Home-based versus hospital-based rehabilitation after myocardial infarction: A randomized trial with preference arms--Cornwall Heart Attack Rehabilitation Management Study (CHARMS).

BACKGROUND: Participation in cardiac rehabilitation after acute myocardial infarction is sub-optimal. Offering home-based rehabilitation may improve uptake. We report the first randomized study of cardiac rehabilitation to include patient preference. AIM: To compare the clinical effectiveness of a home-based rehabilitation with hospital-based rehabilitation after myocardial infarction and to determine whether patient choice affects clinical outcomes. DESIGN: Pragmatic randomized controlled trial with patient preference arms. SETTING: Rural South West England. METHODS: Patients admitted with uncomplicated myocardial infarction were offered hospital-based rehabilitation classes over 8-10 weeks or a self-help package of six weeks' duration (the Heart Manual) supported by a nurse. Primary outcomes at 9 months were mean depression and anxiety scores on the Hospital Anxiety Depression scale, quality of life after myocardial infarction (MacNew) score and serum total cholesterol. RESULTS: Of the 230 patients who agreed to participate, 104 (45%) consented to randomization and 126 (55%) chose their rehabilitation programme. Nine month follow-up data were available for 84/104 (81%) randomized and 100/126 (79%) preference patients. At follow-up no difference was seen in the change in mean depression scores between the randomized home and hospital-based groups (mean difference: 0; 95% confidence interval, -1.12 to 1.12) nor mean anxiety score (-0.07; -1.42 to 1.28), mean global MacNew score (0.14; -0.35 to 0.62) and mean total cholesterol levels (-0.18; -0.62 to 0.27). Neither were there any significant differences in outcomes between the preference groups. CONCLUSIONS: Home-based cardiac rehabilitation with the Heart Manual was as effective as hospital-based rehabilitation for patients after myocardial infarction. Choosing a rehabilitation programme did not significantly affect clinical outcomes.

Home-based cardiac rehabilitation versus hospital-based rehabilitation: a cost effectiveness analysis.

BACKGROUND: Home-based cardiac rehabilitation offers an alternative to traditional, hospital-based cardiac rehabilitation. AIM: To compare the cost effectiveness of home-based cardiac rehabilitation and hospital-based cardiac rehabilitation. METHODS: 104 patients with an uncomplicated acute myocardial infarction and without major comorbidity were randomized to receive home-based rehabilitation (n=60) i.e. nurse facilitated, self-help package of 6 weeks' duration (the Heart Manual) or hospital-based rehabilitation for 8-10 weeks (n=44). Complete economic data were available in 80 patients (48 who received home-based rehabilitation and 32 who received hospital-based rehabilitation). Healthcare costs, patient costs, and quality of life (EQ-5D4.13) were assessed over the 9 months of the study. RESULTS: The cost of running the home-based rehabilitation programme was slightly lower than that of the hospital-based programme (mean (95% confidence interval) difference - 30 pounds sterling (- 45 pounds sterling to - 12 pounds sterling) [-44 euro, -67 euro to -18 euro] per patient. The cost difference was largely the result of reduced personnel costs. Over the 9 months of the study, no significant difference was seen between the two groups in overall healthcare costs (78 pounds sterling, - 1102 pounds sterling to 1191 pounds sterling [-115 euro, -1631 euro to -1763 euro] per patient) or quality adjusted life-years (-0.06 (-0.15 to 0.02)). The lack of significant difference between home-based rehabilitation and hospital-based rehabilitation did not alter when different costs and different methods of analysis were used. CONCLUSIONS: The health gain and total healthcare costs of the present hospital-based and home-based cardiac rehabilitation programmes for patients after myocardial infarction appear to be similar. These initial results require affirmation by further economic evaluations of cardiac rehabilitation in different settings.

Dissecting aneurysm of the pulmonary artery in a case of unoperated patent ductus arteriosus.

A 54-year-old woman with unoperated patent ductus arteriosus developed fatal cardiac tamponade due to a dissecting aneurysm of the pulmonary artery causing haemopericardium. Histology of the pulmonary artery showed the presence of cystic medial necrosis. Previous reports of this condition are reviewed and the role of pulmonary hypertension causing secondary cystic medial necrosis is discussed.

Phaeochromocytoma and catecholamine induced cardiomyopathy presenting as heart failure.

