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Recent eLetters

Displaying 1-10 letters out of 696 published

  1. True and true, but not a paradox

    The journal, Heart, recently published a meta-analysis(1) and a commentary(2) on the association of obesity and mortality in patients with Coronary Heart Disease (CHD). Lavie begins his commentary with a story of two hypothetical patients with CHD. One has a BMI of 23 kg/m2 (normal) and the other has a BMI of 32 kg/m2 (obese).(2) Lavie asks about their prognosis. The meta-analysis by Wang et al(1) suggests that the obese patient has the better prognosis. Given that numerous primary prevention studies document that obesity is a cause of CHD, Lavie labels it a "paradox" that the prognosis would be better for the obese patient.

    It is true that obesity is a cause of CHD, and, as shown by Wang et al,(1) it is true that the obese people with CHD have a better prognosis than the non-obese people with CHD. However, this is not a paradox. The results are a function of the well-described phenomenon called, "collider stratification bias."(3) Consider that a person contracts CHD due to either (a) obesity or (b) factors unrelated to obesity (e.g. genetics or infectious diseases). If the causes unrelated to obesity are more strongly associated with the outcome of interest (i.e. mortality), then obesity appears protective. This is similar to analyses finding that maternal- smoking appears protective against infant mortality if one evaluates only low birth weight babies.(4)

    It is misleading to imply that obesity is protective in people with CHD. In the example by Lavie, the non-obese subject is not similar to the obese subject in ways other than obesity.(2) The non-obese subject with CHD must have contracted CHD from factors unrelated to obesity such as genetics or infectious disease. The apparent "obesity paradox" occurs because of confusion with the groups being compared. The comparison is not between obese people and non-obese people. Rather, the comparison is between people who have CHD presumably due to the ramifications of obesity and people who have CHD due to causes unrelated to obesity. The conclusion is not that obesity is protective, but rather that there are other causes of CHD that are more life-threatening than obesity.

    1. Wang ZJ, Zhou YJ, Galper BZ, Gao F, Yeh RW, Mauri L. Association of body mass index with mortality and cardiovascular events for patients with coronary artery disease: A systematic review and meta-analysis. Heart. 2015. doi: heartjnl-2014-307119. 2. Lavie CJ, De Schutter A, Milani RV. Body composition and the obesity paradox in coronary heart disease: Can heavier really be healthier? Heart. 2015. doi: heartjnl-2015-307966. 3. Banack HR, Kaufman JS. Does selection bias explain the obesity paradox among individuals with cardiovascular disease? Ann Epidemiol. 2015;25(5):342-349. 4. Hernandez-Diaz S, Schisterman EF, Hernan MA. The birth weight "paradox" uncovered? Am J Epidemiol. 2006;164(11):1115-1120.

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  2. Correspondence: A not so typical pericardial effusion case....

    To the Editor: We have read with interest the article of Miranda WR and coauthors1, in which a case of effusive-constrictive pericarditis is presented. This is a comprehensive and educational case that provides clinicians with a valuable message. Some points, however, require additional clarification in order to further strengthen the impact of this case. In particular, it is mentioned in the introduction that the patient was diagnosed with 'idiopathic pericarditis'. Nonetheless, the diagnosis of pericarditis is established in the presence of at least 2 out of the 4 main criteria including chest pain, pericardial friction, typical ECG changes and pericardial effusion.2 CRP elevation and pericardial inflammation in the cardiac magnetic resonance imaging (cMR) both constitute supportive findings. Accordingly, since only one diagnostic criterion was fulfilled (i.e. pericardial effusion), it should probably be more appropriate to 'label' the patient's disorder as 'idiopathic pericardial effusion' rather than 'idiopathic pericarditis'. Concerning treatment, the patient received initially colchicine as an outpatient, despite normal baseline CRP values. However, in the absence increased CRP levels, the efficacy of colchicine is questionable in chronic idiopathic pericardial effusion.3 Furthermore, even in the setting of idiopathic pericarditis, which this patient was presumed to have, colchicine is beneficial when administered in conjunction with either aspirin/non-steroidal anti-inflammatory (NSAID) medications or corticosteroids, but not as monotherapy.3 Another intriguing finding in this case was the demonstration of active pericardial inflammation in cMR. This is a quite unexpected finding in the presence of normal baseline CRP levels. Since pericardiocentesis and drainage catheters are potential triggers of pericardial inflammation, one wonders if pericardiocentesis was the actual cause of pericardial inflammation. Along this line, it would be interesting to know the post- pericardiocentesis serum CRP levels. Last but not least, the patient became asymptomatic and the jugular pressure normalized within 72 hours after aggressive NSAID therapy. This turn of events strongly suggests transient pericardial constriction, namely a reversible cause of pericardial constriction, which is occasionally observed towards the end of the effusive period of pericarditis.4 In conclusion, a final diagnosis of idiopathic pericardial effusion (possibly post-pericarditis) with transitory constriction probably unifies all aspects of this challenging case.

