Recent eLetters
Displaying 1-10 letters out of 566 published
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Considering a possible application to prevent or to treat arterial stiffness
Submit responseI was impressed to read the results of Mulders et al. (1), who provided evidence that first-degree relatives of patients with premature coronary artery disease had increased arterial stiffness (measured by pulse-wave velocity) in the absence of coronary artery disease. The authors also found a relation between arterial stiffness and coronary artery calcification.
As a physician, I wonder about ways to prevent the development of coronary artery disease in these individuals who seem to have this disposition. I found it interesting that patients with premature coronary artery disease had elevated triglyceride levels at baseline measurements. These results match well with recent findings by De Caterina et al. (2) on the APOA5-1131T>C gene variant and its association with premature coronary artery disease. According to these results, the APOA5-1131C allele is not only associated with higher triglyceride levels, but also with the risk of premature coronary artery disease when adjusting for the influence of elevated triglyceride levels (2).
Another study that can be linked well to the results of Mulders et al. (1) is recent evidence on aortic relaxation (3), which is the opposite of arterial stiffness. It has just been shown experimentally by Liu et al. (3) that the use of fibrates causes aortic relaxation and goes along with decreased intracellular calcium levels in cultured vascular smooth muscle cells, suggesting an anti-atherosclerotic effect. Fibrates have also been known for their reduction in low density lipoprotein and triglyceride levels.
Combining the findings of Mulders et al. (1) with the results of the two recent studies (2)-(3) might have a clinical application in terms of preventing arterial stiffness and atherosclerosis in people with a disposition to develop coronary artery disease. In the future, it would probably be necessary to confirm the link between the APOA5-1131C allele (and possible other alleles) and the emergence of atherosclerosis in carriers of the alleles, and to transfer the experimental evidence on aortic relaxation (3) to clinical studies. Given that fibrate drugs can cause a number of adverse side reactions, I would still find it difficult to prescribe them to (healthy) individuals who seem to have a disposition to develop arterial stiffness, as it is not certain that they will actually develop coronary artery disease. In addition, the APOA5-1131C allele also increased the risk of coronary artery disease independent of triglyceride levels (2), so factors other than elevated triglyceride levels also seem to play a role. In any case, more research is needed to offer individuals at risk a good estimate what they can do to prevent coronary artery disease.
1. Mulders TA, van den Bogaard B, Bakker A et al. Arterial stiffness is increased in families with premature coronary artery disease. Heart 2012;98:490-4.
2. De Caterina R, Talmud PJ, Merlini PA, et al. Strong association of the APOA5-1131T>C gene variant and early-onset acute myocardial infarction. Atherosclerosis 2011;214:397-403.
3. Liu A, Yang J, Huang X, et al. Relaxation of rat thoracic aorta by fibrate drugs correlates with their potency to disturb intracellular calcium of VSMCs. Vascul Pharmacol 2012; Epub ahead of print Jan 21.
Conflict of Interest:
None declared
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Re: Quantitative myocardial perfusion analysis using multi-row detector CT in acute myocardial infarction
Submit responseDear Editors:
We are writing in regards to the paper entitled "Quantitative myocardial perfusion analysis using multi-row detector CT in acute myocardial infarction" that is recently published in the April 2012 issue of Heart. We would like to congratulate the authors for a very interesting study that has used all the advanced techniques available in the GE Healthcare CT Perfusion research version software. We are the core laboratory that develop and validate the techniques in that version of the software and are very pleased that they are being used successfully in their work. Instead of references #13-16 in their paper, the correct references that detail our work implemented in the software are as follows:
1. So A et al. Beam hardening correction in CT myocardial perfusion measurement. Phys Med Biol 2009;54(10):3031-3050
2. So A et al. Quantitative myocardial perfusion measurement using CT Perfusion: a validation study in a porcine model of reperfused acute myocardial infarction. Int J Cardiovasc Imaging. Epub 2011 Jul 29
3. So A et al. Non-invasive assessment of functionally relevant coronary artery stenoses with quantitative CT perfusion: preliminary clinical experiences. Eur Radiol 2012;22(10):39-50 Epub 2011 Sep 21
In particular, the beam hardening correction method in the CT Perfusion research version software is based on our work previously published in 2009 (see #1 above) rather than the work of Kitagawa et al as referenced in the paper.
