Recent eLetters
Displaying 1-10 letters out of 552 published
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Unmeasured socioeconomic variables - hallmark to various cardiovascular risk in asian cohort
Submit responseDear Editor
I read with great interest the editorial written by Zaman et al. The paper has also highlighted that it is very difficult in any ethnic group to understand all unmeasured socioeconomic variables which affect overall cardiovascular risk.
Some unmeasured variable potentially could be:
1) Level of education of parents in the family. 2) Profession of father and mother. 3) Financial status of the family. 4) Diet - Personal liking of fast food in the family. Very difficult to measure, however previous research has shown that fast food is often preferred in lower socio-economical class [1]. Also, generally speaking Asian food can vary in its saturated fat content depending upon personal preferences. This will directly affect cardiovascular risk in that population. 5) Location - For example, do Asians in London have better lifestyles than those living in Glasgow? And does this effect overall cardiovascular risk?
In my opinion, Asian community educational programmes geared to healthy lifestyles would be imperative to overall reduce the burden of cardiovascular disease in this group in the UK.
This could potentially include interactive sessions on -
1) Healthy Asian Cooking 2) Dancing (Bollywood/Hollywood) 3) Organised social group Country Walks 4) Talks on various diseases like Diabetes, Obesity, heart attack, risk factors for it. 5) Lastly, they should also know the fact - They are at higher risk of heart attack than any other ethnicity in the UK!
Hopefully, with education we can reduce the overall burden of CAD in Asian population in the UK.
Reference:
1. Smoyer-Tomic K.E., Spence J.C., Raine K.D., Amrhein C., et al. The association between neighborhood socioeconomic status and exposure to supermarkets and fast food outlets (2008) Health and Place, 14 (4), pp. 740-754.
Conflict of Interest:
None declared
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A Miscarriage of Justice in the RATPAC Trial ?
Submit responseHaving read the three papers published around the RATPAC Trial (1,2,3), I have come to the conclusion there has been a major miscarriage of justice. That miscarriage of justice relates to diagnostic equipment used in the standard treatment protocols for the hospitals involved in the RATPAC Trial (Beckman Access, Centaur CP and Roche E170). Point of Care Testing (POCT) was not convincingly vindicated in this trial but the other equipment and methods were deemed by association of the data to be inadequate. A cursory examination of the papers clearly shows : 1. The main reason for the improvement in patient discharge was the decision to change the time interval for testing cardiac markers from 12 hours (or 6 hours in one case) to 90 minutes. 2. The sensitivity of the equipment used for Troponin under the standard protocol was as good as the method used in the POCT protocol (Siemens Stratus) 3. Both POCT and Standard Care Equipment would have required a centrifuged sample so pre-analytical delay should have been the same. 4. The variability of results between sites was more about ED processes than the POCT protocol. Therefore simply using the equipment used in the standard care setting for the 90 minute protocol would, in my opinion, have given basically the same outcomes. Point of care analysis per se was not a major player in this trial. This was all about changing timeframes and processes. I therefore find the conclusion that "Point of care testing panel assessment increases successful discharge home and reduces median length of stay........" misleading. The use of troponin alone by the standard protocol methods has been evaluated elsewhere (4,5) and with great success. It is therefore not surprising that the economic assessment of the RATPAC trial found point of care testing to be expensive. It has been found in this case to be unnecessary. What was also unnecessary was the standard care guideline of a 12 hour delay, though that was the recommendation and guideline at the time, and the contributors were right to be using it. It is an old guideline and troponin methods have improved so much as to make that interval redundant. What this paper highlights is not that POCT can improve turnaround in ED but that protocols need to be kept up to date with technological change and clinical research. This is easier said than done given the complexity of committees looking after guidelines and the conservative nature of change in a clinical setting. I therefore declare a mistrial and absolve the Beckman Access, Roche E170 and Centaur CP of any inference of inadequacy and everyone else of any criticism for what is still a well planned, executed and valuable trial in showing that processes and procedures are more important than equipment and that variations are more about people and the conditions they work under. REFERENCES: 1.Goodacre, SW et al "The Randomised Assessment of Treatment using Panel Assay of Cardiac Markers (RATPAC) trial : a randomised controlled trial of point-of-care cardiac markers in the emergency department" Heart 2011 97:190-196; doi:10.1136/hrt.2010.203166 2. Fitzgerald, P et al "Cost-Effectiveness of Point-of-care Biomarker Assessment for Suspected Myocardial Infarction : The Randomised Assessment of Treatment Panel Assay of Cardiac Markers (RATPAC) Trial" Acad Emerg Med 2011;18(5):488-495 3. Bradburn, M et al "Interhospital Variation in the RATPAC trial (Randomised Assessment of Treatment Panel Assay of Cardiac Markers). Emerg Med J 2011; May 26 doi: 10.1136/emj.2010.108522 4. Keller, T et al "Sensitive Troponin I in Early Diagnosis of Acute Myocardial Infarction" NEJM 2009;361:868-877 5. Reichlin, T et al "Early Diagnosis of Myocardial Infarction with Sensitive Cardiac Troponin Assays" NEJM 2009;361:858-867Conflict of Interest:
None declared
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No additional information with Computed Tomography Coronary Angiography prior to alcohol septal ablation.