    References 1 Miranda WR, Newman DB, Nishimura RA. A not so typical pericardial effusion case....Heart 2015 Jun 17. pii: heartjnl-2015-308115. 2 Imazio M, Gaita F. Diagnosis and treatment of pericarditis. Heart 2015 Apr 8. pii: heartjnl-2014-306362. 3 Brucato A, Brambilla A, Adler Y, Spodick,D. Colchicine for Recurrent Acute Pericarditis. Arch Intern Med 2006;166:696. 4 Haley JH, Tajik AJ, Danielson GK, et al. Transient constrictive pericarditis: causes and natural history. J Am Coll Cardiol 2004;43:271-5.

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  3. Importance of the UK health care model for success in cardiovascular disease control compared the health care model in Turkey

    We read the paper of Bhatnagar P. et al. 1 and were impressed by great success of the UK health care on control of cardiovascular disease (CVD). In the UK during last decade, CVD decreased from top to 2nd row on mortality of men in whom, lipid lowering drugs were the most prescribed medicine. 1 In this report, importance of primary care and increased number of less invasive approaches like angioplasty compared to surgery were pointed out. We compared some data here with performance-based procedure-dependent income model for physicians in Turkey during the last decade. All individuals can apply to a tertiary hospital since absence of compulsory referral system in this model.

    Decreased number of referred patients may not eliminate low risk group and high risk patients may not be treated effectively, then more severely ill patients may be detected in a vicious circle. Since the health autority has started to act in 2002, the number of refered patients from primary care has decreased and operations has increased from 22 %, 1.598.362 to 3 %, 4.684.237 respectively in 2013. 2 Nevertheless, CVD continues to be the biggest killer in Turkey. In this model, increased applications may be seen as a profitable investment. In fact, the total number of private hospitals has gradually increased from 271 in 2002 and to 550 in 2013 in Turkey. 2 Interestingly, instead of encouraging preventive approach, it was tried to settle a mandatory on call arrangement for primary care physicians differently from UK. Fortunately, that was blocked by social consciousness.

    Limited time for diagnostic tests in Turkish model may be a disadvantage for prevention of organ damage in hypertension. One of five patients with previously undiagnosed hypertension, the leading risk for CVD is associated with subclinical target organ damage including cardiac remodelling. 3 Early determination of cardiac remodelling and exercise hypertension have gained more importance, 4 however, they may be ignored in clinical practice. Exercise hypertension may be missed even in large national registiries, therefore, we recently have mentioned its importance in healthy individuals who develope early cardiac remodelling in British registry (LARGE). 4

