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Recent eLetters

Displaying 1-10 letters out of 712 published

  1. Revascularization of chronic total coronary occlusions

    Revascularization of chronic total coronary occlusions

    Christophe Bauters a, b, c, MD; Gilles Lemesle a, c, MD.

    a Centre Hospitalier R?gional et Universitaire de Lille, Lille, France b Inserm U1167, Institut Pasteur de Lille, Universit? de Lille 2, Lille, France c Facult? de M?decine de Lille, Lille, France

    To the Editor,

    We read with great interest the article by Ladwiniec et al. (1) on the prognostic impact of percutaneous interventions (PCI) for chronic total coronary occlusions (CTO). Indeed, there are obvious limitations in the previously published literature that essentially demonstrated a better prognosis after successful CTO PCI than after failed CTO PCI. A propensity -matched approach comparing CTO PCI versus medically treated CTO as performed in the present report, does not have the strength of a randomized trial, but nevertheless has the potential to provide meaningful information for physicians. In the modern era of secondary prevention, the prognosis of patients with stable coronary artery disease (CAD) has been shown to be favorable (2). Although this may make difficult to demonstrate a survival benefit by a new intervention, this is however a global figure and subgroups of patients, such as those with CTO, may do worse than others; therefore, focusing studies on these high-risk stable CAD patients certainly makes sense. The study by Ladwiniec et al. (1) reports interesting trends suggesting that revascularization of a CTO might be beneficial. However, one important point that would need to be clarified is the level of secondary prevention in this study, and whether this level was the same in all groups of patients. There are consistent data in the literature showing that patients with a recent revascularization have higher prescription of secondary prevention drugs (statins, antiplatelets, angiotensin-converting enzyme inhibitors, ?-blockers) than patients without revascularization (3). In addition, information on the use of dual antiplatelet therapy (DAPT) would also be important. Due to the frequent use of drug-eluting stents (DES), and long stented segments, it is conceivable that an extended duration of DAPT was used in a significant proportion of the patients with CTO PCI. Extended DAPT has recently been shown to reduce thrombotic events after DES implantation (4); this impact is not only related to a decrease in very late stent thrombosis but also to a reduction in non-stent-thrombosis-related myocardial infarction. An imbalance toward more intense secondary prevention in the CTO PCI group could potentially explain the trends for the improved outcome. If the information is available, providing data on the combination of secondary prevention drugs at discharge and also during the course of the study would therefore be very useful.

    References

    [1] Ladwiniec A, Allgar V, Thackray S, Alamgir F, Hoye A. Medical therapy, percutaneous coronary intervention and prognosis in patients with chronic total occlusions. Heart 2015;101:1907-14. [2] Bauters C, Deneve M, Tricot O, Meurice T, Lamblin N. Prognosis of patients with stable coronary artery disease (from the CORONOR study). Am J Cardiol 2014;113:1142-5. [3] Meurice T, Tricot O, Lemesle G et al. Prevalence and correlates of non -optimal secondary medical prevention in patients with stable coronary artery disease. Arch Cardiovasc Dis 2015;108:340-6. [4] Mauri L, Kereiakes DJ, Yeh RW et al. Twelve or 30 months of dual antiplatelet therapy after drug-eluting stents. N Engl J Med 2014;371:2155 -66.

    Conflict of Interest:

    None declared

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  2. Adiponectin and Atrial Fibrillation in Older Adults

    We thank Dr. Kawada for his comments regarding our study. Consistent with the sexual dimorphism in circulating adiponectin levels documented in both rodents and humans, plasma concentrations of total and high-molecular -weight (HMW) adiponectin were higher in female than male participants in the Cardiovascular Health Study.[1] Despite such differences, we have not found evidence of effect modification by sex for total or HMW adiponectin for a variety of outcomes in this cohort, including diabetes,[2] mortality,[1] cardiovascular disease,[3] heart failure[4] and now atrial fibrillation (AF).[5] In our view, this lack of support for sex interaction obviates the need for stratified analyses. As relates to Dr. Kawada's query regarding the possible superiority of HMW adiponectin for prediction of AF, we note that although the risk estimates are somewhat higher numerically for the HMW fraction as compared with total adiponectin, the broadly overlapping 95% confidence intervals do not support the presence of a real difference between the two. Last, as detailed in our manuscript and the accompanying editorial, our findings lay out the need for further study into the adiponectin-AF relationship, and we agree with Dr. Kawada that such efforts should include meta- analytic approaches.

