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Circadian Variations of Infarct Size in STEM1

2012; Lippincott Williams & Wilkins; Volume: 110; Issue: 3 Linguagem: Inglês

10.1161/circresaha.111.262816

1524-4571

Borja Ibáñez, Aida Suárez-Barrientos, Pedro López‐Romero,

Heart Rate Variability and Autonomic Control

HomeCirculation ResearchVol. 110, No. 3Circadian Variations of Infarct Size in STEM1 Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessLetterPDF/EPUBCircadian Variations of Infarct Size in STEM1 Borja Ibanez, Aida Suarez-Barrientos and Pedro Lopez-Romero Borja IbanezBorja Ibanez , Aida Suarez-BarrientosAida Suarez-Barrientos and Pedro Lopez-RomeroPedro Lopez-Romero Originally published3 Feb 2012https://doi.org/10.1161/CIRCRESAHA.111.262816Circulation Research. 2012;110:e22To the Editor:We read with interest the recent article by Reiter et al1 regarding the circadian variations of infarct size in acute myocardial infarction (AMI).This article confirms that there is a circadian variation of infarct size in ST-segment elevation myocardial infarction (STEMI) patients according to the time of the day of AMI onset, something recently shown by our group (Suarez-Barrientos et al2). More important, a third independent series by Arroyo Ucar et al3 has been reported almost simultaneously with the current paper by Reiter and colleagues1 showing similar results. The fact that 3 independent series report a circadian variation of infarct size in humans provides robust evidence that this spontaneous phenomenon is real.Despite both studies (Reiter et al1 and Suárez-Barrientos et al2) having found a circadian variation in infarct size, the time of the day of STEMI onset resulting in larger infarcts varies between both series: Reiter et al found that enzyme release is higher when STEMI onset is between 1 and 5 am,1 while our previous study2 showed that the largest infarcts are from patients with STEMI onset in the dark-to-light transition (ie, between 6 am and noon). The latter data are in agreement with previous animal studies.4There are several potential reasons for this apparent disparity: Patients excluded from the final analysis: Reiter et al1 initially evaluated a population of 1031 STEMI patients, and excluded from the analysis ≈85% of the population. Of note, they excluded 568 patients because of TIMI flow >0 or collateral flow, and 104 additional patients for preinfarction angina or postconditioning. In contrast, in our previous study we excluded from the analysis only patients with previous infarctions or not revascularized by any means (15% of exclusions in comparison with 85% by Reiter et al). The final study population in Reiter et al was 165 patients, and that of Suarez-Barrientos et al was 811 patients. We believe that such a high rate of exclusions in the work by Reiter et al represents a source of selection bias that might have affected the final result. When testing a novel hypothesis in a retrospective manner, consecutive patients should be analyzed unbiased and then adjust for any potential source of bias.Statistical adjustment for factors influencing per se infarct size: the statistical analysis in our previous work took into consideration infarct size modifiers (such as time of ischemia, culprit artery, previous treatment with b-blockers, and ACE inhibitors), while Reiter et al1 did not adjust the peak enzyme release for any of these modifiers, being therefore another potential source of bias in the work by Reiter et al.Reiter et al1 followed the same methodology we described for infarct size estimation: peak concentration of cardiac injury biomarkers. We reported the whole set of CK and troponin-I data. However, Reiter et al reported only CK data. They claim that troponin data were similar, but they decided not to show this critical piece of information that would have reinforced the CK results.From all the above, we wonder how the results from Reiter et al would have been if they had performed such a comprehensive statistical adjustment for infarct size modifiers and with a more reasonable rate of patient exclusion from