Echocardiographic evaluation of left ventricular function in ischemic heart disease Mollema, S.A.

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Echocardiographic evaluation of left ventricular function in ischemic heart disease

Mollema, S.A.

Citation

Mollema, S. A. (2010, December 9). Echocardiographic evaluation of left ventricular function in ischemic heart disease. Retrieved from

https://hdl.handle.net/1887/16229

Version: Corrected Publisher’s Version

License: Licence agreement concerning inclusion of doctoral thesis in the Institutional Repository of the University of Leiden

Downloaded from: https://hdl.handle.net/1887/16229

Note: To cite this publication please use the final published version (if

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Chapter 5

impact of time to reperfusion after acute myocardial infarction on myocardial damage assessed by left ventricular longitudinal strain

Matteo Bertini, MD,^1,2 Sjoerd A. Mollema, MD,¹ Victoria Delgado, MD,¹ M. Louisa Antoni, MD,¹ Arnold C.T. Ng, MBBS,¹ Eduard R. Holman, MD, PhD,¹ Giuseppe Boriani,

MD, PhD,^1,2 Martin J. Schalij, MD, PhD,¹ Jeroen J. Bax, MD, PhD¹

1Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands

2Department of Cardiology, University of Bologna, Bologna, Italy Am J Cardiol 2009;104:480-485

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abstract

The relation between cardiac troponin T (cTnT) and regional strain in patients with acute myocardial infarction (AMI) was investigated. Furthermore, the effect of symptoms-to-balloon time on impairment in regional strain after AMI was evaluated. A total of 157 consecutive patients with AMI who underwent primary percutaneous coronary intervention (PCI) were included.

Two-dimensional (2D) echocardiography early after PCI was performed. Speckle-tracking analysis was applied to assess left ventricular (LV) global and regional longitudinal peak systolic strain (LPSS). Infarcted area was defined based on the culprit vessel. Mean LV ejection fraction (LVEF) was 47 ± 7%. Global LPSS was -14.4 ± 3.2%. The infarcted area LPSS was significantly reduced as compared to global LPSS (-11.3 ± 4.5%, p<0.001). The major reflector of cTnT was infarcted area LPSS (β=0.47, p<0.001). The mean symptoms-to-balloon time was 212 ± 92 minutes. Based on this time, the study population was divided in tertiles. In the group with the shortest symptoms-to-balloon time, global LPSS and infarcted area LPSS were less impaired as compared to the groups with longer symptoms-to-balloon time (p<0.01 for both). In conclu- sion, myocardial strain was related to peak levels of cTnT, thus reflecting damage after AMI.

Early reperfusion resulted in reduced myocardial damage in the infarcted area as quantified with strain.

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Impact of time to reperfusion after acute myocardial infarction on myocardial damage assessed by left ventricular longitudinal strain

introduction

After acute myocardial infarction (AMI), magnetic resonance imaging (MRI) is considered the gold standard for the quantification of myocardial damage (i.e. infarct size and transmurality of scar formation) (1). Recently, myocardial strain has been introduced as a sensitive marker of left ventricular (LV) (dys)function (2,3). In addition, Vartdal et al. demonstrated in a head- to-head comparison with contrast-enhanced MRI, in a small study of 30 patients with anterior AMI that assessment of global myocardial strain early after reperfusion therapy is a valuable predictor of infarct size (4). Novel two-dimensional (2D) speckle-tracking echocardiography enables assessment of global and regional myocardial strain, and was validated against MRI and sonomicrometry (5). How regional strain relates with cardiac troponin T (cTnT) release after AMI is unknown (6,7). Furthermore, the effect of onset of symptoms-to-balloon time after AMI on reduction in regional strain is unclear. The aim of the current study was to investigate the relation between cTnT release and regional strain in patients with AMI. In addition, the onset of symptoms-to-balloon time on impairment in regional strain after AMI was evaluated.

mEthods

A total of 191 consecutive patients admitted with AMI with ST-segment elevation, were evaluated.

All patients underwent primary percutaneous coronary intervention (PCI) of the culprit vessel and received optimal medical treatment (8). Only patients with first AMI were included. During PCI, the final TIMI (Thrombolysis In Myocardial Infarction) flow and the number of diseased coronary arteries (stenosis >50% of vessel diameter) were assessed. The time from onset of symptoms to first balloon dilatation (symptoms-to-balloon time) was determined. Based on the symptoms-to-balloon time, the population was divided in 3 tertiles. Peak blood levels of cTnT (reflecting myocardial damage) were obtained. All patients underwent 2D echocardiography within 48 hours of admission and after 3 months to assess LV volumes, LV ejection fraction (LVEF), wall motion score index (WMSI), and severity of mitral regurgitation. Furthermore, speckle-tracking analysis using automated function imaging (AFI) was applied to assess global longitudinal peak systolic strain (global LPSS). In addition, the infarct-related segments (infarcted area) and non-infarct-related segments (remote area) were determined and mean longitudinal peak systolic strain (LPSS) was quantified for the infarcted and remote area.

