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Recent eLetters

Displaying 1-10 letters out of 683 published

  1. 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:

    None declared

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  2. 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:

    None declared

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  3. 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

    Conflict of Interest:

    None declared

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  4. 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:

    None declared

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  5. 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.

    Conflict of Interest:

    None declared

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  6. Re:Physical Activity and Cardiorespiratory Fitness as Underappreciated Modulators of Obesity-Related Risk of Sudden Cardiac Death

    We thank Laukkanen et al. for their interest in our recent report titled "Obesity related risk of sudden cardiac death in the Atherosclerosis Risk in Communities (ARIC) study" (1). We agree that regular moderate physical activity reduces the risk of sudden cardiac death (SCD) and all-cause mortality. Physical activity, but not fitness, was captured in the ARIC study via questionnaires. However, adjustment for this variable in our multivariable analysis did not change the results of the study. In the analysis for BMI, after adjustment for physical activity in addition to all variables in our Model 2, the HR (95% CI) for SCD were 1, 1.24 (0.75-2.04), 1.05 (0.59-1.85), and 1.42 (0.76-2.68) among non- smokers with BMI of 18.5-24.9, 25-29.9, 30-34.9 and 35+, respectively (p for trend 0.45). In the analysis for waist-hip-ratio, after additional adjustment for physical activity in our Model 2, the HR (95% CI) for SCD were 1, 0.98 (0.53-1.81), 1.45 (0.86-2.43), and 1.93 (1.13-3.30) among non -smokers with waist-hip-ratio of reference (<0.8 in women, <0.95 in men), high category 1, 2 and 3, respectively (p for trend 0.005). REFERENCES 1. Adabag S, Huxley RR, Lopez FL, Chen LY, Sotoodehnia N, Siscovick D, Deo R, Konety S, Alonso A, Folsom AR. Obesity related risk of sudden cardiac death in the atherosclerosis risk in communities study. Heart. 2015;101:215-21

    Conflict of Interest:

    None declared

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  7. NICE guidance for the investigation of recent-onset chest pain

    The paper by Patterson et al (1) illustrates why the NICE and ESC guidelines (2,3) recommend no non-invasive testing in patients presenting with undifferentiated chest pain in whom a non-cardiac cause is suspected or the probability of coronary artery disease (CAD) is judged to be very low (NICE <10%, ESC <15%). Table 5 shows there were 351 such patients, of whom 24 were subsequently diagnosed with CAD. Even if we accept that the chest pain in all 24 of these "false negative" cases was in fact caused by myocardial ischaemia, this is equivalent to a diagnostic sensitivity of 93% for clinical judgment in ruling out coronary disease, better than could be achieved by exercise electrocardiography or perfusion imaging in such a low risk population (4).

    It is unclear from the manuscript exactly how "the subsequent CAD diagnosis" was determined and how sound was that determination. There were only 11 hospital admissions with "angina" so it presumably involved some form of non-invasive testing in most cases. The fact that CAD was "excluded" or "inconclusive" in nearly all (>90%) of these patients is entirely predictable given the initial clinical diagnosis of non-cardiac chest pain or low probability CAD. This begs the question what contribution the testing made to patient care? Certainly, the tests were unhelpful in failing to prevent 6 MACE events, although it is hard to know whether this 1.7% event rate should be seen as a cause for "alarm".

    Finally, Patterson et al warn against using the NICE guidance to "justify excluding (low risk) patients from further investigation if CAD is still suspected based on all available clinical information". There was no intention that the guideline should be used in this way but a more selective approach to investigation than apparently used by Patterson et al is surely needed to address increasing concerns about the overuse of noninvasive diagnostic tests in patients with chest pain (5).

    References

    1. Patterson CM, Nair A, Ahmed N, Bryan L, Bell D, Nicol ED. Clinical outcomes when applying NICE guidance for the investigation of recent-onset chest pain to a rapid-access chest pain clinic population. Heart 2015;101:113-118 2. Chest pan of recent onset: Assessment and diagnosis of recent onset chest pain or discomfort of suspected cardiac origin. NICE guidelines [CG95] Published date: March 2010. http://www.nice.org.uk 3. Montalescot G, Sechtem U, Achenbach S, Andreotti F, Arden C, Budaj A, et al. 2013 ESC guidelines on the management of stable coronary artery disease: The Task Force on the management of stable coronary artery disease of the European Society of Cardiology. Eur Heart J. 2013; 34(38):2949-3003 4. Detrano R, Gianrossi R, Mulvihill D, Lehman K, Dubach P, Colombo A, Froelicher V. Exercise-induced ST segment depression in the diagnosis of multivessel coronary disease: a meta analysis. J Am Coll Cardiol 1989;14:1501-8. 5. Ladapo JA, Blecker S, Douglas PS. Physician decision making and trends in the use of cardiac stress testing in the United States: An analysis of repeated cross-sectional data. Ann Intern Med 2014;161:482-490

    Conflict of Interest:

    I chaired the NICE guideline group: Chest pan of recent onset: Assessment and diagnosis of recent onset chest pain or discomfort of suspected cardiac origin. NICE guidelines [CG95] Published date: March 2010. http://www.nice.org.uk

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  8. What about the actual history of the chest pain

    I am rather surprised that the authors did not take into account more clinical features of the history in their model.(1) Pleuritic features and relief when sat up suggest pericarditis, whilst there are of course specific features that suggest reflux oesophagitis; timing is important, as pain lasting less than a minute is really not suggestive of ischaemic disease.

