May 2010 Br J Cardiol 2010;17:103
Terry McCormack
If we consider gastro-oesopageal endoscopy as a similar procedure to transoesophageal echocardiography (TEE) then we might be alarmed at the 30-day mortality of 1:2,000 reported by Quine et al.1 I am not a practitioner of either of those arts, but I am putting on my anaesthetist cap to respond to the article by Mankia et al. discussing intravenous opiate/benzodiazepine sedation in this issue of the journal (see pages 125-7). The endoscopy death rate is especially concerning if you compare the fact that anaesthesia was considered to have been totally responsible for death in less than 1:10,000 operations in the UK.2 Mankia et al. quite rightly suggest that there should be guidelines concerning the safe use of intravenous sedation in TEE, and should be congratulated for highlighting this matter. I would suggest that their gastrointestinal endoscopy colleagues have a lot of experience on which to draw from.
May 2010 Br J Cardiol 2010;17:105-07
Andrew Nicolaides
Cardiovascular disease is the biggest killer in the UK causing 198,000 deaths per year, and stroke is the most common cause of disability in women. Can individuals at increased risk be identified and can heart attacks and strokes be prevented?
March 2010 Br J Cardiol 2010;17:55-6
David A Fitzmaurice
In this issue, Sandler’s paper (see pages 86–8) reinforces the growing body of evidence that should lead to the demise of the routine use of direct current cardioversion (DCCV) for patients with atrial fibrillation. This interesting paper highlights several issues surrounding DCCV within the context of a service re-design within a district general hospital. Despite a state-of-the-art service, the success of DCCV was limited, with sinus rhythm maintained in between the stated 20% (22/110) or even optimistically 40% (22/55) at around one year. I would suggest that this is unacceptable and that we would not allow any other procedure with significant associated morbidity to be undertaken with such a low chance of succeeding.
February 2010 Br J Cardiol 2010;17:8–10
Uazman Alam, Omar Asghar, Sohail Q Khan, Sajad Hayat, Rayaz A Malik
Cardiac auscultation is a critical part of the clinical examination. In antiquity physicians listened to heart sounds directly by placing their ear to the chest. In 1816 Laennec was asked to examine a young ‘corpulent’ woman in Paris, out of embarrassment he rolled a sheaf of paper into a cylinder to listen to her heart sounds, the stethoscope was invented. Initially, Laennec applied his invention to study cardiopulmonary diseases where he correlated bedside findings with autopsy results.(1
February 2010 Br J Cardiol 2010;17:11-12
Nigel J Artis, Tushar Raina, Chris P Gale
The atrioventricular (AV) conducting system of the mammalian heart was described a hundred years ago. Albert Hyman, a cardiologist working in New York City performed studies on the stopped heart. On injection of drugs into the right atrium, usually including adrenaline, the stopped heart continued beating.
November 2009 Br J Cardiol 2009;16:265–7
Khalill Ramjane, Lei Han, Chang Jing
Although patients with acute coronary syndrome (ACS) share key pathophysiological mechanisms, they present with diverse clinical, electrocardiographic and enzyme characteristics and experience a wide range of serious cardiovascular outcomes.
September 2009 Br J Cardiol 2009;16:211–12
Anitha Varghese, Jane Flint
Cardiac rehabilitation (CR) is the process by which patients with cardiac disease, in partnership with a multi-disciplinary team of health professionals, are encouraged and supported to achieve and maintain optimal physical and psychosocial health.”1 The fundamental interventions required for CR should provide the cornerstone of lifelong management in cardiovascular disease – for those who present with the numerous manifestations, those identified as being at increased risk, and, indeed, all of us.