First, the relation between cTnT, as reflector of myocardial damage, and LV longitudinal strain was evaluated. Second, markers of myocardial damage quantified with cTnT were determined. Third, the relation between symptoms-to-balloon time and longitudinal LV strain of the infarcted and remote areas was assessed.

All patients were imaged in left lateral decubitus position using a commercially available system (Vingmed Vivid 7, General Electric-Vingmed, Milwaukee, Wisconsin, USA). Standard 2D images and

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color Doppler data were digitally stored in cine-loop format and the analysis was performed offline using EchoPac version 7.0.0. (General Electric-Vingmed). Images were obtained using a 3.5-MHz transducer from the standard apical views (4- and 2-chamber views). Left ventricular end-systolic and end-diastolic volumes were measured from the apical 4- and 2-chamber views and LVEF was derived using the Simpson’s method (9). Severity of mitral regurgitation was graded semi-quanti- tatively from color-flow Doppler data using the 4-chamber apical views according to the ACC/AHA guidelines (10). Mitral regurgitation was classified as mild (jet area/left atrial area <20%), moderate (jet area/left atrial area 20-40%) and severe (jet area/left atrial area >40%). Segmental wall motion was evaluated and scored as 1: normal; 2: hypokinesia; 3: akinesia; 4: dyskinesia. Global WMSI was calculated using the sum of the segmental scores divided by the number of segments analyzed, as previously described (11,12).

The speckle-tracking software tracks the frame-to-frame movement of natural myocardial acoustic markers, or speckles, on standard gray scale images (13,14). Myocardial strain can then be assessed from temporal differences in the mutual distance of neighboring speckles. The change in length divided by the initial length of the speckle pattern over the cardiac cycle can be used to calculate longitudinal strain, with myocardial shortening represented as negative strain, and myocardial lengthening as positive strain. In the current study, automated function imaging (AFI), a novel algorithm based on speckle-tracking imaging, was applied to evaluate LV longitudinal strain on LV apical views (apical long-axis, 4- and 2-chamber views). With AFI, longitudinal strain is first analyzed on the apical long-axis view where the closure of the aortic valve is defined. The time inter- val between R wave and aortic valve closure is measured and used as a reference for longitudinal strain assessment on the 4- and 2-chamber view loops. After defining the mitral annulus and the LV apex with 3 index points at the end-systolic frame in each apical view, the automated algorithm traces 3 concentric lines on the endocardial border, the mid-myocardial layer and epicardial border, including the entire myocardial wall. The tracking algorithm follows the endocardium from this single frame throughout the cardiac cycle, and allows for a further manual adjustment of the region of interest to ensure a good tracking throughout the cardiac cycle. The LV is divided in 6 segments in each apical view and the tracking quality is validated for each segment. Finally, the automated algorithm provides the LPSS value for each LV segment in a 17-segment model polar plot, with the average value of LPSS for each apical view and the averaged global LPSS value for the complete LV (Figure 1) (15). The culprit vessel was identified as the occluded vessel at coronary angiography (supported by ECG criteria). In the 17-segment model infarcted area and remote area were classified based on culprit vessel and recommendations of American Society of Echocardiography (9,16). The apical segment pointed out by AFI was classified as infarct-related segment if the apex was sup- plied by the culprit vessel as defined from invasive angiography. The following measurements were derived: global LPSS, infarcted area LPSS and remote area LPSS. To assess the reproducibility of AFI- derived global LPSS measurement, 22 patients were randomly selected. Bland-Altman analysis was performed to evaluate the intra- and inter-observer agreement repeating the analysis 1 week later by the same observer and by a second independent observer. Bland-Altman analysis demonstrated

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good intra- and inter-observer agreement, with small bias, not significantly different from zero.

Mean differences ± 2 standard deviations (SD) were 0.04 ± 0.56% for intra-observer agreement and 0.07 ± 2.40% for inter-observer agreement.

