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Is Longitudinal Strain Associated with Left Ventricular Remodeling in Patients with Acute Myocardial Infarction? To the Editor: Recently, Park et al 1 documented a strong association between longitudinal strain (LS) assessed by echocardiography and left ven- tricular (LV) remodeling in 50 patients with acute myocardial infarc- tion (AMI). The investigators, using both conventional Doppler tissue imaging and speckle tracking imaging, showed that patients who developed severe left ventricular remodeling, in a variable time setting after AMI (range 3-47 months), had significantly lower base- line LS and that this variable was a strong independent predictor of the remodeling process. Despite the appealing objective of the study, we would like to comment on 2 notable limitations. First, baseline left ventricular systolic function, as determined by LV ejection fraction and wall motion score index, was significantly different between the 2 groups studied. Ideally, LS should be evaluated as an independent risk factor for future remodeling between 2 groups of patients with relatively comparable LV systolic function. Second and most important is the different time period during which LV remodeling was assessed by echocardiography (with a range of 3-47 months) after the index infarction. Of interest is the fact that the investigators did not include in their multivariable model analysis novel indices of LV diastolic filling, such as E/e= and E/Vp, that have been recently shown as accurate prognostic markers of LV remodeling in the setting of reperfused AMI. 2,3 We have recently commented on an article concerning postinfarct LV remodeling in the modern clinical era and presented our own experience in a population of patients with early effective reperfusion. 4,5 We proposed that E/Vp ratio and brain natriuretic peptide levels are the strongest predictors of LV remodeling. We used conventional Doppler tissue imaging to assess LS in the anterior wall and found no significant association between LS and the net change of LV systolic volume index in a 6-month period after a reperfused anterior AMI. In contrast, we observed that patients in the remodeling group had less evidence of post-systolic shortening in the strain curve in the risk area of the anterior wall (11% vs 39%, P .03). The presence of post-systolic shortening that may reflect stunned myocar- dial tissue remains controversial for the time being and awaits further investigation. 6 We believe that larger studies are needed to evaluate LS as an independent predictor of LV remodeling. Christodoulos E. Papadopoulos, MD Georgios A. Giannakoulas, MD Theodoros D. Karamitsos, MD Haralambos I. Karvounis, MD Ioannis Stiliadis, MD Georgios E. Parharidis, MD First Cardiology Department AHEPA University Hospital Aristotle University of Thessaloniki Greece REFERENCES 1. Park YH, Kang SJ, Song JK, Lee EY, Song JM, Kang DH, et al. Prognostic value of longitudinal strain after primary reperfusion therapy in patients with anterior wall acute myocardial infarction. J Am Soc Echocardiogr 2008;21:262-7. 2. Hillis GS, Ujino K, Mulvagh SL, Hagen ME, Oh JK. Echocardiographic indices of increased left ventricular filling pressure and dilation after acute myocardial infarction. J Am Soc Echocardiogr 2006;19:450-6. 3. Moller JE, Sondergaard E, Seward JB, Appleton CP, Egstrup K. Ratio of left ventricular peak E-wave velocity to flow propagation velocity assessed by color M-mode Doppler echocardiography in first myocardial infarction. Prognostic and clinical implications. J Am Coll Cardiol 2000;35:363-70. 4. Papadopoulos CE, Karvounis HI, Giannakoulas G, Karamitsos TD, Efthimi- adis GK, Parharidis GE. Predictors of left ventricular remodeling after reperfused acute myocardial infarction. Am J Cardiol 2007;99:1024-5. 5. Savoye C, Equine O, Tricot O, Nugue O, Segrestin B, Sautiere K, et al. Myocardial infarction in modern clinical practice (from the REmodelage Ventriculaire [REVE] Study Group). Am J Cardiol 2006;98:1144-9. 6. Sutherland GR, Di Salvo G, Claus P, D’Hooge J, Bijnens B. Strain and strain rate imaging: a new clinical approach to quantifying regional myocardial function. J Am Soc Echocardiogr 2004;17:788-802. doi:10.1016/j.echo.2008.07.012 Prediction of Left Ventricular Remodeling After Primary Reperfusion Therapy in Acute Anterior Wall Myocar- dial Infarction Using Myocardial Deformation Data Reply to the Editor: We thank Dr Papadopoulos and colleagues for pointing out several issues related to our recent publication on the prognostic value of longitudinal strain (LS) after acute anterior wall myocardial infarction (AMI). 1 They expressed concern about significant baseline differences in left ventricular (LV) systolic function (LV ejection fraction and wall motion score index) between patients who did and did not develop LV remodeling. They suggested that LS should be tested between 2 groups of patients with relatively comparable LV systolic function. Their suggestion is ideal, but, in real clinical situa- tions, arbitrary control of LV systolic function after AMI is impossible. However, we note other clinical articles dealing with LV remodel- ing, 2,3 in which baseline differences in LV systolic function were significant, and interestingly enough these indices of systolic function were proved as one of the independent factors associated with LV remodeling. 3 Moreover, despite significant difference of LV ejection fraction and wall motion score index in our study, LS was proved the only independent variable associated with LV remodeling in multi- variate analysis, which could be interpreted as an advantage rather than disadvantage or limitation. Their second concern was the different time periods between the index clinical event (AMI) and follow-up echocardiography. Because LV remodeling is a time-dependent process, we agree with them in that we need a guideline in terms of appropriate follow-up duration. Unfortunately, at present, there is no general consensus, and different time intervals have been used by different investigators. 2 Actually, in clinical practice, hard clinical events, including hospital admission or death, occur during follow-up, which can result in different time periods. In our study the time interval was 15 8 months (mean standard deviation), and we originally thought at least a 12-month follow-up duration was acceptable. Because patients with develop- ment of clinical events or LV remodeling before 12 months were included in this study, the time interval was variable. The last and important issue is potential association between LV filling pressure parameters and LV remodeling. In our study we did not include E/e’ measures, but included deceleration time of early transmitral inflow, which has been proved to be associated with an increased risk of LV dilation after AMI. 4-6 We have failed to demon- strate the predictive role of deceleration time. As Dr Papadopoulos and colleagues mentioned, the strong association between LV filling pressure parameters and LV remodeling has been reported recently by several investigators. 2,7,8 The contradictory findings can be partly explained by marked heterogeneity of patient population or selection bias. Although we selected patients with anterior AMI who received 1077