We hope this clarification would prevent confusion in the mind of readers who read the paper and are stimulated to pursue quantitative myocardial perfusion research.
Best regards,
Aaron So, PhD, Associated Scientist, Lawson Health Research Institute, London, Ontario, Canada
Ting-Yim Lee, PhD, FCCPM, CIHR-GE Healthcare Chair in Functional Imaging; Director, PET/CT Research, Lawson Health Research Institute; Scientist, Robarts Research Institute; Professor, Medical Biophysics, Oncology, Medical Imaging, Western University, London, Ontario, Canada
Conflict of Interest:
T.-Y. Lee has a CT Perfusion software licensing agreement with GE Healthcare, and receives research grant support from GE Healthcare, Astra Zeneca and Celgene. A. So has no disclosure.
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Industry-sponsored cost-effectiveness study of TAVI
Submit responseThe potential cost-effectiveness (CE) of adopting innovative procedures within a publically funded healthcare system is a recurring issue.[1] Trans-catheter aortic valve insertion (TAVI) is not currently provided by the devolved National Health Service (NHS) in Scotland, although a single high quality randomised controlled clinical trial (RCT) has demonstrated that TAVI is a clinically effective intervention for reducing the risk of death in older patients with severe aortic stenosis considered unfit for standard surgery.[2] The recently published CE analysis of TAVI reports an incremental CE ratio (ICER) of 16,000 [pounds sterling] per quality adjusted life year (QALY) gained, which falls below the ICER thresholds applied by the National Institute for Health and Clinical Excellence (NICE) in the UK.[1]
The science-consultancy company 'Oxford Outcomes' constructed their CE model based on New York Heart Association (NYHA) category data obtained in the original RCT.[2] This involved adopting a rather convoluted approach of indirectly estimating EQ-5D (EuroQol) values ('utilities') based on data concerning the relationship between NHYA categories and EQ- 5D in patients with heart failure, and on UK population norms that are now almost 20 years old.[1] Given that individual patients in the original RCT had their EQ-5D values measured directly (at baseline, one, six and 12 months) it is not clear why 'Medtronic' (the TAVI-device manufacturer who funded both the original RCT and the CE analysis) did not release the ED- 5D data to 'Oxford Outcomes'. Other important clinical values are derived from a 'literature review' and estimates made by a 'clinical steering group'. Unfortunately making an informed judgement about the validity of these values is difficult as the literature search strategy is not described and membership of the 'steering group' is not reported.
Historically the assessment of CE in the cardiovascular arena has predominantly related to drug therapies, but the approach is now increasingly being applied to cardiovascular devices.[3] Unfortunately CE studies, with their heavy reliance on statistical modelling based on multiple assumptions, have a poor track record of providing unbiased information for healthcare decision making. In a previous systematic review of almost 500 CE studies, industry-sponsored studies were 2-3 times more likely to report favourable results compared to non-industry funded analyses.[4] This may be because the biomedical industry regards the undertaking and reporting of CE analyses as a marketing tool, rather than as an independent scientific endeavour.[3] Consequently clinicians and policy-makers need to be both cautious and critical in assessing this type of study. In our opinion a further replication of these CE findings are required using the EQ-5D data from the original trial.
[1] Watt M, Mealing S, Eaton J, et al. Cost-effectiveness of transcatheter aortic valve replacement in patients ineligible for conventional aortic valve replacement. Heart 2012;98:370-6.
[2] Leon MB, Smith CR, Mack M, et al. PARTNER Trial Investigators. Transcatheter aortic-valve implantation for aortic stenosis in patients who cannot undergo surgery. N Engl J Med 2010;363:1597-607.
[3] Tarricone R, Drummond M. Challenges in the clinical and economic evaluation of medical devices: the case of transcatheter aortic valve implantation. J Med Marketing 2011;11:221-229.