    The authors state 'we included consenting adults aged >25 years who presented to the ED within 24h of experiencing chest pain suspected to be cardiac in origin by the initial treating physician' and thus I take this to assume they trusted the history of the initial physician as one that suggested cardiac disease - even then, I assume 'cardiac' means ischaemic, not pericarditic or indeed dissection-type of pain.

    Similar work to this paper has been done in stable angina, where the description of angina pain as typical is associated with coronary outcomes.(2) Clearly unstable angina lacks the exertional component of stable angina and is thus harder perhaps from simple history-taking alone to be sure of a diagnosis, but that does not mean chest pain descriptors (character, site, duration) don't play a diagnostic, and hence potentially prognostic role in unstable angina.

    1. Body R, Carley S, McDowell G, Pemberton P, Burrows G, Cook G, Lewis PS, Smith A, Mackway-Jones K. The Manchester Acute Coronary Syndromes (MACS) decision rule for suspected cardiac chest pain: derivation and external validation. Heart 2014;100:18 1462-1468

    2. Zaman MJ, Junghans C, Sekhri N, et al. Presentation of stable angina pectoris among women and South Asian people. CMAJ 2008;179:659-67

    Conflict of Interest:

    None declared

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  9. what was the prevalence of concordant ST segment deviation in type 1 AMI with LBBB?

    The 6.3% prevalence of left bundle branch block(LBBB) among 17,488 subjects with type 1 acute myocardial infarction(AMI) translates into 1101 subjects with this manifestation of AMI(1). This represents a golden opportunity to document the prevalence of concordant ST segment deviation in those 1101 subjects so as to enable a comparison to be made with the study which reported a low prevalence of acute coronary occlusion in patients with LBBB who did not have concordant ST segment deviation(2). An even more important comparison would be a documentation of the sensitivity and specificity of concordant ST segment deviation for type 1 AMI in those 1101 subjects vs the documentation of 16.7% sensitivity and 88.6% specificity in the 120 subjects evaluated by Brown et al(3) References (1)Baron T., Hambraeus K., Sundstrom J et al Type 2 myocardial infarction in clinical practice Heatr 2015;101:101-106 (2)McMahon R., Siow W., Bhindi R et al Left bundle branch block without concordant ST changes is rarely associated with acute coronary occlusion International Journal of Cardiology 2013;167:1339-1342 (3) Brown AJ., Hoole SP., McCormick LM et al Left bundle branch block with acute thrombotic occlusion is associated with increased myocardial jeopardy score and poor clinical outcomes in primary percutaneous coronary activations Heart 2013;99:774-778

    Conflict of Interest:

    None declared

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  10. manchseter medical society

    The documentation of a rising incidence of cardiac resynchronisation therapy(CRT)-related infection(1) calls for a reappraisal of the Class 1 level A recommendation for the use of this modality(2), given the fact that the recommendation antedated the ground breaking introduction of angiotensin-neprilysin inhibition in subjects with comparable severity of systolic heart failure(3). In that study a significant(p < 0.001) reduction in mortality and hospitalisation for heart failure was documented in subjects randomised to angiotensin-neprilysin inhibition vs counterparts randomised to optimum dose enalapril with comparable background therapy(3). Over and above the risk of infection(1), CRT has the added disadvantage of unpredictability of response(4), and, in 36% of cases, poor retention on mean follow up of 2.5 years(5). Accordingly, to justify CRT in the unique subgroup of symptomatic systolic heart failure subjects with left bundle branch block(QRS duration > 150 ms) and sinus rhythm(2) that modality will have to be shown to be superior to angiotensin-neprilysin inhibition when the latter is used in a comparable group of subjects , both groups being on comparable background therapy. References (1) Harrison JL., Prenedergast BD., Sandoe JAI Guidelones for diagnosis management and prevention of implantable cardiac electronic device infection Heart 2014 doi 10.1136/heartjnl-2014-306873 (2) Brignole M., ASuricchio A., Baron Equivas G et al 2013 ESC guidelines on cardiac pacing and cardiac resynchronisation therapy Europace 2013;15:1070-1118 (3) McMurray JJV., Packer M., Desai AS et al Angiotensin-neprilysin inhibition versus enalapril in heart fdailure 2014;371;993-1004 (4) Clelenad J., Freemantle N., Ghio S et al Predicting the long term effects of cardiac resynchronisation therapy on mortality from baseline variables and early response J Am Coll Cardiol 2008;52:430-444 (5) Knight B., Desai A., Coman J Faddis M., Yong P Long term retention of cardiac resynchronisation therapy J Am Coll Cardiol 2004;44:72-77

    Conflict of Interest:

    None declared

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