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Cardiac markers and acute coronary syndromes without ST elevation
- Joseph Tomson, Kim Losh, Dzifa W. Abban (19 June 2007)
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Primary care and rehabilitation have a role in acute coronary syndromes
- Hasnain M Dalal (20 June 2007)
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creating illness
- Donald Macaulay (21 June 2007)
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the confounding effect of left bundle branch block needs to be taken into account
- oscar,m jolobe (21 June 2007)
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The non-superiority of fondaparinux
- Jeremy B Jones, Andrew Docherty (29 June 2007)
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Joseph Tomson, Specialist registrar in cardiology Alexandra hospital, Redditch. B98 7UB, Kim Losh, Dzifa W. Abban
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We read with interest the article on acute coronary syndromes without ST elevation [1]. However we think that the role of cardiac markers in myocardial infarction needs further qualification, especially from a general medical perspective. Cardiac troponins, the most widely used cardiac markers, are no longer known to be cardiac specific as previously thought [2]. Several non-cardiac causes for their elevation have been described [3-5]. In acute medical presentations such as stroke and pulmonary embolism , patients may present with ECG changes and may also have a troponin rise, mimicking acute coronary syndrome without ST elevation. Hence ‘any rise’ in cardiac markers does not essentially qualify as a myocardial infarction. A thorough clinical evaluation of such patients is needed to differentiate those with acute coronary syndromes. References 1. Peters RJ, Mehta S, Yusuf S. Acute coronary syndromes without ST segment elevation.BMJ. 2007; 334(7606):1265-9. 2. Grove ML. Raised cardiac troponins: troponins seem to be sensitive but not specific. BMJ. 2004; 329(7457):111. 3. Ammann P, Pfisterer M, Fehr T, Rickli H. Raised cardiac troponins.BMJ. 2004;328(7447):1028-9. 4. Jensen JK, Atar D, Mickley H.Mechanism of troponin elevations in patients with acute ischemic stroke.Am J Cardiol. 2007;99(6):867-70. 5. Giannitsis E, Muller-Bardorff M, Kurowski V, Weidtmann B, Wiegand U, Kampmann M, et al. Independent prognostic value of cardiac troponin T in patients with confirmed pulmonary embolism. Circulation 2000; 102(2):211-7. Competing interests: None declared |
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Hasnain M Dalal, Genral Practitioner Truro TR1 2LZ
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As a general practitioner I was disappointed to find that the role of primary care and cardiac rehabilitation in the long term treatment of patients with acute coronary syndromes has not been acknowledged by Peters et al [1]. A similar review in the Lancet made the same omission [2]. The importance of cardiac rehabilitation after myocardial infarction has recently been emphasised by NICE guidance [3]. The evidence for the effectiveness of nurse-led CHD (coronary heart disease) secondary prevention clinics in primary care [4] has been included in the QOF(quality and outcomes framework) of the new general practitioner contract. When such primary care based clinics are integrated with cardiac rehabilitation programmes, it is possible to provide optimal long-term treatment for patients with acute coronary syndromes [5]. Reference List (1) Peters RJ, Mehta S, Yusuf S. Acute coronary syndromes without ST segment elevation. BMJ 2007; 334(7606):1265-1269. (2) Boersma E, Mercado N, Poldermans D, Gardien M, Vos J, Simoons ML. Acute myocardial infarction. Lancet 2003; 361(9360):847-858. (3) Skinner JS, Cooper A, Feder GS. Secondary prevention for patients after a myocardial infarction: summary of NICE guidance. BMJ 2007; 334(7603):1112-1113. (4) Campbell NC, Thain J, Deans HG, Ritchie LD, Rawles JM, Squair JL. Secondary prevention clinics for coronary heart disease: randomised trial of effect on health. BMJ 1998; 316(7142):1434-1437. (5) Dalal HM, Evans PH. Achieving national service framework standards for cardiac rehabilitation and secondary prevention. BMJ 2003; 326(7387):481-484. Competing interests: None declared |
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Donald Macaulay, GP Principal Blackburn Health Centre, West Lothian EH47 7LL
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I am concerned at the growing number of patients who are admitted to hospital with a history of chest pain, who have a normal ECG and blood tests that show no evidence of myocardial damage. They may even have had normal exercise electrocardiograms. Many of these patients are either labeled as having acute coronary syndrome without ST segment elevation, angina or ischaemic heart disease. While some of these patients may indeed have ischaemic heart disease it seems to me that many have not and need that reassurance. The authors in their tips for non-specialists stress the importance of a careful focused history as being the most important diagnostic tool but my impression is that my hospital colleagues do not always have the time for this. I wonder if a scoring system or something similar could be developed to prevent healthy patients being misdiagnosed. Nearly every patient who is admitted with chest pain seems to come out on a statin, aspirin, beta- blocker and ACE even if all investigations are normal. The review of the week later on in the BMJ quotes Oakley as saying screening “isn’t to prevent disease but to change identities – to produce patients”. I feel that currently as regards chest pain we are in the business of creating illness. Competing interests: None declared |
