Alcohol use and hypertension. Clinical considerations and implications

Alcohol abuse is a more frequent contributor to hypertension than is generally appreciated. Although hypertension is transitory in most alcoholics and may not be evident after a short period of abstinence, it is potentially dangerous. Paroxysms of hypertension might result in target-organ damage. Hypertension may be the causal link to the increased incidence of stroke and coronary heart disease observed in problem drinkers as well as a contributor to the pathogenesis of alcoholic cardiomyopathy. Because of its transitory nature, however, alcohol-associated hypertension may, regrettably , be dismissed as inconsequential. Thus, a major potential cause of cardiovascular morbidity may go untreated.     

Ethanol: its adverse effects upon the hypothalamic-pituitary-gonadal axis

Considerable evidence has accrued over the last decade to establish that ethanol is a gonadal toxin. Such toxicity is both direct, being expressed at the level of the testes, and indirect, being expressed at the level of the hypothalamus and/or pituitary. As a result of studies performed both in man and in animals, it has been shown that ethanol abuse per se, and not the associated disease that occurs with alcohol abuse, is responsible for the impotence, loss of libido, and testicular atrophy which are seen commonly in chronic alcoholic men. With prolonged alcohol abstinence, recent studies have suggested that spontaneous recovery of normal sexual function is possible in some chronic alcoholics if testicular atrophy has not yet occurred and if their responses to clomiphene and/or luteinizing hormone--releasing factor stimulation are normal. In contrast, abstinent alcoholic men with either overt testicular atrophy or inadequate responses to such pharmacologic challenges fail to recover spontaneously despite continued alcohol abstinence and will require either a penile prosthesis or long-term oral androgen therapy to achieve "acceptable" sexual functioning.     

Alcoholic heart disease

Alcoholic heart disease is caused by a lifestyle in which alcoholics are continue to consume an excessive amount of alcohol over a long period of time. Total abstinence is a very effective way to treat them to prevent the development of the final stage of this disease. In contrast, repetitive drinking of massive amount of alcohol is very harmful and causes exacerbation of this disease. From our clinical studies, six candidates were nominated as symptoms of alcoholic heart disease, namely(1) tachyarrhythmias (incidence: 33%), (2) left ventricular hypokinesis(17%), (3) QT interval prolongation(17%), (4) hyperthickened LV wall(13%), (5) LV dilatation with pump failure: alcoholic cardiomyopathy(0.1%), and (6) sudden cardiac death (unknown %). In the beginning of alcoholic heart disease, the patient usually complains of no symptoms, and physical signs are quite poor. Ordinarily, either transient atrial fibrillation and/or left ventricular hypertrophy which is initially documented by electrocardiography or echocardiography is one of the first signals in the diagnosis. Without such early signals, an early diagnosis is impossible. To make a definite diagnosis of alcoholic heart disease, a clinical follow-up is by all means necessary. Improvement of cardiac function after total abstinence, it's worsening after drinking again, and again improvement after abstinence a second time is a diagnostic clue. In this follow-up study, electrocardiography and echocardiography were employed as important ways to gather date. In treatment, total abstinence is essential. To achieve this therapeutic goal, education of the patient is necessary, because approximately 70 per cent of patients with alcoholic heart disease fail to continue abstinence within two years even if they have good training.     

Alcohol abuse and brain infarction

Recent findings on the relation between alcohol abuse and ischaemic brain infarction are reviewed. Much of the association has hitherto been explained by the effects of confounding factors such as smoking. Alcohol increases blood pressure in both hypertensive and normotensive subjects and alcohol induced hypertension enhances the risk of both hemorrhagic and ischaemic strokes. Analysis of case histories shows that alcohol abuse has precipitated cerebral embolism in conjunction with cardiac diseases including alcoholic cardiomyopathy and paradoxical embolism due to deep vein thrombosis via atrial septal defect. Among young adults, falling when intoxicated with alcohol has caused traumatic dissection of the carotid artery and consequent brain infarction. Alcohol may predispose individuals to cerebral embolism, thrombosis and ischaemia via its effects on the coagulation cascade, platelet count and function and contractility of the cerebral vessels. Further studies are needed to prove that these mechanisms are significant and to identify any other mechanisms which may mediate the risk associated with alcohol abuse. On the basis of current data, alcohol should be considered as an independent risk factor for ischaemic cerebral infarction in young adults.     