Most of continuous variables were normally distributed (as evaluated by the Kolmogorov- Smirnov test). For reasons of uniformity, summary statistics for all continuous variables are therefore presented as mean ± SD. Categorical data are summarized as frequencies and percentages. Differ- ences among groups (according symptoms-to-balloon time tertiles) were assessed by one-way ANOVA with Bonferroni`s post-hoc analysis. Linear regression analysis was used to determine the relations between cTnT and LPSS values (global, infarcted area and remote area), between symptoms-to balloon time and LPSS values (global, infarcted area and remote area), and between the change in LVEF after 3 months (LVEF after 3 months – LVEF at baseline) and LPSS (infarcted area and remote area). In order to identify the best marker of myocardial damage (quantified by cTnT), univariable and multivariable linear regression analysis were performed including clinical (age, gender, number of diseased vessels, symptoms-to-balloon time) and echocardiographic (LVESV, LVEF, infarcted area LPSS, remote area LPSS, WMSI) characteristics of the patients. Only significant (p<0.05) univariable predictors were entered as covariates in the multivariable stepwise model. All figure 1. Example of assessment of global LPSS using AFI analysis. Apical long-axis view where the closure of aortic valve is defined (upper left panel). Four-chamber (upper right panel) and 2-chamber views (lower left panel). The “bull‘s eye” plot, using a 17-segment model, provides the LPSS for each LV segment (lower right panel). AFI: automatic function imaging; LPSS: longitudinal peak systolic strain; LV:

left ventricle.

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statistical tests were 2-sided, and a p value <0.05 was considered significant. SPSS 14.0 (SPSS Inc, Chicago, IL, USA) was used for statistical analysis.

rEsults

Of 191 consecutive patients admitted with AMI, 157 were included. Eight patients were excluded since they had a previous AMI; another 26 patients were excluded because of a poor acoustic window at echocardiography.

Based on symptoms-to-balloon time, the study population was divided in 3 groups (tertiles): <170 minutes (n=55), between 170 and 215 minutes (n=53) and >215 minutes (n=49). All clinical variables were comparable between the 3 groups, except for peak levels of cardiac enzymes. Peak level of cTnT, reflecting myocardial damage, was higher in patients with longer symptoms-to-balloon time (p<0.001, analysis of variance) (Table 1). An overview of the echocardiographic variables is provided in Table 2. For the 3 subgroups, no significant differences were demonstrated in LV volumes (p=NS, analysis of variance). Of note, LVEF was lower in patients with longer symptoms-to-balloon time (p<0.05, analysis of variance). Furthermore, WMSI was higher in patients with longer symptoms-to- balloon time (p<0.01, analysis of variance).

Global LPSS in the overall study population was -14.4 ± 3.2% (Table 2). The LPSS of the infarcted area was significantly reduced as compared to the global LPSS (-11.3 ± 4.5%, p<0.001). Of note, remote area LPSS was relatively increased as compared to the global LPSS (-16.2 ± 3.5%, p<0.001), suggesting compensatory hyperkinesis of the remote myocardium. Global LPSS was significantly related to cTnT (r=0.52, p<0.001). Concerning regional strain, infarcted area LPSS was related to cTnT (r=0.58, p<0.001) whereas LPSS of the remote area was less strongly related to cTnT (r=0.32, p<0.001). Figure 2 shows the correlations between LPSS and peak cTnT.

At univariable linear regression, symptoms-to-balloon time, LVESV, LVEF, infarcted area LPSS, remote area LPSS and WMSI were significantly related to cTnT (Table 3). At multivariable analysis, the only independent markers of myocardial damage (quantified with cTnT) were the infarcted area LPSS value and the WMSI (Table 3). Importantly, the change in LVEF after 3 months was significantly related with infarcted area LPSS (r=-0.37, p<0.001), whereas no relation was observed between the change in LVEF after 3 months and remote area LPSS (r=-0.07, p= NS).

A significant relation was noted between symptoms-to-balloon time and global LPSS (r=0.45, p<0.001; Figure 3). Furthermore, a substantial correlation between symptoms-to-balloon time and infarcted area LPSS was demonstrated (r=0.45, p<0.001). A less strong relation was observed between symptoms-to-balloon time and remote area LPSS (r=0.26, p<0.001). Finally, the LPSS values for the 3 subgroups are shown in Figure 4. Global LPSS and infarcted area LPSS were more reduced in patients with longer symptoms-to-balloon time (ANOVA p<0.001). In the group with the shortest symptoms-to-balloon time (<170 minutes) global LPSS and infarcted area LPSS were higher as compared to the group with patients with symptoms-to-balloon time between 170