    References

    1. Kizer JR, Benkeser D, Arnold AM, Mukamal KJ, Ix JH, Zieman SJ, Siscovick DS, Tracy RP, Mantzoros CS, Defilippi CR, Newman AB, Djousse L. Associations of total and high-molecular-weight adiponectin with all-cause and cardiovascular mortality in older persons: The cardiovascular health study. Circulation. 2012;126:2951-2961

    2. Kizer JR, Arnold AM, Benkeser D, Ix JH, Djousse L, Zieman SJ, Barzilay JI, Tracy RP, Mantzoros CS, Siscovick DS, Mukamal KJ. Total and high-molecular-weight adiponectin and risk of incident diabetes in older people. Diabetes Care. 2012;35:415-423

    3. Kizer JR, Benkeser D, Arnold AM, Djousse L, Zieman SJ, Mukamal KJ, Tracy RP, Mantzoros CS, Siscovick DS, Gottdiener JS, Ix JH. Total and high -molecular-weight adiponectin and risk of coronary heart disease and ischemic stroke in older adults. J Clin Endocrinol Metab. 2013;98:255-263

    4. Karas MG, Benkeser D, Arnold AM, Bartz TM, Djousse L, Mukamal KJ, Ix JH, Zieman SJ, Siscovick DS, Tracy RP, Mantzoros CS, Gottdiener JS, deFilippi CR, Kizer JR. Relations of plasma total and high-molecular- weight adiponectin to new-onset heart failure in adults >/=65 years of age (from the cardiovascular health study). Am J Cardiol. 2014;113:328-334

    5. Macheret F, Bartz TM, Djousse L, Ix JH, Mukamal KJ, Zieman SJ, Siscovick DS, Tracy RP, Heckbert SR, Psaty BM, Kizer JR. Higher circulating adiponectin levels are associated with increased risk of atrial fibrillation in older adults. Heart. 2015;101:1368-1374

    Conflict of Interest:

    None declared

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  3. Total and high molecular weight adiponectin are positively associated with incident atrial fibrillation by a follow-up study

    I read with great interest the report by Macheret et al., (1) who conducted an 11-year prospective study in 3190 older adults, aged 65 years or older, without cardiovascular disease for monitoring incident atrial fibrillation (AF). The authors measured plasma total adiponectin, high molecular weight (HMW) adiponectin and amino-terminal pro-brain natriuretic peptide 1-76 (NT-proBNP1-76). There were 886 incident AF events, and they demonstrated a positive, not U-shaped, association between incident AF and total or HMW adiponectin with causality by adjusting NT-proBNP1-76, adiposity and other confounders. I have some concerns on their study.

    First, the authors speculated some possible mechanism on the risk of increased plasma total and HMW adiponectin for incident AF in older adults. I fundamentally agree with their comments, but sex difference on total and HMW adiponectin should be handled with caution. The authors presented the decreasing trend in the percentage of men, stratified by quartiles of total and HMW adiponectin in their Tables 1 and S1. As there is a sex difference on AF (2), stratified analysis by sex in addition to the adjustment with sex would present useful information.

    Second, the authors selected the Cox proportional hazard model for the risk assessment of AF by plasma total and HMW adiponectin. The authors presented that correlation coefficient between total and HMW adiponectin was 0.94, and I agree with their statistical procedure of precluding simultaneous inclusion into independent variables. Is there no superiority between total and HMW adiponectin for the prediction of AF in older adults?

