Ventricular function in noncardiacs with alcoholic fatty liver: role of ethanol in the production of cardiomyopathy

Since many patients with cardiomyopathy have a history of chronic ethanolism often associated with malnutrition, we have evaluated left ventricular (LV) function in alcoholics with fatty liver, who had no clinical evidence of cardiac or nutritional disease.During an afterload test of LV function the pressor response to angiotensin evoked a threefold rise of enddiastolic pressure in the alcoholic group which was substantially greater than the 4 mm Hg rise in control subjects. The stroke volume and stroke work response in the noncardiac alcoholic was significantly less than in controls. Diminished LV function was corroborated in the noncardiac alcoholic at rest, using a contractility index.To evaluate the dose-response relationship of ethanol in the production of cardiac malfunction, two groups of noncardiac alcoholic subjects were studied acutely at low and moderate dose levels. After 6 oz, ventricular function, myocardial blood flow, and metabolism were not significantly affected. After 12 oz, there was a progressive rise of end-diastolic pressure and decrease of stroke output at a mean blood alcohol level of 150 mg/100 ml, reverting toward control by 4 hr. The coronary effluent transiently evidenced leakage of cell constituents, despite an increase of coronary blood flow, suggesting a direct but reversible cardiac injury. Myocardial extraction of triglyceride was enhanced, whereas FFA uptake was reduced. A possible role of myocardial triglyceride accumulation in heart muscle was considered in pathogenesis.Chronic ingestion of 16 oz of Scotch daily by an alcoholic subject while on a normal diet produced, after 12 wk, a progressive increase of heart rate and size, circulation time, and venous pressure, and a ventricular diastolic gallop. Normal values were restored within 7 wk after interrupting alcohol.These several studies suggest that the cumulative effects of repeated ingestion of ethanol in intoxicating doses can produce diminished LV function before clinical evidence of cardiac abnormality, or heart disease not necessarily related to malnutrition.     

Chronic Heart Failure: Contemporary Diagnosis and Management

Chronic heart failure (CHF) remains the only cardiovascular disease with an increasing hospitalization burden and an ongoing drain on health care expenditures. The prevalence of CHF increases with advancing life span, with diastolic heart failure predominating in the elderly population. Primary prevention of coronary artery disease and risk factor management via aggressive blood pressure control are central in preventing new occurrences of left ventricular dysfunction. Optimal therapy for CHF involves identification and correction of potentially reversible precipitants, target-dose titration of medical therapy, and management of hospitalizations for decompensation. The etiological phenotype, absolute decrease in left ventricular ejection fraction and a widening of QRS duration on electrocardiography, is commonly used to identify patients at increased risk of progression of heart failure and sudden death who may benefit from prophylactic implantable cardioverter-defibrillator placement with or without cardiac resynchronization therapy. Patients who transition to advanced stages of disease despite optimal traditional medical and device therapy may be candidates for hemodynamically directed approaches such as a left ventricular assist device; in selected cases, listing for cardiac transplant may be warranted.ACC = American College of Cardiology; ACEI = angiotensin-converting enzyme inhibitor; ADHF = acute decompensated heart failure; AF = atrial fibrillation; AHA = American Heart Association; ARB = angiotensin II receptor blocker; CABG = coronary artery bypass grafting; CAD = coronary artery disease; CHF = chronic heart failure; CRT = cardiac resynchronization therapy; ICD = implantable cardioverter-defibrillator; LV = left ventricular; LVAD = LV assist device; LVEF = LV ejection fraction; MI = myocardial infarction; MR = mitral regurgitation; SCD = sudden cardiac death; UF = ultrafiltrationChronic heart failure (CHF) is a progressive syndrome that results in a poor quality of life for the patient and places an economic burden on the health care system. Despite advances in the control of cardiovascular diseases such as myocardial infarction (MI), the incidence and prevalence of CHF continue to increase.¹ An accurate estimate of disease burden is difficult to gather because of the vast number of patients with asymptomatic left ventricular (LV) dysfunction. As the population ages, there is an epidemiological shift toward a greater prevalence of clinical heart failure with preserved LV function, the so-called stiff-heart syndrome. In fact, heart failure with preserved systolic function may account for up to two-thirds of cases in patients older than 70 years.² Regardless of age, the lifetime risk of developing heart failure is approximately 20% for all patients older than 40 years.³Despite the growing prevalence, novel screening techniques and therapeutic directions have improved the outlook for patients with heart failure by focusing not only on symptom control but also on ameliorating the pathophysiology toward a corrective phenotype. This review discusses accepted and emerging therapeutic directions, with an emphasis on practical implications. In light of the available literature and clinical trials, the primary emphasis will be on systolic dysfunction, with a separate brief discussion of heart failure with preserved systolic function.     