Submit responseto the editor: Spratt and colleagues describe two cases in which they state that performing a Computed Tomography coronary angiography (CTCA) prior to alcohol septal ablation (ASA) may aid in the selection of the appropriate septal branch for ablation and patients suitable for ASA (1). Visualisation of a dominant septal perforator and its course in the myocardium with CTCA has been described previously (2). Importantly, CTCA has three important limitations being that it is unable to visualise due to limitation of resolution smaller proximal septal branches that can be the target vessel, that it is unable to visualise the perfusion area of the septum and that it cannot display the area of maximal flow acceleration. The combination of coronary angiography and contrast echocardiography has been shown to be superior for these purposes (3) and we therefore believe that performing additional CTCA prior to ASA does not give extra information.
reference 1) Spratt JC, Langrish JP. Identifying the target septal perforator prior to alcohol septal ablation in hypertrophic obstructive cardiomyopathy: a new application for computed tomography coronary angiography. Heart 2011; 97: 1718-1719. 2) Brinjikji W, Harris SR, Froemming AT, Christensen KN, Lachman N, Araoz PA. Descriptive anatomy of the dominant septal perforators using Dual Source CT angiography. Clin Anat 2010; 23(1): 70-8. 3) Faber L, Seggewiss H, Gleichmann U. Percutaneous septal myocardial ablation in hypertrophic obstructive cardiomyopathy: Results with respect to intraprocedural myocardial contrast echocardiography. Circulation 1998; 98: 2415-2421.
Conflict of Interest:
None declared
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Death following "pill-in-the-pocket" treatment with propafenone and verapamil in a CYP2D6 poor metaboliser
Submit responseTo the Editor Daniell [1] reports a case of syncope after "pill-in-the-pocket" treatment with propafenone. He mentions the CYP2D6 metabolism of propafenone and the possible interaction with CYP2D6 inhibitors. We would like to further illustrate the potential risks of propafenone in CYP2D6 poor metabolisers with the case of a 70 year-old woman who died from sudden cardiac arrest after taking 600 mg of propafenone orally for the treatment of atrial fibrillation (AF). The patient was seen on an outpatient basis following a cerebrovascular accident. An ECG showed AF with a rapid ventricular rate. The QTC interval was 430 msec. An echocardiography showed moderate left ventricular hypertrophy (LVH) with left atrial enlargement. Left and right ventricular systolic function and size were normal. She was taking gliclazide (160 mg daily) for diabetes and verapamil (240 mg daily) for hypertension. After three weeks of therapeutic anticoagulation, she received a single oral dose of 600 mg propafenone. She was in sinusal rhythm by the next day. Anticoagulation was maintained. A few months later, asymptomatic AF justified another single dose of propafenone 600 mg orally. The ECG was similar to the previous episode. She developed two hours later, a malaise with profound weakness, sweating, pallor, nausea and vomiting. On arrival, the emergency services noted cardiac arrest with asystole. Cardio- pulmonary resuscitation failed. No specific cause of death could be found. The autopsy showed moderate LVH (<14mm) but no coronary abnormalities. A small scar of myocardial infarction was noted on the lateral wall of the left ventricle. No pulmonary embolism, ischemic or hemorrhagic stroke was found. However, PCR showed homozygosity for CYP2D6*4 resulting in poor drug metabolism. In the absence of Q wave or anamnestic angina, it is unlikely that the small past infarction played a major role in sudden death. LVH is a known risk factor for ventricular arrhythmia but it is mainly reported when the septum is thicker than 14 mm. A contributory proarrhythmic adverse effect of propafenone was suggested. Dose-related proarrhythmic effects such as ventricular tachycardia, flutter, ventricular fibrillation and torsade de pointes have been described [2]. Propafenone's first-pass liver metabolism is mainly related to CYP2D6, two minor pathways being CYP1A2 and CYP3A4. CYP2D6 is subjected to polymorphism and studies in CYP2D6 intermediate and poor metabolisers (PM) have shown that Cmax is increased by nearly 50% and 150% respectively compared to extensive metabolisers after a single oral dose. Pharmacodynamics mirror pharmacokinetics with a prolongation of the PR interval in PM [3]. The PM CYP2D6 genotype and the interaction between propafenone and verapamil, a strong