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Recent eLetters

Displaying 1-10 letters out of 724 published

  1. Regarding sex differences in cardiovascular ageing: let's not forget iron

    The interesting paper of Merz and Cheng did not mention iron as a plausible non-hormonal factor, which might in part explain the sex differences in cardiovascular aging [1].

    Mounting evidence suggests that the metabolic derangements and detrimental cardiovascular effects usually attributed to menopause represent only a mere consequence of the older age of menopausal women, rather than related to the loss of ovarian function. In fact, heart protection by premenopausal levels of female hormones, that is the oestrogen hypothesis, is not consistent with epidemiological findings that premenopausal hysterectomy essentially cancels the protection even in patients with preservation of functioning ovaries [2]. On the contrary, these data [2] suggest that an intact uterus has an important role in the protection of premenopausal women, and this is likely related to the beneficial effect of iron depletion in menstruating women (i.e. the iron hypothesis suggested since 1981 by Sullivan [3]).

    A protective effect of iron depletion may be related to the decreased availability of redox-active iron within atherosclerotic lesions. Serum ferritin concentrations, commonly used as a surrogate for iron stores, are significantly lower in premenopausal menstruating women (25-50 ng/mL) compared to men (140-150 ng/mL) of similar age, but slowly increase after menopause. Interestingly, average menstrual blood loss each year (780 mL) approximates blood loss from donating approximately two 500 mL units of whole blood [4]. It is noteworthy that phlebotomy of one unit of whole blood twice a year among predominantly white middle-aged and elderly men with peripheral arterial disease, resulted in a significant decrease in overall mortality, myocardial infarction and stroke over a several year period, compared to the control group not phlebotomized [4]. Not surprisingly, during the trial, the average serum ferritin concentration in the iron reduction group was approximately 60 ng/mL compared to 110 ng/mL in the control group [4]. On the contrary, it has become evident that supplemental iron use among elderly woman may be significantly and dose dependently associated with increased total mortality [5].

    In conclusion, higher vascular wall iron, contained in macrophages, might in part explain the sex difference in cardiovascular ageing. Moreover, donating blood twice a year by men and possibly postmenopausal women might decrease CVD morbidity and mortality. Furthermore, unnecessary iron supplements should be avoided and iron fortification of our food supply should be questioned. Finally, randomized trials of iron depletion for the primary and secondary prevention of vascular disease need to be done.

    1. Merz AA, Cheng S. Sex differences in cardiovascular ageing. Heart 2016 Feb [Epub ahead of print]. 2. Kannel WB, Levy D. Menopause, hormones, and cardiovascular vulnerability in women. Arch Intern Med 2004;164:479-81. 3. Sullivan JL. Iron and the sex difference in heart disease risk. Lancet 1981;1:1293-4. 4. Zacharski LR, Shamayeva G, Chow BK. Effect of controlled reduction of body iron stores on clinical outcomes in peripheral arterial disease. Am Heart J 2011;162:949-957.e1. 5. Mursu J, Robien K, Harnack LJ. Dietary supplements and mortality rate in older women: the Iowa Woman's Health Study. Arch Intern Med 2011;171:1625-1633.

    Conflict of Interest:

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  2. Author Reply: Sex Differences in Cardiovascular Ageing

    We thank Dr. Goldstein for bringing to our attention the iron hypothesis as a potential non-hormonal factor contributing to sex differences in cardiovascular aging. We also find intriguing the possibility that iron depletion in menstruating women may be cardio- protective. We had previously been aware of the potential role of iron as a byproduct of heme-oxygenase activity in mediating cardiometabolic risk,[1] with a number of community studies having reported equivocal findings when examining the relation between either iron or ferritin with respect to outcomes.[2-5] It is our impression that heterogeneity in prior study results may be related to differences in participant sampling methods, the iron measures used (ferritin, total iron binding capacity, transferrin saturation, serum iron, and dietary iron intake), and presence of potential confounding variables that could influence both iron levels and a given outcome of interest (e.g. inflammation, genetic variants). Given that iron accumulation patterns have been observed to vary by age and race as well as sex,[6] we agree that further studies investigating the role of iron as a potential contributor to cardiovascular risk are warranted. In particular, interventional studies could evaluate sex-based differences and also account for variables that could influence both iron levels and a given outcome of interest (e.g. blood donation and/or phlebotomy patterns, supplemental intake of iron, dietary patterns including heme vs. non-heme iron intake, and factors that might elevate ferritin as part of the acute phase response). We look forward to learning more about the potential contribution of iron depletion to sex differences in cardiovascular disease, in particular, as additional evidence emerges from this understudied field.