[4] Bell CM, Urbach DR, Ray JG, Bayoumi A, Rosen AB, Greenberg D, Neumann PJ. Bias in published cost effectiveness studies: systematic review. BMJ 2006;332:699-703.
Conflict of Interest:
None declared
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A Comparison of ECG scores for Area at Risk
Submit responseVersteylen et al (1) recently evaluated several area at risk (AAR) methods in patients with acute ST elevation myocardial infarction (STEMI) using 4 physiologic principles, and concluded that cardiac magnetic resonance imaging (CMRI) methods out-perform angiographic methods, which are better than electrocardiographic (ECG) methods. However this study utilized the antiquated Aldrich score, rather than the updated ECG index, described by Wilkins et al (2).
The Aldrich score is based upon the extent of inferior ST elevation and total number of leads with ST elevation in anterior infarcts. Recent studies have shown that it is an unstable marker of AAR (3) and correlates poorly with SPECT imaging (4). The modified score by Wilkins et al (2), incorporates the number of leads with abnormal Q waves, ST elevation and/or peaked T waves in anterior infarcts, and the extent of excess Q wave duration and inferior ST elevation in inferior infarcts. Compared with the Aldrich score, this method produced better correlations with QRS- derived final infarct size (2).
To further evaluate the Wilkins method, we compared Aldrich and Wilkins AAR estimates in 47 acute STEMI patients who had undergone CMRI with delayed hyperenhancement, and observed the following, as regards conformity to the 4 physiologic principles proposed by these authors (1):
1. For the concept that AAR is always ? infarct size (IS), the Wilkins method conformed in 76% of patients, compared to 59% for the Aldrich score.
2. In patients with transmural infarcts, Bland-Altman plots showed better agreement between AAR and IS using the Wilkins method (95% CI - 18.42 to 8.125), compared to Aldrich score (95% CI -18.54 to 15.37).
3. Increasing correlation between AAR size and IS was observed with increasing infarct transmurality for the Wilkins method but not the Aldrich score.
4. In the correlation of myocardial salvage and mean transmurality, 78% of patients were within the ?30% margin of the inverse 'line of identity' using the Wilkins method as compared to 60% for the Aldrich score.
Accordingly, compared with its antecedent ECG index, the Wilkins method better fulfils the principles outlined by Versteylen et al, perhaps to degree equivalent to angiographic AAR methods.
References: 1. Versteylen MO, Bekkers SC, Smulders MW, et al. Performance of angiographic, electrocardiographic and MRI methods to assess the area at risk in acute myocardial infarction. Heart 2012;98:109-15. 2. Wilkins ML, Maynard C, Annex BH, et al. Admission prediction of expected final myocardial infarct size using weighted ST-segment, Q wave, and T wave measurements. J Electrocardiol 1997;30:1-7. 3. Bouwmeester S, van Hellemond IE, Maynard C, et al. The stability of the ST segment estimation of myocardial area at risk between the prehospital and hospital electrocardiograms in patients with ST elevation myocardial infarction. J Electrocardiol 2011;44:363-9. 4. Christian TF, Gibbons RJ, Clements IP, Berger PB, Selvester RH, Wagner GS. Estimates of myocardium at risk and collateral flow in acute myocardial infarction using electrocardiographic indexes with comparison to radionuclide and angiographic measures. J Am Coll Cardiol 1995;26:388- 93.
Conflict of Interest:
None declared
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Important cost categories not included: TAVI probably less cost-effective
Submit responsePatients eligible for the TAVI intervention are old (>75), face a high mortality risk and generally have multiple comorbidities [1]. Health care consumption of this group of patients can therefore expected to be high [2,3]. As a consequence, life extension in this group would probably result in additional health care consumption in so-called life years gained. Health care consumption in life years gained could be due to treatment of a large variety of diseases related to old age and/or consumption of long-term care due to disabilities.