Prediction of Left Ventricular Remodeling After Primary Reperfusion Therapy in Acute Anterior Wall Myocardial Infarction Using Myocardial Deformation Data

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Is Longitudinal Strain Associated with Left VentricularRemodeling in Patients with Acute MyocardialInfarction?

To the Editor:

Recently, Park et al1 documented a strong association betweenlongitudinal strain (LS) assessed by echocardiography and left ven-tricular (LV) remodeling in 50 patients with acute myocardial infarc-tion (AMI). The investigators, using both conventional Doppler tissueimaging and speckle tracking imaging, showed that patients whodeveloped severe left ventricular remodeling, in a variable timesetting after AMI (range 3-47 months), had significantly lower base-line LS and that this variable was a strong independent predictor ofthe remodeling process.

Despite the appealing objective of the study, we would like tocomment on 2 notable limitations. First, baseline left ventricularsystolic function, as determined by LV ejection fraction and wallmotion score index, was significantly different between the 2 groupsstudied. Ideally, LS should be evaluated as an independent risk factorfor future remodeling between 2 groups of patients with relativelycomparable LV systolic function. Second and most important is thedifferent time period during which LV remodeling was assessed byechocardiography (with a range of 3-47 months) after the indexinfarction.

Of interest is the fact that the investigators did not include in theirmultivariable model analysis novel indices of LV diastolic filling, suchas E/e= and E/Vp, that have been recently shown as accurateprognostic markers of LV remodeling in the setting of reperfusedAMI.2,3 We have recently commented on an article concerningpostinfarct LV remodeling in the modern clinical era and presentedour own experience in a population of patients with early effectivereperfusion.4,5 We proposed that E/Vp ratio and brain natriureticpeptide levels are the strongest predictors of LV remodeling. We usedconventional Doppler tissue imaging to assess LS in the anterior walland found no significant association between LS and the net changeof LV systolic volume index in a 6-month period after a reperfusedanterior AMI. In contrast, we observed that patients in the remodelinggroup had less evidence of post-systolic shortening in the strain curvein the risk area of the anterior wall (11% vs 39%, P � .03). Thepresence of post-systolic shortening that may reflect stunned myocar-dial tissue remains controversial for the time being and awaits furtherinvestigation.6

We believe that larger studies are needed to evaluate LS as anindependent predictor of LV remodeling.