inhibitor of CYP3A4, may have led to increased propafenone bioavailability. This, taken together with her previous myocardial infarction and moderate LVH, might have increased the patient's susceptibility to the dose-dependant proarrhythmogenic effects of propafenone. The benefit of the "pocket pill" strategy proposed for cardiac arrhythmia [4] in vulnerable patients might well be hampered by pharmacogenetic and/or drug-drug interactions leading to unexpected and unfavourable issues. Determining the genotype or phenotype of patients treated with drugs that have narrow therapeutic margins (such as class I antiarrhythmics) may allow the prescription of an adapted dose regimen for CYP2D6 PM. References 1. Daniels HW. Syncope following "pill-in-the-pocket" treatment of atrial fibrillation with propafenone plus quinidine. Heart 2011;97:1626. 2 Capucci A, Boriani G. Propafenone in the treatment of cardiac arrhythmias. A risk-benefit appraisal. Drug Safety 1995; 12: 55-72. 3. Zhou SF. Polymorphism of human cytochrome P450 2D6 and its clinical significance: Part I. Clin Pharmacokinet 2009;48:689-7234. 4. Alboni P, Botto GL, Baldi N, Luzi M, Russo V, Gianfranchi L et al. Outpatient treatment of recent-onset atrial fibrillation with the "pill-in -the-pocket" approach. N Engl J Med 2004; 351: 2384-91
Conflict of Interest:
None declared
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The neglected role of blood pressure in acute heart failure syndrome
Submit responseI read with interest Harinstein et al's review of clinical assessment in acute heart failure syndromes (AHFS) . Initial assessment of AHFS included evaluation of important prognostic factors which influence treatment such as the presence of atrial fibrillation, acute pulmonary oedema and renal function. This is in accordance with the 6 axis model described by Professor Gheorghiade. An important factor in the 6 axis model which has been neglected is the role of blood pressure in the presentation and evaluation of AHFS. Blood pressure plays a critical role in the prognosis of acute heart failure and should be a central consideration in management decisions. Previous work by Prof Gheorghiade describes the central role of blood pressure in acute heart failure. Blood pressure is an independent predictor of mortality and morbidity in heart failure. AHFS can present with low, normal and high blood pressure and each of these groups have different pathophysiology and respond differently to treatment. It is important to distinguish between them in the evaluation of AHFS. High blood pressure in AHFS tends to be due to a reactive hypertension caused by high sympathetic tone whereas low blood pressure reflects poor cardiac output . Studies have shown that elevated systolic blood pressure (SBP) is common in patients hospitalized with AHFS. These patients have a lower post-discharge mortality, lower rates of rehospitalisation and shorter duration of stay that those with low systolic blood pressure. However they also have a increased risk of morbid events. It is hypothetised that blood pressure may distinguish those with early or mid stage disease (high SBP) from those with advanced disease (low SBP) . Congestive symptoms were more likely in high blood pressure at admission however during discharge low SBP had more congestive symptoms. Patients with high blood pressure may respond to heart failure treatment differently to low SBP however high blood pressure in AHFS is underrepresented in clinical trials of heart failure drugs. Use of ACE inhibitors and Beta blockers in these patients may have beneficial anti- hypertensive effect whereas they are less used in heart failure with hypotension. Hypotension may represent low cardiac output and maintaining adequate blood pressure is a treatment priority in the management of these types of AHFS. High SBP had better response to treatment however the re- hospitalisation rates and risk of morbid events were similar to low SBP. Better treatment response in high SBP gave physician a false sense of security that these patients were not as ill as hypotensive AHFS. This may have resulted in less aggressive management. There were lower rates of left ventricular function assessment and aldosterone use in high SBP. Acute heart failure is often inadequately managed in hospitals resulting in poor prognosis and re-hospitalisation. One of the factors influencing good management is careful evaluation of blood pressure. The role of this important factor is often poorly understood and underestimated. Yet it is a clinical feature which makes a substantial difference to treatment response.