    Barnett and Piccini (3) also recommended further research to confirm the possible mechanism on the association, which would lead to the prevention of AF in older adults. Anyway, studies presenting the positive or no association between adiponectin and incident AF would be summarized by meta-analysis in the future(4,5).

    References

    1. Macheret F, Bartz TM, Djousse L, et al. Higher circulating adiponectin levels are associated with increased risk of atrial fibrillation in older adults. Heart 2015;101:1368-74.

    2. Rienstra M, Van Veldhuisen DJ, Hagens VE, et al. Gender-related differences in rhythm control treatment in persistent atrial fibrillation: data of the Rate Control Versus Electrical Cardioversion (RACE) study. J Am Coll Cardiol 2005;46:1298-306.

    3. Barnett AS, Piccini JP Sr. Adiponectin: an accurate biomarker for patients at risk for atrial fibrillation? Heart 2015;101:1351-2.

    4. Knuiman M, Briffa T, Divitini M, et al. A cohort study examination of established and emerging risk factors for atrial fibrillation: the Busselton Health Study. Eur J Epidemiol 2014;29:181-90.

    5. Rienstra M, Sun JX, Lubitz SA, et al. Plasma resistin, adiponectin, and risk of incident atrial fibrillation: the Framingham Offspring Study. Am Heart J 2012;163:119-124.e1.

    Conflict of Interest:

    None declared

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  4. Genomics in cardiology: new findings in old syndromes?

    Last year, in response to Priest and Ashley's paper on genomics in cardiology[1], we urged close collaboration of congenital cardiologist and geneticist for some adults with congenital heart conditions, who had not been tested in childhood.[2] The converse is also pertinent. A recent case (23-year-old female) with chromosome 1p36 deletion* (previous PDA and VSD closure in childhood) presented at another hospital with TIA's; echocardiography demonstrated impaired left ventricular function (40%) the cause of which was not clear. There were no residual septal defects and no arrhythmias were documented on extended ambulatory monitoring. Cardiac involvement in 1p36 deletion is well described, predominantly ASD (28%), VSD (23%), valvar anomalies (20.5%) and PDA (12.8%)[3]. 1p36 is one of the most common distal terminal deletion syndromes. It is a contiguous gene deletion syndrome involving haploinsufficiency of several genes, which is associated with a multisystem disorder including developmental delay and mental retardation. Yet it was only in 2008 that an association with left ventricular non-compaction (LVNC) was observed in a cohort of 60 patients (23%).[3] LVNC is a distinct cardiomyopathy characterised by abnormal persistence of left ventricular trabeculations; it may be associated with left ventricular hypertrophy or dilatation, or both; Important sequelae do occur - heart failure, ventricular arrhythmias, complete heart block, and thromboembolic disease arising from the recesses between trabeculae. We undertook a CT heart (MRI intolerant) in the patient referred to our GUCH service. She had dominant apical non compaction poorly characterised on 2D or 3D echo, fulfilling the criteria for a diagnosis of LVNC. Anticoagulation has been recommended.

    Deletion of 1p36 was first described in the early 1980's. Further advances have identified mutations in the PRDM16 gene within the 1p36 region, encoding a transcription factor. It is suggested that a gene deletion within the 1p36 region may be one cause of LVNC and dilated cardiomyopathy.[4] Cardiologists and Geneticists working together, sharing new knowledge in their particular specialities, is beneficial for them and their patients. We have striven (unfunded) to create that service. This case is an example of that practice. Commissioners please take note.

    *She also has a terminal 5p15.3 trisomy which has not been associated with LVNC.

