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Recent eLetters

Displaying 1-10 letters out of 688 published

  1. 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.

    Conflict of Interest:

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  2. 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.

    Conflict of Interest:

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  3. Coffee brewing technique as a confounder in observational studies

    Choi and colleagues describe an association between moderate coffee consumption and lower prevalence of subclinical coronary atherosclerosis [1]. This is consistent with a growing body of evidence that supports this finding. A similar large prospective study of over 400 000 participants, demonstrated that coffee consumption was inversley associated with both total and cause-specific mortality, specifically heart disease [2]. These findings were independent of the caffeine content of the coffee, suggesting that other compounds might be important. Coffee contains many other compounds that might be responsible for the observations of these studies, including antioxidants, but the naturally occurring diterpenes, cafestol and kahweol, are of significant interest. Both are found in Arabica beans and released during the brewing process of regular and decaffeinated coffee. The amount in coffee preparations varies enormously depending on the brewing method used. Instant and drip-filtered coffee contains insignificant quantities of diterpenes, which are removed by industrial processing and the lipid binding properties of filter paper respectively. In contrast, high concentrations occur in French press, Scandinavian boiled and Turkish-style coffees [3]. Diterpenes have pleiotropic effects including elevating serum lipids, anti-oxidant, anti- inflammatory, pro-apoptotic, and anti-angiogenic properties [2-4]. Whilst this work contributes to the evidence that coffee may confer health benefits, future studies need to account for coffee brewing technique as a significant confounding variable.

    1 Choi Y, Chang Y, Ryu S, et al. Heart Published Online First: 2 March 2015 doi:10.1136/heartjnl-2014- 306663.

    2 Freedman ND, Park Y, Abnet CC, et al. Association of coffee drinking with total and cause-specific mortality. N Engl J Med 2012;366:1891-904.

    3 Urgert R, van der Weg G, Kosmeijer-Schuil TG, et al. Levels of the cholesterol-elevating diterpenes cafestol and kahweol in various coffee brews. J Agric Food Chem 1995;43:2167-2172.

    4 C?rdenas C, Quesada AR, Medina MA. Anti-angiogenic and anti- inflammatory properties of kahweol, a coffee diterpene. PLoS One. 2011;6(8):e23407.

    Conflict of Interest:

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  4. Air pollution and cardiovascular disease

    I read a paper by Xie et al. with interest (1). There is also a review article in the same issue by Chin on the mechanism on the relationship between air pollution and cardiovascular events (2), and expert position paper was also published (3). Xie et al. handled large samples in Beijing and conducted their survey with special emphasis on fine particulate matter (PM2.5) concentration and ischaemic heart disease (IHD) morbidity and mortality. The authors clarified that a 10 microgram/cubic meter increase in PM2.5 was associated with a 0.27% increase in IHD morbidity and a 0.25% increase in mortality on the same day. In addition, they estimated that 7703 cases and 1475 deaths were observed during the 3 years by exceeding environmental criteria by WHO on M2.5. I have some comments on this relationship.

    Beelen et al. (4) reported a meta-analysis for the effect of long- term exposure to air pollution on cardiovascular mortality (overall and cause-specific), and concluded that there was no significant association. Yamamoto et al. (5) reported a systematic review on the association between air pollution and cardiovascular disease in South Asia, and they could not elucidate air pollution as a significant risk factor for cardiovascular disease (CVD). Heinrich et al. (6) mentioned that each study of meta-analysis showed different number of samples and sex distribution, which was related to the study outcomes. In addition to difference of follow-up period and ethnicity, indicators of air pollution are speculated to become a key factor on the relationship.

    CVD is composed of specific causes such as cerebrovascular disease, IHD and myocardial infarction, and sub-analysis with enough number of samples are needed to confirm the causality of the association. Namely, a systematic review should be conducted by specifying the types of air pollution and classification of CVD.