酒精性心肌病临床观察及护理

[目的]了解酒精性心肌病的临床特征、超声心动图检查结果,总结护理经验。[方法]收集62例酒精性心肌病病人的临床表现、超声心动图检查结果、治疗措施及护理对策等。[结果]酒精性心肌病以心脏扩大、心力衰竭和心律失常为主要表现,彩色多普勒超声心动图对诊断、治疗效果、预后评价均具有非常重要的意义,戒酒是治疗的关键。在护理该类病人时病情观察及健康教育很重要,告诫并督促病人戒酒,将获得较好的预后。[结论]医护人员应该提高对该病的认识,做到早诊断、早治疗、早戒酒。     

Psychiatric outcome in alcoholic liver transplant patients

We investigated drinking behaviour and psychiatric outcome ofpatients with alcoholic liver disease after liver transplantation,to help assess the advisability of the procedure in these patients.English-speaking patients (n = 20) transplanted for alcoholicliver disease and informants, and patients transplanted fornon-alcoholic liver disease (n = 54), were assessed by semi-structuredinterviews and standardized questionnaires 1–6 years followingtransplantation. All alcoholics were abstinent for several monthsafter transplantation, but only one patient remained totallyabstinent. Sixteen of the 20 alcoholics later returned to regulardrinking; the mean daily alcohol consumption was 3.5 units.Forty percent of the group were drinking above the recommendedsafe levels for the general population and over 50% were ‘binge’drinking intermittently. The alcoholic liver transplant patientsdid not have higher levels of psychiatric or physical morbiditythan controls. Patients with alcoholic liver disease returnto drinking after a period of abstinence following liver transplantation,although at lower levels than before. Their vulnerability toalcohol abuse is not explained by higher levels of physicalor psychiatric morbidity.     

Improved function of the failing rat heart by regulated expression of insulin-like growth factor I via intramuscular gene transfer

Current methods of gene transfer for heart disease include injection into heart muscle or intracoronary coronary delivery, approaches that typically provide limited expression and are cumbersome to apply. To circumvent these problems, we selected a transgene, insulin-like growth factor-I (IGF-I), which may, in theory, have favorable effects on heart function when secreted from a remote site. We examined the feasibility and efficacy of skeletal muscle injection of adeno-associated virus 5 encoding IGF-I under Tet regulation (AAV5.IGFI-tet) to treat heart failure. Myocardial infarction (MI) was induced in rats by coronary occlusion; 1 week later, rats with impaired left ventricular (LV) function received 2×10(12) genome copies (GC) of AAV5.IGFI-tet in the anterior tibialis muscle, and 4 weeks later, were randomly assigned to receive doxycycline in drinking water to activate IGF-I expression (IGF-On; n=10), or not to receive doxycycline (IGF-Off; n=10). Ten weeks after MI (5 weeks after activation of IGF-I expression), LV size and function were assessed by echocardiography and physiological studies. IGF-On rats showed reduced LV end-systolic dimension (p=0.03) and increased LV ejection fraction (p=0.02). In addition, IGF-On rats showed, before and during dobutamine infusion, increases in cardiac output (p=0.02), stroke work (p=0.0001), LV + dP/dt (p<0.0001), LV relaxation (LV - dP/dt; p=0.03), and systolic arterial blood pressure (p=0.0003). Mean arterial pressure and systemic vascular resistance were unchanged. Activation of IGF-I expression reduced cardiac fibrosis (p=0.048), apoptosis (p<0.0001), and caspase-3/7 activity (p=0.04). Serum IGF-I was increased 5 weeks after transgene activation (p=0.008). These data indicate that skeletal muscle injection of AAV5.IGFI-tet enables tetracycline-activated expression, increases serum IGF-I levels, and improves function of the failing heart.     