    References

    1. 1. Priest J.R, Ashley E.A. Genomics in clinical practice. Heart Published Online First: 25 Jul 2014 doi:10.1136/heartjnl-2014-306111
    2. 2. Rafiq I, Freeman L. Clinical genomics and the adult with congenital heart disease: new opportunities. Heart Published Online First: 6 Oct 2014. doi: 10.1136/heartjnl-2014-306802
    3. 3. Battaglia, A, Hoyme, H. E, Dallapiccola, B, et al. Further delineation of deletion 1p36 syndrome in 60 patients: a recognizable phenotype and common cause of developmental delay and mental retardation. Pediatrics 121: 404-410, 2008.
    4. 4. Arndt A.K, Schafer S, Drenckhahn J.D, et al. Fine mapping of the 1p36 deletion syndrome identifies mutation of PRDM16 as a cause of cardiomyopathy. Am J Hum Genet 2013 Jul 11;93(1):67-77.

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  5. Increasing professional and societal awareness of the uncertainty underpinning hypertrophic cardiomyopathy (HCM)

    I read with great interest the above guidelines published for this rare inherited heart disorder. Over the past few years, much work has gone into elucidating possible risk factors and markers which can help predict sudden cardiac death in such patients. Namely, we have already established that myocardial fibrosis, age and certain mutations in cardiac genes are markers indicative of a higher risk of sudden cardiac death for these individuals (1).

    Whilst biochemically, we have a clear understanding of the mutations and the pathological mechanisms which appear to lead to asymmetrical septal hyertrophy and consequent left ventricular outflow obstruction, the current difficulties instead lie with early identification, and ways in which this can be enhanced through modern imaging techniques (2). Indeed, since the disease is inherited in an autosomal dominant pattern, one pertinent question that should be carefully considered is whether those who already with affected family members should undergo early gene mutation analysis and trans-thoracic echocardiography to enhance the possibility of early detection. Moreover, once already detected, how frequently would echocardiography surveillance be indicated (to monitor for progression of hyertrophy) and justifiable from an economical point of view ? One could rationalise that such imaging may not be entirely yielding as the largest cause of death in HOCM patients remains potentially fatal ventricular arrhythmias, and thus may vindicate that primary interventions such as ICD implantation and symptom monitoring are the most prudent steps initially to mimimising cardiac death in this population.

    The fact that in the past few years, several athletes have nearly succumbed to this potentially catastrophic condition, including a high- profile Tottenham footballer, raises many issues regarding the validity of echocardiography alone in helping to diagnose and risk stratify HCM patients. Indeed, because professional athletes undergo 'compensatory' left ventricular hypertrophy in response to high-intensity aerobic training, it may practically difficult to distinguish the hyertrophy that is attributable to pathology (HCM) or instead a physiological change (3). Therefore, further work is needed to establish the best imaging modality for these patients. While recent work is being faceted towards gadolinum- enhancement MRI and the benefits this could have in detecting myocardial fibrosis and hypertrophy, we are in the present moment unfortunately limited by its availability and cost-effectiveness.

    Ultimately, whilst further work is targeted at risk stratification and studying the biochemical changes which lead to HCM, a low threshold for suspecting HCM must be maintained amongst healthcare professionals, including primary care and secondary care physicians. In particular, young patients presenting with chest pain, syncopal episodes and shortness of breath unexplained by alternative pathology, should undergo detailed evaluation and referred to specialist cardiology services in secondary care promptly.

    References:-

    1) Christiaans I, van Engelen K, van Langen IM, Birnie E, Bonsel GJ, Elliott PM, Wilde AA. Risk stratification for sudden cardiac death in hypertrophic cardiomyopathy: systematic review of clinical risk markers. Europace Journal 2010. 4 (12): 667-76.

    2) Frey N1, Luedde M, Katus HA. Mechanisms of disease: hypertrophic cardiomyopathy. Nature Review Cardiology 2011. 9(2):91-100

    3) S Basavarajaiah, M Wilson, S Junagde, G Jackson, G Whyte, and S Sharma. Physiological left ventricular hypertrophy or hypertrophic cardiomyopathy in an elite adolescent athlete: role of detraining in resolving the clinical dilemma. British Journal of Sports Medicine 2006 (8): 727-729.