    1. Bhatnagar P, Wickramasinghe K, Williams J, et al. The epidemiology of cardiovascular disease in the UK 2014. Heart 2015;0:1-8. doi:10.1136/heartjnl-2015-307516. 2. Kose MR, Basara BB, Guler C, Yentur GK. Turkish Republic, Ministry of Health. Annual Health Statistics, Ankara, 2013. 3. Korhonen PE, Kautiainen H, Jarvenpaa S, Kantola I. Target organ damage and cardiovascular risk factors among subjects with previously undiagnosed hypertension. Eur J Prev Cardiol 2013; 21:980-8. 4. Yalcin F, Abraham TP, Gottdiener JS. Letter regarding the article by Lee PT, et al. Left ventricular wall thickness and the presence of asymmetric hypertrophy in healthy young army recruits: data from the LARGE heart study. Circ Cardiovasc Imaging 2013;6:e28.

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  4. Review underestimates cardiovascular disease prevalence

    Dear Editor

    In their review of the epidemiology of cardiovascular disease (CVD) in the UK, Bhatnagar et al considerably underestimate the prevalence of CVD.[1] They used data from the Clinical Practice Research Datalink (CPRD), an extract of primary care electronic health records (EHRs) of a representative sample of patients registered with UK general practices, and data from the Quality & Outcomes Framework (QOF), the UK general practice pay for performance scheme. However data from two other sources demonstrate a higher incidence or prevalence of CVD than that obtained from CPRD or QOF.

    For example, using CPRD data, Bhatnagar et al report a prevalence of stroke of 2.53% in men and 1.99% in women. This is higher than the overall stroke prevalence of 1.7% quoted by the authors using QOF data, probably because data and care quality is better in CPRD practices. However the Health Survey for England (HSfE) 2013 report includes time trends in CVD prevalence up to 2011,[2] and the corresponding figures, based on patient- reported doctor-diagnosed disease, are 2.7% and 2.1%. Patient reports of stroke prevalence have been well-validated in longitudinal cohort studies.[3-5]

    Record linkage studies have also shown that primary care EHRs underestimate the prevalence of CVD. For example, using data from CPRD, hospital admissions from Hospital Episode Statistics, and the national registry of acute coronary syndromes (Myocardial Ischaemia National Audit Project, MINAP), and the mortality registry, Herrett et al showed that the crude incidence of acute myocardial infarction was 25% lower using only Clinical Practice Research Datalink data compared with using all three sources. Payne et al showed considerably higher CVD incidence rates when general practice and hospital data was combined.[6]

    We have used HSfE data to model the prevalence of CVD in small populations,[7] and have shown strong evidence of spatial clustering of CVD under-diagnosis, particularly in deprived inner city areas.[8] In order to reduce CVD mortality further and tackle health inequalities, there should be much higher awareness of under-diagnosis in primary care.

    References

    1. Bhatnagar P, Wickramasinghe K, Williams J, Rayner M, Townsend N. The epidemiology of cardiovascular disease in the UK 2014. Heart 2015. Link: http://heart.bmj.com/content/early/2015/05/06/heartjnl-2015- 307516.abstract.

    2. Health & Social Care Information Centre. Health Survey for England - 2013, Trend tables 2014. Link: http://www.hscic.gov.uk/catalogue/PUB16077/HSE2013-Adult-trend-tbls.xls.

    3. Walker MK, Whincup PH, Shaper AG, Lennon LT, Thomson AG. Validation of Patient Recall of Doctor-diagnosed Heart Attack and Stroke: A Postal Questionnaire and Record Review Comparison. American Journal of Epidemiology 1998;148(4):355-61. Link: http://aje.oxfordjournals.org/cgi/content/abstract/148/4/355

    4. Glymour MM, Avendano M. Can Self-Reported Strokes Be Used to Study Stroke Incidence and Risk Factors?: Evidence From the Health and Retirement Study. Stroke 2009;40(3):873-79. Link: http://stroke.ahajournals.org/cgi/content/abstract/40/3/873

    5. Kazumasa Y, Ai I, Hiroyasu I, Manami I, Shoichiro T. Self-reported stroke and myocardial infarction had adequate sensitivity in a population- based prospective study JPHC (Japan Public Health Center)?_"based Prospective Study. Journal of clinical epidemiology 2009;62(6):667-73. Link: http://www.sciencedirect.com/science/article/pii/S0895435608002345

    6. Payne RA, Abel GA, Simpson CR. A retrospective cohort study assessing patient characteristics and the incidence of cardiovascular disease using linked routine primary and secondary care data. BMJ Open 2012;2(2). Link: http://bmjopen.bmj.com/content/2/2/e000723.abstract.