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oscar,m jolobe, retired geriatrician manchester medical society, c/o john rylands university library, oxford road, manchester , M13 9PP
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The account of the electrocardiographic(ECG) criteria and management of acute coronary syndromes without ST segment elevation(1) remains incomplete in the absence of any mention of the confounding effect of a clinical presentation accompanied by an ECG characterised by left bundle branch block(LBBB)(2), be it old or new, especially when non-compliant with Sgarbossa's criteria(3), which, themselves, though highly specific, have poor sensitivity(4). Where the onset of LBBB is undetermined, and Sgarbossa's criteria are not met, the dilemna which faces the clinician is whether or not to follow the treatment options for myocardial infarction, including thrombolysis(5), and arguably, primary angioplasty as well, or whether to restrict oneself to the treatment options for non ST segment elevation acute coronary syndromes (1) References (1) Peters RJG., Mehta S., Yusuf S Acute coronary syndromes without ST segment elevation British Medical Journal 2007:334:1265-9 (2) Brady WJ., Lentz B., Barlotta K., Harrigan RA., Chan T ECG patterns confounding the diagnosis of acute coronary syndrome: left bundle branch block, right ventricular paced rhythms, and left ventricular hypertrophy Emergency Medicine Clinics of North America 2005:23:999-1025 (3)Sgarbossa EB., Pinski L., Gates KB et al Early electrocardiographic diagnosis of acute myocardial infarction in the presence of ventricular paced rhythm American Journal of Cardiology 1996:77:423-4 (4) Haywood LJ Left bundle branch block in acute myocardial infarction, benign or malignant?(Editorial Comment) Journal of the American College of Cardiology 2005:46:39-41 (5) Shlipak MG., Lyons WL., Go AS et al Should the electrocardiogram be used to guide therapy for patients with left bundle branch block and suspected myocardial infarction? Journal of the American Medical Association 1999:281:714-9 Competing interests: None declared |
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Jeremy B Jones, SHO Wishaw General Hospital, Wishaw, Scotland, ML2 0DP, Andrew Docherty
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We read with interest the recommendations made for fondaparinux by Peters and colleagues in their clinical review of ACS without ST segment elevation[1]. However, we feel that the recommendations made by Peters are inconsistent with the evidence they present. Moreover, the recommendations are not reflected in current clinical guidelines and are not representative of practice throughout the UK. The recommendations for fondaparinux are based on a single randomised trial that compared fondaparinux with the low molecular weight heparin, enoxaparin[2]. The authors correctly highlight that there was no recorded difference in the efficacy of fondaparinux and enoxaparin. However, the headline major bleeding figure presented by Peters (relative risk reduction of 50% with fondaparinux) is somewhat misleading when viewed in context. Overall, the absolute risk reduction in major bleeds with fondaparinux was only of the order of 1.9% and was reported at day 9. At day 4, when most patients would be expected to have stopped their anticoagulant, there was little difference in the major bleeding rates between the two groups. Moreover, the reported differences in bleeding rates were not apparent when the data was reviewed for patients under 65 years old. In addition, it is now well established that enoxaparin dosing should be modified according to age and renal function to reduce the risk of bleeding, something not done in this study. In the same study, forty percent of patients underwent percutaneous coronary intervention (PCI). In this groups of patients, enoxaparin was associated with lower efficacy endpoints and similar major bleeding rates. Most notably, there was a marked increase in catheter thrombosis in the patients treated with fondaparinux. Using a relative risk figure as favoured by Peters previously, the increased risk of these events was greater than 200% when compared to enoxaparin. The recommendation to use “a small dose of unfractionated heparin” to modify this risk is not evidence based and does not reflect recommendation from any clinical guidelines. We suggest that these findings highlight that fondaparinux is not a suitable anticoagulant for patients in whom an early invasive management strategy is considered. We feel that this excludes fondaparinux from the management of ACS patients at this time. 1. Peters RJ, Mehta S, Yusuf S. Acute coronary syndromes without ST segment elevation. BMJ 2007; 334(7606):1265–1269. 2. The OASIS-5 Investigators. Comparison of fondaparinux compared to enoxaparin in acute coronary syndromes without ST segment elevation. N Engl J Med 2006;354:1464–1476. Competing interests: None declared |
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