    Conflict of Interest:

    None declared

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  6. Re:Correspondence: A not so typical pericardial effusion case

    To the Editor:

    We have read over and agree with the insightful comments of Lazaros at al. Our clinical vignette mainly focused on the hemodynamic abnormalities and post-pericardiocentesis diagnosis. Therefore, some of the clinical details had to be omitted for purposes of brevity. A pericardial rub was present during our patient's initial evaluation, and she later developed chest pain consistent with pericardial irritation, confirming the diagnosis of "pericarditis". However, we do agree with the authors that the diagnosis is one that requires at least 2 out of 4 main criteria. With respect to treatment, nonsteroidal anti-inflammatory agents were not prescribed by the outside institution due a reported bleeding diathesis (which was later ruled out after hematologic evaluation at our institution), but we totally agree that colchicine should not be prescribed as monotherapy for acute pericarditis. The C-reactive protein was normal post-pericardiocentesis which, in the past, was thought to rule out an active inflammatory process. However, we have seen a number of patients with signs of pericardial inflammation on MRI scanning, despite normal serum inflammatory makers who have either responded to anti- inflammatory treatment or have been found to have an inflamed pericardium at the time of surgery. This indicates to us that MRI imaging may be more sensitive than serum markers in diagnosing pericardial inflammation. Finally, we agree that this was a case of "transient constriction" [1] which was unmasked after removal of a hemodynamically significant pericardial effusion. We do thank Lazaros et al for their comments.

    References:

    1 Feng D, Glockner J, Kim K, et al. Cardiac magnetic resonance imaging pericardial late gadolinium enhancement and elevated inflammatory markers can predict the reversibility of constrictive pericarditis after antiinflammatory medical therapy: a pilot study. Circulation 2011;124:1830 -7.

    Conflict of Interest:

    None declared

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  7. Re:The key role of the right ventricle in the pathogenesis of acute pulmonary oedema

    We thank Drs. MacIver and Clark for their comments regarding the role of the right ventricle in the development of acute pulmonary edema. We agree that a relative mismatch in stroke volume from the right and left sides of the heart can contribute to alveolar congestion [1]. Although we did mention preload as an important contributor to development of hypertensive acute heart failure (AHF), we chose to simplify the discussion of right heart circulation, treating it as more of a passive conduit rather than an active precipitant for the purposes of our short, specific review. We believe this is appropriate for the intent of our discussion as it is the specific acute insult of systemic hypertension on the left ventricle that causes an imbalance in stroke volume, not an isolated increase right heart function relative to left. Stated another way, it is uncoupling of the left ventricular-vascular relationship in the setting of acute hypertension and a chronically remodeled heart that leads to an imbalance in right and left stroke volume rather than an amplification of right ventricular contractile force induced by catecholamine effects, in and of itself. Evidence for the importance of this can be seen in optimal therapeutic management of hypertensive AHF, in which rapid reduction in afterload via vasodilation produces dramatic improvement of dyspnea and resolution of acute pulmonary edema [2, 3, 4]. While the net effect most certainly reflects a re-alignment of stroke volume mismatch, the same degree of benefit is not seen with treatments that predominantly target preload reduction. Such insight suggests that, while right ventricle function can indeed be an important player in the pathogenesis of congestion, its clinical relevance for patients with hypertensive AHF may be largely academic but this mechanism should be included in any comprehensive review of all potential contributors to the complex issue of pulmonary congestion in heart failure..

    1 MacIver DH, Clark AL. The vital role of the right ventricle in the pathogenesis of acute pulmonary edema. Am J Cardiol 2015;115:992-1000. 2 Peacock WF, Chandra A, Char D, et al. Clevidipine in acute heart failure: Results of the A Study of Blood Pressure Control in Acute Heart Failure-A Pilot Study (PRONTO). Am Heart J 2014;167:529-36. 3 Levy P, Compton S, Welch R, et al. Treatment of severe decompensated heart failure with high-dose intravenous nitroglycerin: a feasibility and outcome analysis. Ann Emerg Med 2007;50:144-52. 4 Cotter G, Metzkor E, Kaluski E, et al. Randomised trial of high-dose isosorbide dinitrate plus low-dose furosemide versus high-dose furosemide plus low-dose isosorbide dinitrate in severe pulmonary oedema. Lancet 1998;351:389-93.