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and 215 minutes (-16.0 ± 2.4 versus -14.3 ± 2.9%, and -13.7 ± 3.6 versus -11.3 ± 4.5%, respectively, both p<0.01). Similarly, in the group of patients with symptoms-to-balloon time between 170 and 215 minutes, global LPSS and infarcted area LPSS were higher as compared to the group with the longest (>215 minutes) symptoms-to-balloon time (-14.3 ± 2.9 versus -12.5 ± 3.2%, and -11.3 ± 4.5 versus. -8.7 ± 4.0%, respectively, p<0.01 for both). Importantly, no difference was demonstrated between the subgroups for remote area LPSS.

table 1. Clinical characteristics

symptoms-to-balloon time (minutes) overall

population (n=157)

<170 (n=55)

170-215 (n=53)

>215 (n=49)

anova p value

Age (years) 60 ± 11 60 ± 11 61 ± 10 60 ± 11 NS

Male/female 123/34 44/11 39/14 40/9 NS

Hypertension 50 (32%) 21 (38%) 14 (26%) 15 (31%) NS

Diabetes mellitus 17 (11%) 2 (4%) 7 (13%) 8 (16%) NS

Smoker 85 (54%) 27 (49%) 31 (58%) 27 (55%) NS

Positive family history of CAD 65 (41%) 22 (40%) 23 (43%) 20 (41%) NS

Peak level of cardiac troponin T (µgr/l) 7.3 ± 6.7 5.1 ± 4.0 7.1 ± 5.4 10.1 ± 9.1 <0.001 PCI parameters

Symptoms-to-balloon time (minutes) 212 ± 92 139 ± 24 195 ± 14 312 ± 101 <0.001^* Culprit vessel (LAD/non-LAD)

(%)

77/80 (49/51)

23/32 (42/58)

28/25 (53/47)

29/20 (59/41)

NS Number of normal coronary arteries 1.3 ± 0.7 1.2 ± 0.8 1.4 ± 0.7 1.4 ± 0.7 NS Final TIMI flow during PCI 3.0 ± 0.3 3.0 ± 0.2 3.0 ± 0.0 2.9 ± 0.3 NS CAD: coronary artery disease; LAD: left anterior descending coronary artery; MI: myocardial infarction;

PCI: percutaneous coronary intervention; TIMI: Thrombolysis In Myocardial Infarction.

*By definition.

table 2. Echocardiographic characteristics

symptoms-to-balloon time (minutes) overall

population (n=157)

<170 (n=55)

170-215 (n=53)

>215 (n=49)

anova p value Left ventricular end-diastolic

volume (ml)

128 ± 31 129 ± 32 125 ± 31 131 ± 32 NS

Left ventricular end-systolic volume (ml)

68 ± 20 66 ± 20 65 ± 20 72 ± 20 NS

Left ventricular ejection fraction (%)

47 ± 7 50 ± 6 47 ± 8 45 ± 7 <0.05

Mitral regurgitation >grade 2 7 (4%) 3 (5%) 3 (6%) 1 (2%) NS

Wall motion score index 1.5 ± 0.2 1.4 ± 0.2 1.5 ± 0.2 1.6 ± 0.2 <0.01 Global longitudinal peak

systolic strain (%)

-14.4 ± 3.2 -16.0 ± 2.5 -14.3 ± 2.9 -12.5 ± 3.2 <0.001 Longitudinal peak systolic

strain of the infarcted area (%)

-11.3 ± 4.5 -13.7 ± 3.6 -11.3 ± 4.5 -8.7 ± 4.0 <0.001

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figure 2. Relations between cTnT and global LPSS (r=0.52, p<0.001; panel A), LPSS of infarcted area (r=0.58, p<0.001; panel B), and LPSS of remote area (r=0.32, p<0.001; panel C). cTnT: cardiac troponin T;

LPSS: longitudinal peak systolic strain.

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discussion

The current study provides new insights into the pathophysiology of AMI exploring the link between time to reperfusion and myocardial damage quantified by strain. The main findings can be summarized as follows: 1) the best reflector of enzymatic infarct size (release of cTnT) was infarcted area LPSS; 2) early reperfusion resulted in reduced infarct size with more preserved LPSS in the infarcted area; conversely, early reperfusion did not alter LPSS of the remote area.

Myocardial damage during AMI can be accurately quantified with cTnT, as shown in animal experiments with post-mortem analysis and recently confirmed in clinical practice (6,7,17,18).