    References

    1. Xie W, Li G, Zhao D, et al. Relationship between fine particulate air pollution and ischaemic heart disease morbidity and mortality. Heart 2015;101:257-63.

    2. Chin MT. Basic mechanisms for adverse cardiovascular events associated with air pollution. Heart 2015;101:253-6.

    3. Newby DE, Mannucci PM, Tell GS, et al. Expert position paper on air pollution and cardiovascular disease. Eur Heart J 2015;36:83-93.

    4. Beelen R, Stafoggia M, Raaschou-Nielsen O, et al. Long-term exposure to air pollution and cardiovascular mortality: an analysis of 22 European cohorts. Epidemiology 2014;25:368-78.

    5. Yamamoto SS, Phalkey R, Malik AA. A systematic review of air pollution as a risk factor for cardiovascular disease in South Asia: limited evidence from India and Pakistan. Int J Hyg Environ Health 2014;217:133-44.

    6. Heinrich J, Thiering E, Rzehak P,et al. Long-term exposure to NO2 and PM10 and all-cause and cause-specific mortality in a prospective cohort of women. Occup Environ Med 2013;70:179-86.

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  5. Lower heart rate better in early AF

    Since the study shows a lower heart rate in paroxysmal or persistent AF is associated with lesser chance of progression to permanent AF, would rigorous treatment of heart rate with beta blockers in paroxysmal or persistent AF reduce the chance of their progression to permanent AF ?

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  6. WHEN THE RECOMMENDATION OF THE GUIDELINES ABOUT FRACTIONAL FLOW RESERVE WILL BE FOLLOWED?

    We have read with great interest the article written by Zhang et al[1] and we want to congratulate the authors on his contribution in this relevant issue. Since the first publication in 1995 by Pijls et al, fractional flow reserve has constantly progressed with undoubted success. After initially being validated as alternative to the non-invasive tests, the DEFER trial showed that a strategy of PCI based in FFR achieves better outcomes than the PCI guided by angiography in stable patients with one- vessel disease. In the following years this hypothesis was also confirmed in multivessel disease with the FAME and FAME-2 trials and even in non-ST elevation acute coronary syndromes with the subgroup of patients of the FAME and the recently published FAMOUS-NSTEMI trial. Finally, in FAME the possibility of differing between the angiographic and functional concepts of multivessel disease was also demonstrated. The article written by Zhang resumes perfectly the advantages of this technique. However, despite the robust evidence supporting its value and after having received the highest level of recommendation in the European and ACC/AHA guidelines, its utilization is still low and in many centres even anecdotal. It has also been recently published a disappointing median time lag of 14 years needed between guideline recommendation to 90 % practice uptake for class I therapies in acute coronary syndromes[2]. Although issues associated with reimbursement have been argued, there exist additional reasons which play an important role in the low percentage of FFR: as an example in Spain where most of the activity is performed in public hospitals without difficulties associated to reimbursement, in 2013 only 4.097 cases were reported, which represented 2,9% of the coronary angiographies and 6,2% of the PCIs[3]. We believe that fractional flow reserve has changed the conception of the cardiac catheterization laboratory and nowadays a complete diagnosis, risk stratification and adequate treatment in a one- stage manner can be offer to the still high number of patients with stable caronary disease who have not been adequately studied before the catheterization and to most of the non-ST elevation acute coronary syndromes, avoiding in many cases a second visit to the lab satisfying their expectancies and reducing unnecessary delays and costs.

    Reference List

    (1) Zhang D, Lv S, Song X, Yuan F, Xu F, Zhang M, Yan S, Cao X. Fractional flow reserve versus angiography for guiding percutaneous coronary intervention: a meta-analysis. Heart 2015.

    (2) Putera M, Roark R, Lopes RD, Udayakumar K, Peterson ED, Califf RM, Shah BR. Translation of acute coronary syndrome therapies: From evidence to routine clinical practice. Am Heart J 2015; 169(2):266-273.

