ISSN:0954-6820    

DOI:10.1046/j.1365-2796.1996.381742000.x

出版商:Blackwell Science Ltd    

年代:1996

数据来源: WILEY

摘要:

Kemp E (Department of Nephrology, Odense University Hospital, Odense, Denmark). Xenotransplantation (Review).J Intern Med1996;239: 287–97.Xenotransplantation means transplantation of organs and tissues from animals to human beings. Today, with use of new and more conventional immunosuppressive substances, it is possible to achieve good long‐term survival of organs and cells transplanted between closely related species; for example, between baboon and man. However, large‐scale treatment by xenotransplantation is still not possible because a transplantation between species such as pig and man will still not be successful. Nevertheless, many researchers have tried to solve these problems, and it is hoped that transgenic animals in combination with newer immunosuppressive treatment will make xenotransplantation a realistic possibility. The time horizon for clinically successful xenotransplantation with pig organs is unknown at the moment. Nevertheless, many investigators think that the breakthrough will occur in a few years

ISSN:0954-6820    

DOI:10.1046/j.1365-2796.1996.380747000.x

出版商:Blackwell Science Ltd    

年代:1996

数据来源: WILEY

摘要:

Johnell O (Department of Orthopaedics, Malmö University Hospital, Malmö, Sweden). Advances in osteoporosis: better identification of risk factors can reduce morbidity and mortality (Review).J Intern Med1996;239:299–304.Osteoporosis is a common disease of postmenopausal women and the elderly. Low bone mass results from genetic, nutritional and lifestyle factors, decreased oestrogen levels, certain medical conditions, and the use of certain drugs. The overall incidence and age‐and sex‐related incidences of osteoporosis are increasing worldwide. Osteoporotic fractures can cause considerable pain, disability, loss of independence and deterioration in quality of life. Many patients lose the ability to perform the activities of daily living. Mortality and morbidity after hip fracture increase with age. Prevention of osteoporosis and osteoporotic fractures is an urgent priority to reduce the burden placed on health care and social welfare

ISSN:0954-6820    

DOI:10.1046/j.1365-2796.1996.429781000.x

出版商:Blackwell Science Ltd    

年代:1996

数据来源: WILEY

摘要:

Swedberg Ket al. (Department of Medicine, Östra University Hospital, Göteborg, Sweden). Heart failure – from pathophysiology to therapy (Minisymposium).J Intern Med1996;239: 305–43.Population studies, together with data from clinical records, reveal a range of estimated heart failure prevalence of 1–10%. Estimated incidence rates vary around 1% per annum. In community studies, the five‐year mortality is between 50–60%, while in patients requiring hospital admission, the annual mortality is 10–20% in those with mild–moderate symptoms and as high as 40–60% in severe heart failure.Many definitions of heart failure have been formulated. Making a diagnosis is a complex process. Heart failure is not a diagnosis or even one syndrome, but is a cluster of syndromes. The diagnosis is therefore only part of the assessment process. Essential parts for the diagnosis include symptomatology, objective evidence of important cardiac dysfunction and evaluation of the response to therapy. The cardinal symptom is exertional breathlessness. At present, echocardiography remains the most useful tool for confirming cardiac dysfunction, but determination of atrial natriuretic peptide or magnetic resonance imaging may supersede it. Heart failure has been viewed primarily as an oedematous disorder, in which fluid retention occurs because the heart cannot pump adequate quantities of blood to the kidneys. This model led to the utilization of diuretics for heart failure, but it failed to recognize that heart failure is a chronic progressive disorder that impairs both the quality and quantity of life, even when oedema is adequately controlled.A new model has been developed in which the development and progression of heart failure is viewed as resulting from the interplay of haemodynamic and neurohormonal mechanisms. Both mechanisms support the inotropic state of the heart following an injury to the myocardium, but when sustained for long periods, these mechanisms act to enhance ventricular wall stress, and, thereby, impair ventricular performance. As the heart failure evolves, endogenous mechanisms that are normally activated to control wall stress become exhausted, and peripheral vasoconstriction and sodium retention develop. Unopposed activation of haemodynamic stresses and neurohormonal systems leads to further destruction of myocardium and progression of the underlying disease. The acceptance of this haemodynamic–neurohormonal model has led to the development of vasodilators and neurohormonal antagonists which have been shown to be useful alone  – or added to diuretics – in the treatment of heart failure.Non‐pharmacological therapy includes counselling of life style and, for patients with moderate heart failure, light exercise. Within the last decade, pharmacological therapy was improved considerably. Asymptomatic patients with left ventricular dysfunction benefit from acetylsalicylic acid (ASA) and beta‐blockers. In patients with progressive dilatation of the left ventricle and with an established left ventricular dysfunction treatment with angiotensin‐converting enzyme (ACE) inhibitors has beneficial effects on mortality and morbidity.In symptomatic patients and those with clear systolic left ventricular dysfunction in addition to digitalis and diuretics, ACE inhibitors are clearly indicated in addition to ASA. Beta‐blockers may be added but the true benefit is not established. The initiation of both ACE inhibitors and beta‐blockers should be careful and the dose titrated slowly. Antiarrhythmic class I agents should be avoided unless clear indications are present, e.g. life‐threatening arrhythmias. Amiodarone might be considered as an alternative.The prognosis for patients with heart failure remains serious and the search for e