In the article by Watt et al. [4] only a limited set of cost categories is included, which results in too favourable estimates of the cost effectiveness of TAVI. Current NICE guidelines do not advocate the inclusion of medical costs in life years gained of diseases not directly related to the intervention under study [5]. Ignoring costs that are relevant for the NHS is difficult to defend using scientific arguments [6- 8]. It also results in favoring interventions that primarily increase length of life over interventions that mainly improve quality of life [9]. Broadening the perspective beyond the NHS, as Watts et al. suggest, would probably result in even less favourable cost effectiveness estimates as the target group of TAVI does not participate in the labour market anymore and therefore consumes more than they produce [9]. While there may be uncomfortable implications of including more cost categories that warrant discussion, this can never be a reason to exclude foreseeable costs.
References
1. Leon MB, Smith CR, Mack M, et al. Transcatheter aortic-valve implantation for aortic stenosis in patients who cannot undergo surgery. New Engl J Med 2010; 363: 1597-607
2. Yang Z, Norton EC, Stearns SC.J Gerontol B Psychol Sci Soc Sci. 2003 Jan;58(1):S2-10.Longevity and health care expenditures: the real reasons older people spend more.
3. Basu A, Arondekar BV, Rathouz PJ.Scale of interest versus scale of estimation: comparing alternative estimators for the incremental costs of a comorbidity. Health Econ. 2006 Oct;15(10):1091-107.
4. Watt M, Mealing S, Eaton J, Piazza N, Moat N, Brasseur P, Palmer S, Busca R, Sculpher M.Cost-effectiveness of transcatheter aortic valve replacement in patients ineligible for conventional aortic valve replacement. Heart. 2012 Mar;98(5):370-6. Epub 2011 Nov 10.
5. ISPOR. Pharmacoeconomic Guidelines Around The World. Available at: http://www.ispor.org/PEguidelines/index.asp. Accessed 08/18, 2011.
6. Rappange DR, van Baal PH, van Exel NJ, Feenstra TL, Rutten FF, Brouwer WB. Unrelated medical costs in life-years gained: should they be included in economic evaluations of healthcare interventions? Pharmacoeconomics 2008;26(10):815-830.
7. Meltzer D. Response to "Future costs and the future of cost- effectiveness analysis". J.Health Econ. 2008 Jul;27(4):822-825.
8. Feenstra TL, van Baal PH, Gandjour A, Brouwer WB. Future costs in economic evaluation. A comment on Lee. J.Health Econ. 2008 Dec;27(6):1645- 9; discussion 1650-1.
9. Meltzer D. Accounting for future costs in medical cost- effectiveness analysis. J.Health Econ. 1997 Feb;16(1):33-64.
Conflict of Interest:
None declared
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"High platelet reactivity to both aspirin and clopidogrel" is indicative of a generalized high platelet reactivity phenotype
Submit responseYoung-Hoon Jeong, MD, PhD,1,2 Kevin P Bliden , MBA,1 Yongwhi Park, MD, PhD,2 Udaya S. Tantry, PhD,1 Paul A. Gurbel, MD1
1Sinai Center for Thrombosis Research, Baltimore, Maryland; and 2Division of Cardiology, Department of Internal Medicine, Gyeongsang National University Hospital, Jinju, Korea.
The study by Breet et al.1 supported our previous suggestion that a cutoff of aspirin reaction units (ARU) >550 was too high to identify high on-treatment platelet reactivity (HPR).2 The cutoff defined by the highest quartile (461 ARU) from our study2 is remarkably similar to the 454 ARU cutoff value associated with 1-year outcomes in the Breet et al. study.1 Moreover, across ARU quartiles, reactivity to ADP and collagen significantly increased.2
In a new analysis of 558 patients undergoing percutaneous coronary intervention during aspirin and clopidogrel therapy, we could observe that 5microM ADP- and 0.5mg/mL arachidonic acid (AA)-induced aggregation correlated well (r =0.625) (Figure A). In addition, receiver-operating characteristics curve analysis showed that 19.5% AA-induced aggregation corresponded to 5microM ADP-induced aggregation >46% cutoff for HPR3 (Figure B). These data agree strongly with the HPR cutoff of 20.0% AA- induced aggregation associated with 1-year outcomes in the Breet et al. study.1 Moreover, patients with HPR to ADP had a 2.4-fold greater prevalence of HPR to AA, and there was high concordance between two criteria (~74%) (Figure A), suggesting that HPRs as determined by ADP- and AA-induced platelet aggregation may not be different indicators of the risk stratification, but identify a global phenotype of hyperreactive platelets.
