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• W2965485004 abstract "HomeCirculation ResearchVol. 125, No. 4Response by Stiermaier and Eitel to Letter Regarding Article, “Combined Intrahospital Remote Ischemic Perconditioning and Postconditioning Improves Clinical Outcome in ST-Elevation Myocardial Infarction: Long-Term Results of the LIPSIA CONDITIONING Trial” Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessLetterPDF/EPUBResponse by Stiermaier and Eitel to Letter Regarding Article, “Combined Intrahospital Remote Ischemic Perconditioning and Postconditioning Improves Clinical Outcome in ST-Elevation Myocardial Infarction: Long-Term Results of the LIPSIA CONDITIONING Trial” Thomas Stiermaier and Ingo Eitel Thomas StiermaierThomas Stiermaier From the University Heart Center Lübeck, Medical Clinic II (Cardiology/Angiology/Intensive Care Medicine), Germany; and German Center for Cardiovascular Research, Partner Site Hamburg/Kiel/Lübeck. Search for more papers by this author and Ingo EitelIngo Eitel From the University Heart Center Lübeck, Medical Clinic II (Cardiology/Angiology/Intensive Care Medicine), Germany; and German Center for Cardiovascular Research, Partner Site Hamburg/Kiel/Lübeck. Search for more papers by this author Originally published1 Aug 2019https://doi.org/10.1161/CIRCRESAHA.119.315537Circulation Research. 2019;125:e18–e19In Response:We thank Dr Olafiranye for the interest in our work regarding the long-term protective effects of ischemic conditioning in patients with ST-segment–elevation myocardial infarction.1 Our post hoc analysis of a randomized trial (LIPSIA CONDITIONING) showed a significant reduction of new congestive heart failure after combined remote ischemic conditioning (RIC) and postconditioning in addition to primary percutaneous coronary intervention compared with a control group receiving standard treatment.2 Postconditioning only in addition to primary percutaneous coronary intervention resulted in a nonsignificant reduction of heart failure events.2 At the time of new congestive heart failure, left ventricular ejection fraction (LVEF) was significantly reduced in all patients experiencing this end point while no cases were related to heart failure with preserved LVEF. As mentioned correctly by Dr Olafiranye,1 initial LVEF did not differ between the study arms, and the proportion of patients with an LVEF <50% was also similar in the 3 groups (RIC and postconditioning, n=103; postconditioning only, n=105; control group, n=97). The incidence of new congestive heart failure in this subgroup with impaired initial LVEF reflects the results in the overall study population: RIC and postconditioning, n=2 of 103 (1.9%); postconditioning only, n=5 of 105 (4.8%); control group, n=6 of 97 (6.2%). However, considering the overall frequency of new congestive heart (RIC and postconditioning, n=6; postconditioning only, n=8; control group, n=17), these numbers illustrate that events were not restricted to patients with preexisting impairment of LVEF but also occurred in patients with at least preserved LVEF immediately after infarction. Therefore, we agree with Dr Olafiranye that the prevention of postinfarction heart failure after ischemic conditioning was not related to immediate effects on cardiac function, which is also confirmed by similar myocardial damage and functional outcome in the treatment groups. However, it is conceivable that ischemic conditioning prevents progression to heart failure by inhibiting adverse left ventricular remodeling, albeit our data cannot prove this hypothesis in the absence of systematic follow-up of cardiac function in all patients. The acute loss of myocardium changes ventricular hemodynamics, which can result in a dilated left ventricle with impaired contractile function including also the apparently healthy myocardium. The complex process of adverse remodeling involves not only myocytes and the extracellular matrix but also the capillary microcirculation. Although infarct size and microvascular damage (microvascular obstruction and intramyocardial hemorrhage) are the best