Showing papers by "Philip A. Poole-Wilson published in 2000"

Acute coronary findings at autopsy in heart failure patients with sudden death: results from the assessment of treatment with lisinopril and survival (ATLAS) trial.

Abstract: Background—Sudden unexpected death frequently occurs in chronic heart failure. The importance of acute coronary events in triggering sudden death (SD) is unclear. Methods and Results—We evaluated at autopsy the prevalence of acute coronary findings (coronary thrombus, ruptured plaque, or myocardial infarction [MI]) and their relation to SD. Autopsy results in 171 patients in the randomized ATLAS trial were reviewed. The prevalence of acute coronary findings was 33%: in 54% of patients with significant coronary artery disease (CAD) who died suddenly, 32% who died of myocardial failure, but in non-CAD patients, they were present in only 5% and 10% respectively. The percentage of patients classified as dying of MI was 28% in the autopsy group versus 4% in the nonautopsied group (P<0.0001). Of the autopsied group with acute MI, 97% (31 of 32 patients) with SD and 40% (6 of 15 patients) with myocardial failure did not have the MI diagnosed during life. When undiagnosed MI was classified as “sudden unexpected” ...

A Rapid Access Heart Failure Clinic provides a prompt diagnosis and appropriate management of new heart failure presenting in the community

Abstract: Background and aims The diagnosis of heart failure is an important clinical problem and yet reported diagnostic accuracy in primary care is less than 50%. We established a Rapid Access Heart Failure Clinic (RAHFC) in a district general hospital serving a population of 292000 in SE London, UK, to diagnose and manage new cases of heart failure presenting for the first time in the community. Methods Patients with suspected new onset heart failure were referred by their Primary Care Physician without appointment for clinical assessment on the same or next working day. Assessment by a specialist registrar in cardiology included history, examination, chest X-ray, electrocardiogram (ECG) and echocardiogram. When a diagnosis of heart failure was made appropriate treatment, including angiotensin converting enzyme inhibitors (ACEI), was started. Results Over 15 months 383 patients were seen (0.4 cases/100000 population/weekday) 178/383 (46%) were considered to have definite or possible heart failure at the initial assessment in the RAHFC. A normal ECG (negative predictive value 94%) and chest X-ray virtually excluded the diagnosis of heart failure. After subsequent specialist investigations and follow-up, including a trial of therapy where appropriate, 101/383 (26%) were finally diagnosed as clinical heart failure. ACEI therapy was commenced in 56/57 (98%) of patients in whom it was considered appropriate. Conclusion The RAHFC provided rapid assessment, prompt diagnosis and early introduction of life prolonging therapy for patients presenting with suspected heart failure in the community.

Low doses vs. high doses of the angiotensin converting-enzyme inhibitor lisinopril in chronic heart failure: a cost-effectiveness analysis based on the Assessment of Treatment with Lisinopril and Survival (ATLAS) study

Abstract: Objective A cost-effectiveness analysis of high and low doses of the angiotensin-converting enzyme (ACE) inhibitor lisinopril in the treatment of chronic heart failure. Methods A cost-effectiveness analysis using data from a randomized controlled trial, ATLAS, where 3164 patients with chronic heart failure were allocated to a high-dose (daily target dose 32.5–35 mg) or low-dose strategy (daily target dose 2.5–5.0 mg) of lisinopril. Differential costs were based on resource use data collected in the trial costed using UK unit costs. Cost-effectiveness analysis related differential costs to differential life-years during a 4-year trial follow-up. Results The mean total number of hospital in-patient days per patient was 18.5 in the high dose group and 22.5 in the low dose group. Over the whole duration of the trial, the mean (S.D.) daily dose of lisinopril in the high-dose group was 22.5 mg (15.7mg) compared to 3.2 mg (2.5 mg) in the low-dose group. The mean difference in cost per patient was £397 lower in the high-dose group [95% CI (high-dose–low-dose) −£1263 to £436]. Mean life-years per patient were 0.085 years higher in the high-dose group [95% CI (high-dose–low-dose) −0.0074 to 0.1706). Based on mean costs and life-years, high-dose therapy dominates low-dose (less costly and more effective). Allowing for uncertainty in mean costs and life-years, the probability of high-dose therapy being less costly than low dose was 82%. If a decision maker is willing to pay at least £3600 per life-year gained, the probability of high-dose being more cost-effective was 92%. Conclusions The ATLAS Study showed that the treatment of heart failure with high-doses of lisinopril has a high probability of being more cost-effective than low-dose therapy.

Commentary on "Effects of ischaemia and reperfusion on calcium exchange and mechanical function in isolated rabbit myocardium".

Abstract: Rereading and commenting upon an article written 18 years ago is almost to intrude on the prerogatives of history. Wallowing in nostalgia may be a satisfying activity but is not a plausible method for identifying, posing or answering scientific questions. I reread this paper with trepidation but was relieved, perhaps the correct sentiment, to find that it still addressed an important issue. More surprising was the realisation of how limited has been the progress made over the last two decades. In 1974, as a young research worker, I was fortunate to work in the laboratories of Glen Langer in Los Angeles, supported by the British Heart Foundation. Previously in London I had been investigating the net change in potassium homeostasis in cardiac and skeletal muscle, in vivo, in response to alterations of acid–base balance. Glen Langer had developed a technique which allowed the measurement not just of tissue content of an ion but of ion fluxes. The technique allowed examination of the effect of acid–base changes on potassium fluxes so as to explain the previously observed net changes [1]. Later this same technique was adapted to measure the flux of calcium isotopes (45Ca2+ and 47Ca2+) into and out of the myocardium [2]. Bourdillon developed the system further so that measurements could be made during and after a period of ischaemia. That formed the basis of the paper published in Cardiovascular Research [3]. The technique used was the arterially perfused intraventricular septum of the rabbit heart. A small cannula is inserted into the first septal artery which in the rabbit comes off shortly after the origin of the left anterior descending coronary artery. Non perfused tissue is cut away so that a small triangular of piece of myocardium …