Sudden Death Associated with Alcohol Consumption

Evaluation of a binge drinker who died suddenly after a weekend of heavy beer consumption, and had been resuscitated successfully, revealed no evidence of clinically detectable heart disease. Baseline electrophysiological testing was normal. Following intravenous ethanol infusion, paired ventricular extrastimuli from the right ventricle induced a rapid polymorphic ventricular tachycardia requiring cardioversion. Repeat electrophysiological testing 24 hours later without alcohol infusion was again normal. The patient was discharged on no medications and was instructed to refrain from drinking alcohol. Approximately 3 months later the patient died suddenly after heavy beer consumption. Alcohol should be considered in the evaluation of survivors of cardiac arrest and alcohol challenge may be useful in their evaluation.     

急性酒精干预对长期嗜酒者左心功能的超声心动图观察

目的 通过超声心动图观察急性酒精摄入对长期哮酒者左心功能的影响，评价其早期诊断酒精性心肌病的价值。方法 嗜酒组42例，对照组18例，分别测定急性饮酒及及饮酒后1h、2h、3h每搏输出量将结果进行统计学处理。结果 饮酒前嗜酒组与对照组左室收缩功能无明显差异，但哮酒组急性酒精摄入前后EF、SV无变化，CO增大，其中21例EF、SV下降；对照组EF、SV、CO均增大。左室舒张功能E值无变化，A值明显升高，酒后1h、2h、3hE／A下降。结论 虽饮酒前与对照组相比，哮酒组左室收缩功能无明显变化，E／A＞1，但哮酒组急性酒精摄入后左室收缩、功能均有不同程度下降，急性酒精摄入实验可作为酒精性心肌病早期敏感指标之一。     

Cardiac hypertrophy induced by thyroid hormone is independent of loading conditions and beta adrenoceptor blockade

This study was designed to determine whether thyroid hormone (T4) produces cardiac hypertrophy and alters ventricular function by direct effects on the heart or by alterations in adrenergic stimulation or changes in the peripheral circulation. Rats were treated with captopril (4 mg/ml of drinking water), propranolol (0.5 mg/ml of drinking water), hydralazine (80 mg/l of drinking water) or the combination of captopril and propranolol with and without T4 (15 micrograms/100 g b.w. i.p.). After 10 days, T4 increased (P less than .01) heart rate, left ventricular (LV) dP/dt and LV weight/body weight, but did not alter LV systolic pressure (SP) or enddiastolic pressure (EDP). Compared to treatment with T4 alone, captopril plus T4 decreased LV SP (P less than .05) and LV EDP (P less than .01); however, heart rate, LV dP/dt and LV weight/body weight were unchanged. Treatment with T4 plus propranolol decreased heart rate and LV EDP (P less than .05) compared to T4 alone; however, LV SP, LV dP/dt and LV weight/body weight were unchanged (P greater than .05). Hydralazine did not alter (P greater than .05) heart rate, LV SP, LV EDP or prevent the development of increased LV weight/body weight when given with T4; however, LV dP/dt was slightly decreased (P less than .05). Treatment with the combination of captopril and propranolol did not alter (P greater than .05) heart rate, LV SP, LV EDP or LV dP/dt and also failed to prevent the development of increased LV weight/body weight and LV dP/dt when given with T4.(ABSTRACT TRUNCATED AT 250 WORDS)     

Differentiation of athlete's heart from pathological forms of cardiac hypertrophy by means of geometric indices derived from cardiovascular magnetic resonance.