Low-dose ethanol consumption allows strength recovery in chronic alcoholic myopathy

Chronic skeletal myopathy may affect one third of chronic alcohol misusers. It is generally accepted that abstinence allows partial recovery, and that continued high-dose ethanol consumption progressively deteriorates muscle function. However, the effect of low-dose ethanol consumption in alcoholic myopathy has not been studied. We studied 58 chronic alcoholic male patients with biopsy-proven chronic alcoholic myopathy over 5 years. We evaluated ethanol intake, biochemical and nutritional parameters, and assessed muscle strength. Eighteen patients who remained abstinent showed marked improvement in muscle strength. As expected, the 19 patients who persisted in high-dose ethanol consumption further diminished in their muscle strength. In the 11 patients who maintained low-dose (相似文献   

Role of cardiac magnetic resonance imaging in assessment of nonischemic cardiomyopathies

Diagnosis of nonischemic cardiomyopathy is a challenging process that influences patient morbidity and mortality. Currently, the well known World Health Organization classification has been revisited by an American Heart Association expert consensus panel. The contemporary classification is compatible with the rapid evolution in molecular genetics and evolving diagnostic tools such as cardiac magnetic resonance imaging (MRI). Magnetic resonance imaging is a robust diagnostic tool that offers various techniques to assess the function, morphology, perfusion, and scarring of myocardial tissue thus providing better understanding of the underlying causes of nonischemic cardiomyopathies. In this review, we discuss the current role of cardiac MRI in the evaluation of nonischemic cardiomyopathy, in the context of the current American Heart Association classification of these disorders.     

News in brief

Heart failure is a major cause of morbidity and mortality in chronic kidney disease (CKD). Rather than merely secondary to traditional vascular factors, CKD is also an independent risk factor for heart failure, termed uremic cardiomyopathy (UCM). Echocardiography commonly reveals structural left ventricular hypertrophy in CKD, without clarifying whether it is adaptive or maladaptive. Corresponding functional assessments have been mostly conducted at rest. To unravel the extents and mechanisms UCM, a next step involves the adoption of direct measurements of CKD-induced cardiac pumping incapacity at peak exercise. This could potentially lead to future novel interventions to ameliorate or reverse UCM.     

Ethanol and galactose metabolism as influenced by 4-methylpyrazole in alcoholics with and without nutritional deficiencies. Preliminary report of a new approach to pathogenesis and treatment in alcoholic liver disease.

4-Methyl pyrazole (4-MP, a specific inhibitor of alcohol dehydrogenase) reduced ethanol elimination by 30-50% and completely removed the ethanol-induced inhibition of galactose elimination in 2 control subjects. Ethanol elimination was accelerated in 2 alcoholics with adequate nutrition, but the effect of 4-MP was comparable to that in controls. In 2 other alcoholic subjects, who reported poor nutritional intake, intermediate rates of ethanol elimination were observed and 4-MP had almost no effect on ethanol or galactose elimination. These results suggest that alcohol abuse may result in an increased contribution to ethanol elimination by pathways other than that involving alcohol dehydrogenase (ADH) and that the decreased contribution from ADH, possibly potentiated by inadequate nutrition, may diminish the ethanol-induced shift in the NAD-coupled redox state. Since liver damage produced by alcohol abuse is believed to be related to changes from the normal redox state caused by ethanol, these results may explain why alcoholic liver damage is uncommon in alcoholics living on a marginal diet. Since 4-MP effectively eliminates the ethanol-induced shift in the redox state, a therapeutic trial with 4-MP in alcoholics with a high risk for liver disease is indicated.     