Harinstein M E, Flaherty J D, Fonarow G C, Mehra M R, Lang R M, Raymond K J, Cleland J G, Knight B P, Pang P S, Bonow R O, GHEORGHIADE M Clinical assessment of acute heart failure syndromes: emergency department through the early post-discharge period Heart 2011 97:1607-1618; doi:10.1136/hrt.2011.222331
Gheorghiade M, Abraham W T, Albert N M, Greenberg B H, O'Connor C, Yancy C W, Young J B, Fonorow G C, Systolic Blood Pressure at Admission, Clinical Characteristics, and Outcomes in Patients Hospitalized With Acute Heart Failure JAMA. 2006;296(18):2217-2226. doi: 10.1001/jama.296.18.2217
Gheorghiade M, Abraham WT, Albert NM, et al., OPTIMIZE-HF Investigators and Coordinators. Systolic blood pressure at admission, clinical characteristics, and outcomes in patients hospitalized with acute heart failure. JAMA. 2006;296(18):2217-2226.
Flaherty JD, Bax JJ, De Luca L, et al., Acute Heart Failure Syndromes International Working Group. Acute heart failure syndromes in patients with coronary artery disease early assessment and treatment. J Am Coll Cardiol. 2009;53(3):254-263
Gheorghiade M, Zannad F, Sopko G, et al. Acute heart failure syndromes: current state and framework for future research. Circulation.2005;112:3958
Conflict of Interest:
None declared
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Re:CT or MRI for post-procedural aortic stenting?
Submit responseFurther to Kenny et al's response to our editorial view (1) of their original paper (2), we completely agree that long-term surveillance after coarctation stenting is required to detect complications but would re- iterate that this must also apply to balloon dilation and surgical repairs too. Given that these patients will need life-long follow up and continued imaging it is important that such imaging carries a low risk to the patient and is sensitive to vascular complications that may arise both at the site of repair and at the aortic valve and ascending aorta.
While MRI scanning cannot detect circumferential stent fracture, it occurs in the setting of a resistant lesion and by its very occurrence is accompanied by a recurrent gradient that is detectable on echocardiography or MRI velocity scanning. Current MRI imaging sequences are now able to provide good wall definition even with stainless steel stents and as MRI becomes more widely available should allow a reduction in the need for CT scanning in this setting just to detect aneurysm formation. We use CT now only when urgency dictates and MRI is not readily available for logistic reasons.
As Kenny et al acknowledge, the assessment of coarctation by MRI scanning is comprehensive and without any risks from radiation and we believe should become the preferred modality supplemented by interval echocardiography and clinical examination.
1. Rosenthal E, Bell A. Optimal imaging after coarctation stenting. Heart 2010; 96:1169-71.
2. Chakrabarti S, Kenny D, Morgan G, et al. Balloon expandable stent implantation for native and recurrent coarctation of the aorta : prospective computed tomography assessment of stent integrity, aneurysm formation and stenosis relief. Heart 2010; 96:1212-16.
Conflict of Interest:
None declared
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Screening for 22q11.2 microdeletion in adults with tetralogy of Fallot
Submit responseTo the Editor: We read with interest the paper by van Engelen et al.,1 analysing the prevalence of 22q11.2 deletion syndrome (22q11.2DS) in adults with tetralogy of Fallot (TOF) and with pulmonary atresia(PA)/ventricular septal defect (VSD). We agree with the experience that many adult patients with TOF have not been tested for 22q11.2DS in the past, so that awareness of the syndrome is needed among clinicians who care adults with congenital heart defects (CHDs). Nevertheless, we disagree to introduce as general practice the large-scale screening of all TOF patients irrespective of their clinical phenotype. Personal experience in paediatric patients with 22q11.2DS has evidenced that the deletion is virtually never found in non-syndromic patients with conotruncal defects.2 In addition, it has been evidenced that distinct subtypes of conotruncal heart defects are likely to be found in association with 22q11.2DS. In regard to TOF, patients with 22q11.2DS have often right/cervical aortic arch with/without aberrant left subclavian artery, hypoplasia or absence of the infundibular septum, absence of the pulmonary valve, and hypoplasia and discontinuity of the pulmonary arteries.2 Among children with TOF and PA, the 35% is carrying a 22q11.2DS, and distinctive recognizable patterns of CHDs include major aorto-pulmonary collateral arteries, sometimes with discontinuity of the pulmonary arteries.2 The review of the literature about clinical characteristics of adults with 22q11.2DS is showing that extracardiac anomalies can help clinician to suspect 22q11.2DS.3 Particularly, previous series reported that facial anomalies can be detected in 99-100% of the cases, ranging from subtle to characteristic. Additional evidenceable signs include hypernasal speech (90%), intellectual disability of any degree and/or learning difficulties (93-97%). The rare occurrence of extremely mild clinical expression of 22q11.2DS in a parent of an affected child can now be explained with the molecular mechanisms of genetic compensation (presence of a 22q11.2 deletion on one chromosome and 22q11.2 duplication on the other allele of chromosome 22).4 In conclusion, the search for 22q11.2DS is important in adult patients with TOF and with PA/VSD, since recognition of the syndrome has clinical and reproductive implications, but genetic testing, in our opinion, should be reserved to patients with associated "classic" or "subtle" extracardiac anomalies, and to those with distinct anatomic cardiac subtypes.