predictors for postinfarction ventricular remodeling, alterations in the infarcted border zone and in the remote, noninfarcted myocardium have also been reported as determinants of postinfarction cardiac function and clinical outcome.3 It can be speculated that ischemic conditioning prevents subtle myocardial alterations and microvascular dysfunction in the noninfarcted myocardium, which subsequently lowers the risk of adverse ventricular remodeling. The fact that cardioprotection by ischemic conditioning and postinfarction remodeling are both presumably triggered by complex humoral and neuronal signaling cascades supports a potential link as well. The potent anti-inflammatory cytokine interleukin-10, for example, seems to play a key role in both processes. Experimental studies in mice showed that upregulation of interleukin-10 following RIC resulted in late protection against myocardial ischemia-reperfusion injury and interleukin-10 also contributed to improved LVEF and postinfarction left ventricular remodeling by inhibiting fibrosis.4,5 Likewise, other overlapping or complementary signaling pathways are conceivable. Of note, the potential prevention of ventricular remodeling after ischemic conditioning is a long-term effect and might explain the reduction of new congestive heart failure during follow-up. In contrast, Dr Olafiranye mentions a potential mechanism for the prevention of early postinfarction heart failure events, which were also numerically reduced in the combined RIC and postconditioning treatment arm in our study, via an increase in circulating nitrite.1In conclusion, ischemic conditioning is a promising approach to prevent progression to postinfarction heart failure with encouraging preliminary clinical results. A better understanding of the mechanisms underlying ischemia-reperfusion injury, cardioprotection by ischemic conditioning, and postinfarction adverse ventricular remodeling is required to improve conditioning protocols and patient selection.DisclosuresNone.FootnotesFor Disclosures, see page e19.References1. Olafiranye O. Letter by Olafiranye regarding article “ combined intrahospital remote ischemic perconditioning and postconditioning improves clinical outcome in ST-elevation myocardial infarction: long-term results of the LIPSIA CONDITIONING trial”.Circ Res. 2019; 125:e16–e17. doi: 10.1161/CIRCRESAHA.119.315526LinkGoogle Scholar2. Stiermaier T, Jensen JO, Rommel KP, de Waha-Thiele S, Fuernau G, Desch S, Thiele H, Eitel I. Combined intrahospital remote ischemic perconditioning and postconditioning improves clinical outcome in ST-elevation myocardial infarction: long-term results of the LIPSIA CONDITIONING trial.Circ Res. 2019; 124:1482–1491. doi: 10.1161/CIRCRESAHA.118.314500LinkGoogle Scholar3. Reinstadler SJ, Stiermaier T, Liebetrau J, Fuernau G, Eitel C, de Waha S, Desch S, Reil JC, Pöss J, Metzler B, et al. Prognostic significance of remote myocardium alterations assessed by quantitative noncontrast T1 mapping in ST-segment elevation myocardial infarction.JACC Cardiovasc Imaging. 2018; 11:411–419. doi: 10.1016/j.jcmg.2017.03.015CrossrefMedlineGoogle Scholar4. Cai ZP, Parajuli N, Zheng X, Becker L. Remote ischemic preconditioning confers late protection against myocardial ischemia-reperfusion injury in mice by upregulating interleukin-10.Basic Res Cardiol. 2012; 107:277. doi: 10.1007/s00395-012-0277-1CrossrefMedlineGoogle Scholar5. Krishnamurthy P, Rajasingh J, Lambers E, Qin G, Losordo DW, Kishore R. IL-10 inhibits inflammation and attenuates left ventricular remodeling after myocardial infarction via activation of STAT3 and suppression of HuR.Circ Res. 2009; 104:e9–e18. doi: 10.1161/CIRCRESAHA.108.188243LinkGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetails August 2, 2019Vol 125, Issue 4 Advertisement Article InformationMetrics © 2019 American Heart Association, Inc.https://doi.org/10.1161/CIRCRESAHA.119.315537PMID: 31518209 Originally publishedAugust 1, 2019 PDF download Advertisement SubjectsMortality/SurvivalMyocardial Infarction" @default.
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