Pathogenesis, diagnosis, and treatment of alcoholic liver disease

Alcohol-related liver disease is a major cause of morbidity and mortality in the United States. Alcoholic liver disease encompasses a clinicohistological spectrum, including fatty liver, alcoholic hepatitis, and alcoholic cirrhosis. Fatty liver is a benign and reversible condition, but progression to alcoholic hepatitis and cirrhosis is life-threatening. Alcoholic hepatitis is diagnosed predominantly on clinical history, physical examination, and laboratory testing, although liver biopsy is often necessary to secure the diagnosis. The major focus of management is abstinence from alcohol, supportive care, treatment of complications of infection and portal hypertension, and maintenance of positive nitrogen balance through nutritional support. Corticosteroid therapy is controversial but should be considered in patients with a discriminant function greater than 32 and/or presence of spontaneous hepatic encephalopathy in the absence of infection, gastrointestinal bleeding, and renal failure. The only curative therapy for advanced alcoholic cirrhosis is liver transplantation. Several recent advances in understanding the pathogenesis of alcoholic liver disease may lead to novel future treatment approaches, including inhibition of tumor necrosis factor a, antioxidant therapy, stimulation of liver regeneration, and stimulation of collagen degradation.     

Apheresis in the treatment of idiopathic dilated cardiomyopathy

Dilated cardiomyopathy (DCM) causes significant morbidity and mortality and is the number one indication for cardiac transplantation in the United States. A large percentage of cases of DCM have no identifiable cause with evidence suggesting that these may represent an autoimmune disorder triggered by viral myocarditis. There is a growing body of literature suggesting that a number of immunoadsorption techniques, as well as plasma exchange, may have a role in the treatment of idiopathic DCM. The hypothesized autoimmune mechanism behind idiopathic DCM as well as the published evidence for the use of apheresis in this disorder are reviewed. The available evidence suggests that apheresis may be an effective treatment, but additional research is needed to identify markers that will predict response and the most effective apheresis technique. J. Clin. Apheresis 2012. © 2012 Wiley Periodicals, Inc.     

The efficacy of low-dose antivenom therapy on morbidity and mortality in snakebite cases

Similar to the cases seen around the world, snakebite causes mortality and morbidity in Turkey. The venom of different types of snake in the region of Çukurova causes serious systemic and local tissue damage.     

Intercurrent complications in chronic alcoholic men admitted to the intensive care unit following trauma

Objective A chronic alcoholic group following trauma was investigated to determine whether their ICU stay was longer than that of a non-alcoholic group and whether their intercurrent complication rate was increasedDesign Prospective study.Setting An intensive care unit.Patients A total of 102 polytraumatized patients were transferred to the ICU after admission to the emergency room and after surgical treatment. Of these patients 69 were chronic alcoholics and 33 were allocated to the non-alcoholic group. The chronic-alcoholic group met the DSM-III-R and ICD-10 criteria for alcohol dependence or chronic alcohol abuse/harmful use. The daily ethanol intake in these patients was 60 g. Diagnostic indicators included an alcoholismrelated questionnaire (CAGE), conventional laboratory markers and carbohydrate-deficient transferrin.Measurement and results Major intercurrent complications such as alcohol withdrawal syndrome (AWS), pneumonia, cardiac complications and bleeding disorders were documented and defined according to internationally accepted criteria. Patients did not differ significantly between groups regarding age, TRISS and APACHE score on admission. The rate of major intercurrent complications was 196% in the chronic alcoholic vs 70% in the non-alcoholic group (P=0.0001). Because of the increased intercurrent complication rate, the ICU stay was significantly prolonged in the chronic-alcoholic group by a median period of 9 days.Conclusions Chronic alcoholics are reported to have an increased risk of morbidity and mortality. However, to our knowledge, nothing is known about the morbidity and mortality of chronic alcoholics in intensive care units following trauma. Since chronic alcoholics in the ICU develop mor major complications with a significantly prolonged ICU stay following trauma than non-alcoholics, it seems reasonable to intensify research to identify chronic alcoholics and to prevent alcohol-related complications.     

