International Journal of Cardiology 187 (2015) 459–461

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International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard

Letter to the Editor

Influence of ischemic postconditioning on myocardial dysfunction measured by speckle tracking echocardiography in patients with ST-elevation myocardial infarction Shanmuganathan Limalanathan a,d,f,⁎, Jan Eritsland a,d, Nils-Einar Kløw b,f, Michael Abdelnoor c, Pavel Hoffmann e, Geir Øystein Andersen a,d a

Department of Cardiology, Unit of Epidemiology and Biostatistics, Oslo University Hospital Ullevål, Oslo, Norway Department of Radiology, Unit of Epidemiology and Biostatistics, Oslo University Hospital Ullevål, Oslo, Norway c Center for Clinical Research, Unit of Epidemiology and Biostatistics, Oslo University Hospital Ullevål, Oslo, Norway d Center for Heart Failure Research, Oslo, Norway e Section for Interventional Cardiology, Oslo, Norway f Faculty of Medicine, University of Oslo, Oslo, Norway b

a r t i c l e

i n f o

Article history: Received 11 February 2015 Accepted 17 March 2015 Available online 18 March 2015 Keywords: Speckle tracking ST-elevation myocardial infarction Ischemic postconditioning Myocardial strain Post-systolic shortening

Timely performed reperfusion and adjuvant drug therapy are essential in the treatment of acute ST elevation myocardial infarction (STEMI). Reperfusion of the infarct-related artery (IRA) may, paradoxically, result in further injury of the ischemic myocardium by mechanisms collectively termed ischemia/reperfusion (I/R) injury [1]. Cardioprotection by ischemic postconditioning (IPost), performed by interrupted blood-flow to the ischemic myocardium at the time of reperfusion, has shown diverging effects on measures of infarct size and left ventricular (LV) function in clinical trials [2]. Previous studies have shown good correlation between myocardial strain measured by 2-dimensional (2-D) speckle tracking echocardiography and infarct size and LV function [3]. Furthermore, post-systolic shortening has been suggested to be associated with ischemic segments with potential for recovery in patients with non-STEMI [4]. However, little is known about a possible effect of IPost on myocardial strain in the acute stage of STEMI. ⁎ Corresponding author at: Department of Cardiology, Oslo University Hospital Ullevål, N-0407 Oslo, Norway. E-mail addresses: [email protected], [email protected] (S. Limalanathan).

http://dx.doi.org/10.1016/j.ijcard.2015.03.192 0167-5273/© 2015 Published by Elsevier Ireland Ltd.

The aim of this study was to investigate the effect of IPost on LV dysfunction, measured by myocardial strain and post-systolic shortening in patients with acute PCI-treated STEMI. The study population consisted of patients with first time STEMI, symptom duration ≤6 h and successful PCI, recruited from the randomized POSTEMI study [5]. IPost was performed by 4 cycles of 1 min balloon occlusion of IRA, starting 1 min after opening and separated by 1 min reperfusion intervals, followed by stenting. In the control group, reperfusion was followed by immediately stenting. An early (median 2 days) conventional grayscale echocardiography was performed with a digital ultrasonic device system (Vivid 9, GE Vingmed Ultrasound, Horten, Norway). The average frame rate was 56 ± 14 frames/s. The recorded grayscale images were analyzed by Echopac software version 112. The end-systole was manually defined by aortic valve closure in the apical long-axis view. The regions of interest were manually obtained by marking the endocardial border of the LV. Global longitudinal peak strain and peak systolic strain were measured from the three standard apical views. Post-systolic shortening was defined as the difference between peak strain and peak systolic strain [6] and post-systolic index (PSI) was calculated manually (Fig. 1a, b). One echo-cardiographer performed all examinations and analyses. Repeated analyses of 20 randomly selected patients were performed by a second observer and reliability analyses revealed an interclass correlation coefficient for peak systolic strain of 0.93 (95% CI 0.82–0.97). Assessment of infarct size and LV ejection fraction (LVEF) was performed by cardiac magnetic resonance (CMR) examination after 4 months. The CMR protocol has been described previously [7]. Continuous and categorical variables are presented as median values with interquartile range (IQR) and proportions, respectively. Differences between groups were analyzed by Mann–Whitney test for continuous variables and chisquare test for categorical variables. A p-value b0.05 was considered statistically significant. Linear regression analyses were used to control for potential confounders of the association between IPost and peak systolic strain and post-systolic index, respectively. A total of 133 consecutive STEMI patients included in the POSTEMI trial were evaluated and 33 patients were excluded from the echo

