Objective-To evaluate whether nurse run clinics in general practice improve secondary prevention in patients with coronary heart disease. 1.47, 1.10 to 1.96). There was no eVect on smoking cessation (0.78, 0.47 to 1.28). Of six possible components of secondary prevention, the baseline mean was 3.27. The adjusted mean improvement attributable to intervention was 0.55 of a component (0.44 to 0.67). Improvement was found regardless of practice baseline performance. Conclusions-Nurse run clinics proved practical to implement in general practice and eVectively increased secondary prevention in coronary heart disease. Most patients gained at least one eVective component of secondary prevention and, for them, future cardiovascular events and mortality could be reduced by up to a third.

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Objective: To determine secondary preventive treatment and habits among patients with coronary heart disease in general practice. Design: Process of care data on a random sample of patients were collected from medical records. Health and lifestyle data were collected by postal questionnaire (response rate 71%). Setting: Stratified, random sample of general practices in Grampian.

Within their first year secondary prevention clinics improved patients' health and reduced hospital admissions.

Study objective -Seasonality of coronary heart disease (CHD) was examined to determine whether fatal and non-fatal disease have the same annual rhythm. Design -Time series analysis was carried out on retrospective data over a 10 year period and analysed by age groups (<45 to >75 years) and gender. (under 45 years) admitted to hospital there was a dominant spring peak and an autumn trough. A bimodal pattern of spring and winter peaks was evident for hospital admissions in older male age groups: with increasing age the spring peak diminished and the winter peak increased. In contrast, female hospital admissions showed a dominant winter/summer pattern of seasonal variation. In male and female CHD deaths seasonal variation showed a dominant pattern of winter peaks and summer troughs, with the winter peak spreading into spring in the two youngest male age groups. CHD incidence in women showed a winter/summer rhythm, but in men the spring peak was dominant up to the age of 55. Conclusions -The male, age related spring peak in CHD hospital admissions suggests there is an androgenic risk factor for myocardial infarction operating through an unknown effector mechanism. As age advances and reproduction becomes less important, the well defined winter/summer pattern of seasonal variation in CHD is superimposed, and shows a close relationship with the environment, especially temperature, or the autumn and early winter fall in temperature. (J Epidemiol Community Health 1995;49:575-582) Studies of seasonal variation in coronary heart disease (CHD) are almost entirely based on data derived from national registers of deaths. Studies based on seasonal variation of CHD hospital admissions are few. Dunnigan et all found a bimodal pattern of seasonal variation with spring and winter peaks in a study of 47 281 admissions to all Scottish hospitals in 1962-66 in the diagnostic category ICD 420

Reduction of a rapid ventricular rate in atrial fibrillation results in a longer diastolic filling period and a higher left ventricular stroke volume but this is offset by reduced contractility and fewer beats per minute; the net effect on cardiac output is uncertain. Sequences of stroke distances were measured by Doppler ultrasound in 60 resting patients with atrial fibrillation to determine the relation between ventricular rate and linear cardiac output. The slope of the cardiac output/ventricular rate relation was positive in all 20 patients with a ventricular rate less than 90 beats per minute and negative in 16 (40%) of 40 patients with a ventricular rate greater than 90 beats per minute. In atrial fibrillation the ventricular rate can be regarded as "controlled" when the cardiac output/ventricular rate slope is positive and "uncontrolled" when the slope is negative--that is when reduction of ventricular rate would lead to increased cardiac output. As so defined, ventricular rate at rest was controlled in every patient when the ventricular rate was less than 90, controlled in 44 (73%) patients when the ventricular rate was 90-140 beats per minute, and uncontrolled in every case when it was greater than 140 beats per minute. Achieving a target ventricular rate of 90 beats per minute in patients with atrial fibrillation at rest would result in control with the least compromise of cardiac output.

IMPORTANCE YARS2 mutations have been associated with a clinical triad of myopathy, lactic acidosis, and sideroblastic anemia in predominantly Middle Eastern populations. However, the identification of new patients expands the clinical and molecular spectrum of mitochondrial disorders. OBJECTIVES To review the clinical, molecular, and genetic features of YARS2-related mitochondrial disease and to demonstrate a new Scottish founder variant. DESIGN, SETTING, AND PARTICIPANTS An observational case series study was conducted at a national diagnostic center for mitochondrial disease in Newcastle upon Tyne, England, and review of cases published in the literature. Six adults in a well-defined mitochondrial disease cohort and 11 additional cases described in the literature were identified with YARS2 variants

Since autonomic tone affects the likelihood of the occurrence and perpetuation of atrial fibrillation, variation of the rate of occurrence of attacks would be expected in parallel with the known diurnal variation of autonomic activity.5 In this study we noted the times of day that episodes of atrial fibrillation occurred. We also compared the ventricular rates at the onset of paroxysms, and noted the number of prolonged paroxysms, in patients with and without digoxin therapy. Patients and methodsWe selected Holter recordings showing paroxysmal atrial fibrillation in 72 consecutive patients who were being investigated for clinical reasons. All patients were in sinus rhythm at the start and end of the recordings, which lasted for 48 hours. For the purposes of this study paroxysmal atrial fibrillation was defined as the occurrence of at least five beats of supraventricular origin, with a totally irregular ventricular response, with no visible P or flutter waves, the arrhythmia lasting less than 24 hours. Seventy two patients (32 men and 40 women; mean age 72 (range 34-93) had arrhythmias which fulfilled these criteria. Associated diagnoses were as follows: none 45, ischaemic heart disease 12, sinoatrial disease 11, valvar heart disease two, hypertension two. Thirty one patients were taking digoxin, 11 were taking a ,B adrenergic blocker (five with digoxin), and nine were taking a calcium channel blocker (three with digoxin). We calculated the serum concentration of digoxin from the serum creatinine concentration and the body weight, using a nomogram based on the pharmacokinetics of digoxin.6 The calculated serum digoxin concentration was 0 ,ug/l in 41, up to 1 jg/l in 11, and over 1 jug/l in 20 patients.The time of onset of each paroxysm was noted together with the ventricular rate, calculated from the first 5-10 beats of each paroxysm. In the case of prolonged bouts of atrial fibrillation lasting 30 minutes or more, the duration of the attack and the ventricular rate immediately before it ended were noted.