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Explaining the recent declines in coronary deaths in Australia and beyond
- Simon Capewell, Dr Julia Critchley & Dr Martin O' Flaherty (10 February 2009)
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Improving survival post myocardial infarction – does this translate to an increasing incidence of atrial fibrillation?
- Kok-Hoon Tay, Kok-Hoon Tay, Deirdre A Lane, and Gregory Y H Lip (19 February 2009)
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Simon Capewell, Chair of Clinical Epidemiology University of Liverpool, L69 3GB, Dr Julia Critchley & Dr Martin O' Flaherty
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We congratulate Tom Briffa and colleagues on their interesting analysis (BMJ 2009; 338: 341). We agree that secondary prevention medications (aspirin, betablockers, ACE inhibitors and statins) make a useful contribution to case fatality reduction in myocardial infarction survivors. Furthermore, exercise-based rehabilitation and smoking cessation are also important. [1,2] But what impact do these therapies have on the overall decrease in coronary heart disease deaths? Our cell based IMPACT model has been used to determine the contribution of treatments and risk factor reduction to mortality falls in diverse populations including the UK, European and Mediterranean countries, New Zealand and the USA [3-8]. This validated model suggests that 50%-75% of the falls in cardiac deaths can actually be attributed to population level improvements in the major cardiovascular risk factors (mainly smoking, cholesterol, and blood pressure), whilst the remaining 25 -50% of the mortality fall can be attributed to medical interventions. [3- 8] These findings are consistent with earlier MONICA studies which included Australasia.[2] Important contributions consistently come not only from secondary prevention medications, but also from the initial treatments for acute coronary syndrome and also for heart failure. Conversely, revascularisation for chronic disease makes a surprisingly small contribution.[3-13] Health care resources are becoming scarcer. Countries will therefore need to increasingly focus on the comparative effectiveness and cost- effectiveness of different interventions, particularly scrutinising the most expensive therapies.[9,13] With Best Wishes S Capewell
REFERENCES 1. Critchley, J. A. and Capewell, S. A Systematic Review of the Mortality Risk reduction When Patients With Coronary Heart Disease Stop Smoking. JAMA 2003-290; 86-97. 2. Kuulasmaa K, Tunstall-Pedoe H, Dobson A, Fortman S, Sans S. Estimation of contribution of changes in classic risk factors to trends in coronary event rates across the WHO MONICA Project populations. Lancet 2000; 355:675-87. 3. Laatikainen T, Critchley J, Vartiainen E, Salomaa V, Ketonen M, Capewell S. Explaining the decline in coronary heart disease mortality in Finland between 1982 and 1997. Am. J. Epidemiol. 2005; 162:764-73. 4. Ford ES, Ajani UA, Croft JB, Critchley JA, Labarthe DR, Kottke TE et al. Explaining the Decrease in US deaths from Coronary Disease, 1980 -2000. NEJM 2007; 356:2388-2398. http://dx.doi.org/10.1056/NEJMsa053935. (2 Feb 2009, date last accessed). 5. Unal B, Critchley J, Capewell S. Modelling the decline in CHD deaths in England and Wales, 1981-2000: comparing contributions from primary prevention and secondary prevention. BMJ 2005; 331:614-5. doi:10.1136/bmj.38561.633345.8F. 6. Palmieri L, Bennett K, Giampaoli S, Capewell S. Explaining the decrease in coronary heart disease mortality in Italy between 1980 and 2000. Am JPH 2009; in press 7. Lena Björck, Annika Rosengren, Kathleen Bennett , George Lappas , Simon Capewell. Modelling the Decreasing Coronary Heart Disease Mortality in Sweden between 1986 and 2002. Eur Heart J 2009 [in press -08-01753R1] 8. Capewell S, Beaglehole R, Seddon M, McMurray J J. Contribution of modern treatment to the decline in coronary heart disease mortality in Auckland, New Zealand between 1982 and 1993. Circulation 2000. 102; 1511-1516. 9. Unal B, Critchley J, Capewell S. Small changes in United Kingdom cardiovascular risk factors could halve coronary heart disease mortality. J Clin Epi 2005; 58:733-40. 10. Capewell S, Unal B, Critchley J, McMurray JJV. Over 20,000 avoidable coronary deaths in England and Wales in 2000: the failure to give effective treatments to many eligible patients. Heart 2006; 92:521- 523. 11. Capewell S, O'Flaherty M. Maximising secondary prevention therapies in patients with coronary heart disease. Heart 2008; 94(1):8-9. 12. Capewell S, O'Flaherty M, Ford ES, Critchley JA. Potential reductions in coronary heart disease mortality by treating more patients in the United States. Am J Cardiology 2009 [in press]. 13. Unal B, Critchley JA, Capewell S. Explaining the decline in coronary heart disease mortality in England and Wales between 1981 and 2000. Circulation 2004; 109(9);1101-7. Competing interests: None declared |
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Kok-Hoon Tay, Research Fellow University Department of Medicine, City Hospital, Dudley Road, Birmingham, B18 7QH, Kok-Hoon Tay, Deirdre A Lane, and Gregory Y H Lip