    Conflict of Interest:

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  8. Plasma N-terminal-pro-brain natriuretic peptide as a useful biomarker for predicting all-cause death in patients with heart failure regardless of the levels of left ventricular ejection fraction

    I read with great interest the report by Kang et al., (1) who conducted one-year prospective study in 1670 patients with heart failure (HF). The authors measured plasma N-terminal-pro-brain natriuretic peptide (NT-proBNP), and left ventricular ejection fraction (LVEF) was used for binary classification of HF. Although patients with keeping LVEF showed significantly lower NT-proBNP level than those with reduced LVEF, all- cause death did not differ between two groups. In addition, plasma NT- proBNP and obesity were significant predictors of all-cause death regardless of the levels of LVEF. I have some concerns on their study.

    First, the authors selected the Cox proportional hazard model using forward selection method (Wald statistic) with 20 independent variables for predicting all-cause mortality. As LVEF was not selected as a significant variable, and Kaplan-Meier survival curves, stratified by LVEF, have small meaning in their study. Instead, the effect of obesity on all-cause death should be speculated. I suspected that obesity at baseline was partly caused by edema, although there was a decreasing trend of body mass index as plasma NT-proBNP increased. It seems appropriate that the authors selected body mass index instead of body fat mass as the indicator of obesity. On this point, further consideration is needed.

    Second, the authors conducted receiver operating characteristic curve analysis for predicting all-cause of death by using four models. I understand the disadvantage of model 1 with LVEF3, and model 2 with plasma NT-proBNP seems satisfactory for predicting all-cause of death. But model 3 with 5 clinical factors is also useful for the prediction. I suppose that body mass index would contribute for the statistical result.

    Their study presented that only use of LVEF for predicting all-cause death in patients with HF has a risk in clinical procedure. Although the authors explained one reference as presenting a tendency towards potential harm for survival by NT-proBNP guided therapy, (2) I think that the study design differs between two studies. Anyway, I recommend the authors additional survival analysis by excluding data of death in early period of time from the baseline to avoid unsuspected reason of death.

    References

    1. Kang SH, Park JJ, Choi DJ, et al. Prognostic value of NT-proBNP in heart failure with preserved versus reduced EF. Heart 2015 Aug 28. doi: 10.1136/heartjnl-2015-307782

    2. Maeder MT, Rickenbacher P, Rickli H, et al. N-terminal pro brain natriuretic peptide-guided management in patients with heart failure and preserved ejection fraction: findings from the Trial of Intensified versus standard medical therapy in elderly patients with congestive heart failure (TIME-CHF). Eur J Heart Fail 2013;15:1148-56.

    Conflict of Interest:

    None declared

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  9. Habitual chocolate consumption and risk of cardiovascular disease among healthy men and women: Pre-determined research or/ "made-to-order" research ?

    As a part of a low-fat diet regular consumption of chocolate (containing plant sterols [PS] and cocoa flavanols [CF] ) improve cardiovascular health by lowering cholesterol and improving blood pressure [1]. Exact mechanism remains uncertain. Chocolates are a rich source of catechins, a protective molecule against heart diseases, cancer, and other medical conditions. Catechin content highest in dark, bitter chocolate and lowest in light or milk chocolate. Chocolates & cocoa products also contain addictive compounds such as n-acylethanolamines (cannabis), phenylethylamine (stimulants), also provides copper, which inhibits the action of Hesperidin (an essential flavanone). High copper activity increases the risk for vascular degeneration such as varicose veins, hemorrhoids, aneurysms, bruising, heart disease, and stroke. Copper level highest in dark, bitter chocolate and lowest in light or milk chocolate[2].There is a inverse relationship between chocolate consumption and CVD risk through reducing BP. The inverse relation appeared stronger for stroke than for MI. For consistent results randomized clinical trials (RCT) are required [3]. This observational study is similar to data dredging ; Data dredging, bias, or confounding [4]. This observational study has several limitations; self-reported data is the major limitation, and the results cannot provide evidence of causality, also correlation does not equal causation. The study highlights, how reporting observational study facts can be dangerous and why critical analysis of evidence is required . Because of wide coverage of this report in media, chocolate manufacturers have been taking advantage of these findings to target conscious consumers for health benefits, but the main agenda of the chocolate manufacturers is business i.e to earn money by selling chocolate.