M.Cristina Digilio,1 Bruno Marino,2 Bruno Dallapiccola1 1 Medical Genetics, Bambino Gesu' Paediatric Hospital, IRCCS, Rome, Italy; 2 Department of Pediatrics, Pediatric Cardiology, La Sapienza University, Rome, Italy
Correspondence to Dr M.Cristina Digilio, Medical Genetics, Bambino Gesu' Paediatric Hospital, IRCCS, Piazza S.Onofrio 4, 00165 Rome, Italy; mcristina.digilio@opbg.net
REFERENCES 1. van Egelen K, Topf A, Keavney BD, et al. 22q11.2 deletion syndrome is under-recognized in adult patients with tetralogy of Fallot and pulmonary atresia. Heart 2010;96:621-4. 2. Marino B, Digilio MC, Toscano A, et al. Anatomic patterns of conotruncal defects associated with deletion 22q11. Genet Med 2001;3:45-8. 3. Fung WLA, Chow EWC, Webb GD, Gatzoulis MA, Bassett AS. Extracardiac features predicting 22q11.2 deletion syndrome in adult congenital heart disease. Int J Cardiol 2008;131:51-8. 4. Carelle-Calmels N, Saugier-Veber P, Girard-Lemaire F, et al. Genetic Compensation in a Human Genomic Disorder. N Engl J Med 2009;360:1211-6.
Conflict of Interest:
None declared
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Involving primary care and cardiac rehabilitation in a reorganized service could improve outcomes
Submit responseThe full National Heart Failure Audit report[1] and a recent editorial in the Lancet endorse the report's conclusion that it 'provides a powerful incentive to reorganize heart failure care in the UK'.[1,2] The suggested solution is to provide specialist care similar to that given to people after heart attacks citing that such specialized units 'could do for heart failure what coronary care units have done for myocardial infarction.'[2] There is no mention of how primary care could be involved and there is only a passing reference to rehabilitation. Since 2004 general practitioners in the UK have been rewarded for maintaining heart failure registers through the quality and outcomes framework of the GMS contract. In many parts of the UK there are community based heart failure specialist nurses who make an important contribution in caring for patients with heart failure - providing lifestyle advice and supervising the gradual titration of beneficial drugs such as angiotensin converting inhibitors and beta blockers. It would make sense to link these community-based services with the services in hospitals. The forward in the audit report acknowledges that 'it is vital that there is close collaboration between primary and secondary care if the improved outlook for heart failure patients is to be realised'. [1] The benefits of nurse led secondary prevention clinics for coronary heart disease in primary care are proven[3]and a recent updated Cochrane review of exercise in heart failure has demonstrated improved outcomes.[4] It is possible to link clinics in primary care with cardiac rehabilitation programmes [5] and commissioners can now access new NHS support for cardiac rehabilitation to design better services for heart failure.(http://www.dh.gov.uk/en/Publicationsandstatistics/Publications/PublicationsPolicyAndGuidance/Browsable/DH_117504)
Hasnain Dalal, Peninsula Medical School (Primary Care), Truro, TR1 3HD Jenny Wingham, Royal Cornwall Hospitals Trust, Truro Patrick Doherty, York St John University Robert JP Lewin, University of York, York Rod S Taylor,Penisula Medical School(Primary Care), Exeter
Reference List
(1) NHS Information Centre and the British Society for Heart Failure. National Heart Failure Audit 2010. 2010. Ref Type: Report
(2) Crunch time for heart failure care in England and Wales. Lancet 2010; 376(9758):2041.
(3) 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.