    References

    1. Fredenburgh LE, Merz AA, Cheng S. Haeme oxygenase signalling pathway: implications for cardiovascular disease. Eur Heart J. 2015 Jun 21;36(24):1512-8. doi: 10.1093/eurheartj/ehv114. Epub 2015 Mar 31. Review. PubMed PMID: 25827602; PubMed Central PMCID: PMC4475572.

    2. Salonen JT, Nyyssonen K, Korpela H, Tuomilehto J, Sepp?nen R, Salonen R. High stored iron levels are associated with excess risk of myocardial infarction in eastern Finnish men. Circulation. 1992 Sep;86(3):803-11. PubMed PMID: 1516192.

    3. Baer DM, Tekawa IS, Hurley LB. Iron stores are not associated with acute myocardial infarction. Circulation. 1994 Jun;89(6):2915-8. PubMed PMID: 8205708.

    4. Mu?oz-Bravo C, Guti?rrez-Bedmar M, G?mez-Aracena J, Garc?a- Rodr?guez A, Navajas JF. Iron: protector or risk factor for cardiovascular disease? Still controversial. Nutrients. 2013 Jul 1;5(7):2384-404. doi: 10.3390/nu5072384. Review. PubMed PMID: 23857219; PubMed Central PMCID: PMC3738979.

    5. Basuli D, Stevens RG, Torti FM, Torti SV. Epidemiological associations between iron and cardiovascular disease and diabetes. Front Pharmacol. 2014 May 20;5:117. doi: 10.3389/fphar.2014.00117. eCollection 2014. Review. PubMed PMID: 24904420; PubMed Central PMCID: PMC4033158.

    6. Zacharski LR, Ornstein DL, Woloshin S, Schwartz LM. Association of age, sex, and race with body iron stores in adults: analysis of NHANES III data. Am Heart J. 2000 Jul;140(1):98-104. PubMed PMID: 10874269.

    Conflict of Interest:

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  3. The enigma of high adiponectin levels and adverse outcomes in older people: a consequence of proinflammatory state and autoimmune activation?

    The excellently analyzed paper from the Cardiovascular Health Study on higher circulating adiponectin being associated with elevated risk of atrial fibrillation (AF) in the elderly [1), calls for focusing attention on this and analogous paradoxical manifestations accumulating in the medical literature. The investigation by Macheret and associates involved 886 incident AF events in a cohort of older -predominantly female- adults. It demonstrated a positive and linear, rather than inverse or U-shaped, association between circulating adiponectin and incident AF, independent of numerous potential confounders. Females were particularly involved, although sex-stratified analysis was not provided, African-Americans were much less susceptible than Whites, as were overweight/obese than lean people.

    Paradoxal behaviour of high adiponectin levels considered as a pro- inflammatorily converted protein had been published from the Turkish Adult Risk Factor study since 2008 repeatedly. Independently from obesity and hyperinsulinemia, serum adiponectin disclosed epidemiologic evidence of attenuation of anti-inflammatory activities (2). Serum adiponectin proved to confer no protection against hypertension and was found to diverge in women from men regarding protection against future coronary disease risk (3).

    Adiponectin is not the only plasma protein to show paradoxical outcome. HDL-cholesterol and its constituents apolipoprotein(apo) A-I, A- II, and apoE have formed relevant underlying mechanisms for hypertension, metabolic syndrome, type-2 diabetes, coronary heart disease, chronic kidney disease and osteoarthritis. Not cholesterol itself, but cholesterol -overloaded high-density lipoprotein particles were independently associated with progression of carotid atherosclerosis in a cardiovascular disease-free Chinese population. High apo A-I levels, rather than conferring protection against incident type-2 diabetes, independently predicted it among Turks. The apoB/LDL-cholesterol ratio, a measure of small dense low-density lipoprotein particles, was highly predictive of diabetes in Finnish men.