PURPOSE: Determination of the underlying etiology of left ventricular hypertrophy (LVH) is a common, challenging, and critical clinical problem. The authors aimed to test whether pathological LVH, such as occurs in hypertrophic cardiomyopathy (HCM), hypertensive heart disease, or aortic stenosis, and physiological LVH in athletes, can be distinguished by means of left ventricular volume and geometric indices, derived from cardiovascular magnetic resonance imaging. METHODS: A total of 120 subjects were studied on a 1.5 Tesla MR (Sonata, Siemens Medical Solutions, Erlangen, Germany) scanner, comprising healthy volunteers (18), competitive athletes (25), patients with HCM (35), aortic stenosis (24), and hypertensive heart disease (18). Left ventricular mass index, ejection fraction, end-diastolic, end-systolic and stroke volume index, diastolic wall thickness, wall thickness ratio and diastolic and systolic wall-to-volume ratios were determined. RESULTS: Left ventricular (LV) mass indices were similar for all forms of LVH (p > 0.05), which were at least 35% higher than those obtained in healthy volunteers (p < 0.05). Multiple logistic regression showed that the percentage of correctly predicted diagnoses was 100% for athlete's heart, 80% for hypertrophic cardiomyopathy, 54% for aortic stenosis, and 22% for hypertensive heart disease. Using a receiver operating curve-determined cut-off value for diastolic wall-to-volume ratio of less than 0.15 mm x m2 x ml(-1), athletes' hearts could be differentiated from all forms of pathological cardiac hypertrophy with 99% specificity. CONCLUSIONS: Athlete's heart can be reliably distinguished from all forms of pathological cardiac hypertrophy using CMR-derived LV volume and geometric indices, but pathological forms of LVH present with overlapping cardiac hypertrophy phenotypes. This capability of CMR should be of high clinical value.     

New onset heart failure in a 29-year-old: A case report of isolated left ventricular noncompaction

A previously healthy 29-year-old patient presented with new onset congestive heart failure. Based on findings on transthoracic echocardiogram (TTE) and cardiac magnetic resonance imaging (MRI) at an outside center, the patient was diagnosed as having a dilated cardiomyopathy with structural abnormalities in the ventricular septum and left ventricular (LV) apex suspicious for myocardial tumor. After referral to our center for further management, repeat TTE revealed findings characteristic of left ventricular non-compaction (LVNC) with severely depressed overall LV systolic function. Review of the outside cardiac MRI supported the diagnosis of LVNC. Final management consisted of traditional medical therapy for congestive heart failure, an implantable cardiac defibrillator (ICD), warfarin anticoagulation for the prevention of thromboembolism and referral for cardiac transplant.     

超声心动图在诊断酒精性心肌病中的应用价值

目的探讨超声心动图在诊断酒精性心肌病中的应用价值。方法应用彩色多普勒超声心动图检测32例长期大量饮酒所致酒精依赖患者静息状态下的心内结构、血流和功能,从心脏各房室内径、室壁厚度、室壁回声、各室壁运动幅度、室壁增厚率、左室射血分数、各瓣膜形态结构、血流及功能等指标进行多方面观察,结合病史做出超声提示。结果左室舒张末期内径不同程度增大者32例,左室舒张末内径增大并左房内径增大者24例,以左心室增大为主的全心增大者6例,左室壁对称性轻度肥厚者9例,左室心肌内出现散在斑点状中强回声17例,左室心内膜增厚,回声增强10例,左心功能减低者20例(62.5%),左心功能减低合并不同程度肺循环高压者4例,左心增大伴左室心尖部附壁血栓者1例。结论超声心动图在酒精性心肌病的诊断中具有重要的临床应用价值,是临床医师诊断酒精性心肌病的重要辅助检查手段。     

Electrocardiographic left ventricular hypertrophy Cornell product is a feasible predictor of cardiac prognosis in patients with chronic heart failure

Background

Left ventricular hypertrophy (LVH) is an independent risk factor for cardiovascular disease and is associated with heart failure development. The Cornell product is an easily measured electrocardiographic parameter for assessing LVH. However, it is undetermined whether the Cornell product can predict the cardiac prognosis of chronic heart failure (CHF) patients.