the actual analysis.Borja Ibanez Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC) Madrid, Spain Cardiovascular Institute Hospital Clínico San Carlos Madrid, SpainAida Suarez-Barrientos Cardiovascular Institute Hospital Clínico San Carlos Madrid, SpainPedro Lopez-Romero Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC) Madrid, SpainDisclosuresNone.FootnotesLetters to the Editor will be published, if suitable, as space permits. They should not exceed 1000 words (typed double-spaced) in length and may be subject to editing or abridgment. References 1. Reiter R, Swingen C, Moore L, Henry TD, Traverse JH. Circadian dependence of infarct size and left ventricular function after ST elevation myocardial infarction. Circ Res. 2011; 110: 105– 110.LinkGoogle Scholar2. Suarez-Barrientos A, Lopez-Romero P, Vivas D, Castro-Ferreira F, Nunez-Gil I, Franco E, Ruiz-Mateos B, Garcia-Rubira JC, Fernandez-Ortiz A, Macaya C, Ibanez B. Circadian variations of infarct size in acute myocardial infarction. Heart. 2011; 97: 970– 976. CrossrefMedlineGoogle Scholar3. Arroyo Úcar E, Dominguez-Rodriguez A, Abreu-Gonzalez P. Influence of diurnal variation in the size of acute myocardial infarction. Med Intensiva. 2011; Sep5. [Epub ahead of print]. Google Scholar4. Durgan DJ, Pulinilkunnil T, Villegas-Montoya C, Garvey ME, Frangogiannis NG, Michael LH, Chow CW, Dyck JR, Young ME. Short communication: ischemia/reperfusion tolerance is time-of-day-dependent: mediation by the cardiomyocyte circadian clock. Circ Res. 2010; 106: 546– 550.LinkGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Oyama Y, Walker L and Eckle T (2021) Targeting circadian PER2 as therapy in myocardial ischemia and reperfusion injury, Chronobiology International, 10.1080/07420528.2021.1928160, 38:9, (1262-1273), Online publication date: 2-Sep-2021. du Pré B, Van Veen T, Crnko S, Vos M, Deddens J, Doevendans P and Van Laake L (2017) Variation within Variation: Comparison of 24-h Rhythm in Rodent Infarct Size between Ischemia Reperfusion and Permanent Ligation, International Journal of Molecular Sciences, 10.3390/ijms18081670, 18:8, (1670) Oster H, Challet E, Ott V, Arvat E, de Kloet E, Dijk D, Lightman S, Vgontzas A and Van Cauter E (2016) The Functional and Clinical Significance of the 24-Hour Rhythm of Circulating Glucocorticoids, Endocrine Reviews, 10.1210/er.2015-1080, 38:1, (3-45), Online publication date: 1-Feb-2017. Mahmoud K, Nijsten M, Wieringa W, Ottervanger J, Holmes D, Hillege H, van 't Hof A and Lipsic E (2014) Independent association between symptom onset time and infarct size in patients with ST-elevation myocardial infarction undergoing primary percutaneous coronary intervention, Chronobiology International, 10.3109/07420528.2014.992527, 32:4, (468-477), Online publication date: 21-Apr-2015. Rotter D, Grinsfelder D, Parra V, Pedrozo Z, Singh S, Sachan N and Rothermel B (2014) Calcineurin and its regulator, RCAN1, confer time-of-day changes in susceptibility of the heart to ischemia/reperfusion, Journal of Molecular and Cellular Cardiology, 10.1016/j.yjmcc.2014.05.004, 74, (103-111), Online publication date: 1-Sep-2014. Ammirati E, Cristell N, Cianflone D, Vermi A, Marenzi G, De Metrio M, Uren N, Hu D, Ravasi T, Maseri A and Cannistraci C (2013) Questing for Circadian Dependence in ST-Segment–Elevation Acute Myocardial Infarction, Circulation Research, 112:10, (e110-e114), Online publication date: 10-May-2013. Bonney S, Hughes K, Harter P, Mittelbronn M, Walker L and Eckle T (2013) Cardiac Period 2 in myocardial ischemia: Clinical implications of a light dependent protein, The International Journal of Biochemistry & Cell Biology, 10.1016/j.biocel.2012.12.022, 45:3, (667-671), Online publication date: 1-Mar-2013. Traverse J, Reiter R and Henry T (2012) Response to Ibanez et al, Circulation Research, 110:3, (e23-e23), Online publication date: 3-Feb-2012. February 3, 2012Vol 110, Issue 3 Advertisement Article InformationMetrics © 2012 American Heart Association, Inc.https://doi.org/10.1161/CIRCRESAHA.111.262816PMID: 22302758 Originally publishedFebruary 3, 2012 PDF download Advertisement