Phaeochromocytoma is rare and usually presents as paroxysmal or sustained hypertension; none the less, it can also cause severe acute pulmonary oedema in normotensive individuals. Six patients with phaeochromocytoma presenting in Cornwall and West Devon between 1982 and 1986 are described. Five of them died of pulmonary oedema within 24 hours of the onset of symptoms. At necropsy all five had normal sized hearts and in the four hearts examined by histology there was evidence of catecholamine induced heart disease in the form of focal myocardial necrosis. The sixth patient presented with arterial spasms and pulmonary oedema. Surgical removal of the causative tumour was successful in this patient.

Problems in the investigation of an apparent outbreak of coagulase-negative staphylococcal septicaemia following cardiac surgery.

Two hundred and twenty-six hospital staff and patients were investigated for the carriage of gentamicin-resistant coagulase-negative staphylococci (CNS) during an apparent outbreak of infection after cardiac surgery. Of the four index strains from infected wounds, three were indistinguishable. The carriage of similar organisms was widespread, particularly among ITU staff (72%) and patients. Ninety-one of the 296 gentamicin-resistant isolates were further investigated, and of these 33 were indistinguishable from index strains even with the use of specialized techniques. Our experience indicates that in outbreaks of infection caused by gentamicin-resistant CNS, resources should be focused on the interruption of transmission and prevention of introduction of these organisms to susceptible patients.

HLA antigen associations in hypertrophic cardiomyopathy.

Histocompatibility antigen testing has been carried out in 20 unrelated normotensive English Caucasoids with hypertrophic cardiomyopathy and in 17 relatives, six of whom also had the disease. A strong association with the HLA-DRw6 antigen complex was found (P = 0.0036) but it was no longer significant after correction for the 52 antigens tested (P = 0.1701).

Left vocal cord paralysis and dysphagia in mitral valve disease.

Two cases of severe mitral stenosis with both hoarseness, caused by left vocal cord palsy, and dysphagia are described. This combination in the same patient has not, to our knowledge, been previously described. Previous studies have firmly established that vocal cord paralysis in mitral stenosis is a result of compression of the left recurrent laryngeal nerve as it passes around the aortic arch. It is suggested that dysphagia may also develop as a result of neurological damage, in this case to autonomic nerve plexuses supplying the oesophagus, leading to abnormal peristalsis and enabling external compression by a tense left atrium sufficient to cause symptoms

Determinants of high blood pressure in salt-deprived renal hypertensive rats: role of changes in plasma volume, extracellular fluid volume and plasma angiotensin II.

1. Rats with indwelling aortic and right atrial cannulae were maintained on a sodium-free diet before and after renal arterial constriction combined with contralateral nephrectomy. Control animals underwent the same protocol except that non-constricting clips were used. 2. Plasma volumes in the salt-deprived animals were lower than previously determined values in animals with free access to sodium. After clipping plasma volume increased in the hypertensive animals. Extracellular fluid volume was increased equally in both normotensive and hypertensive animals on the second postoperative day only. 3. Before clipping and contralateral nephrectomy plasma angiotensin II values were higher than normal. After the operation angiotensin II concentrations fell to normal over a period of 14 days without significant differences between experimental and control groups. 4. It is concluded that high blood pressure after clipping may be in part maintained by increases in plasma volume. However, the results strongly suggest that other renal mechanisms are likely to be of major pathogenic importance.

The role of the kidney in hypertension.

The role of the kidney in hypertension is reviewed in terms of sodium and water homeostasis, of the secretion of renin inappropriate to the state of sodium and water balance and of other renal humoral factors which might be implicated in the hypertensive process. Fundamental to the long-term maintenance of hypertension is an alteration in the relationship between renal perfusion pressure and the excretion of sodium and water. This alteration may be brought about as a result of renal structural damage, sympathetically mediated renal vasoconstriction or the action of renal or extrarenal hormones which modulate sodium and water excretion. When renin is secreted in excess of the prevailing level of sodium and water balance, the generated angiotensin contributes to the hypertension directly through peripheral and renal vasoconstriction. The level of blood pressure in two hypertensive patients with chronic renal failure was found to be highly correlated with the level of plasma renin activity as this was lowered by the administration of a beta-blocking drug. In rats deprived of sodium, renal artery constriction and contralateral nephrectomy was followed by hypertension without any elevation of plasma angiotensin and with a minimal expansion of plasma volume unaccompanied by expansion of extracellular fluid volume. The possible role of this small volume change and of other possible factors in producing hypertension is discussed. Studies in the nephrectomised rat confirmed eariler reports that renal medullayr auto-explants inhibited renoprival hypertension, but neither the identity nor mode of action of the medullary hypotensive factor were further clarified.