Methods and results

We performed standard 12-lead electrocardiography and calculated the Cornell product in 432 consecutive CHF patients. LV geometry was assessed as normal, concentric remodeling, concentric or eccentric hypertrophy. The Cornell product was significantly higher in patients with eccentric hypertrophy, and increased with advancing New York Heart Association functional class. During a median follow-up of 660 days, there were 121 cardiac events including 36 cardiac deaths and 85 re-hospitalizations for worsening heart failure. Multivariate Cox proportional hazard analysis showed that the Cornell product was an independent predictor of cardiac events in CHF patients. Patients in the highest quartile of Cornell product had a higher prevalence of LV eccentric hypertrophy (22, 29, 33 and 67 % for quartiles one through four). Kaplan–Meier analysis demonstrated that the highest quartile of Cornell product was associated with the greatest risk among CHF patients.

Conclusion

The Cornell product is associated with LV eccentric hypertrophy and can be used to predict future cardiac events in CHF patients.     

Dynamic three-dimensional visualization of the left ventricle by intracardiac echocardiography

Cardiac function and hemodynamics are routinely evaluated during catheterization in patients with heart disease. Although intracardiac echocardiography (ICE) has been employed in guiding electrophysiology procedures, it has not been effectively used in assessing hemodynamics. We tested the utility of ICE in measuring left ventricular (LV) volume throughout the cardiac cycle. In four normal dogs (weight = 26 to 37 kg), a 10-F sheath was inserted through the femoral artery and placed inside the LV along its major axis. An ICE catheter (9 F, 9 MHz) was then inserted through the sheath into the LV. The ICE catheter was pulled back inside the sheath in 1-mm intervals starting from the apex, and 2-D tomographic images were continuously acquired while gating to respiration. Subsequently, the ICE catheter was replaced by a conductance catheter to measure single-beat volume signals. Stroke volume was determined by thermodilution for validation. All measurements were made in each dog while pacing the atrium at two different cycle lengths (range = 300 to 500 ms). The endocardial boundary was digitized from the ICE images throughout the cardiac cycle and LV volume was computed by integrating multiple segments along the major axis (range = 55 to 70 mm). We found that ICE accurately reconstructed LV 3-D anatomy. Stroke volume by ICE was in excellent agreement with thermodilution (error = 3.8 +/- 3.0%, r = 0.99, n = 8) and was highly reproducible. Morphology of LV volume signals correlated well with corresponding instantaneous volume signals derived by conductance (r = 0.93, n = 8). In conclusion, ICE accurately reconstructs LV anatomy and volume throughout the cardiac cycle in the normal heart. This approach could facilitate interventional diagnostic and therapeutic procedures.     

高血压及冠心病患者左心房扩大与心功能的相关性

背景临床观察发现高血压及冠心病患者普遍存在左心房扩大,但左房扩大的发生机制及临床意义尚未完全明了.目的探讨高血压及冠心病患者左心房内径的变化的临床意义及其与心功能的相关性.设计以诊断为依据的病例对照研究.地点、对象和方法选择在成都军区昆明总医院就诊的360例高血压患者、286例冠心病患者及255例健康人为研究对象.应用彩色多普勒超声心动图仪、三导心电图仪及24h动态心电图仪,测定左房内径、左室舒张末内径(1eft ventricular diastolic diameter,LVDd)、左室后壁厚度(1eftventricular posterior wallthickness,LVPWT)、室间隔厚度(septalthink-ness,WST)、每搏输出量(stroke volume,SV)、每分输出量、射血分数值、E/A比值.以观察左房扩大及左室肥厚与心功能的相关性.主要观察指标各组患者左房内径的变化,左房内径与左心室肥大及心功能的关系.结果高血压组及冠心病组左房内径分别为(30.13±5.54),(31.35±5.84)mm较正常对照组[(26.82±6.11)mm]显著增加.高血压组及冠心病组伴LAD扩大者射血分数[(49.12±12.11)%]及E/A(0.86±0.2)显著降低.结论高血压组及冠心病患者左房内径较正常者增加,1/3以上高血压组及冠心病组患者伴有左房扩大.左房内径扩大与左心室肥大及心功能减退有关;左房内径扩大可能是高血压组及冠心病病情进展及心功能减退的标志.     