    7. Public Health England (Association of Public Health Observatories). Browsing Disease prevalence models: modelled estimates of prevalence of CHD by GP Practice. 2009. Link: http://www.apho.org.uk/resource/view.aspx?RID=48308.

    8. Soljak M, Samarasundera E, Indulkar T, Walford H, Majeed A. Variations in cardiovascular disease under-diagnosis in England: national cross-sectional spatial analysis. BMC Cardiovascular Disorders 2011;11(1):12. Link: http://www.biomedcentral.com/1471-2261/11/12.

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  5. Progression of myocardial fibrosis in Hypertrophic cardiomyopathy

    We have read with interest the article by Choi and colleagues entitled "Myocardial fibrosis progression on cardiac magnetic resonance in hypertrophic cardiomyopathy" published on Heart" (1). In this study, the Authors evaluated the increment of the extent of late gadolinium enhancement (LGE) in patients with hypertrophic cardiomyopathy (HCM). This study reproduces our previous paper entitled "Progression of myocardial fibrosis assessed with cardiac magnetic resonance in hypertrophic cardiomyopathy", published in 2012 (2) and cited in the current ESC guidelines for HCM. Choi found a fast progression of fibrosis in HCM, confirming our previous results. However, there are some differences between the studies that deserve a discussion. Choi and colleagues used a cut-off of >4% of LGE to assess the increment of fibrosis, whereas we used a cut-off of ?1 gram increment. In HCM the left ventricular mass may change significantly from the baseline to the follow-up magnetic resonance and a change in % of ventricular mass may not necessarily be consequence of a real increase in LGE but only secondary to variation of left ventricular mass.

    We found that apical HCM had higher LGE rate of progession, but this was not found by Choi who underlines this difference asserting that our"results are in clear contrast with common belief that the prognosis of apical HCM is generally good". However, in both studies the prognosis was not evaluated and the populations are different because Choi and colleagues excluded apical HCM with apical anuerysm. Apical anuerysms may be the evolution of the fast progression of LGE in apical HCM and are associated to worse prognosis (3). Yet, there are some recent evidences demonstrating the worse prognosis of apical HCM than other patterns of hypertrophy in caucasian patients (4). European and Asiatic apical HCM might be different diseases, with similar phenotype but different rate of progression of LGE and maybe prognosis. Unfortunately, because of the lack of genotype in both the studies, we cannot assess whether the different rate of LGE progression between the two populations of apical HCM is secondary to geographical/ethnic differences or to a selection bias performed by the Authors.

    References 1. Choi HM, Kim KH, Lee JM, Yoon YE, Lee SP, Park EA, Lee W, Kim YJ, Cho GY, Sohn DW, Kim HK. Myocardial fibrosis progression on cardiac magnetic resonance in hypertrophic cardiomyopathy. Heart. 2015;101:870-876. 2. Todiere G, Aquaro GD, Piaggi P, Formisano F, Barison A, Masci PG, Strata E, Bacigalupo L, Marzilli M, Pingitore A, Lombardi M. Progression of myocardial fibrosis assessed with cardiac magnetic resonance in hypertrophic cardiomyopathy.J Am Coll Cardiol. 2012;60:922-929. 3. Maron MS, Finley JJ, Bos JM, Hauser TH, Manning WJ, Haas TS, Lesser JR, Udelson JE, Ackerman MJ, Maron BJ.Prevalence, clinical significance, and natural history of left ventricular apical aneurysms in hypertrophic cardiomyopathy. Circulation. 2008;118:1541-1549 4. Klarich KW, Attenhofer Jost CH, Binder J, Connolly HM, Scott CG, Freeman WK, Ackerman MJ, Nishimura RA, Tajik AJ, Ommen SR.Risk of death in long-term follow-up of patients with apical hypertrophic cardiomyopathy. Am J Cardiol. 2013;111:1784-1791