(4) Davies EJ, Moxham T, Rees K, Singh S, Coats AJ, Ebrahim S et al. Exercise training for systolic heart failure: Cochrane systematic review and meta-analysis. Eur J Heart Fail 2010; 12(7):706-715.
(5) Dalal HM, Evans PH. Achieving national service framework standards for cardiac rehabilitation and secondary prevention. BMJ 2003; 326(7387):481-484
Conflict of Interest:
All authors except Patrick Doherty are members of the REACH HF Study Group which has received funding from the NIHR as a Programme Development Grant to conduct research in heart failure and cardiac rehabilitation
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chest radiography for validation of heart failure diagnosis
Submit responseRemarkably, chest radiography was notable by its absence from the "mandatory fields for completion" in the 2008-2009 national heart failure audit(1) notwithstanding the documentation that clinical markers of congestion have high positive predictive value(PPV) for validation of acute heart failure(2). According to one review, pulmonary vascular redistribution is associated with a PPV of 75% and a negative predictive value(NPV) of 52% for the presence of acute heart failure. Correspondingly, interstitial oedema is associated with PPV and NPV of 78% and 53%, respectively(2). Accordingly the national heart failure audit was a missed opportunity for evaluating the diagnostic accuracy of these two radiographic parameters in the real world References (1) Cleland JG., McDonagh T., Rigby AS et al The national heart failure audit for England and Wales 2008-2009 Heart 2011;97:876-886 (2)Gheorghiade M., Follath F., Ponikowski P et al Assessing and grading congestion in acute heart failure: a scientific statement from the Acute Heart Failure Committee of the Heart Failure Association of the European Society of Cardiology and Endorsed by the European Society of Intensive Care Medicine European Journal of Heart Failure 2010;12:423-33
Conflict of Interest:
None declared
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Overnight dehydration increases the risk of a morning infarct
Submit responseDear Sir, It was with great interest that I read the recent article by A. Suarez- Barrientos and colleagues (1). However, I think there is one very important aspect left out of this very good clinical investigation and that is blood volume. One of the principal problems of heart pumping is having enough blood volume to do this with. If there is insufficient volume then the heart has to alter its rate of contraction, which can change filling time, or the force of contraction, which will depend on the overall peripheral resistance and the viscosity of the blood which will increase rates of cardiac hypertrophy and remodelling. It would appear then to be a problem of physiological fluid (haemo-) dynamics.
In the study reported here the authors wrote that "the infarct size was found to be significantly larger with STEMI onset in the dark-to-light transition period (6:00 to noon)". This is the first section of the day after an overnight period of sleep. Fluid consumption is not usually recommended during this period yet there is substantial loss of water which leads to overnight dehydration of both the intra and extracellular compartments (2). Therefore, at the end of the sleep period there would be an overall decreased blood volume, which would imply reduced perfusion throughout the vascular system, with perhaps an increase in viscosity, and thus extra work for the heart. It would therefore not be surprising to see an increased number of infarcts occuring in this period. One of the indicators of insufficient blood volume is an increase in plasma levels of the hormones making up the renin-angiotensin-aldosterone system (RAS) (3). Although none of these hormones are treated in the current article I imagine if they were measured they would be increased in the period 6.00 to noon. Furthermore, antagonists of the RAS are used extensively in the treatment of heart failure (4). It could be suggested therefore that one way to reduce the risk of myocardial infarction in the morning would be improved tissue perfusion through increased water intake, perhaps before going to bed and at intervals during sleep.
References.
1. Su?rez-Barrientos A, L?pez-Romero P, Vivas D, Castro-Ferreira F, N??ez-Gil I, Franco E, Ruiz-Mateos B, Garc?a-Rubira JC, Fern?ndez-Ortiz A, Macaya C, Ibanez B. Circadian variations of infarct size in acute myocardial infarction. Heart. 2011 Apr 27. [Epub ahead of print] 2. Colwell CS. Preventing dehydration during sleep. Nat Neurosci. 2010;13:467-74. 3. Thornton SN. Thirst and hydration: physiology and consequences of dysfunction. Physiol Behav. 2010;100:15-21. 4. Zannad F, McMurray JJ, Krum H, van Veldhuisen DJ, Swedberg K, Shi H, Vincent J, Pocock SJ, Pitt B; EMPHASIS-HF Study Group. Eplerenone in patients with systolic heart failure and mild symptoms. N Engl J Med. 2011;364:11-21.
Conflict of Interest:
None declared
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