It is a matter of debate whether the VerifyNow-ASP assay can determine reliably the extent of AA-induced aggregation. In the Aspirin- Induced Platelet Effect (ASPECT) study,4 the estimation of HPR to AA was highly assay-dependent, and no significant correlations in HPR to AA existed between AA-induced LTA and VerifyNow-ASP. The presence of uninhibited cyclooxygenage-2 in whole blood that contributed to thromboxane A2 production may explain different prevalence of HPR to AA in VerifyNow-ASP as compared with LTA.
To date, no convincing data are available regarding the utility of measuring platelet response to multiple agonists in stratifying the risk for ischemic events. High platelet reactivity to multiple agonists may not be due to independent responses, but rather indicate a global high platelet reactivity phenotype.2 Whether personalized antiplatelet therapy based on platelet response to multiple agonists is more beneficial than measuring response to a single agonist deserves further investigation.
REFERENCES
1. Breet NJ, van Werkum JW, Bouman HJ, et al. High on-treatment platelet reactivity to both aspirin and clopidogrel is associated with the highest risk of adverse events following percutaneous coronary intervention. Heart 2011;97:983-90.
2. Dichiara J, Bliden KP, Tantry US, et al. Platelet function measured by VerifyNowTM identifies generalized high platelet reactivity in aspirin treated patients. Platelets 2007;18: 414-23.
3. Bonello L, Tantry US, Marcucci R, et al. Working Group on High On -Treatment Platelet Reactivity. Consensus and future directions on the definition of high on-treatment platelet reactivity to adenosine diphosphate. J Am Coll Cardiol 2010;56:919-33.
4. Gurbel PA, Bliden KP, DiChiara J, et al. Evaluation of dose- related effects of aspirin on platelet function: results from the Aspirin-Induced Platelet Effect (ASPECT) study. Circulation 2007;115:3156- 64.
We want to attach a figure file.
Conflict of Interest:
HPRs as determined by ADP- and AA-induced platelet aggregation may not be different indicators of the risk stratification, but identify a global phenotype of hyperreactive platelets. In addition, It is a matter of debate whether the VerifyNow-ASP assay can determine reliably the extent of arachdonic acid-induced aggregation.
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It is usually the cigarettes that did it
Submit responseIt should be remembered that in INTERHEART, nine risk factors accounted for 90% of the population attributable risk of a myocardial infarction in men and 94% in women - these did not include family history.[1] Thus, on a population basis, I would disagree with the authors that 'A positive family history of premature coronary artery disease (CAD) is an important risk factor for cardiovascular disease (CVD)'. It is however obvious that 'The associated risk increases further when relatives are affected at a younger age' - and thus the paper asks an important question in trying to ascertain whether arterial stiffness might play a role in risk prediction within families with genuinely premature CAD.
On that point of genuineness, rarely do my colleagues ask the patient whether that relative who suffered a heart attack in their 50s smoked or had diabetes. The 'positive family history' of CAD is often thus anything but - it was the smoking that more usually causes the myocardial infarction rather than any arterial stiffness that family member might have had.
Reference 1. Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study. Yusuf S, Hawken S, Ounpuu S, Dans T, Avezum A, Lanas F, McQueen M, Budaj A, Pais P, Varigos J, Lisheng L; INTERHEART Study Investigators. Lancet. 2004 Sep 11-17;364(9438):937-52.
Conflict of Interest:
None declared
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RAMIT: Making sense of its findings and flaws
Submit responseWest and colleagues'[1] recently published randomised controlled trial (RCT) exemplifies successful failure. Because and not despite of its null findings and flaws, RAMIT provides lessons for the future of prevention. Skeptics and proponents of traditional hospital-based cardiac rehabilitation (CR) should not use the study's findings or flaws to defend their respective positions but harness its failure constructively for innovation in designing more accessible and effective services.