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We read with interest the paper by Briffa et al [1] who observe an improved survival following acute myocardial infarction (AMI). This may reflect the advances in how we manage patients with AMI including application of optimised medical treatments (antiplatelet therapy, ACE inhibitors, beta-blockers, thrombolytic therapy) and increased coronary artery revascularization. In addition, primary angioplasty is increasingly used in many centres, and such treatment is associated with improved outcomes, compared to acute treatment with thrombolysis [2]. Whilst Briffa et al [1] make important observations, the generalisability of the data should be considered, since their study population were generally younger [aged 35-64 years] which may not be truly representative of today’s general population susceptible of developing AMI, given the average age of a first AMI in men is 66 years and 70 years for women [3]. The fact remains that many patients are now surviving AMI with shorter hospital admissions, but with more survivors, this leaves increasing numbers of post-AMI subjects with damaged hearts and possibly, impaired left ventricular (LV) function. The latter is commonly associated with arrhythmias, such as atrial fibrillation (AF). AF is also the most commonly encountered cardiac arrhythmia that complicates AMI, with an incidence between 6% and 21% [4]. Such patients often have a worse outcome, with increased mortality, stroke and thromboembolism during the early phase post-AMI [4]. Heart failure and impaired LV function is also commonly associated with AF, and such patients also have a higher mortality and morbidity, particularly from stroke and thromboembolism [5]. On a broader scale, subjects aged >40 years have a 1 in 4 lifetime risk for developing AF and even in the absence of MI or congestive cardiac failure, the lifetime risk is still high – at 16% [6]. AF is increasing in incidence and Miyasaka et al [7] suggest that the number of persons with AF is projected to be 12.1 million by 2050, assuming there is no further increase in age-adjusted incidence of AF, but it could be as many as 15.9 million if the increase in incidence continues at the current rate. Given that the mean age of the general population is increasing, perhaps reflecting better medical treatments for conditions such as AMI (hence, improving survival – as suggested by Briffa et al[1]), we would propose that the improvement in MI survival over the last decade is likely to be an important contributor to the increased risk of developing AF. With our ageing population, this will undoubtedly impose an enormous economic burden as AF already costs 0.9%-2.4% of our National Health Service (NHS) UK and this figure could be rising [8]. Given that AF in association with previous MI is associated with an increased risk of stroke [9], the decline in AMI mortality may parallel the increase in AF, and possibly, an increase in stroke related to AF where previous AMI and/or impaired LV function is present. The importance of recognising AF in such post-AMI survivors is crucial. REFERENCES 1. Briffa T, Hickling S, Knuiman M, Hobbs M, Hung J, Sanfillippo FM, Jamrozik K, Thompson PL. Long term survival after evidence treatment of acute myocardial infarction and revascularisation: follow-up of population based PERTH MONICA cohort, 1984-2005. BMJ 2009;338:b36. 2. Keeley EC, Boura JA, Grines CL. Primary angioplasty versus intravenous thrombolytic therapy for acute myocardial infarction: a quantitative review of 23 randomised trials. Lancet. 2003;361:13-20. 3. American Heart Association. Heart Disease and Stroke Statistics—2005 Update. Dallas, Texas: American Heart Association, 2005. 4. Schmitt J, Duray G, Gersh BJ, Hohnloser SH. Atrial fibrillation in acute myocardial infarction: a systematic review of the incidence, clinical features and prognostic implications. Eur Heart J. 2008 Dec 24. [Epub ahead of print]. 5. Wolf PA, Abbott RD, Kannel WB. Atrial fibrillation as an independent risk factor for stroke: the Framingham study. Stroke 1991;22:983-988. 6. Lloyd-Jones DM, Wang TJ, Leip EP, Larson MG, Levy D, Vasan RS, D'Agostino RB, Massaro JM, Beiser A, Wolf PA, Benjamin EJ. Lifetime risk for development of atrial fibrillation: the Framingham Heart Study. Circulation 2004;110:1042-6. 7. Miyasaka Y, Barnes ME, Gersh BJ, Cha SS, Bailey KR, Abhayaratna WP, Seward JB, Tsang TSM. Secular trends in incidence of atrial fibrillation in Olmsted County, Minnesota, 1980 to 2000, and implications on the projections for future prevalence. Circulation 2006;114:119-125. 8. Stewart S, Murphy N, Walker A et al. Cost of an emerging epidemic; an economic analysis of atrial fibrillation in the UK. Heart 2004;90:286- 292. 9. Siu CW, Jim MH, Ho HH, Miu R, Lee SW, Lau CP, Tse HF. Transient atrial fibrillation complicating acute inferior myocardial infarction: implications for future risk of ischemic stroke. Chest. 2007;132:44-9. Competing interests: None declared |
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