Severe cardiac disease in pregnancy, part II: impact of congenital and acquired cardiac diseases during pregnancy

PURPOSE OF REVIEW: Part II of this review gives an overview of the different maternal cardiac problems during pregnancy and their management, and developments over recent years. RECENT FINDINGS: Many studies published over the last 5 years provided new insights on different cardiac diseases in pregnancy. Publications discussed in this part of the review on cardiac disease in pregnancy, for example, provide epidemiological data on heart disease during pregnancy in general, and cardiomyopathy and ischemic heart disease in particular. In addition, we discussed the implications of a history of peripartum cardiomyopathy for a subsequent pregnancy, interventional strategies during pregnancy in women with ischemic heart disease, and the role of echocardiography in the evaluation of cardiac disease in pregnancy. SUMMARY: The prevalence of the different causes of heart disease has shifted towards congenital heart disease by the end of the millennium. In developing countries, relatively rare diseases like rheumatic fever are still common, so these diseases are increasingly 'exported' to developed countries. The group of women with congenital heart disease represents most women with heart disease during pregnancy, followed by rheumatic heart disease. With the exception of patients with Eisenmenger's syndrome, pulmonary vascular obstructive disease, and Marfan's syndrome with aortopathy, maternal death during pregnancy is rare in women with heart disease. Although the risk for mortality is low in pregnant women with preexistent cardiac disease, these women are at increased risk for serious morbidity such as heart failure, arrhythmias, and stroke.     

Vascular endothelial dysfunction in diabetic cardiomyopathy: pathogenesis and potential treatment targets

Cardiovascular complications account for significant morbidity and mortality in the diabetic population. Diabetic cardiomyopathy, a prominent cardiovascular complication, has been recognized as a microvascular disease that may lead to heart failure. Pathogenesis of diabetic cardiomyopathy involves vascular endothelial cell dysfunction, as well as myocyte necrosis. Clinical trials have identified hyperglycemia as the key determinant in the development of chronic diabetic complications. Sustained hyperglycemia induces several biochemical changes including increased non-enzymatic glycation, sorbitol-myoinositol-mediated changes, redox potential alterations, and protein kinase C (PKC) activation, all of which have been implicated in diabetic cardiomyopathy. Other contributing metabolic abnormalities may include defective glucose transport, increased myocyte fatty acid uptake, and dysmetabolism. These biochemical changes manifest as hemodynamic alterations and structural changes that include capillary basement membrane (BM) thickening, interstitial fibrosis, and myocyte hypertrophy and necrosis. Diabetes-mediated biochemical anomalies show cross-interaction and complex interplay culminating in the activation of several intracellular signaling molecules. Studies in both animal and human diabetes have shown alteration of several factors including vasoactive molecules that may be instrumental in mediating structural and functional deficits at both the early and the late stages of the disease. In this review, we will highlight some of the important vascular changes leading to diabetic cardiomyopathy and discuss the emerging potential therapeutic interventions.     

Epidemiology of heart failure in sub-Saharan Africa

Heart failure has emerged as a dominant form of cardiovascular disease in Africa, and has great social and economic relevance owing to its high prevalence, mortality and impact on young, economically active individuals. The causes of heart failure in Africans remain largely nonischemic. Hypertension, cardiomyopathy, rheumatic heart disease, chronic lung disease and pericardial disease are the main contributors to the etiology of cardiac failure in sub-Saharan Africa, accounting for over 90% of cases. Hypertensive heart disease complications occur more frequently in Africans and the majority of affected patients are younger. Endemic cardiomyopathies include dilated cardiomyopathy, peripartum cardiomyopathy and endomyocardial fibrosis. Nonendemic cardiomyopathies apparently occur with the same frequency as in other parts of the world, and include hypertrophic cardiomyopathy and arrhythmogenic right ventricular dysplasia/cardiomyopathy. Coronary artery disease and its complications remain uncommon in Africa, but the situation is changing due to modifications in lifestyle, risk-prone behavior, diet, cultural attitudes and other consequences of rapid urbanization. As the prevalence of heart failure is expected to rise substantially in sub-Saharan Africa, the authors call for population-based studies and registries of the epidemiology of heart failure in Africans and the urgent study of interventions that will decrease morbidity and mortality from the causes of heart failure, with a focus both on nonischemic and ischemic risk factors.     