Signal-Averaged Electrocardiography in Elderly Subjects With and Without Heart Disease

Prevalence of abnonnal signal-averaged electrocardiography in normal populations ap pears to be low, but has not been studied previously in an asymptomatic elderly population. To study the prevalence of abnormal ventricular late potentials in an elderly population, a group of 51 subjects with no evidence of cardiac disease and ranging In age from 62 to 102 years underwent signal-averaged electrocardiography. Results were compared to a group of 179 patients similar in age but with complex ventricular arrhythmias, and to a group of 25 asymptomatic volunteers under the age of 50. The prevalence of an abnormal signal-averaged ECG was 14% in the normal elderly subjects, and 31 % in the patients (P = 0.01), and 4 % in the young subjects (P = NS). We conclude that the prevalence of abnormal ventricular late potentials in elderly patients without heart disease is similar to levels reported in other populations of normal controls, but elderly patients with cardiac disease have a significantly higher prevalence of abnormal signal-averaged ECG studies than the normals.     

Ethanol and heart disease. An underestimated contributing factor

With the number of chronic heavy users of ethanol in the United States estimated to be 15 to 20 million and the evidence increasing that ethanol causes serious cardiac metabolic disturbances, ethanol abuse is obviously a serious problem and most likely is an important contributing factor to cardiac morbidity and mortality. However, a direct cause-and-effect relationship between the biochemical dysfunctions produced by ethanol and the clinical entity of alcoholic cardiomyopathy has not been clearly established. What is lacking is a method to differentiate the damage secondary to ethanol abuse from that secondary to other causes. Sorely needed is a biochemical or anatomic marker (perhaps evaluated by serial myocardial biopsy) for alcoholic cardiomyopathy and a study to detect which cases of dilated cardiomyopathy indeed are due to ethanol-induced damage. Further longterm studies are also needed to demonstrate the benefits of abstinence upon large groups of patients, the effects of abstinence upon sudden death, and the effects of discontinuance of ethanol use for patients in the early stages of alcoholic cardiomyopathy. Ethanol is probably an underestimated contributing factor to cardiac disease. The importance of determining ethanol's impact on cardiovascular morbidity and mortality is underscored by the facts that alcoholic heart disease is completely avoidable and is largely reversible by abstinence.     

The health effects of moderate alcohol intake in humans: an epidemiologic review

A large body of scientific evidence associates the moderate intake of alcohol with reduced mortality among middle-aged and older people in industrialized societies. This association is due largely to a reduced risk of death from coronary heart disease, which appears to outweigh any possible adverse effects of moderate drinking. The regular consumption of small amounts of alcohol is more healthful than the sporadic consumption of larger amounts. No beneficial effect of moderate drinking on mortality has been demonstrated in young adults (premenopausal women and men who have not reached their forties). It is theoretically possible that moderate drinking in young adulthood might reduce the risk of later heart disease; however, this has not been clearly demonstrated. For some individuals (e.g., those who cannot keep their drinking moderate, pregnant women, and those who are taking medications that may interact adversely with alcoholic beverages), the risks of alcohol consumption, even in moderation, outweigh any potential benefits. Because even small amounts of alcohol can impair judgment and coordination, no one should drink alcoholic beverages, even in moderation, before driving a motor vehicle or performing other activities that involve attention and skill.     