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  6. Atrial fibrillation in acute pericarditis: an overblown association

    Imazio et al. investigated the incidence and prognosis of presumably new onset atrial fibrillation (AF) and flutter (AFl) in acute pericarditis [1]. They showed that only 4% of the patients with acute pericarditis developed new onset atrial arrhythmias [1]. The mean age of patients who experienced AF in this study was 67 years. Notably, the age-stratified AF prevalence in this study remains comparable to that in the general population of a developed country [2-3]. The study findings strongly suggested that acute pericarditis by itself may not be significantly arrhythmogenic.

    It apparently remains a common prevailing myth that acute idiopathic pericarditis predisposes to AF due to an accompanying inflammatory state. On the contrary, arrhythmias in acute idiopathic or viral pericarditis are often related to alternate associated comorbidities such as ageing, ventricular dysfunction, myocardial ischemia and/or factors predisposing to left atrial abnormality [4-7]. This is supported by the data from several prior controlled investigations [4-6]. Non-idiopathic forms of pericarditis such as suppurative pericarditis and the ones complicated by development of effusions or major hemodynamic alterations may be at a higher risk for developing AF due to accompanying septic state and fluid volume shifts. This perhaps may be partly the reason for why some studies had shown higher rates of AF in patients with bacterial and tuberculous pericarditis [8]. Similarly, in the current study presence of pericardial effusion was associated with a higher risk of AF. Also, patients with postoperative pericarditis and post-pericardiotomy syndrome may have a higher incidence of AF due to the similar reasons associated with any other form of post-surgical AF.

    In summary, the presence of AF in acute idiopathic pericarditis should not be perceived as a causal association and rather may reflect unmasking of AF in a patient with prior asymptomatic paroxysmal AF or simply reflect the presence of a prior underlying risk substrate for AF such as left atrial enlargement or left ventricular systolic or diastolic dysfunction. This well-designed study further in fact further clarifies that the use of anticoagulation, when warranted, in patients with acute pericarditis may not be as deleterious as it was previously thought.

    References: 1. Imazio M, Lazaros G, Picardi E, Vasileiou P, Orlando F, Carraro M, Tsiachris D, Vlachopoulos C, Georgiopoulos G, Tousoulis D, Belli R, Gaita F. Incidence and prognostic significance of new onset atrial fibrillation/flutter in acute pericarditis. Heart. 2015 Apr 29. pii: heartjnl-2014-307398. doi: 10.1136/heartjnl-2014-307398. 2. Ball J, Carrington MJ, McMurray JJ, Stewart S. Atrial fibrillation: profile and burden of an evolving epidemic in the 21st century. Int J Cardiol. 2013;167(5):1807-24. 3. Lip GY, Brechin CM, Lane DA. The global burden of atrial fibrillation and stroke: a systematic review of the epidemiology of atrial fibrillation in regions outside North America and Europe. Chest. 2012;142(6):1489-98. 4. Spodick DH. Arrhythmias during acute pericarditis. A prospective study of 100 consecutive cases. JAMA. 1976;235:39-41. 5. Spodick DH. Significant arrhythmias during pericarditis are due to concomitant heart disease. J Am Coll Cardiol. 1998;32:551-2. 6. Spodick DH: The Pericardium: A Comprehensive Textbook, Marcel Dekker, New York 1997. 7. Chhabra L, Spodick DH. Letter by Chhabra and Spodick regarding the article, "Clinical Profile and Influences on Outcomes in Patients Hospitalized for Acute Pericarditis" by Kyt? et al. Circulation. 2015. In Press. 8.Syed FF, Ntsekhe M, Wiysonge CS, et al. Atrial fibrillation as a consequence of tuberculous pericardial effusion. Int J Cardiol. 2012; 158:152-4.