Myocardial damage is a surrogate of infarct size, and integrates transmurality of necrosis and the extension of damage in the different myocardial segments. Strain imaging may also pro- vide an accurate method to estimate infarct size. Indeed, Vartdal et al. recently showed that assessment of global myocardial strain early after reperfusion therapy is a valuable predictor of infarct size (4). In the current study, global LPSS was significantly related with cTnT confirming these previous findings. In addition, a good relation was noted between cTnT and infarcted area LPSS. Moreover, at the multivariable linear regression analysis the best marker of cTnT release was infarcted area LPSS. These results underline that the strain of the injured myocardium is an index of damage. In addition, WMSI was also a strong reflector of cTnT release but not as strong as infarcted area LPSS. Possibly, this is related to the absence of wall motion abnormalities in small infarctions or in very early reperfused infarctions, where the strain is already reduced. A further explanation may be that WMSI is a qualitative parameter derived from visual analysis of segmental motion, whereas strain is a quantitative parameter that permits discrimination between active deformation and passive motion. Of interest, the relatively increased strain in table 3. Multivariable linear regression analysis to identify markers of myocardial damage as quantified with cardiac troponin T

Dependent variable:

Peak cardiac troponin T

univariable analysis

multivariable analysis

β p value β p value

Independent variables

Age (years) 0.076 0.17

Female gender 0.061 0.22

Number of normal coronary arteries 0.050 0.53

Symptoms-to-balloon time (minutes) 0.23 0.002 - -

Left ventricular end-systolic volume (ml) 0.26 <0.001 - -

Left ventricular ejection fraction (%) -0.27 <0.001 - -

Longitudinal peak systolic strain of the infarcted area (%)

0.58 <0.001 0.47 <0.001

Longitudinal peak systolic strain of the remote area (%)

0.32 <0.001 - -

Wall motion score index 0.45 <0.001 0.19 0.012

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figure 3. Relations between symptoms-to-balloon time and global LPSS (r=0.45, p<0.001; panel A), infarcted area LPSS (r=0.45, p<0.001; panel B), and remote area LPSS (r=0.26, p<0.001; panel C). LPSS:

longitudinal peak systolic strain.

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the remote area reflected the compensatory hyperkinesis of the non-infarcted tissue to main- tain global systolic LV function. In addition, only infarcted area LPSS was significantly related to the change in LVEF after 3 months; therefore, consistently with previous observations, a good marker of myocardial damage was related to the change of LV systolic function. Dura- tion of coronary occlusion during AMI is the principal determinant of myocardial damage. In experimental studies after 90 minutes of coronary occlusion the extent of cell death involves 40-50% of the area at risk (20). In the clinical context, AMI is frequently characterized by tem- porary occlusion and reperfusion of the coronary artery, and therefore it may be difficult to estimate the exact duration of coronary occlusion. However, early reperfusion therapy leads to smaller myocardial damage (21). Boersma et al. analyzed the relation between treatment delay and short-term mortality using data from several randomized trials collecting a large number (n=50,246) of patients (21). The authors concluded that the beneficial effect of reperfusion in AMI is substantially larger in patients presenting within 2 hours after onset of symptoms as compared to patients presenting after 2 hours. The benefits of early reperfusion include less LV remodeling, improvement of myocardial electrical stability and improved long-term survival figure 4. Global LPSS, infarcted area LPSS and remote area LPSS in the 3 different groups in relation to symptoms-to-balloon time <170 minutes (white bars), 170 to 215 minutes (grey bars), and >215 minutes (black bars). LPSS: longitudinal peak systolic strain.

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(22,23). At present, data concerning the relation between time to reperfusion and myocardial strain are lacking. In the current study, a significant relation between symptoms-to-balloon time and global LPSS was noted. The relation between these 2 parameters was not perfect, which is probably related to the presence of collateral blood flow, the coronary artery involved, sponta- neous reperfusion and concomitant antiplatelet therapy (e.g. glycoprotein IIb-IIIa inhibitors).

A recent study demonstrated that symptoms-to-balloon time was a significant determinant of transmurality in patients with AMI (24). The current findings highlight that infarcted area LPSS is not only reduced as compared to remote area LPSS but is also significantly influenced by the time to reperfusion. Indeed, infarcted area LPSS was progressively larger in the groups of patients with shorter as compared to the groups with longer time to reperfusion.

Some limitations of the present study need attention. Additional comparison with contrast-enhanced MRI for precise delineation of scar tissue would have been preferred, but these data were not available; previous studies however, showed good correlation between contrast-enhanced MRI and cTnT for quantification of myocardial scar tissue (6,7,17,18). Data on long-term outcome were not obtained and further investigations on the prognostic value of strain after AMI are needed.

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