Regarding doubts raised by the findings over the benefits of CR in the modern age, commendably and post-hoc, the study was powered to detect differences in mortality at 7-9years and in all likelihood risk factors at one-year. Yet, its failure to find benefits in these outcomes potentially points to the need for CR interventions to evolve from time-limited, exercise-focused programmes into more accessible and individually tailored ones. Such programmes could equally address all modifiable risk factors,[2] as necessary, and include long-term follow-up with ongoing support.[3]
While the RAMIT design was originally a large-scale RCT it was ultimately flawed because it was stopped early for unclear reasons having enrolled around 22% (n=1813) of the targeted sample size in approximately 3years. Also, over 20% of the intervention group dropped out and did not complete the rehabilitation programme and any contamination among controls is unclear. Such barriers are common amongst CR trials and clinical programmes and suggest that flexible programmes that overcome indifference, transport and work-related issues are important to pursue and develop.
RAMIT's findings also highlight the need for better description of the intervention. As CR programmes are complex interventions, CONSORT recommends they be described comprehensively with "precise details" of content. This not only improves trial quality but also uptake of evidence by clinicians.[4] In RAMIT, specific content of the intervention for each risk factor and corresponding behaviour change techniques used are poorly described.
Finally, the benefits of trials should not be reduced to headline effects. Findings, whether positive or negative, can yield useful insights to improve interventions and methodology. A focus on increasing participation in evidence-based risk factor management strategies that are individualised and multidimensional will help researchers keep pace with advances in medical management.
References 1. West RR, Jones DA, Henderson AH. Rehabilitation after myocardial infarction trial (RAMIT): multi-centre randomised controlled trial of comprehensive cardiac rehabilitation in patients following acute myocardial infarction. Heart 2012 (Published on December 22, 2011 as 10.1136/heartjnl-2011-300302). 2. Wood DA, Kotseva K, Connolly S, et al, on behalf of EUROACTION Study Group. Nurse-coordinated multidisciplinary, family-based cardiovascular disease prevention programme (EUROACTION) for patients with coronary heart disease and asymptomatic individuals at high risk of cardiovascular disease: a paired, cluster randomised controlled trial. Lancet 2008;371:1999-2012. 3. Redfern J, Maiorana A, Neubeck L, Clark AM, Briffa T. Achieving coordinated Secondary Prevention of coronary heart disease for All in Need (SPAN). Int J Cardiol 2011;146(1):1-3. 4. Clark AM, Redfern J, Thompson D, Briffa T. More data, better data or improved evidence translation: what will improve cardiovascular outcomes? Int J Cardiol 2012;155:347-349.
Conflict of Interest:
None declared
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The future of Cardiac Rehabilitation in the UK
Submit responseDear Sir,
The recent paper by West et al [1] was critiqued by the current cohort of students taking the MSc Preventive Cardiology at Imperial College London. The following opinions summarise the consensus reached in a group discussion.
Although all programmes included were reported to conform to contemporary 1995 BACR guidelines for phase three rehabilitation, these varied markedly, as highlighted by the variability in healthcare disciplines involved, and programme duration, described by the authors. Indeed, although the discipline of cardiac rehabilitation was founded in the late 1960's, the evolution of this model of care has varied widely, as demonstrated by the diversity of centres in this study. The heterogeneity of programme delivery in this trial therefore limits the conclusions that can be drawn about the value of cardiac rehabilitation compared to usual care. More recent guidelines from the BACR in 2007 [2] define more stringent core competencies and a trial conducted today might provide a more valid assessment of comprehensive prevention and rehabilitation programmes.
The authors state that the required sample size was estimated at 8000 from power calculations for their primary endpoint of 2-year all-cause mortality. The final inclusion of 1817 participants means the trial was unable to answer this question. Centres that were unwilling to randomise patients were included as 'elective hospitals'. This sub-analysis of centres not participating in the trial is a non-randomised comparison, and therefore using these observational data in order to 'enlarge the sample size' is inappropriate. Given the small sample size it is not surprising that no significant reduction was demonstrated in the primary endpoint. Given the heterogeneity of these programmes, it is also unsurprising that no significant reductions were seen in one year outcomes for smoking, diet and medication adherence. However, a common theme to all programmes was the emphasis they placed on physical exercise. Therefore, it is surprising that despite exercise being the cornerstone of these programmes, physical activity levels were significantly lower in patients receiving cardiac rehabilitation.