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analyses due to insufficient image quality. Patient characteristics of included and excluded patients are summarized in Table 1. No significant between-group differences were found in peak troponin T level, infarct size or LVEF assessed by CMR after 4 months. Post-systolic shortening was present in 98 out of 100 patients. Median peak systolic strain was reduced to − 13.1 (IQR − 16.3, − 11.2), n = 100. No significant differences were found in peak systolic strain or post-systolic index in IPost group compared to controls (Fig. 1c and d). Linear regression analyses showed that age, symptom-to-balloon time and anterior wall

infarction had substantial confounding effect (25%) on the association between IPost and peak systolic strain. The association between IPost and peak systolic strain remained non-significant, however, after adjustment for these confounders. Similarly, age, symptom-to-balloon time and anterior wall infarction had substantial confounding effects (12%) on the association between IPost and post-systolic index, however also this association remained non-significant after adjustment. The main result of the study was that IPost did not influence LV function, measured as peak systolic strain and post-systolic index in STEMI

Fig. 1. Myocardial strain measurements in STEMI patients. a: Cartoon illustrating peak strain, peak systolic strain and post-systolic shortening. Post-systolic index = (peak strain − peak systolic strain / peak strain) × 100. b: Myocardial longitudinal strain curves from apical long axis view from a patient with left anterior descending artery occlusion. Post-systolic shortening was present in anteroseptal segments. c and d: Myocardial strain measurements in STEMI patients randomized to ischemic postconditioning (IPost) (n = 45) or control (n = 55). Median values and interquartile range of peak systolic strain (panel c) and post-systolic index (panel d), measured by speckle tracking echocardiography, are given.

S. Limalanathan et al. / International Journal of Cardiology 187 (2015) 459–461

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Table 1 Patient characteristics of STEMI patients randomized to ischemic postconditioning (IPost) or control. Patients excluded from the study are shown for comparison. Variable

IPost (n = 45)

Control (n = 55)

Excluded (n = 33)

Age (years) Male gender (%) Treated hypertension (%) Diabetes (%) Current smoking (%) Symptom-to-balloon time (min) Anterior wall infarction (%) At admission Systolic blood pressure (mm Hg) Heart rate (beats/min) Peak troponin-T (ng/L)

63 (56–72) 82 22 2 49 190 (115–268)

56 (52–64) 87 22 0 55 166 (125–219)

66 (59–71) 78 44 3 47 238 (141–310)

48

52

50

140 (134–160)

145 (134–170)

140 (125–164)

75 (65–85) 5826 (4221–9270) 13.9 (9.3–18.4) 59 (52–65)

75 (64–89) 6064 (3300–11,095) 13.3 (6.3–22.9) 54 (48–62)

77 (61–84) 5503 (3412–11,350) 15.6 (8.6–24.4) 52 (39–63)

Infarct size (% of LV mass)a Ejection fraction (%)a

Data are presented as median values (interquartile range) or percentage. a Measured by cardiac magnetic resonance imaging.