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  7. Survival in South Asian and White European patients after acute myocardial infarction: new evidence of heterogeneity

    Dear Editor Gholap et al confirmed a surprising observation that South Asians, compared to White British populations, have lower or similar, rather than higher mortality, following myocardial infarction, as Fischbacher et al first demonstrated in Scotland.(1;2) As the chief investigator of that Scottish study I found the result perplexing given South Asians' high prevalence of type 2 diabetes. A literature review showed the mortality following MI in Scottish South Asians was similar to international reports and concluded that White Scottish people had unusually high post-MI mortality.(2) This showed how studies on minorities may, paradoxically, throw light on health of the majority.

    Possibly, compared to White Scottish people, South Asians may have having smaller, less lethal MIs given their tendency to diffuse atherosclerosis. We hypothesised that South Asians may reach hospitals quicker than the White Scottish populations given they tended to live in the inner city. Given heterogeneity in South Asian populations (Indians, Pakistanis; men, women) we were keen to disaggregate them. We have published our results, and they show further surprises. The survival following MI was, compared to White Scottish people, similar in Indian men and women, but better in Pakistanis, especially women. Our conclusions were unaltered by adjustment for socio-economic factors, travel times, hospitalisation for diabetes, or cardiovascular procedures. We had no cardiovascular risk factor data but Gholap et al's data show these are not explanatory.

    The results are reassuring from a clinical and public health perspective but they remain surprising. Possibly, they relate to lower cardiovascular risk factors over a lifetime, as many of South Asians came to the UK as adults having had little exposure to risk factors when young. It will be interesting to see whether the new generations of South Asians will also enjoy this 'protection', given their lifelong exposure to cardiovascular risk factors and a high risk of diabetes.

    In the Netherlands ethnic minority groups (defined by parental and own birthplace) have relatively worse outcomes, with gaps increasing over time.(4) Overall, in the UK we can be proud of these results as they reflect, at least partially, equitable health care.

    Reference List

    1 Gholap NN, Khunti K, Davies MJ, Bodicoat DH, Squire IB. Survival in South Asian and White European patients after acute myocardial infarction. Heart 2015; 101/8: 630-636. 2 Fischbacher CM, Bhopal R, Povey C, Steiner M, Chalmers J, Mueller G et al. Record linked retrospective cohort study of 4.6 million people exploring ethnic variations in disease: myocardial infarction in South Asians. BMC Public Health 2007; 7/1: 142. 3 Bansal N, Fischbacher CM, Bhopal RS, Brown H, Steiner MF, Capewell S et al. Myocardial infarction incidence and survival by ethnic group: Scottish Health and Ethnicity Linkage retrospective cohort study. BMJ Open 2013; 3/9. 4 van Oeffelen AAM, Agyemang C, Stronks K, Bots ML, Vaartjes I. Prognosis after a first hospitalisation for acute myocardial infarction and congestive heart failure by country of birth. Heart 2014; heartjnl-2013.

    Word count 345

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  8. Culprit or multivessel revascularisation in cardiogenic shock

    Georg Fuernau, Holger Thiele

    Medical Clinic II-Department of Cardiology, Angiology and Intensive Care Medicine, University Heart Center Luebeck, University of Luebeck, Luebeck, Germany

    Keywords: acute myocardial infarction, cardiogenic shock, multivessel percutaneous coronary intervention

    Corresponding author: Georg Fuernau, M.D. Medical Clinic II (Cardiology/Angiology/Intensive Care Medicine) University Heart Center Luebeck University Hospital Schleswig-Holstein, Ratzeburger Allee 160 23538 Luebeck, Germany Mail: georg.fuernau@gmx.at Tel.: +49 451 500 2501; Fax: +49 451 500 6437