Therefore the authors are right to question the value of cardiac rehabilitation, as delivered in this trial, compared to usual care. And the same question could be asked about cardiac rehabilitation programmes today and their ability to deliver all aspects of secondary prevention of cardiovascular disease.
1. West RR, Jones DA, Henderson AH. Rehabilitation after myocardial infarction trial (RAMIT): multi-centre randomised controlled trial of comprehensive cardiac rehabilitation in patients following acute myocardial infarction. Heart. 2011 Dec 22. [Epub ahead of print]? 2. BACR. Standards and core components for cardiac rehabilitation 2007. Available at http://www.bcs.com/documents/affiliates/bacr/BACR%20Standards%202007.pdf
Rashid MA, Arefaine Abraha N, Bhatti N, Chinedu-Ezepue N, Dhomun G, Gill V, Nusrat M, Nwa-Amadi M, Paracha A, Pelina A, Sheikh M, Tornada A, Tueny M, Vedanthachari R, Lock C, Roszczynska A, Xuereb C.
Conflict of Interest:
None declared
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Exercise training as an essential component of cardiac rehabilitation.
Submit responseDear Editor,
We read with interest, but also great concern, the paper by West, et al.1 on their multi-centre randomized cardiac rehabilitation study, suggesting negligible results. This study was covered in the Belgian press and already led to questions about further reimbursement of such multi- disciplinary programs. We agree that re-evaluation of cardiac rehabilitation in the era of early revascularisation and thoroughly changed secondary prevention, is timely. However, this study does not involve a standard exercise training component. Patients only trained once a week or biweekly; this is nowhere near the general recommendations for physical activity in primary or secondary prevention. Intensity, modality and duration of training sessions are not described, and exercise testing pre and post rehabilitation to assess treatment effect is lacking. Also, significantly fewer patients were exercising after 1 year, suggesting exercise underdosage. We disagree with their presumption that improved secondary prevention precludes multi-disciplinary rehabilitation programs. The recently published EUROASPIRE III showed that cardiovascular prevention is still poorly implemented in daily practice. West et al. themselves reported a suboptimal preventive approach; only 54-62% of patients were taking a statin or beta-blocker at follow-up. The authors also failed to mention two recent studies demonstrating that cardiac rehabilitation led to a 45% reduction in long-term mortality in a registry of 2395 post-PCI patients.2 In a registry of 18809 patients with acute coronary syndrome, failure to comply with lifestyle and exercise recommendations was associated with an early almost 4-fold increased risk of adverse cardiovascular events.3 These patients were extremely well treated in terms of pharmacological prevention. The authors also concluded that cardiac rehabilitation had no effect on psychological morbidity or quality of life, but generic measures, such as the SF36, may have lacked sensitivity to detect actual changes in patient-reported outcomes. Previous work has shown that cardiac rehabilitation has a significant beneficial effect on psychological morbidity.4 To our opinion, the most important conclusion from this study is incorporated in the last line of the abstract; maybe it is time to re- think cardiac rehabilitation in the UK.
References
1. West RR, Jones DA, Henderson AH. Rehabilitation after myocardial infarction trial (RAMIT): multi-centre randomised controlled trial of comprehensive cardiac rehabilitation in patients following acute myocardial infarction. Heart 2011; doi:10.1136/heartjnl-2011-300302 2. Goel K, Lennon RJ, Tilbury RT et al. Impact of cardiac rehabilitation on mortality and cardiovascular events after percutaneous coronary intervention in the community. Circulation 2011;123:2344-2352. 3. Chow CK, Jolly S, Rao-Melacini P et al. Association of diet, exercise, and smoking modification with risk of early cardiovascular events after acute coronary syndromes. Circulation 2010;121:750-758. 4. Denollet J, Brutsaert DL. Reducing emotional distress improves prognosis in coronary heart disease: 9-year mortality in a clinical trial of rehabilitation. Circulation 2001;104:2018-2023.
Conflict of Interest:
None declared
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