    It may thus be concluded that the enigma of high adiponectin levels and adverse outcomes in older people is most likely a consequence of proinflammatory state and autoimmune activation. Diverse factors such as sex, age, race/ethnicity, susceptibility to impaired glucose tolerance modulate this phenomenon, formed on one hand by autoimmune components composed of protective plasma proteins turned proinflammatory, on the other hand by proteins sustaining epitope damage and partially escaping immunoassay (4).

    References

    1. Macheret F, Bartz TM, Djusse L. et al. Higher circulating adiponectin levels are associated with increased risk of atrial fibrillation in older adults. Heart 2015;101:1368-1374

    2. Onat A, Hergenc G, Dursunoglu D, et al. Relatively high levels of serum adiponectin in obese women, a potential indicator of anti- inflammatory dysfunction: Relation to sex hormone-binding globulin. Int J Biol Sci 2008;4:208-14

    3. Onat A, Aydin M, Can G, et al. High adiponectin levels fail to protect against risk of hypertension and, in women, against coronary disease: involvement in autoimmunity? World J Diabet 2013;4:219-25

    4. Onat A, Can G. Enhanced proinflammatory state and autoimmune activation: a breakthrough to understanding chronic diseases. Curr Pharm Design 2014; 20:575-84

    Conflict of Interest:

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  4. Carotid Artery Stenting Outcomes in Dataset Registries: A Cause of Concern or an Opportunity for Improvement?

    Roffi et al.1 report that contemporary outcomes following carotid stenting (CAS) in large-scale registries were comparable to carotid endarterectomy (CEA). They also concluded that, over time, complication rates following CAS had decreased.1

    We recently reviewed outcomes after >1,500,000 procedures in 21 administrative dataset registries where procedural death/stroke rates were reported for both CEA and CAS.2 One key finding was that CAS was associated with in-hospital/30-day death/stroke rates which exceeded the 3% American Heart Association (AHA) risk threshold for asymptomatic patients in 9/21 registries (43%). In symptomatic patients, death/stroke rates exceeded the 6% AHA risk threshold in 13/18 (72%) registries and exceeded 10% in 5/18 registries (28%).2 We also found no evidence of a decline (over time) in procedural risks after CAS.2

    There is no doubt that CAS experts are now reporting excellent and durable outcomes, and it is also true that CAS offers benefits (over CEA) in terms of avoiding cranial nerve injury. However, there is a discrepancy between what is being reported in randomised trials and what is happening in the 'real world', especially in symptomatic patients. Some argue that most strokes following CAS are non-disabling (i.e. not clinically important), but Thomas Brott (CREST Principal Investigator) has stated that any perioperative stroke is associated with poorer long term survival, just as with perioperative myocardial infarction.3

    In conclusion, we agree with Marco Roffi that with better patient selection, improvements in stent design/protection devices and (most importantly) centralization of CAS procedures into high-volume centres, procedural risks following CAS will become similar to CEA. But, is the movement into 'higher volume' centres really happening? Sadly, evidence suggests that in the USA, if nowhere else, many CAS practitioners perform only 1-3 procedures each year,4 making it impossible to ever overcome the learning curve.

    The future is certainly looking brighter for CAS, but key opinion leaders now need to 'step up to the plate' to ensure that patients are only treated by experienced CAS practitioners with audited outcomes within AHA risk thresholds. This will not be popular, but evidence suggests that until it does, nothing will change.

    References

    1. Roffi M, Kulcsar Z, Carrera E, et al. Carotid artery stenting. Heart 2016 Mar 4. pii: heartjnl-2015-307638. doi: 10.1136/heartjnl-2015- 307638 [Epub ahead of print]

    2. Paraskevas KI, Kalmykov EL, Naylor AR. Stroke/Death Rates Following Carotid Artery Stenting and Carotid Endarterectomy in Contemporary Administrative Dataset Registries: A Systematic Review. Eur J Vasc Endovasc Surg. 2016;51:3-12.

    3. von Allmen R. Dismantling the different myths around the CREST trial. Vascular News. 2012;53(1):10. Available at: http://www.vascularnews.com/vn-newspaper- pdfs?DocumentScreen=detail&cl=371&ccs=655. Accessed on March 23, 2016.