    We read with great interest the manuscript by Park and co-workers published epub ahead of print in Heart [1]. The authors investigated an important and controversial issue, interventional treatment of multi- vessel disease in patients with cardiogenic shock complicating acute myocardial infarction. Yet, we have some concerns if the population studied in this manuscript reflects a population with real cardiogenic shock. Although using established definitions for cardiogenic shock (systolic blood pressure <90 mmHg for >30 min or the need for supportive management to maintain systolic blood pressure >90 mmHg and evidence of end-organ hypoperfusion) the one-year mortality (~16%) in the study by Park et al. was much lower than in all other studies investigating cardiogenic shock. In other trials mortality rates of 50% up to 63% after 1 year were reported [2, 3]. Therefore, we believe that the population studied is a cohort at minor risk and the results cannot be extrapolated to patients with severe cardiogenic shock. Furthermore, the discussion is slightly selective with not all trials being cited comparing multi-vessel versus culprit lesion only PCI in cardiogenic shock. The current evidence has recently been reviewed [4]. To clarify the important question of multi-vessel vs. culprit lesion percutaneous coronary intervention in patients with cardiogenic shock complicating myocardial infarction a randomized European multi-center study is currently recruiting patients (Culprit Lesion Only PCI Versus Multivessel PCI in Cardiogenic Shock - CULPRIT-SHOCK; ClinicalTrials.gov Identifier: NCT01927549). Conflict of Interest: None declared

    References

    1 Park JS, Cha KS, Lee DS, et al. Culprit or multivessel revascularisation in ST-elevation myocardial infarction with cardiogenic shock. Heart 2015. pii: heartjnl-2014-307220. doi: 10.1136/heartjnl-2014- 307220. [Epub ahead of print].

    2 Thiele H, Zeymer U, Neumann FJ, et al. Intra-aortic balloon counterpulsation in acute myocardial infarction complicated by cardiogenic shock (IABP-SHOCK II): final 12 month results of a randomised, open-label trial. Lancet 2013;382:1638-45.

    3 Aissaoui N, Puymirat E, Tabone X, et al. Improved outcome of cardiogenic shock at the acute stage of myocardial infarction: a report from the USIK 1995, USIC 2000, and FAST-MI French nationwide registries. Eur Heart J 2012;33:2535-43.

    4 Thiele H, Ohman EM, Desch S, et al. Management of cardiogenic shock. Eur Heart J 2015. pii: ehv051. [Epub ahead of print].

    Conflict of Interest:

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  9. Paradoxical low-flow low-gradient aortic stenosis: advanced severe disease, a new entity or a progression of disease?

    I read the research by Dahl et al. with great interest (1). The authors have suggested paradoxical low-flow low-gradient aortic stenosis is a distinct entity, and not an advanced stage of severe aortic stenosis. Indeed, they have observed only 5% of these patients had high-gradient severe disease prior to the index assessment (1).

    Recent studies have demonstrated that paradoxical low-flow low- gradient is a heterogeneous subgroup of patients with aortic valve calcification (based on computed tomography), echocardiographic and cardiovascular magnetic resonance features between those observed in concordant non-severe and severe disease (2-4). Moreover, more than 80% of patients with paradoxical low-flow low-gradient severe aortic stenosis experienced progression of aortic stenosis severity, with half of them to high-gradient severe disease (5). Instead of an advanced stage of severe disease or a distinct entity, these studies have suggested paradoxical low -flow low-gradient severe aortic stenosis is a stage in transition from non-severe to severe disease.

    Consistent with this hypothesis, all the patients in the current study have progressed from non-severe disease, albeit at different rates and with different remodelling patterns (Figures 1, 2 and 3 (1)). In this regard, paradoxical low-flow low-gradient severe aortic stenosis (and for that matter, the other flow and gradient patterns) reflects the complex interaction between aortic valve calcification and heterogeneous hypertrophic response, rather than a new entity.

