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• W2901709989 abstract "HomeCirculation: Cardiovascular InterventionsVol. 11, No. 9Reperfusion Treatment in Late Presentation Acute Myocardial Infarction Free AccessEditorialPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessEditorialPDF/EPUBReperfusion Treatment in Late Presentation Acute Myocardial InfarctionTiming Is Not Everything Mohammad Alkhalil, MRCP and Robin P. Choudhury, DM Mohammad AlkhalilMohammad Alkhalil Acute Vascular Imaging Centre (M.A., R.P.C.), Radcliffe Department of Medicine, University of Oxford, United Kingdom Royal Victoria Hospital, Belfast Health and Social Care Trust, United Kingdom (M.A.). Search for more papers by this author and Robin P. ChoudhuryRobin P. Choudhury Acute Vascular Imaging Centre (M.A., R.P.C.), Radcliffe Department of Medicine, University of Oxford, United Kingdom Division of Cardiovascular Medicine (R.P.C.), Radcliffe Department of Medicine, University of Oxford, United Kingdom Search for more papers by this author Originally published14 Sep 2018https://doi.org/10.1161/CIRCINTERVENTIONS.118.007287Circulation: Cardiovascular Interventions. 2018;11:e007287This article is a commentary on the followingBenefit From Reperfusion With Primary Percutaneous Coronary Intervention Beyond 12 Hours of Symptom Duration in Patients With ST-Segment–Elevation Myocardial InfarctionSee Article by Nepper-Christensen et alContemporary management of ST-segment–elevation myocardial infarction (STEMI) is built around timely reperfusion therapies that aim to reduce infarct size and optimize patient outcome.1 Duration of ischemia, as a key determinant of infarct size, has been recognized since the 1970s, guided by the wave front phenomenon, whereby myocyte death is proportionate to the duration of coronary artery occlusion and starts from the endocardium.2 This knowledge has pushed pharmacological and catheter-based coronary interventions to minimize delay to reperfusion. Nonetheless, the relationship between the probability of death and ischemia time (defined as time from symptoms onset to reperfusion therapy) is nonlinear.3 In trials of thrombolysis, the maximal benefit was delivered within the first 2 hours.4 Therefore, the survival benefit from opening occluded artery is crucially related to time in the very early course of STEMI presentation; however, this relationship breaks down in patients presenting late.3,5Remarkably, a time threshold to define late presentation (>12 hours) for primary percutaneous coronary intervention (PCI) was inferred from data derived from outcomes with lytic therapies, generating debate as to whether such an approach is appropriate.6 The LATE study (Late Assessment of Thrombolytic Efficacy) showed no morality benefits in patients presenting beyond 12 hours using thrombolytic therapy.7 Yet, mechanical recanalization of the infarct-related artery in the BRAVE-2 trial (Beyond 12 Hours Reperfusion Alternative Evaluation), albeit underpowered, showed prognostic benefit in patients with late STEMI presentation up to 48 hours.8 On the contrary, establishing flow in the epicardial coronary artery with PCI in very late presenters (3–28 days) in the OAT (Occluded Artery Trial) did not improve mortality or left ventricle ejection fraction during 4-year follow-up compared with medical therapy.5It seems likely that time from symptom onset is, in part, a proxy for the downstream status of the myocardium. Duration of ischemia is related to extent of infarction and its complications, such as intramyocardial hemorrhage.9 However, time from symptom onset relies on accurate recollection and does not take into account individual variations such as intermittent or partial coronary occlusion, the extent of collateral circulation, degree of ischemic preconditioning, and the metabolic status within the ischemic myocardium.10 These deficiencies could be potentially be addressed if the myocardium could be accurately and promptly characterized, for example, by imaging.Imaging studies have consistently shown that substantial salvageable myocardium can occur in some patients, even with time onset from symptoms >48 hours.11 More importantly, the relationship between time from onset of symptoms and imaging surrogates of infarct severity was weak at most, highlighting the importance of other features beyond symptom duration