    4. Choi JC, Johnston SC, Kim AS. Early outcomes after carotid artery stenting compared with endarterectomy for asymptomatic carotid stenosis. Stroke. 2015;46:120-125.

    Conflict of Interest:

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  5. Complete multivessel revascularization in STEMI. Reply to the letter by Shah et al.

    To the Editor:

    We read with interest the letter by dr Shah [1] regarding our recent meta-analysis: "Complete revascularisation in ST-elevation myocardial infarction and multivessel disease: meta-analysis of randomised controlled trials" [2]. The meta-analysis was designed to compare complete multivessel PCI (MV-PCI) with non-complete MV-PCI in ST-elvation myocardial infarction (STEMI) and MV disease. Complete MV-PCI was defined as revascularisation to non-infarct-related artery lesions during index procedure, non-complete MV-PCI-encompassed culprit-only revascularization (COR) and staged approaches. First of all, we appreciate the comments by Shah and are glad that our research has become of interest to a large international readership. At the same time we believe that 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.

    Shah suggests that because the majority of staged procedures were performed within days to weeks of their index procedures, they would be considered more like complete than incomplete revascularizations over a 12 -month follow-up. This is a simply arbitrary reclassification, given the large time discrepancy between the two approaches in all included studies that were however not designed to define an optimal timing, nor it was the primary focus of our paper. As a result, Shah speculates that staged PCI should became anyhow bundled in the same group with complete revascularization. This arbitrary re-reclassification is also in contrast with the natural history of the untreated coronary lesions. These patients present a different risk profile from those allocated to staged PCI; as a reflection of this, the untreated lesions over time in the second group have led to an accrual over time of the MI rates in the IRA- only treated patients; a difference in time in this group is pivotal to demonstrate the impact of leaving a non culprit plaque untreated; same applies to staged procedures. The approach in our analysis therefore reflects 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. Our study was not designed to compare in the same setting complete revascularization (CR) vs index hospitalization CR vs later date CR vs IRA only revascularization; neither was any study conducted to date.

    Secondly, Shah is concerned about the validity of the findings due to inconsistency driven by inclusion of the entire complete revascularization cohort from the Complete versus Culprit-Lesion Only Primary PCI Trial (CvLPRIT), while in the Supplementary Table 5 CR was performed during the index procedure for 97 patients [3]. Current meta-analysis was performed according to intention-to-treat (ITT) which is recommended as the least biased way to estimate intervention effects in randomized trials [4]: principles of ITT analyses are, first of all, to classify participants in the intervention groups to which they were randomized, regardless of the intervention they actually received, therefore inclusion of post-hoc analyses which is the case for Supplementary Table 5, is not only forbidden by design of the meta-analysis but may also lead to attrition bias with patients dropping out from the initial randomization group and consequently to results that are unequal in regard to exposure and/or outcome. In the methods section of the CvLPRIT one reads that "if randomized to complete revascularization, it was mandated that the IRA be treated first. If there were no clinical contraindications, complete revascularization was recommended at the same sitting to reduce multiple vascular punctures, avoid prolonged hospitalization, and attenuate potential patient dropout". Decision for the procedure to be staged was based on clinical reasons and left to the operator, which we cannot answer for.

    Thirdly, Shah cited part of the methods from the study by Maamoun et al. [5] and concluded this study was an observational cohort; this remark is however incorrect because what is reported also in the abstract is: "A total of 78 patients (72 males and 6 females) with ST-elevation MI presented within 12 h from the onset of symptom who had at least two angiographically-documented diseased coronary arteries (luminal diameter narrowing ?70%) and received primary PCI were included. They were randomly assigned to receive either PCI for culprit vessel only in the initial procedure (SR group) followed by another session of angioplasty to other diseased vessels (within 7 days), or (CR group) consisted of 42 patients who had received complete revascularization during the initial procedure after intracoronary administration of nitroglycerin to avoid stenting of functionally nonsignificant lesions". We have no reasons to believe it was otherwise.

