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Rapid Responses: Rapid Responses published:
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not powerful at all ..
- L Sam Lewis (18 September 2005)
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Prevention is Better than Cure
- Navneet Singh (19 September 2005)
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Cholesterol and blood pressure role in modelling questioned.
- Eddie Vos (21 September 2005)
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Realistic assumptions...
- Peter R Bates (21 September 2005)
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What about the economics?
- Adam Jacobs (23 September 2005)
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Re: not powerful at all ..
- Belgin Unal, Julia Critchley, Simon Capewell (24 September 2005)
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Re: Cholesterol and blood pressure role in modelling questioned.
- Belgin Unal, Julia Critchley, Simon Capewell (24 September 2005)
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L Sam Lewis, GP Surgery, Newport, Pembrokeshire, SA42 0TJ
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Belgin Unal et al. discover a self-evident truth using an unnecessarily complex model, and then use the words ‘more powerful’ to fundamentally mislead. Clearly if the whole population stopped smoking more lives would be saved than if we simply stopped IHD patients from smoking Reducing risk factors in the whole population rather than in a subset ( IHD cases) will obviously result in a greater absolute number of lives saved IF both groups were at the same individual risk … But the truth is that the same intervention ( eg: stopping smoking, lowering cholesterol ) will have the greatest absolute benefit in the individual at the highest risk ( assuming, as do Belgin Unal et al., that the relative Risk Reduction is the same across all at-risk categories - it may yet be the case that high-risk people have HIGHER relative risk reductions, such as from cholesterol-lowering ). Lives saved = number of people treated x individual risk reduction It is precisely because IHD patients are at highest risk that we are enjoined to target them first. This will produce the greatest absolute number of lives saved per person treated - my definition of ‘powerful’. If resources allow we should extend our efforts to ever more of the general population in the order of individual risk assessment. If we intend our efforts to be ‘powerful’ we would pay heed to the numbers needed to treat, and the costs per life saved – which this paper does not. Dr L S Lewis, MRCP Newport Surgery Pembrokeshire Competing interests: Cost vs. benefit |
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Navneet Singh, Locum SHO - General Medicine Various NHS Hospitals
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This study confirms the common proverbial saying "Prevention is better than Cure". The fact that when applied to general population, smaller reductions in various cardiovascular risk factors leads to significant reductions in overall mortality is well known. The reinforcement of this fact by this study should make the government to target the school going younger generation, for identifying and aggressively managing the common cardiovascular risk factors such as smoking, sedentary lifestyle and obesity. This would require more active involvement of the media, the school authorities and the parents in promoting awareness towards a healthier lifestyle for this generation. This would definitely improve the outcomes on a long-term basis. The effort should be on a scale comparable to the vaccination programmes for common preventable childhood infectious disorders. Competing interests: None declared |
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Eddie Vos, maintains health-heart.org Sutton (Qc) Canada J0E 2K0
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The modeling regarding 'deaths postponed'
from cardiovascular causes is incomplete since it does not consider total
mortality. The model basically looks at smoking (no argument there),
blood pressure lowering and cholesterol lowering by diet
and statins.
The fundamental unanswered question about blood pressure is: does artery hardening and decline cause an increase in blood pressure or, conversely, is blood pressure in fact causal to heart disease and the deaths it causes? There are to my knowledge no placebo controlled blood pressure lowering drug trials in women where a mortality benefit was found, for example the MRC trial (1) while there may be increased myocardial infarction in men from antihypertensives (2). The fundamental cause or effect question about cholesterol is similar and there are indeed no intervention data that prove that dietary cholesterol or saturated fat reduction has a mortality benefit in anyone (3). Regarding women, it is now absolutely clear that statins will not reduce all-cause mortality (4) as is the case in anyone over the age of 70, as per the PROSPER trial (5). The one conclusion in which the modelling supports the trial data is the inefficacy of statins, and where only 145 deaths were calculated to be postponed in England and Wales for each year of use in people without overt heart disease simply to lower their cholesterol. Therefore, the assumption of causality of the aforementioned parameters of the model should be questioned. Cholesterol and blood pressure simply may not be 'causal' and confounders that may be, like homocysteine, omega-3 fatty acid intake and others must be figured in for modelling to give reliable outcomes. vos{at}health-heart.org 1. No authors listed. MRC trial of treatment of mild hypertension: principal results. Medical Research Council Working Party. Br Med J (Clin Res Ed). 1985 Jul 13;291(6488):97-104. MEDLINE 2861880. 2. Merlo J, Ranstam J, Liedholm H, Hedblad B, Lindberg G, Lindblad U, et al. Incidence of myocardial infarction in elderly men being treated with antihypertensive drugs: population based cohort study. BMJ. 1996;313:457-61. MEDLINE 8776312. 3. Hooper L, Summerbell CD, Higgins JP, Thompson LR, Capps NE et al.
Dietary fat intake and prevention of cardiovascular disease: systematic
review. BMJ 2001;322:757-63. MEDLINE 11282859.