ISSN:0954-6820    

DOI:10.1046/j.1365-2796.1996.458459794000.x

出版商:Blackwell Science Ltd    

年代:1996

数据来源: WILEY

ISSN:0954-6820    

DOI:10.1046/j.1365-2796.1996.460795000.x

出版商:Blackwell Science Ltd    

年代:1996

数据来源: WILEY

摘要:

Dargie HJ, McMurray JJV, McDonagh TA (Department of Cardiology, Western Infirmary, Glasgow, and Department of Cardiology, Western General Hospital, Edinburgh, UK). Heart failure –  implications of the true size of the problem (Minisymposium: Heart failure).J Intern Med 1996;239:309–15.We review current knowledge on the true size of the clinical condition known as ‘heart failure’ in terms of epidemiological information and in relation to the true clinical burden.Population studies, together with data from physician and general practitioner records, reveal a range of estimated heart‐failure prevalence of 1–10%. Estimated incidence rates vary from approximately 0–1% per annum. Reasons for variation include age, sex and, possibly, methodology.In community studies, the five‐year mortality is between 50–60% while, in patients requiring hospital admission, the annual mortality is 10–20% in those with mild–moderate symptoms, and as high as 40–60% in severe heart failure.While angiotensin‐converting enzyme (ACE) inhibitor treatment does significantly improve mortality in all grades of symptomatic heart failure, the annual mortality in severe patients was still 36% in CONSENSUS I.It is obvious that the term ‘heart failure’ is insufficiently descriptive or specific to be an acceptable label for all patients who might benefit from treatment.As ‘clinical’ heart failure is often an advanced and irreversible state, studies of its antecedents are important in developing strategies aimed at retarding the progression from the asymptomatic to the symptomatic conditions. The true prevalence of the most common antecedent, left ventricular dysfunction, has re

ISSN:0954-6820    

DOI:10.1046/j.1365-2796.1996.461800000.x

出版商:Blackwell Science Ltd    

年代:1996

数据来源: WILEY

摘要:

Cleland J, Habib F (Medical Research Council (UK) Clinical Research Initiative in Heart Failure, West Medical Building, University of Glasgow, Glasgow, and Royal Post‐Graduate Medical School, Hammersmith Hospital, London, UK). Assessment and diagnosis of heart failure (Minisymposium: Heart failure).J Intern Med 1996;239:317–25.Diagnosis is the first essential step in the provision of good management of heart failure. Diagnosis of heart failure by clinical means alone may be fairly accurate in advanced heart failure but will only be correct in about 50% of milder cases; little better than guessing. The number of patients with mild heart failure in whom the diagnosis is not even considered is unknown. In at risk groups, such as those who have had a myocardial infarction, symptoms alert the clinician to a possible diagnosis of heart failure which must be confirmed by further investigation. The echocardiogram is the single most useful diagnostic tool for heart failure in widespread use at the present.Once it is established that the patient has heart failure, its cause must be sought out. As the majority of patients with heart failure are elderly, concomitant diseases may complicate management and should be sought out. European Society Guidelines on the Diagnosis of Heart Failure have been published and provide a minimum data set of investigations that should be carried out in all patie

ISSN:0954-6820    

DOI:10.1046/j.1365-2796.1996.462801000.x

出版商:Blackwell Science Ltd    

年代:1996

数据来源: WILEY

摘要:

Packer, M (Division of Circulatory Physiology, Columbia University, College of Physicians and Surgeons, New York, USA). New concepts in the pathophysiology of heart failure: beneficial and deleterious interaction of endogenous haemodynamic and neurohormonal mechanisms (Minisymposium: Heart failure).J Intern Med1996;239:327–33.During most of the last 50 years, physicians have viewed heart failure primarily as an oedematous disorder, in which fluid retention occurs because the heart cannot pump adequate quantities of blood to the kidneys. This conceptual model led to the successful utilization of diuretics for heart failure, but it failed to permit physicians to recognize that heart failure is a chronic progressive disorder that impairs both the quality and quantity of life, even when oedema is adequately controlled.To accommodate this new understanding, a new model has been developed, in which the development and progression of heart failure is viewed as resulting from the interplay of haemodynamic and neurohormonal mechanisms. Both mechanisms support the inotropic state of the heart following an injury to the myocardium, but when sustained for long periods, their ability to augment cardiac contractility wanes, and, instead, these same mechanisms act to enhance ventricular wall stress, thereby impairing ventricular performance. As the heart‐failure state evolves, endogenous mechanisms that are normally activated to control wall stress become exhausted, and peripheral vasoconstriction and sodium retention develop. Unopposed activation of haemodynamic stresses and neurohormonal systems leads to further destruction of the myocardium and progression of the underlying disease.The acceptance of this haemodynamic– neurohormonal model has led to the development of vasodilators and neurohormonal antagonists that have been shown to be useful alone, or when added to diuretics, in the treatment of heart fa

ISSN:0954-6820    

DOI:10.1046/j.1365-2796.1996.463796000.x

出版商:Blackwell Science Ltd    

年代:1996

数据来源: WILEY

摘要:

Kjekshus J, Swedberg K (Department of Medicine, The National Hospital, University of Oslo, Oslo, Norway, and Department of Medicine, Östra University Hospital, Göteborg University, Göteborg, Sweden). Treatment of heart failure (Minisymposium: Heart failure).J Intern Med1996;239:335–43.Effective treatment of heart failure depends on a correct functional and aetiological diagnosis. In asymptomatic patients with cardiac dysfunction following myocardial infarction, treatment is directed to prevent recurrent infarction by aggressive lipid lowering with statins and antiplatelet drugs. Beta blockers are important to reduce sudden death. In symptomatic heart failure, clinical improvement is obtained by inhibition of the renin–angiotensin and sympathetic system. Angiotensin‐converting‐enzyme inhibitors in combination with diuretics reduce morbidity and mortality caused by progression of the myocardial dysfunction and recurrent myocardial infarction. Drugs that activate the neurohormonal systems are clearly counteractive. Digitalis has a definite favourable effect on systems, and in patients with atrial fibrillation, but its effect on mortality is still unsettled. Beta blockers in routine treatment of symptomatic heart failure still remains controversial, but may benefit selecte

ISSN:0954-6820    

DOI:10.1046/j.1365-2796.1996.464797000.x

出版商:Blackwell Science Ltd    

年代:1996

数据来源: WILEY

摘要:

Objectives.To investigate the effects of smoking on blood pressure and proteinuria in hypertensive diabetic patients with nephropathy.Design.Controlled, randomized, cross‐over study.Setting.Tertiary care centre, University Hospital of Düsseldorf, Germany.Subjects.A total of 25 subjects were recruited, each of whom smoked at least 20 cigarettes a day: 10 normotensive healthy volunteers and 15 hypertensive type 1 (insulin‐dependent) diabetic outpatients with diabetic retinopathy and persistent micro‐ or macroalbuminuria; 10 diabetic patients had normal autonomic function test, whilst five patients showed signs of autonomic neuropathy.Interventions.Controlled smoking or nonsmoking over a period of 8 h on separate days.Main outcome measures.Blood pressure was measured every 10 min with an automatic device and urine samples were collected every 3 h.Results.Systolic blood pressure increased during smoking in controls (mean) (11.5 mmHg,P=0.0001) and in diabetic patients without autonomic neuropathy (7.9 mmHg;P=0.018), but not in patients with autonomic neuropathy (‐2.4 mmHg;P=0.792). Diastolic blood pressure increased during smoking in controls (6.2 mmHg;P=0.019) but not in diabetic patients (2.5 mmHg;P=0.204. 0.2 mmHg;P=0.956). During smoking, median proteinuria and albuminuria increased in diabetic patients without autonomic neuropathy (8.1 mg mmol‐1creatinine,P=0.002;and 2.6 mg mmol creatinine,P=0.084). No significant changes in albuminuria or proteinuria occurred in the other two groups.Conclusions.Smoking increases blood pressure values in healthy subjects and in hypertensive patients with diabetic nephropathy and without autonomic neuropathy. This effect of smoking may be partly responsible for the faster progression of diabetic nephropathy in smoking diabeti

ISSN:0954-6820    

DOI:10.1046/j.1365-2796.1996.468809000.x

出版商:Blackwell Science Ltd    

年代:1996

数据来源: WILEY