    Finally, Shah advises that the trial by Ghani et al. [6] should have had as well been included in the meta-analysis. While report by Ghani et al. comprises a follow-up study, the main results derive from the article by Dambrink et al. [7]. This study was intentionally excluded as not pertinent to the design of the meta-analysis. Dambrink et al. randomized STEMI patients to invasive and conservative treatment after primary angioplasty. In the invasive- group, "ischaemia-guided additional revascularisation was performed during the in-hospital phase after primary PCI or in an out-patient setting but no later than three weeks after STEMI", therefore nowhere close to complete MV-PCI during index procedure. The last claim of other studies intentionally omitted, undermining the validity of this meta-analysis, we leave to the discretion of the Heart Editor and the Readership.

    References

    1. Rahman Shah. Letter to the Editor regarding heartjnl-2014- 307293.R2 - Complete Revascularization in ST-Elevation Myocardial Infarction and Multivessel Disease. Meta-Analysis of Randomized Controlled Trials. 17.03.2016

    2. Kowalewski M, Schulze V, Berti S, Waksman R, Kubica J, Kolodziejczak M, Buffon A, Suryapranata H, Gurbel PA, Kelm M, Pawliszak W, Anisimowicz L, Navarese EP. Complete revascularisation in ST-elevation myocardial infarction and multivessel disease: meta-analysis of randomised controlled trials. Heart 2015;101:1309-1317.

    3. Gershlick AH, Khan JN, Kelly DJ, et al. Randomized trial of complete versus lesion-only revascularization in patients undergoing primary percutaneous coronary intervention for STEMI and multivessel disease: the CvLPRIT trial. J Am Coll Cardiol. 2015;65:963-72.

    4. Newell DJ. Intention-to-treat analysis: implications for quantitative and qualitative research. Int J Epidemiol 1992;21:837-841.

    5. Maamoun W, Elkhaeat N, Elarasy R. Safety and feasibility of complete simultaneous revascularization during primary PCI in patients with STEMI and multivessel disease. Egyptian Heart J 2011;63:39-43.

    6. Ghani A1, Dambrink JH, van 't Hof AW, et al. Treatment of non- culprit lesions detected during primary PCI: long-term follow-up of a randomised clinical trial. Neth Heart J. 2012 Sep; 20(9): 347-353

    7. Dambrink JH, Debrauwere JP, van 't Hof AW, Ottervanger JP, Gosselink AT, Hoorntje JC, de Boer MJ, Suryapranata H. Non-culprit lesions detected during primary PCI: treat invasively or follow the guidelines? EuroIntervention 2010;5:968-975.

    Conflict of Interest:

    None declared

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  6. Complete vs Culprit-only Revascularization for Patients with ST-Segment Elevation Myocardial Infarction

    To the Editor: We read with great interest the recent meta-analysis by Kowalewski et al.[1] The authors should be congratulated for their work. However, we would like to make few comments about some issues with the meta-analysis. First, complete revascularizations (CRs) done as staged procedures (SPs) were analyzed with the incomplete revascularization group, but endpoints were measured at a median follow-up of 12 months. Because the majority of SPs were performed within days to weeks of their index procedures, clinical wisdom suggests they would behave more like CRs than incomplete revascularizations over a 12-month follow-up. Therefore, we believe that from statistical and clinical points of view, CRs performed as SPs should have been included in the complete revascularization group, as was done in other meta-analyses and randomized trials.[2] Furthermore, the authors did not consistently analyzed CRs performed as SPs with the incomplete arm. In the Complete versus Culprit-Lesion Only Primary PCI Trial (CvLPRIT), CR was performed during the index procedure for 97 patients (Supplementary Table 5 in the CvLPRIT trial),[2] but this group (for this meta-analysis)was combined with patients receiving CRs as SPs, bringing the total to 150. This inconsistency significantly impacts the validity of the meta-analysis. In addition, the title indicates the study was a meta-analysis of randomized trials, yet it included the study by Maamoun et al, an observational cohort study,[3] as evidenced by a statement in the Methods section. Maamoun et al state, "Group 1 consisted of 36 patients presented in the 1st year of the study and had undergone primary PCI for culprit vessel only in the initial procedure followed by another session of angioplasty to other diseased vessels and group 2 consisted of 42 patients presented in the 2nd year of the study and had received complete revascularization during the initial procedure." Finally, the authors did not include a trial by Ghani et al.[4] No reason for this omission was mentioned in the Methods or Discussion. Therefore, we wonder if other studies were also omitted, undermining the validity of this meta-analysis. References: 1. 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;101(16):1309-17. 2. Gershlick AH, Khan JN, Kelly DJ, et al. Randomized trial of complete versus lesion-only revascularization in patients undergoing primary percutaneous coronary intervention for STEMI and multivessel disease: the CvLPRIT trial. J Am Coll Cardiol. 2015;65:963-72. 3. Maamoun W, Elkhaeat N, Elarasy R. Safety and feasibility of complete simultaneous revascularization during primary PCI in patients with STEMI and multivessel disease. Egyptian Heart J 2011;63:39-43. 4. Ghani A1, Dambrink JH, van 't Hof AW, et al. Treatment of non-culprit lesions detected during primary PCI: long-term follow-up of a randomised clinical trial. Neth Heart J. 2012 Sep; 20(9): 347-353.