Alcohol, the heart and cardiovascular system

Any advice about the consumption of alcohol must take into account not only the relation between alcohol and cardiovascular disease but also the well-known association of heavy consumption of alcohol with a large number of health risks. Numerous observational studies have consistently demonstrated a reduction of coronary heart disease with moderate consumption of alcohol. Consumption of 1 or 2 drinks per day is associated with a reduction in risk of dying from coronary heart disease of approx. 30-50%. A drink equivalent amounts to a 12-ounce bottle of beer, a 4-ounce glass of wine, and a 1.5-ounce shot of 80-proof spirits. It has been repeatedly demonstrated that there is a J-shaped relation between alcohol consumption and total mortality. The lowest mortality occurs in those who consume 1 or 2 drinks per day. A stepwise decline in coronary heart disease death occurs with increasing drinks per day. Because coronary heart disease accounts for 1/3 or more of total death, people with no alcohol consumption have higher total mortality than those drinking 1 to 2 drinks per day. Conversely, mortality due to a large number of other diseases increases with an increasing number of drinks consumed per day. The protective effects of alcoholic against coronary heart disease are mainly related to an increase in HDL cholesterol. A number of other mechanisms have been proposed including effects of alcohol on blood clotting and non-alcoholic components of alcoholic beverages, particularly in red wine and dark beer, which may have antioxidant properties. Harmful effects of alcohol on the cardiovascular system include congestive cardiomyopathy, systemic hypertension and cerebral vascular incidents. There is a direct correlation between the amount of alcohol consumed during lifetime and a reduction in left ventricular ejection fraction.     

Alcohol and the liver

Since ethanol metabolism predominantly takes place in the liver it is not surprising that hepatic intermediary metabolism is strikingly influenced. Alcohol is metabolized via three enzyme systems: alcohol dehydrogenase (ADH), microsome ethanol oxidizing system (MEOS) and catalase. The ADH reaction produces reducing equivalents as NADH which results in various metabolic disorders such as hyperproteinemia IV and V, hypoglycaemia, lactacidosis, hyperuricaemia, and certain forms of porphyria. The metabolism of hormones is also disturbed. Alcohol fatty liver is a direct consequence of NADH production. Alcoholic liver disease comprises of fatty liver, alcoholic hepatitis and cirrhosis. Risk factors of alcoholic liver disease are the amount of alcohol consumed, drinking pattern, female gender and certain genetic predispositions. Alcoholic hepatitis is characterized by a typical clinical and laboratory feature, and specific heaptic morphology. Poor prognostic factors are continuous alcohol consumption, cholestatis and perivenular fibrosis. Alcoholic cirrhosis has similar complications as cirrhosis of other etiology. Therapy includes abstinence, antioxidative drugs, steroids, and S-adenosylmethionine. Liver transplantation is of long-term benefit.     

Predictors of Mortality and Hospitalization for Cardiac Causes in Patients with Heart Failure and Nonischemic Heart Disease: A Subanalysis of the ALPHA Study

Background: Several studies have searched for predictors of clinical outcome in patients with heart failure (HF). However, since they were collected in clinical trials, most data were subject to selection biases and do not specifically apply to patients with nonischemic heart disease. This study examined the impact of several variables on combined all-cause mortality and hospitalization for cardiac causes, in consecutive ambulatory patients with HF included in the ALPHA registry.
Methods and Results: This analysis included 446 patients with HF and nonischemic heart disease, in New York Heart Association functional class II or III, and a left ventricular (LV) ejection fraction below 40%. In 126 patients (73%) the disease was idiopathic dilated cardiomyopathy, in 72 (16%) hypertensive, in nine (2%) valvular, and in 39 (9%) of other etiologies. The median age was 61 years (range 51–69 years) and 349 (78%) patients were men. Over a median follow-up of 31 months (range 23–40), 82 patients (18%) died or were hospitalized for cardiac causes. In a proportional hazard (Cox) regression model, maximal oxygen consumption (HR 0.9, P = 0.001), LV end-diastolic diameter (HR 1.07, P < 0.001), resting systolic blood pressure (HR 0.97, P < 0.005), and hemoglobin (HR 0.86, P < 0.05) were independent predictors of the combined study endpoint.
Conclusions: In an unselected population of patients with HF and nonischemic heart disease, a reduced exercise capacity, large LV end-diastolic diameter, low systolic blood pressure, and hemoglobin were correlated with long-term all-cause mortality or hospitalization for cardiac causes. These observations may help stratifying and tailoring the treatment of patients with HF and nonischemic heart disease.