    (3) Garcia dB, Hernandez HF, Rumoroso C, Jr., Trillo NR. Spanish Cardiac Catheterization and Coronary Intervention Registry. 23rd official report of the Spanish Society of Cardiology Working Group on Cardiac Catheterization and Interventional Cardiology (1990-2013). Rev Esp Cardiol (Engl Ed) 2014; 67(12):1013-1023.

    Conflict of Interest:

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  7. Re:"Type 2" myocardial infarction: Evidence-based or guesswork diagnosis

    We would like to thank Dr Y-Hassan for his valuable comments [1] on our manuscript on type 2 myocardial infarction (AMI) [2]. As pointed out in our article we share Dr Y-Hassan?s criticism against the vague diagnostic criteria for type 2 AMI in the Universal Definition of Myocardial Infarction [3,4] It may be difficult in many cases to distinguish type 2 AMI from type 1 AMI and other non-ischaemic conditions associated with myocardial damage (which includes Tako-Tsubo cardiomyopathy (TC)). Complementary imaging studies are often necessary for the correct classification and in our study echocardiography and coronary angiography were performed in 73.9% and 75.1% of patients, respectively. Nevertheless, as Dr Y-Hassan suggests, TC may have been missed in a certain number of cases classified as myocardial infarction and we believe, that TC, especially the apical sparing variants, probably are more common than has been previously thought. However, the current diagnostic criteria for TC are neither clear nor evidence based and the real prevalence of TC mimicking AMI remains fairly unknown [5]. A substantial proportion of type 2 AMI has minor troponin elevations and no or only very minor visible impact on left ventricular function, which is not compatible with a TC diagnosis. Therefore, we disagree with Dr Y- Hassan that it is likely that most of the cases classified as type 2 AMI would in fact be TC. To date, the differentiation between type 2 AMI and other non-ischemic conditions remains challenging and might be improved by more frequent use of more advanced imaging techniques such as CMR or PET, but their availability in real life is limited. Furthermore, it is still unclear whether such differentiation has any therapeutic or prognostic impact or is just more of an academic interest. Almost all evidence on how to manage AMI are based on studies on classical type 1 AMI. Therefore, we think that the attempt to distinguish type 1 AMI from other forms of myocardial infarction/injury is a major step forward. However, we fully agree with Dr Y-Hassan that there is an urgent need of more stringent, evidence based, and clinically applicable diagnostic criteria. References: 1. Y-Hassan S. "Type 2" myocardial infarction: Evidence-based or guesswork diagnosis. E-letter 1. Baron T, Hambraeus K, Sundstr?m J, Erlinge D, Jernberg T, Lindahl B. Type 2 myocardial infarction in clinical practice. Heart 2015;101:101-6 3. Thygesen K, Alpert JS, White HD.; Joint ESC/ACCF/AHA/WHF Task Force for the Redefinition of Myocardial Infarction. Universal definition of myocardial infarction. Eur Heart J 2007;28:2525-38. 4. Thygesen K, Alpert JS, Jaffe AS, et al.; JointESC/ACCF/AHA/WHF Task Force for Universal Definition of Myocardial Infarction. Third universal definition of myocardial infarction. J Am Coll Cardiol 2012;60:1581-98. 5. Prasad A, Lerman A, Rihal CS. Apical ballooning syndrome (Tako-Tsubo or stress cardiomyopathy): a mimic of acute myocardial infarction. Am Heart J. 2008;155:408-17.