July 2009 Br J Cardiol 2009;16:159–61
Christopher P Gale, Alex D Simms, Brian A Cattle, Phil D Batin, John S Birkhead, Darren S Greenwood, Alistair S Hall, Robert M West
The Myocardial Ischaemia National Audit Project (MINAP) represents one of the largest observational databases of acute coronary syndrome (ACS) events.1-3 Since its inception in 2000, it has accumulated rich data (including timing and method of admission, emergency and subsequent treatments, and long-term mortality data through linkage to the UK Statistics Authority) for over 650,000 ACS events from all acute hospitals (n=228) in England and Wales (figure 1). Initially designed to monitor standards set by the National Service Framework for Coronary Heart Disease4 with the generation of annual reports of hospital-level ST elevation myocardial infarction (STEMI) performance,5 the provision of contemporary online performance analyses has facilitated improvements in the care of ACS patients.6 Moreover, MINAP is more than a resource for the purposes of audit, it is also a key research tool for the evaluation of cardiovascular care and outcomes.7,8 Although it is primarily focused on clinical need, its research potential has been recognised by several grant-giving bodies, and a committee (the MINAP Academic Group [MAG]) dedicated to overseeing MINAP research has been established.3 The Clinical Performance Group (University of Leeds), a multi-disciplinary team comprising clinical cardiologists, health service researchers and health economists draws on MINAP data to investigate clinical care at multiple levels (patient, population, process and healthcare professional).
May 2009 Br J Cardiol 2009;16:113–15
Ian Kelt, Neal Uren
The British Society of Rheumatology have published guidelines on the management of rheumatoid arthritis, which call for an increased awareness of rheumatoid arthritis as an independent risk factor for ischaemic heart disease.(1) This increased cardiovascular risk is related to the severity and duration of inflammation, and the magnitude of additional cardiovascular risk in severe rheumatoid arthritis has been compared with that seen in diabetes mellitus.(1)
Life expectancy is reduced due to an excess of cardiovascular death, with increased standardised mortality ratios ranging from 1.28 to 3.00 in rheumatoid patients compared with the general population.(2) Women with rheumatoid arthritis are twice as likely to suffer from a myocardial infarction as those without.(2) There is also an increased risk of congestive cardiac failure,2 asymptomatic coronary heart disease and sudden cardiac death.(3)
May 2009 Br J Cardiol 2009;16:117–18
David Gray
“My interest is in the future because I am going to spend the rest of my life there.” – C F Kettering
Cardiovascular diseases are a massive public health problem in both the developed and developing world. UK statistics show, according to death certification, half a million people die annually, about 180,000 due to circulatory disease, 130,000 from neoplastic disease and 70,000 due to respiratory disease. With advancing age, the likelihood of dying from circulatory disease increases. So let’s face it, most of us are going to die from clogged blood vessels, most commonly some manifestation of coronary disease. Add in the millions who will live with symptoms of coronary disease and the numbers stack up even higher.
In 1948, the US public health service financed an epidemiological study on a previously unprecedented scale to investigate why millions of Americans were dying prematurely from heart disease. The result was the Framingham study, from which we have a pretty good idea of what increases our chances of developing coronary disease – smoking, cholesterol, blood pressure and diabetes – well recognised now but unknown until 40 years ago. In fact, Framingham introduced cardiovascular risk and cardiovascular risk factors into the medical vocabulary in a landmark paper in 1961.
A risk scoring system soon followed. Despite listing several important caveats, the Framingham risk score was widely adopted around the world, largely because of its novelty, simplicity and practicality. Some four decades later, there is mounting criticism of the Framingham risk score. First, because it does not predict cardiovascular risk ‘accurately’ enough – when applied to different populations, the score tends to overestimate risk in low-risk populations and underestimate risk in high-risk populations. Second, because it does not take into account other factors such as family history or socio-economic status.
New risk scoring systems have been proposed, each claiming to predict, with greater accuracy than Framingham, the risk of a future cardiovascular event, at least in the population in which each was developed. Will ‘better’ scoring systems help us manage our patients better?
“A good forecaster is not smarter than everyone else – he merely has his ignorance better organised.”
You need to be a member to print this page.
Find out more about our membership benefits
You need to be a member to download PDF's.
Find out more about our membership benefits