ALDH2 in alcoholic heart diseases: molecular mechanism and clinical implications

Alcoholic cardiomyopathy is manifested as cardiac hypertrophy, disrupted contractile function and myofibrillary architecture. An ample amount of clinical and experimental evidence has depicted a pivotal role for alcohol metabolism especially the main alcohol metabolic product acetaldehyde, in the pathogenesis of this myopathic state. Findings from our group and others have revealed that the mitochondrial isoform of aldehyde dehydrogenase (ALDH2), which metabolizes acetaldehyde, governs the detoxification of acetaldehyde formed following alcohol consumption and the ultimate elimination of alcohol from the body. The ALDH2 enzymatic cascade may evolve as a unique detoxification mechanism for environmental alcohols and aldehydes to alleviate the undesired cardiac anomalies in ischemia-reperfusion and alcoholism. Polymorphic variants of the ALDH2 gene encode enzymes with altered pharmacokinetic properties and a significantly higher prevalence of cardiovascular diseases associated with alcoholism. The pathophysiological effects of ALDH2 polymorphism may be mediated by accumulation of acetaldehyde and other reactive aldehydes. Inheritance of the inactive ALDH2*2 gene product is associated with a decreased risk of alcoholism but an increased risk of alcoholic complications. This association is influenced by gene-environment interactions such as those associated with religion and national origin. The purpose of this review is to recapitulate the pathogenesis of alcoholic cardiomyopathy with a special focus on ALDH2 enzymatic metabolism. It will be important to dissect the links between ALDH2 polymorphism and prevalence of alcoholic cardiomyopathy, in order to determine the mechanisms underlying such associations. The therapeutic value of ALDH2 as both target and tool in the management of alcoholic tissue damage will be discussed.     

Increased concentrations of a transferrin variant after alcohol abuse

Isoelectric focusing in agarose gel has been used for separation of different molecular forms of transferrin (Tf) in sera and plasma from alcoholics and controls. One special form of transferrin with isoelectric point 5.7 (= Tf5.7) was quantified by using zone immunoelectrophoresis assay (ZIA). This method was also used for quantification of total transferrin (Tftot). Significant differences in the ratio Tf5.7/Tftot between the groups were obtained and the diagnostic sensitivities, specificities and predictive values of positive tests were 100, 97, 93.8%, respectively. Thus the results showed that this principle seems to be much better for detection of alcoholic abuse than currently used assays as gamma-glutamyltransferase, etc. Samples taken on days following hospitalization showed that the Tf5.7 values decreased over a two-week period of abstinence. Possible explanations for the abnormal quotient after ethanol abuse are discussed.     

Focal fatty liver lesions in alcoholic liver disease: A broadened spectrum of CT appearances

The CT examinations of 26 consecutive alcoholic patients with focal fatty infiltration of the liver were analyzed. Five different patterns of focal fatty infiltration were noted. In most alcoholic patients these appearances present no diagnostic problem and further confirmation can be obtained by repeating the CT scan within 1–2 weeks to see if interval resolution occurs following enforced abstinence. In select instances, more invasive and definitive procedures such as superselective angiography or liver biopsy may be necessary to differentiate these findings from other more serious diseases they may closely resemble, such as primary or secondary liver neoplasms.     

Arrhythmogenic right ventricular cardiomyopathy in a patient with schizophrenia

People with schizophrenia are at greater risk of cardiovascular morbidity and mortality than the general population. Arrhythmogenic right ventricular cardiomyopathy is a recognized cause of sudden cardiac death in young people. This report discusses the necessity for close cardiac evaluation to reduce incidence of sudden death in people with schizophrenia.     

The effects of alcohol on blood pressure and electrolytes

The interaction between alcohol abuse, changes in blood pressure, and electrolyte abnormalities is complex. Some effects of alcohol are seen only with acute ingestion, some during withdrawal, and some only in chronic drinkers. Careful attention to the interactions between the metabolism of various electrolytes can prevent unnecessary morbidity and mortality in alcoholic patients.