    Conflict of Interest:

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  8. Where are the Surgeons? A Safety Opportunity Missed

    The introduction of a Patient Safety Checklist is a welcome addition for interventional cardiologists and is a concept practiced by surgeons in all disciplines for a number of years since the original WHO Patient Safety Checklist was proven to be of benefit in a global and multidisciplinary setting (1). The European Association for Cardiothoracic Surgery embraced this ideal in 2012 (1) with the publication of safety checklists which were specific to the nature of surgery undertaken, comprehensive and failsafe. The purpose of checklists is to ensure patient safety, confirming that the team is prepared for the procedure ahead and that all are ready for any eventuality. The checklist published by Cahill et al has an obvious omission in this regard - ensuring that those involved in the procedure are aware of the contact details and availability of a cardiac surgeon if needed. While less important (but sometimes needed) in coronary interventions where surgical complications are rare, TAVI and other procedures such as pacing lead extraction may require the attendance of the cardiac surgical team more frequently in the event of major issues arising and preparedness is crucial in emergency situations. The BCIS/SCTS Position Statement on TAVI (2009) mandates the need for surgical cover on site and immediate access to cardiopulmonary bypass. There is an opportunity in the checklist for the cardiology team to check that they have current contact and availability details for the cardiac surgical team so that if required help can be summoned without delay. With more and more TAVI procedures being performed transfemorally cardiac surgeons are not always physically present during procedures and robust cover arrangements need to be in place and details of cover confirmed. The checklist is the ideal opportunity for this to be done and avoids unnecessary delays when minutes count. The omission of a specific place on the checklist to ensure that such details are known misses an essential step in ensuring patient safety. However, as is clear from the introduction of safety checklists in the surgical arena the most significant hurdle to overcome is one of apathy following their introduction. If this can be overcome and the motivation of those using it maintained through strong leadership then this will surely be an effective contribution to patient safety.

    1. Haynes AB, Weiser TG, Berry WR, Lipsitz SR, Breizat AH, Dellinger EP, Herbosa T, Joseph S, Kibatala PL, Lapitan MC, Merry AF, Moorthy K, Reznick RK, Taylor B, Gawande AA. A surgical safety checklist to reduce morbidity and mortality in a global population. N Engl J Med 2009;360:491- 499. 2. Clark S.C., Dunning J., Alfieri O.R., Elia S., Hamilton L.R., Kappetein A.P., Lockowandt U., Sarris G.E., Kolh P.H. EACTS Guidelines for the Use of Patient Safety Checklists. European Journal of Cardiothoracic Surgery 2012; 41 (5): 993-1004

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  9. The role of FFR in clinical practice

    Only recently the FAME-2 trial1 showed for the first time that, in patients with stable coronary artery disease (SCAD) and "significant" myocardial ischemia, there is a prognostic advantage of PCI over optimal medical therapy (OMT), and that this advantage is consistent in patients with either single or multi-vessel coronary artery disease. The clinical outcome of patients with coronary stenoses not associated with significant ischemia is favorable with OMT alone, which is therefore a safe and convenient therapeutic strategy. Among patients with SCAD the risk of death and MI is proportional to the extent of ischemic myocardium/number of diseased vessels. Only patients with significant ischemia benefit from revascularization. Several studies however, including the COURAGE and BARI-2D trials2,3, failed to demonstrate a mortality benefit of PCI over OMT, most likely because of the inclusion on these studies of low risk patients with only limited ischemia or even no ischemia. It's common practice, in most cath-labs, to stent intermediate coronary stenoses only based on an angiographic estimation of severity. This meta- analysis and the FAME-2 trial shows, instead, that revascularization with PCI is safer and only confers a survival benefit when a given coronary lesion is associated with significant myocardial ischemia, as proven by FFR measurements. The use of FFR technique, which is simple and relatively safe, should be therefore implemented in every day practice.

    1- Fractional flow reserve-guided PCI for stable coronary artery disease. De Bruyne B, Fearon WF, Pijls NH, Barbato E, Tonino P, Piroth Z, Jagic N, Mobius-Winckler S, Rioufol G, Witt N, Kala P, MacCarthy P, Engstr?m T, Oldroyd K, Mavromatis K, Manoharan G, Verlee P, Frobert O, Curzen N, Johnson JB, Limacher A, N?esch E, J?ni P; FAME 2 Trial Investigators. N Engl J Med. 2014 Sep 25;371(13):1208-17.