    Conflict of Interest:

    None declared

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  7. Assessing effect of remote ischaemic preconditioning on clinical outcomes in patients undergoing cardiac bypass surgery

    Assessing effect of remote ischaemic preconditioning on clinical outcomes in patients undergoing cardiac bypass surgery

    To the Editor : In a recent article of Candilio et al.1 assessing the effect of remote ischaemic preconditioning (RIPC) on postoperative outcomes in patients undergoing cardiac surgery, they showed that RIPC reduced the amount of perioperative myocardial injury by 26% and the incidence of acute kidney injury by 48%.The authors discuss the limitations of their work.In our view, the following important issues in this study seemed not to be well addressed.

    Perioperative dexmedetomidine infusion was not included in data analysis.Actually,perioperative dexmedetomidine infusion is common among patients undergoing cardiac surgery. Dexmedetomidine, a highly selective?2 adrenoreceptor agonist, has advantages for reducing renal injury. Perioperative dexmedetomidine infusion effectively reduces the incidence and severity of acute kidney injury in cardiac surgery.2 Preoperative Contrast angiography was not included in data analysis.

    Preoperative Contrast angiography is not rare among patients undergoing coronary artery bypass grafting surgery.The contrast-induced nephropathy is independently associated with increased postoperative risks of adverse renal events 3.

    Aminoglycoside, a commonly administered antibiotic in the operating room, independently associated with increased risks of postoperative acute renal injury(AKI) through intracellular processes such as mitochondrial dysfunction and reduction of protein synthesis.4

    We are concerned that if there is any disbalance in these factors would have confounded the interpretation of the results.

    1.Candilio L, Malik A, Ariti C, et al. Effect of remote ischaemic preconditioning on clinical outcomes in patients undergoing cardiac bypass surgery:a randomised controlled clinical trial. Heart 2015;101:185-92

    2.Jin Sun Cho, Jae-Kwang Shim, Sara Soh , et al.Perioperative dexmedetomidine reduces the incidence and severity of acute kidney injury following valvular heart surgery. Kidney Int 2015; advance online publication, 7 October 2015;doi:10.1038/ki.2015.306

    3.Persson PB, Hansell P, Liss P. Pathophysiology of contrast medium- induced nephropathy. Kidney Int 2005; 68:14-22.

    4. Sharfuddin AA, Weisbord SD, Palevsky PM, Molitoris BA. Acute kidney injury. In: Taal MW, Chertow GM, Marsden PA,Skorecki K, Yu ASL, Brenner BM, eds. Brenner and Rector's The Kidney. Philadelphia, USA: Elsevier, 2012; 1044-99

    Feng Xue, 1Hai chen Chu,1Wei Zhang2

    1.Department of Anesthesiology, the Affiliated Hospital of Qingdao University ,Qingdao ,China

    2.Department of nephrology ,the Affiliated Hospital of Qingdao University , Qingdao ,China

    Correspondence:

    Wei Zhang, Department of Nephrology, The Affilitated Hospital of Qingdao University,Qingdao266003, China. E-mail:xfwwww@163.com

    Contributors: Feng Xue read the manuscript of Candilio et al.; analysed their methods and data; suggested comment points and drafted this manuscript; responsible for this manuscript; and approved the final manuscript. Hai chen Chu read the paper of Candilio et al.;analysed their data; revised the comment points and this manuscript; and approved the final manuscript.Wei Zhang read the manuscript of Candilio et al.; analysed their methods and data; revised the comment points and this manuscript; and approved the final manuscript.