5. Shepherd J, Blauw GJ, Murphy MB, Bollen EL, Buckley BM, et al. Pravastatin in elderly individuals at risk of vascular disease (PROSPER): a randomised controlled trial. Lancet. 2002 360(9346):1623-30. MEDLINE 12457784. Competing interests: None declared |
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Peter R Bates, Consultant Physician Jersey General Hospital JE2 3PA
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Readers of this article might be bamboozled into thinking that pharmacological intervention to reduce cholesterol levels is ineffective at a population level. Digging into the assumptions of the IMPACT model shows that the low apparent impact of statins for primary prevention occurs because the model assumes a 3% uptake of statin treatment for primary prevention in the population for which such treatment is indicated. This figure is derived from a single study conducted in Nottingham general practices between 1996 and 1998. The study in question did not even differentiate statins prescribed for primary or secondary prevention. This study also showed rapidly changing statin usage (a four- fold increase in statin precribing within 2 years). Interpretation and extrapolation of this data to the whole of the UK in 2000 (or even 2003, as suggested in the discussion) must be tenuous at best. I suggest the authors may wish to question the realism of some of their own assumptions. Even using the authors' own (unspecified) assumptions regarding the numbers eligible for such treatment, increasing the uptake of statins for primary prevention to, say, 80% would increase the estimate of annual deaths prevented or postponed by statins used for primary prevention to 145*80/3=3867. This would provide a proven evidence-based intervention, in contrast to the exhortation given by the authors to focus on attempts to encourage healthier diets. Making different assumptions about statin prescribing would also quickly erode the number of prevented or postponed deaths the authors attribute to dietary changes, since these are calculated as the residual of prevented deaths after those attributable to statins have been estimated. For example, if statin uptake for primary prevention were 30%, the estimated deaths prevented by statins used for primary prevention would be 1450 per annum and by dietary change 4710-1450=3260, rather than the 145 and 4565 suggested in the paper. Competing interests: I have received research funding, educational and travel grants from pharmaceutical manufacturers of lipid-lowering drugs |
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Adam Jacobs, Director Dianthus Medical Limited, London SW19 3TZ
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I read with interest the paper by Unal et al, and I am more than happy to believe their conclusion that primary prevention can postpone more coronary heart disease deaths than secondary prevention. However, I am less convinced by their conclusion that 'Comprehensive CHD strategies should therefore focus on primary prevention'. In reaching that conclusion, they seem to have overlooked the economics of CHD prevention. Primary prevention may have a greater population effect than secondary prevention, but it also needs many more individuals to be targeted or treated, which comes at a greater cost. Thus although primary prevention may be more effective, Unal et al present no data to make us believe it is more cost effective, which must be taken into account if it is to be made a national priority. The cost effectiveness of some measures at the population level, such as tobacco control, may not be in doubt, but I hope that Unal et al's paper will not be seen by itself as a justification to prioritise primary prevention measures more generally. Competing interests: None declared |
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Belgin Unal, Associate proffesor The University of Dokuz Eylul, Izmir, Turkey, Julia Critchley, Simon Capewell
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A comprehensive strategy for coronary heart disease prevention should consider primary and secondary prevention in both individuals and populations. Our study emphasizes the importance of primary prevention in the population level. The model based on available trends data on risk factors and coronary heart disease deaths. Our findings support the fact that in populations with a relatively high incidence of coronary heart disease, such as England and Wales, targeting entire population would produce larger effects than focusing on high-risk populations1-3. References 1.Rose G. The Strategy of Preventive Medicine. Oxford: Oxford University Press, 1992. 2.Kottke TE, Gatewood LC, Wu SC, Park HA. Preventing heart disease: is treating the high risk sufficient? J.Clin.Epidemiol. 1988;41:1083-93. 3.Puska P, Tuomilehto J, Nissinen A, Vartiainen E. The North Karelia Project. 20 year results and experiences. Helsinki: The National Public Health Institute (KTL), Finland, 1995. Competing interests: None declared |
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Belgin Unal, Associate professor The University of Dokuz Eylul, Izmir, Turkey, Julia Critchley, Simon Capewell
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Regarding the causal relationship between blood pressure or cholesterol and coronary heart disease, ethically it may not be possible to carry out a placebo controlled randomized trial. However there is sufficient evidence from cohort studies1;2. Data availability and quality are the main issues for any modelling study3. Impact of many other minor risk factors including homocysteine and omega-3 fatty acid intake could be estimated only if there was a reliable trend data on them. References 1.Law M, Wald N, Morris J. Lowering blood pressure to prevent myocardial infarction and stroke: a new preventive strategy. Health Technol.Assess. 2003;7:1-94. 2.Law MR, Wald NJ, Thompson SG. By how much and how quickly does reduction in serum cholesterol concentration lower risk of ischaemic heart disease? BMJ 1994;308:367-72. 3.Unal B, Critchley J, Capewell S. Missing, mediocre, or merely obsolete? An evaluation of UK data sources for coronary heart disease. J Epidemiol Community Health 2003;57:530-5. Competing interests: None declared |
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