    Longitudinal studies with multi-modality imaging approaches (echocardiography, computed tomography and cardiovascular magnetic resonance) will be essential to fully examine this complex interaction between the valve and the myocardium; and to identify unique characteristics that determine progression in the different flow-gradient patterns.

    References 1. Dahl JS, Eleid MF, Pislaru SV, Scott CG, Connolly HM, Pellikka PA. Development of paradoxical low-flow, low-gradient severe aortic stenosis. Heart. 2015 Mar 20 [Epub ahead of pring]. 2. Chin C, Khaw J, Luo E, Tan SW, White A, Newby DE, et al. Echocardiography Underestimates Stroke Volume and Aortic Valve Area: Implications for Patients With Small-Area Low-Gradient Aortic Stenosis. Can J Cardiol. 2014;30(9):1064-72. 3. Barone-Rochette G, Pi?rard S, Seldrum S, de Meester de Ravenstein C, Melchior J, Maes F, et al. Aortic Valve Area, Stroke Volume, Left Ventricular Hypertrophy, Remodeling, and Fibrosis in Aortic Stenosis Assessed by Cardiac Magnetic Resonance Imaging: Comparison Between High and Low Gradient and Normal and Low Flow Aortic Stenosis. Circ Cardiovasc Imaging. 2013;6(6):1009-17. 4. Clavel M-A, Messika-Zeitoun D, Pibarot P, Aggarwal S, Malouf JF, Araoz P, et al. The complex nature of discordant severe calcified aortic valve disease grading. J Am Coll Cardiol. 2013;62(24):2329-38. 5. Maes F, Boulif J, Pi?rard S, de Meester C, Melchior J, Gerber B, et al. Natural History of Paradoxical Low-Gradient Severe Aortic Stenosis. Circ Cardiovasc Imaging. 2014;7(4):714-22.

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  10. Re:Comment on: An epidemiological appraisal of the association between heart rate variability and particulate air pollution: a meta-analysis

    We thank Buteau and colleague (Buteau et al. 2014) for their interest in our meta-analysis on Heart Rate Variability (HRV) and air pollution (Pieters et al. 2012). Their concern about combining studies from different types of regression models ignores the strength of our meta -analysis to combine all the available evidence on HRV and air pollution published before February 2012. Combining the available evidence is critically important for the goal of computing a summary effect. Nevertheless, Buteau is right that the percentage change calculated from linear and logarithmic models are not exactly the same. However, we disagree that the use of linear models impacted the overall estimates of our meta-analysis based on both logarithmic and linear models. We re-ran our analysis with exclusion of the linear studies (n=6). In this sensitivity analysis, using only studies with logarithmic models (n=23), the combined estimate for an increase of 10 ?g/m? in PM2.5 was associated with significant reduction in the frequency domain parameters including low frequency (-1.77%, 95% CI: -2.82 to -0.72%), high frequency (-2.46%, 95% CI: -3.79 to -1.12%) and time domain parameters SDNN (-0.98%, 95% CI: -1.44 to -0.52%) and RMSSD (-2.62%, 95% CI: -3.65 to -1.61%). These overall estimates did not differ meaningfully from the originally reported estimates combining both linear and logarithmic estimates.

    We agree that meta-analysis should be interpreted in the context of their limitations. Meta-analysis which are based on the information given in the publication, cannot provide the same detail as combining the original data of all studies. Being too stringent to leave out studies based on the models used may also introduce a potential bias towards the overall evidence. However, sensitivity of the findings as presented now, is indeed useful.

    References: Stephane Buteau, Mark S. Goldberg Comment on: An epidemiological appraisal of the association between heart rate variability and particulate air pollution: a meta-analysis Heart published online December 29, 2014

    Pieters N, Plusquin M, Cox B, Kicinski M, Vangronsveld J, Nawrot TS. An epidemiological appraisal of the association between heart rate variability and particulate air pollution: a meta-analysis. Heart. 2012;98:1127-35.

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