or single time point assessment of flow of in the culprit epicardial coronary artery (above).10,11In this issue of Circulation: Cardiovascular Interventions, Nepper-Christensen et al12 report cardiac magnetic resonance (CMR) measurements in patients presenting late with STEMI (12–48 hours). CMR can characterize acute myocardial injury and is becoming the multiparametric imaging method of choice for the assessment of patients after STEMI.13 In order to evaluate the efficacy of PCI, the authors, based in a large-volume single-center recruited individuals, with signs of instability based on clinical presentation and the ECG. Instability was defined as evidence of ongoing ischemia, ongoing or recurrent pain with or without symptoms or signs of shock, heart failure, or malignant arrhythmias according to guidelines.1 Reperfusion therapy is currently recommended for such patients, but it is not known how delayed reperfusion influences patient outcome.1 Here, the authors demonstrated lower myocardial salvage index in this high-risk subgroup compared with patients presenting early (<12 hours) of symptoms onset (P=0.021). Yet, late-presenting patients had a significant degree of salvageable myocardium 0.58 (0.39–0.71) with two-thirds of patients achieving a myocardial salvage index ≥0.5, highlighting the potential benefits of PCI in this subgroup. Moreover, late-presenting patients had larger infarct size (P=0.037) and more likelihood of developing microvascular obstruction than early presenters (72% versus 50%; P=0.002). However, this may not necessarily reflect a time-related effect given baseline differences between 2 groups. Late presenters had more anterior STEMI and were less likely to receive GP (glycoprotein) IIb/IIIa inhibitors. Such differences, in particular the use of GP IIb/IIIa, are known to affect infarct size and may have underestimated the benefits of intervening on late presenters.14 Other baseline differences such as percentage of thrombus aspiration and femoral access may be reflective of change in guidelines given the time lag in recruiting patients between 2 groups, early versus late presenters, limiting definitive conclusions from this study.Despite the inevitable drawbacks from an observational study, the authors highlight the important finding of a lack of association between time to reperfusion and CMR measures of infarct severity. Furthermore, ischemia time was not of value in predicting significant salvageable myocardium in this high-risk group. Interestingly, ischemia time had no interaction with coronary artery status before percutaneous intervention. This is in contrast to the findings from Busk et al,11 in which significantly lower myocardial salvage index was reported in late presenters with occluded coronary artery (44% [23–73] versus 57% [42–86]; P=0.03). This discrepancy maybe related to the nonselective inclusion in the study by Busk et al,11 diluting any potential favorable effects of performing PCI in late-presenting patients. Nevertheless, identifying the subgroup of patients who are more likely to benefit from PCI based on pure symptoms could also be challenged. The SWISS II study (Swiss Interventional Study on Silent Ischemia Type II) demonstrated clinical benefits from revascularization in asymptomatic patients with recent STEMI but with silent ischemia.15 Therefore, the absence of chest pain does not always reflect lack of ischemia, and other tools to characterize late presentations are still required. Thus, asymptomatic late presenters may miss an important therapeutic opportunity should we only rely on symptoms-guided approach to identify patients who require immediate PCI.Advances in cardiac imaging, especially with CMR, have enhanced our understanding of the pathophysiology of acute myocardial infarction.13,16 As highlighted above, the degree of myocardial recovery may not solely be dependent on the apparent duration of ischemia. In an individual patient, these features cannot be ascertained in isolation, nor can their collective effects be discerned. Given the heterogeneity in myocardial injury and response to therapy,10,17 accurate determination of myocardial status in patients presenting late with acute myocardial infarction may be a useful means of stratification.Recently, novel CMR mapping techniques have been shown to reflect myocardial composition, with