    2- Optimal medical therapy with or without PCI for stable coronary disease. Boden WE, O'Rourke RA, Teo KK, Hartigan PM, Maron DJ, Kostuk WJ, Knudtson M, Dada M, Casperson P, Harris CL, Chaitman BR, Shaw L, Gosselin G, Nawaz S, Title LM, Gau G, Blaustein AS, Booth DC, Bates ER, Spertus JA, Berman DS, Mancini GB, Weintraub WS; COURAGE Trial Research Group. N Engl J Med. 2007 Apr 12;356(15):1503-16.

    3- A randomized trial of therapies for type 2 diabetes and coronary artery disease. BARI 2D Study Group, Frye RL, August P, Brooks MM, Hardison RM, Kelsey SF, MacGregor JM, Orchard TJ, Chaitman BR, Genuth SM, Goldberg SH, Hlatky MA, Jones TL, Molitch ME, Nesto RW, Sako EY, Sobel BE. N Engl J Med. 2009 Jun 11;360(24):2503-15.

    Conflict of Interest:

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  10. Effects of remote ischemic preconditioning on clinical outcomes after cardiac surgery

    In recent article of Candilio and colleagues assessing effect of remote ischemic preconditioning (RIPC) on postoperative outcomes in patients undergoing cardiac surgery, they showed that RIPC reduced amount of perioperative myocardial injury by 26% and incidence of acute kidney injury by 48%, respectively. They should be applauded for trying to control most of risk factors affecting postoperative myocardial and kidney injury. However, to differentiate the effects of one factor on study endpoints, all of the other factors have to be standardised. In this study, several important issues were not well addressed. First, perioperative hemoglobin levels were not included in data analysis. Actually, preoperative anemia is common among patients undergoing cardiac surgery and is associated with independently increased risks of postoperative adverse myocardial and renal events.2 Furthermore, the lowest hemoglobin level during cardiopulmonary bypass has been associated independently with the postoperative low-output syndrome, renal failure and mortality.3 Additionally, their study design did not include the detail of intraoperative complications and managements, such as hemodynamic instability, blood loss and blood transfusion. It has been shown that postoperative myocardial injury correlates with changes in blood pressure and heart rate during cardiac surgery.4 Furthermore, it is well know that perioperative blood transfusion is associated with increased troponin I release after cardiac surgery, and increased risks of postoperative short- and long-term mortality. Thus, we cannot exclude possibility that existence of any imbalance in the above factors would have confounded interpretation of their results. Finally, the study by Candilio and colleagues was not powered to show a difference in postoperative short-term clinical outcomes that occurred during the follow-up period. Thus, it is unclear whether favorable effect of RIPC on myocardial and kidney injury after cardiac surgery can be translated to postoperative benefits on mortality and severe adverse events. To address this issue, we agree the authors that the large-scale clinical trials are still required. These new studies should have enough power for postoperative mortality and severe adverse events. If further studies show consistent beneficial effect of RIPC on postoperative myocardial and kidney injury and mortality following cardiac surgery, the implications for practice are immense. REFERENCES 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 Kulier A, Levin J, Moser R, et al; Investigators of the Multicenter Study of Perioperative Ischemia Research Group; Ischemia Research and Education Foundation. Impact of preoperative anemia on outcome in patients undergoing coronary artery bypass graft surgery. Circulation 2007; 116:471 -9 3 Loor G, Li L, Sabik JF 3rd, et al. Nadir hematocrit during cardiopulmonary bypass: end-organ dysfunction and mortality. J Thorac Cardiovasc Surg 2012; 144:654-62. 4 Ketenci B, Enc Y, Ozay B, et al. Myocardial injury during off-pump surgery. The effect of intraoperative risk factors. Saudi Med J 2008; 29:203-8.

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