    Conflict of Interest:

    None declared

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  8. Causes of sleep deprivation in cardiac patients in hospital settings

    Tanu Pramanik Senior Lecturer (Psychology) Effect of sleep deprivation on cardiac patients is an well documented clinical entity which the authors of the current article established with experimental data and therefore deserve sincere applause(1). WHO guideline: The World Health Organization guidelines say that for a good sleep, sound level should not exceed 30 dB(A) for continuous background noise, and 45 dB(A) for individual noise events.(2) Clinical Psychologists point of view: Many clinical psychologists and sleep medicine experts consider that normal sleep should be regarded as one of the basic human rights, because chronic sleep disturbance due to any kind of noise pollution is a well-documented cause of several psychosomatic disorders(3). Cardiologists point of view: Major part of effective treatment result depends on restful sleep for the patients suffering from cardiac arrhythmia , myocardial infarction and related cardiac ailments.These autonomic responses to noise during sleep can be obtained for much lower peak noise intensities as during wake states. These effects, mainly involving increased heart rate and vaso-constriction, have been found to habituate over successive noise-exposed nights as opposed to long exposure times. This could indicate an effect on cardiovascular response over the long term exposure (4). During sleep, heart rate is related to changes in the parasympathetic-sympathetic balance with an increase in sympathetic tone associated with activation and with electroencephalogram (EEG) arousal. Catecholamine levels and sympathetic activity decrease during sleep.This association has been observed not only with sleep deprivation but also with regard to sleep disruption.(5) Brief awakenings from sleep for only a few seconds are associated with temporary elevation in blood pressure and heart rate that results from an autonomic reflex.(6) Currently, we proposed a well organized case control study to explore effect of sleep fragmentation on cardiac arrhythmia patients due to noise generated from cell phone and cardiac monitors in intensive coronary units.We are concerned that otherwise negligible noise pollution may cause delayed recovery of vulnerable cardiac patients. References: 1. e0265 Analysis of 24 h sleep deprivation on arrhythmia and heart rate variability:Wei-Ren Chen, and Xiang-Min Shi:Heart 2010 96:A83; doi:10.1136/hrt.2010.208967.265 2. Berglund B, Lindvall T, Schwela DH. Guidelines for Community Noise. World Health Organization 1999. Available from: http://www.who.int/docstore/peh/noise/guidelines2.html . [Accessed on 2010 March 28]. 3. Tanu Pramanik.Re: wind turbine noise: Response to:- Editorials:Wind turbine noise.BMJ 2012; 344 doi: http://dx.doi.org/10.1136/bmj.e1527 (Published 08 March 2012) Cite this as: BMJ 2012;344:e1527. 4. Muzet A, Ehrhart J, Eschenlauer R, Lienhard JP. Habituation and age differences of cardiovascular responses to noise during sleep. In Sleep 1980;212-5. 5. Sforza E, Chapotot F, Lavoie S, Roche F, Pigeau R, Buguet A. Heart rate activation during spontaneous arousals from sleep: Effect of sleep deprivation. Clin Neurophysiol 2004;115:2442-51. 6. Bonnet MH, Arand DL. Clinical effects of sleep fragmentation versus sleep deprivation. Sleep Med Rev 2003;7:297-310.

    Conflict of Interest:

    None declared

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  9. Response to the letter regarding the article "Early beta-blocker use and in-hospital mortality in patients with Takotsubo cardiomyopathy"