Christodoulos E. Papadopoulos, MDGeorgios A. Giannakoulas, MDTheodoros D. Karamitsos, MDHaralambos I. Karvounis, MD

Ioannis Stiliadis, MDGeorgios E. Parharidis, MDFirst Cardiology DepartmentAHEPA University Hospital

Aristotle University of ThessalonikiGreece

REFERENCES

1. Park YH, Kang SJ, Song JK, Lee EY, Song JM, Kang DH, et al. Prognosticvalue of longitudinal strain after primary reperfusion therapy in patientswith anterior wall acute myocardial infarction. J Am Soc Echocardiogr2008;21:262-7.

2. Hillis GS, Ujino K, Mulvagh SL, Hagen ME, Oh JK. Echocardiographicindices of increased left ventricular filling pressure and dilation after acute

myocardial infarction. J Am Soc Echocardiogr 2006;19:450-6.

3. Moller JE, Sondergaard E, Seward JB, Appleton CP, Egstrup K. Ratio of leftventricular peak E-wave velocity to flow propagation velocity assessed bycolor M-mode Doppler echocardiography in first myocardial infarction.Prognostic and clinical implications. J Am Coll Cardiol 2000;35:363-70.

4. Papadopoulos CE, Karvounis HI, Giannakoulas G, Karamitsos TD, Efthimi-adis GK, Parharidis GE. Predictors of left ventricular remodeling afterreperfused acute myocardial infarction. Am J Cardiol 2007;99:1024-5.

5. Savoye C, Equine O, Tricot O, Nugue O, Segrestin B, Sautiere K, et al.Myocardial infarction in modern clinical practice (from the REmodelageVentriculaire [REVE] Study Group). Am J Cardiol 2006;98:1144-9.

6. Sutherland GR, Di Salvo G, Claus P, D’Hooge J, Bijnens B. Strain and strainrate imaging: a new clinical approach to quantifying regional myocardialfunction. J Am Soc Echocardiogr 2004;17:788-802.

doi:10.1016/j.echo.2008.07.012

Prediction of Left Ventricular Remodeling After PrimaryReperfusion Therapy in Acute Anterior Wall Myocar-dial Infarction Using Myocardial Deformation Data

Reply to the Editor:

We thank Dr Papadopoulos and colleagues for pointing outseveral issues related to our recent publication on the prognosticvalue of longitudinal strain (LS) after acute anterior wall myocardialinfarction (AMI).1 They expressed concern about significant baselinedifferences in left ventricular (LV) systolic function (LV ejectionfraction and wall motion score index) between patients who did anddid not develop LV remodeling. They suggested that LS should betested between 2 groups of patients with relatively comparable LVsystolic function. Their suggestion is ideal, but, in real clinical situa-tions, arbitrary control of LV systolic function after AMI is impossible.However, we note other clinical articles dealing with LV remodel-ing,2,3 in which baseline differences in LV systolic function weresignificant, and interestingly enough these indices of systolic functionwere proved as one of the independent factors associated with LVremodeling.3 Moreover, despite significant difference of LV ejectionfraction and wall motion score index in our study, LS was proved theonly independent variable associated with LV remodeling in multi-variate analysis, which could be interpreted as an advantage ratherthan disadvantage or limitation.

Their second concern was the different time periods between theindex clinical event (AMI) and follow-up echocardiography. BecauseLV remodeling is a time-dependent process, we agree with them inthat we need a guideline in terms of appropriate follow-up duration.Unfortunately, at present, there is no general consensus, and differenttime intervals have been used by different investigators.2 Actually, inclinical practice, hard clinical events, including hospital admission ordeath, occur during follow-up, which can result in different timeperiods. In our study the time interval was 15 � 8 months (mean �standard deviation), and we originally thought at least a 12-monthfollow-up duration was acceptable. Because patients with develop-ment of clinical events or LV remodeling before 12 months wereincluded in this study, the time interval was variable.