changes in relaxation times related to pathological processes at the level of the tissue.18,19 Moreover, these mapping techniques can characterize injured myocardium, allowing assessments of both severity of injury and potential for recovery,18,19 making them ideally suited to evaluate and quantify myocardial injury. Progress in the CMR technology and availability may eventually lead to CMR characterization of myocardial status before primary PCI in patients presenting late. Such an apparently radical notion is akin to brain imaging before reperfusion therapies in stroke or to emergency abdominal computed tomography to select patients for laparotomy after major blunt abdominal trauma and could move the treatment of late presentation acute STEMI toward a more personalized approach.DisclosuresNone.FootnotesThe opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.https://www.ahajournals.org/journal/circinterventionsRobin P. Choudhury, DM, Division of Cardiovascular Medicine, Radcliffe Department of Medicine, John Radcliffe Hospital, University of Oxford, Oxford OX3 9DU, United Kingdom. Email robin.[email protected]ox.ac.ukReferences1. Ibanez B, James S, Agewall S, Antunes MJ, Bucciarelli-Ducci C, Bueno H, Caforio ALP, Crea F, Goudevenos JA, Halvorsen S, Hindricks G, Kastrati A, Lenzen MJ, Prescott E, Roffi M, Valgimigli M, Varenhorst C, Vranckx P, Widimský P; ESC Scientific Document Group. 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation: the Task Force for the management of acute myocardial infarction in patients presenting with ST-segment elevation of the European Society of Cardiology (ESC).Eur Heart J. 2018; 39:119–177. doi: 10.1093/eurheartj/ehx393.CrossrefMedlineGoogle Scholar2. Reimer KA, Jennings RB. The “wavefront phenomenon” of myocardial ischemic cell death. II. Transmural progression of necrosis within the framework of ischemic bed size (myocardium at risk) and collateral flow.Lab Invest. 1979; 40:633–644.MedlineGoogle Scholar3. Gersh BJ, Stone GW, White HD, Holmes DRPharmacological facilitation of primary percutaneous coronary intervention for acute myocardial infarction: is the slope of the curve the shape of the future?JAMA. 2005; 293:979–986. doi: 10.1001/jama.293.8.979CrossrefMedlineGoogle Scholar4. Boersma E, Maas AC, Deckers JW, Simoons ML. Early thrombolytic treatment in acute myocardial infarction: reappraisal of the golden hour.Lancet. 1996; 348:771–775. doi: 10.1016/S0140-6736(96)02514-7CrossrefMedlineGoogle Scholar5. Hochman JS, Lamas GA, Buller CE, Dzavik V, Reynolds HR, Abramsky SJ, Forman S, Ruzyllo W, Maggioni AP, White H, Sadowski Z, Carvalho AC, Rankin JM, Renkin JP, Steg PG, Mascette AM, Sopko G, Pfisterer ME, Leor J, Fridrich V, Mark DB, Knatterud GL; Occluded Artery Trial Investigators. Coronary intervention for persistent occlusion after myocardial infarction.N Engl J Med. 2006; 355:2395–2407. doi: 10.1056/NEJMoa066139CrossrefMedlineGoogle Scholar6. Cohen M, Boiangiu C, Abidi M. Therapy for ST-segment elevation myocardial infarction patients who present late or are ineligible for reperfusion therapy.J Am Coll Cardiol. 2010; 55:1895–1906. doi: 10.1016/j.jacc.2009.11.087CrossrefMedlineGoogle Scholar7. Late Assessment of Thrombolytic Efficacy (LATE) study with alteplase 6–24 hours after onset of acute myocardial infarction.Lancet. 1993; 342:759–766.CrossrefMedlineGoogle Scholar8. Ndrepepa G, Kastrati A, Mehilli J, Antoniucci D, Schömig A. Mechanical reperfusion and long-term mortality in patients with acute myocardial infarction presenting 12 to 48 hours from onset of symptoms.JAMA. 2009; 301:487–488. doi: 10.1001/jama.2009.32CrossrefMedlineGoogle Scholar9. Basso C, Thiene G. The pathophysiology of myocardial reperfusion: a pathologist’s perspective.Heart. 2006; 92:1559–1562. doi: 10.1136/hrt.2005.086959CrossrefMedlineGoogle Scholar10. Elmariah S, Smith SC, Fuster V. Late medical versus interventional therapy for stable ST-segment elevation myocardial infarction.Nat Clin Pract Cardiovasc Med. 2008; 5:42–52. doi: 10.1038/ncpcardio1056CrossrefMedlineGoogle Scholar11. Busk M, Kaltoft A, Nielsen SS, Bøttcher M, Rehling M, Thuesen L, Bøtker HE, Lassen JF, Christiansen EH, Krusell LR, Andersen HR, Nielsen TT, Kristensen SD. Infarct size and myocardial salvage after primary angioplasty in patients presenting with symptoms for <12 h vs. 12-72 h.Eur Heart J. 2009; 30:1322–1330. doi: 10.1093/eurheartj/ehp113CrossrefMedlineGoogle Scholar12. Nepper-Christensen L, Lønborg J, Høfsten DE, Ahtarovski KA, Bang LE, Helqvist S, Kyhl K, Køber L, Kelbæk H, Vejlstrup N, Holmvang L, Engstrøm T. Benefit from reperfusion with primary percutaneous coronary intervention beyond 12 hours of symptom duration in patients with ST-segment–elevation myocardial infarction.Circ Cardiovasc Interv. 