    References:

    1.Robin R. Allen, LeaAnn Carson, Catherine Kwik-Uribe, Ellen M. Evans, John W. Erdman, Jr, Daily Consumption of a Dark Chocolate Containing Flavanols and AddedSterol Esters Affects Cardiovascular Risk Factors in a NormotensivePopulation with Elevated Cholesterol J. Nutr. April 2008 138: 725-731

    2.Chocolate Science and Technology, Emmanuel Ohene Afoakwa. WILEY- BLACKWELL, ISBN 978-1-4051-9906-3.

    3.Brian Buijsse; Cornelia Weikert; Dagmar Drogan; Manuela Bergmann;Heiner Boeing, Chocolate Consumption in Relation to Blood Pressure and Risk of Cardiovascular Disease in German Adults. Eur Heart J. 2010;21(13):1554-1556.

    4.Smith GD, Ebrahim S. Data dredging, bias, or confounding. BMJ 2002;325(7378):1437-8

    Conflict of Interest:

    None declared

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  10. Misinterpretation risks with a superficial reading of a meta-analysis. Reply to the letter by Nairooz et al.

    Nairooz and Naidu [1] claim that definitions of complete and non- complete MV-PCI in our meta-analysis[2] (multivessel percutaneous coronary intervention) might have been missed or misinterpreted in one included study. As a matter of fact, CvLPRIT trial randomized STEMI (ST-elevation myocardial infarction) patients to either complete revascularization (including all N-IRAs [non-infarct related artery]) or IRA-only treatment. Indeed, by study design, complete revascularization was recommended during index procedure, truly reflecting the inclusion criteria of our meta- analysis. Nairooz and Naidu are once more wrong when they argue that different time frames between index PCI and second procedure across the studies might have influenced the outcomes. While small number of studies conducted so far precludes detailed analyses, to assess the optimal timing of the second procedure, was not indeed the objective of the current meta- analysis. Nairooz and Naidu claim that staged PCI became anyhow bundled in the same group with IRA-only revascularization. These patients are similarly different to complete MV-PCI; indeed, the risk of MI in the IRA- only treated patients accrues over time; a difference in time in this group is pivotal also to demonstrate the impact of leaving a non culprit plaque untreated; the approach in our analysis therefore reflects the true clinical practice and indeed is based on coronary- and risk profile evaluation of the patients with non culprit plaques. An arbitrary,fixed time-frame second revascularisation for all patients with non culprit lesions is not only infeasible in clinical setting but ,indeed, dangerous treating in the same way patients with different coronary artery lesions; as a sensitivity analysis, a stratified meta-analysis by intervention in the control group was performed as well and results reported, showing consistency of results. Our study was not designed to compare same setting complete revascularization (CR) vs index hospitalization CR vs later date CR vs IRA only revascularization; neither was any study conducted to date. The criticism about methodology or clinical meaningfulness of a meta- analysis should be based upon specific clinical knowledge of the topic, and, above all, careful reading of the meta-analysis design.

    References:

    1. Nairooz R, Naidu SS. Complete revascularization in STEMI. Heart 2015 [Epub ahead of print] 2. Kowalewski M, Schulze V, Berti S, et al. Complete revascularisation in ST-elevation myocardial infarction and multivessel disease: meta-analysis of randomised controlled trials. Heart. 2015 Jun 2.

    Conflict of Interest:

    None declared

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