and inflammatory cytokines are the proposed mechanisms of systolic dysfunction. The activation of cardiac renin-angiotensin system and salt retention play the role in the development of cardiac hypertrophy and impaired diastolic function. QT interval prolongation, which is observed in 40–50 % of cirrhotic patients, occurs as a result of the derangement in membrane fluidity and ion channel defect. The increased recognition of this disease will prevent the complications of overt heart failure after procedures such as transjugular intrahepatic portosystemic shunt (TIPS) and liver transplantation. Better understandings of the pathogenesis and pathology of cirrhotic cardiomyopathy is crucial in developing more accurate diagnostic tools and specific treatments of this condition.     

Tako-tsubo cardiomyopathy: a rare and badly known clinical entity

Tako-tsubo cardiomyopathy or "transient left ventricular (LV) apical ballooning" clinically presents like acute myocardial infarction without angiographic stenosis on coronary angiogram and a transient (reversible) LV apical ballooning. We discuss here about a 56-year-old woman complains of first constrictive chest pain with ST elevation in leads V2-V6 and minimal enzymatic release. Coronary angiogram demonstrates vessels without stenosis and the left ventriculogram an extensive LV apical wall motion abnormalities. LV dysfunction will only be transient since 24 hours after admission echographic images demonstrate quite complete recovery of LV systolic function. The pain disappears 12 hours after admission and the creatine kinase level normalize after 48 hours.