2018; 11:e006842. doi: 10.1161/CIRCINTERVENTIONS.118.006842LinkGoogle Scholar13. Dall’Armellina E, Karamitsos TD, Neubauer S, Choudhury RP. CMR for characterization of the myocardium in acute coronary syndromes.Nat Rev Cardiol. 2010; 7:624–636. doi: 10.1038/nrcardio.2010.140CrossrefMedlineGoogle Scholar14. Stone GW, Maehara A, Witzenbichler B, Godlewski J, Parise H, Dambrink JH, Ochala A, Carlton TW, Cristea E, Wolff SD, Brener SJ, Chowdhary S, El-Omar M, Neunteufl T, Metzger DC, Karwoski T, Dizon JM, Mehran R, Gibson CM; INFUSE-AMI Investigators. Intracoronary abciximab and aspiration thrombectomy in patients with large anterior myocardial infarction: the INFUSE-AMI randomized trial.JAMA. 2012; 307:1817–1826. doi: 10.1001/jama.2012.421CrossrefMedlineGoogle Scholar15. Schoenenberger AW, Kobza R, Jamshidi P, Zuber M, Abbate A, Stuck AE, Pfisterer M, Erne P. Sudden cardiac death in patients with silent myocardial ischemia after myocardial infarction (from the Swiss Interventional Study on Silent Ischemia Type II [SWISSI II]).Am J Cardiol. 2009; 104:158–163. doi: 10.1016/j.amjcard.2009.03.019CrossrefMedlineGoogle Scholar16. Fernández-Jiménez R, Barreiro-Pérez M, Martin-García A, Sánchez-González J, Agüero J, Galán-Arriola C, García-Prieto J, Díaz-Pelaez E, Vara P, Martinez I, Zamarro I, Garde B, Sanz J, Fuster V, Sánchez PL, Ibanez B. Dynamic edematous response of the human heart to myocardial infarction: implications for assessing myocardial area at risk and salvage.Circulation. 2017; 136:1288–1300. doi: 10.1161/CIRCULATIONAHA.116.025582LinkGoogle Scholar17. Yousef ZR, Redwood SR, Bucknall CA, Sulke AN, Marber MS. Late intervention after anterior myocardial infarction: effects on left ventricular size, function, quality of life, and exercise tolerance: results of the Open Artery Trial (TOAT Study).J Am Coll Cardiol. 2002; 40:869–876.CrossrefMedlineGoogle Scholar18. Liu D, Borlotti A, Viliani D, Jerosch-Herold M, Alkhalil M, De Maria GL, Fahrni G, Dawkins S, Wijesurendra R, Francis J, Ferreira V, Piechnik S, Robson MD, Banning A, Choudhury R, Neubauer S, Channon K, Kharbanda R, Dall’Armellina E. CMR native T1 mapping allows differentiation of reversible versus irreversible myocardial damage in ST-segment-elevation myocardial infarction: an OxAMI Study (Oxford Acute Myocardial Infarction).Circ Cardiovasc Imaging. 2017; 10:e005986. doi: 10.1161/CIRCIMAGING.116LinkGoogle Scholar19. Dall’Armellina E, Piechnik SK, Ferreira VM, Si QL, Robson MD, Francis JM, Cuculi F, Kharbanda RK, Banning AP, Choudhury RP, Karamitsos TD, Neubauer S. Cardiovascular magnetic resonance by non contrast T1-mapping allows assessment of severity of injury in acute myocardial infarction.J Cardiovasc Magn Reson. 2012; 14:15. doi: 10.1186/1532-429X-14-15CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited ByGramegna M, Baldetti L, Beneduce A, Pannone L, Falasconi G, Calvo F, Pazzanese V, Sacchi S, Pagnesi M, Moroni F, Ajello S, Melisurgo G, Agricola E, Camici P, Scandroglio A, Landoni G, Ciceri F, Zangrillo A and Cappelletti A (2020) ST-Segment–Elevation Myocardial Infarction During COVID-19 Pandemic, Circulation: Cardiovascular Interventions, 13:8, Online publication date: 1-Aug-2020.Related articlesBenefit From Reperfusion With Primary Percutaneous Coronary Intervention Beyond 12 Hours of Symptom Duration in Patients With ST-Segment–Elevation Myocardial InfarctionLars Nepper-Christensen, et al. Circulation: Cardiovascular Interventions. 2018;11 September 2018Vol 11, Issue 9 Advertisement Article InformationMetrics © 2018 American Heart Association, Inc.https://doi.org/10.1161/CIRCINTERVENTIONS.118.007287PMID: 30354604 Originally publishedSeptember 14, 2018 KeywordsischemiaST-segment–elevation myocardial infarctionmyocardial infarctionreperfusionEditorialsPDF download Advertisement SubjectsCatheter-Based Coronary and Valvular InterventionsPercutaneous Coronary Intervention" @default.
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