    We would like to thank Professor Madias for his comments and interest in our study.[1] We appreciate the editors of Heart for giving us the opportunity to reply. The Diagnosis Procedure Combination database in Japan contains hospital administrative claims data and discharge abstracts representing approximately 50% of all inpatient admissions to acute-care hospitals in Japan.[2] As per the request by Professor Madias, we additionally extracted data on diabetes mellitus (DM) and hypertension (HTN) in our 2672 study patients with Takotsubo cardiomyopathy (TC), using the International Classification of Diseases, 10th Revision codes (DM, E10- 14.x; HTN, I10.x). Of the 2672 patients, 367 (13.7%) had a diagnosis of DM and 1201 (44.9%) had a diagnosis of HTN as a comorbidity at admission. We also performed a 1:4 propensity score-matching analysis including DM and HTN as covariates, and obtained results consistent with those in our main analysis [1] (30-day in-hospital mortality, early beta-blocker group 2.4% [10/413] vs. control group 2.5% [42/1652]; P=1.000). The proportions of DM and HTN in our study patients with TC were comparable to those recently reported by Professor Madias.[3] However, it remains uncertain whether the prevalence of DM was lower in patients with TC compared with general population in Japan because the contemporary data on the prevalence of DM in the general population were not available in our dataset.

    References 1. Isogai T, Matsui H, Tanaka H, et al. Early beta-blocker use and in- hospital mortality in patients with Takotsubo cardiomyopathy. Heart 2016 Feb 15. pii: heartjnl-2015-308712. doi:10.1136/heartjnl-2015-308712. [Epub ahead of print]. 2. Isogai T, Yasunaga H, Matsui H, et al. Out-of-hospital versus in- hospital Takotsubo cardiomyopathy: Analysis of 3719 patients in the Diagnosis Procedure Combination database in Japan. Int J Cardiol 2014;176:413-7. 3. Madias JE. Low prevalence of diabetes mellitus in patients with Takotsubo syndrome: A plausible 'protective' effect with pathophysiologic connotations. Eur Heart J Acute Cardiovasc Care 2016;5:164-70.

    Conflict of Interest:

    None declared

  10. Takotsubo syndrome in a Japanese patient cohort: an opportunity to tap into a great resource!

    To the Editor: The report by Isogai al,1 published online ahead of print on February 15, 2016 in the Journal, about the 2672 patients (81.5% women) who had suffered Takotsubo syndrome (TTS) between 2010 and 2014, deriving from the "Diagnosis Procedure Combination nationwide inpatient database in Japan" is an invaluable resource, since it comprises all patients with this pathology admitted to acute-care hospitals in the entire nation, where TTS was originally described. The authors, employing score-matching and instrumental variable analyses, analyzed 2110 patients from 615 hospitals (422 who received ?-blocker therapy on hospitalization day 1 or 2, and 1688 patients who did not receive ?-blockers), and found that there was no difference between these 2 subgroups in regards to 30-day mortality.

    It has been reported recently that a history of diabetes mellitus (DM) has a low prevalence in patients admitted with TTS.2 The hypothesized pathophysiological connotation of this observation is that DM may have a "protective" effect for the expression of TTS under stress, via a mediating (ameliorating) effect of the underlying diabetic neuropathy (and presumably autonomic nervous system [ANS] neuropathy), which provides a "bridling" CNS effect on "the catecholamine-mediated mechanism, which has been implicated in the pathogenesis of TTS.1 The authors, in their article's Table 1, provided details of the prevalence of chronic (malignancy, chronic pulmonary disease, chronic liver disease, chronic renal failure, peptic ulcer disease, thyrotoxicosis, rheumatic disease, psychiatric disease), and acute diseases for the unmatched, and the "1:4 propensity score-matched" groups of the entire cohort,1 but curiously have not included information about hypertension (HTN) or DM in their patients with TTS. Since the authors have access to data in the "Diagnosis Procedure Combination nationwide inpatient database in Japan", it will be of interest to provide the readers of the Journal with information on the prevalence of HTN and DM in their 2672 patients with TTS.

    Conflicts of Interest None.

    References

    1.Isogai T, Matsui H, Tanaka H, Fushimi K, Yasunaga H. Early ?- blocker use and in-hospital mortality in patients with Takotsubo cardiomyopathy. Heart. 2016 Feb 15. pii: heartjnl-2015-308712. doi: 10.1136/heartjnl-2015-308712. [Epub ahead of print]. 2. Madias JE. Low prevalence of diabetes mellitus in patients with Takotsubo syndrome: a plausible 'protective' effect with pathophysiologic connotations Eur Heart J Acute Cardiovasc Care (2015) [Epub ahead of print; 11 Feb, pii: 2048872615570761].

    Conflict of Interest:

    None declared

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