Conflict of interest None. Fig. 1 (continued).

patients treated by primary PCI. Thus, based on the current observations, applying IPost in STEMI patients will not improve early recovery of LV function. This is to our knowledge the first clinical study to evaluate the influence of IPost on myocardial strain and post-systolic shortening. These findings extend the previously reported results of the POSTEMI-trial where no effect of IPost was found on infarct size, myocardial salvage or LV function after 4 months of follow-up [5]. Acute ischemia results in reduction of contractile function and an increase in post-systolic shortening of the involved myocardium [6]. Controversy exists as to whether post-systolic shortening may be a marker of the potential for recovery of ischemic, but viable segments after PCI treatment [8] or whether the presence of post-systolic shortening is only another expression of impaired systolic function [9]. We found a reduction in peak systolic strain, and a high rate of postsystolic shortening in our study compared to a reference population [10], but the postconditioning procedure was not able to improve these early signs of impaired myocardial function. A possible limitation of the results may be a potential selection bias due to the exclusion of patients with poor image quality. In conclusion, IPost did not influence myocardial dysfunction, measured as peak systolic strain or post-systolic shortening in patients with STEMI treated by primary PCI. Sources of funding The POSTEMI-trial was supported by the Norwegian Health and Rehabilitation Foundation and Center for Heart Failure Research, University of Oslo, Norway.

References [1] D.M. Yellon, D.J. Hausenloy, Myocardial reperfusion injury, N. Engl. J. Med. 357 (2007) 1121–1135. [2] M. Abdelnoor, I. Sandven, S. Limalanathan, J. Eritsland, Postconditioning in ST-elevation myocardial infarction: a systematic review, critical appraisal, and meta-analysis of randomized clinical trials, Vasc. Health Risk Manag. 10 (2014) 477–491. [3] K. Munk, N.H. Andersen, C.J. Terkelsen, et al., Global left ventricular longitudinal systolic strain for early risk assessment in patients with acute myocardial infarction treated with primary percutaneous intervention, J. Am. Soc. Echocardiogr. 25 (2012) 644–651. [4] C. Eek, B. Grenne, H. Brunvand, et al., Postsystolic shortening is a strong predictor of recovery of systolic function in patients with non-ST-elevation myocardial infarction, Eur. J. Echocardiogr. 12 (2011) 483–489. [5] S. Limalanathan, G.Ø. Andersen, P. Hoffmann, N.E. Kløw, M. Abdelnoor, J. Eritsland, Effect of ischemic postconditioning on infarct size in patients with ST-elevation myocardial infarction treated by primary PCI, results of the POSTEMI randomized trial, J. Am. Heart Assoc. 23 (2014) e000679. [6] T. Kukulski, F. Jamal, L. Herbots, et al., Identification of acutely ischemic myocardium using ultrasonic strain measurements. A clinical study in patients undergoing coronary angioplasty, J. Am. Coll. Cardiol. 5 (2003) 810–819. [7] S. Limalanathan, G.Ø. Andersen, P. Hoffmann, N.E. Kløw, M. Abdelnoor, J. Eritsland, Rationale and design of the POSTEMI (POstconditioning in ST-Elevation Myocardial Infarction) Study, Cardiology 116 (2010) 103–109. [8] M.A. Brown, R.M. Norris, M. Takayama, H.D. White, Post-systolic shortening: a marker of potential for early recovery of acutely ischaemic myocardium in the dog, Cardiovasc. Res. 21 (1987) 703–716. [9] C.J. Terkelsen, S.H. Poulsen, B.L. Nørgaard, et al., Does postsystolic motion or shortening predict recovery of myocardial function after primary percutaneous coronary intervention? J. Am. Soc. Echocardiogr. 20 (2007) 505–511. [10] H. Dalen, A. Thorstensen, S.A. Aase, et al., Segmental and global longitudinal strain and strain rate based on echocardiography of 1266 healthy individuals: the HUNT study in Norway, Eur. J. Echocardiogr. 11 (2010) 176–183.

Influence of ischemic postconditioning on myocardial dysfunction measured by speckle tracking echocardiography in patients with ST-elevation myocardial infarction.

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