The last and important issue is potential association between LVfilling pressure parameters and LV remodeling. In our study we didnot include E/e’ measures, but included deceleration time of earlytransmitral inflow, which has been proved to be associated with anincreased risk of LV dilation after AMI.4-6 We have failed to demon-strate the predictive role of deceleration time. As Dr Papadopoulosand colleagues mentioned, the strong association between LV fillingpressure parameters and LV remodeling has been reported recentlyby several investigators.2,7,8 The contradictory findings can be partlyexplained by marked heterogeneity of patient population or selection

bias. Although we selected patients with anterior AMI who received

1077

1078 Letters to Editor Journal of the American Society of EchocardiographySeptember 2008

successful reperfusion therapy within 12 hours after pain onset, otherinvestigators have included patients without reperfusion therapy3 orthose with percutaneous intervention done between days 1 and 7from chest pain.2,8 Failure to demonstrate significant associationbetween LV remodeling and time to reperfusion in these studies,2,3,8

the most important variable proved in many clinical trials, mightrepresent inherent limitations of variable inclusion criteria. Thus,considering the complicated relationship among LV filling pressure,LV damage, and LV remodeling, the exact pathophysiologic mecha-nism linking these changes remains to be elucidated. The primarygoal of our study was to determine whether myocardial velocity ordeformation data are useful to predict or identify reversible myocar-dial dysfunction, which remains an important but elusive goal ofechocardiographic quantification of regional myocardial function.9

We absolutely agree with Papadopoulos et al that larger longitudinalfollow-up studies using strict inclusion criteria are necessary to clarifythe clinical role of regional echocardiographic quantification of myo-cardial function.

Jae-Kwan Song, MDDivision of CardiologyAsan Medical Center

University of Ulsan College of MedicineSeoul, South Korea

REFERENCES

1. Park YH, Kang SJ, Song JK, Lee EY, Song JM, Kang DH, et al. Prognosticvalue of longitudinal strain after primary reperfusion therapy in patientswith anterior-wall acute myocardial acute myocardial infarction. J Am Soc

Echocardiogr 2008;21:262-7.

2. Hillis GS, Ujino K, Mulvagh SL, Hagen ME, Oh JK. Echocardiographicindices of increased left ventricular filling pressure and dilation after acutemyocardial infarction. J Am Soc Echocardiogr 2006;19:450-6.

3. Savoye C, Equine O, Tricot O, Nugue O, Segrestin B, Sautiere K, et al. Leftventricular remodeling after anterior wall acute myocardial infarction inmodern clinical practice (from the REmodelage VEntricularie [REVE]Study Group). Am J Cardiol 2006;98:1144-9.

4. Cerisano G, Bolognese L, Carrabba N, Buonamici P, Santoro GM, Anto-niucci D, et al. Doppler-derived mitral deceleration time: an early strongpredictor of left ventricular remodeling after reperfused anterior acutemyocardial infarction. Circulation 1999;99:230-6.

5. Poulsen SH, Jensen SE, Egstrup K. Longitudinal changes and prognosticimplication of left ventricular diastolic function in first acute myocardialinfarction. Am Heart J 1999;137:910-8.

6. Temporelli PL, Giannuzzu P, Nicolosi GL, Latini R, Franzosi MG, Gentile F,et al, for the GISI-3 Echo Substudy Investigators. Doppler-derived mitraldeceleration time as a strong prognostic marker of left ventricular remod-eling and survival after myocardial infarction. J Am Coll Cardiol 2004;43:1646-53.

7. Ueno Y, Nakamura Y, Kinoshita M, Fujita T, Sakamoto T, Okamura H. Anearly preditor of left ventricular emodeling after reperfused anterior acutemyocardial infarction: ratio of peak E wave velocity/flow propagationvelocity and mitral E wave deceleration time. Echocardiography 2002;19:555-63.

8. Papadopoulos CE, Karvounis HI, Giannakoulas G, Karamitsos TD, Efthimi-adis GK, Parharidis GE. Predictors of left ventricular remodeling afterreperfused acute myocardial infarction. Am J Cardiol 1024-5.

9. Becker M, Lenzen A, Ocklenburg C, Stempel K, Kuhl H, Neizel M, et al.Myocardial deformation imaging based on ultrasonic pixel tracking toidentify reversible myocardial dysfunction. J Am Coll Cardiol 2008;51:1473-81.

doi:10.1016/j.echo.2008.07.013