Author + information
- Received March 20, 2015
- Revision received June 9, 2015
- Accepted June 18, 2015
- Published online May 1, 2016.
- Jonathan W. Weinsaft, MDa,b,∗ (, )
- Jiwon Kim, MDa,b,
- Chaitanya B. Medicherla, BAa,
- Claudia L. Ma, BAa,
- Noel C.F. Codella, PhDc,
- Nina Kukar, MDd,
- Subhi Alaref, MDa,
- Raymond J. Kim, MDe and
- Richard B. Devereux, MDa
- aGreenberg Cardiology Division, Department of Medicine, Weill Cornell Medical College, New York, New York
- bDepartment of Radiology, Weill Cornell Medical College, New York, New York
- cIBM T.J. Watson Research Center, Yorktown Heights, New York
- dMemorial Sloan Kettering Cancer Center, New York, New York
- eDuke Cardiovascular Magnetic Resonance Center, Durham, North Carolina
- ↵∗Reprint request and correspondence:
Dr. Jonathan W. Weinsaft, Cardiac Magnetic Resonance Imaging Program, Weill Medical College of Cornell University, 525 East 68th Street, Starr-4, New York, New York 10021.
Objectives The goal of this study was to determine the prevalence of post–myocardial infarction (MI) left ventricular (LV) thrombus in the current era and to develop an effective algorithm (predicated on echocardiography [echo]) to discern patients warranting further testing for thrombus via delayed enhancement (DE) cardiac magnetic resonance (CMR).
Background LV thrombus affects post-MI management. DE-CMR provides thrombus tissue characterization and is a well-validated but an impractical screening modality for all patients after an MI.
Methods A same-day echo and CMR were performed according to a tailored protocol, which entailed uniform echo contrast (irrespective of image quality) and dedicated DE-CMR for thrombus tissue characterization.
Results A total of 201 patients were studied; 8% had thrombus according to DE-CMR. All thrombi were apically located; 94% of thrombi occurred in the context of a left anterior descending (LAD) infarct-related artery. Although patients with thrombus had more prolonged chest pain and larger MI (p ≤ 0.01), only 18% had aneurysm on echo (cine-CMR 24%). Noncontrast (35%) and contrast (64%) echo yielded limited sensitivity for thrombus on DE-CMR. Thrombus was associated with stepwise increments in basal → apical contractile dysfunction on echo and quantitative cine-CMR; the echo-measured apical wall motion score was higher among patients with thrombus (p < 0.001) and paralleled cine-CMR decrements in apical ejection fraction and peak ejection rates (both p < 0.005). Thrombus-associated decrements in apical contractile dysfunction were significant even among patients with LAD infarction (p < 0.05). The echo-based apical wall motion score improved overall performance (area under the curve 0.89 ± 0.44) for thrombus compared with ejection fraction (area under the curve 0.80 ± 0.61; p = 0.01). Apical wall motion partitions would have enabled all patients with LV thrombus to be appropriately referred for DE-CMR testing (100% sensitivity and negative predictive value), while avoiding further testing in more than one-half (56% to 63%) of patients.
Conclusions LV thrombus remains common, especially after LAD MI, and can occur even in the absence of aneurysm. Although DE-CMR yielded improved overall thrombus detection, apical wall motion on a noncontrast echocardiogram can be an effective stratification tool to identify patients in whom DE-CMR thrombus assessment is most warranted. (Diagnostic Utility of Contrast Echocardiography for Detection of LV Thrombi Post ST Elevation Myocardial Infarction; NCT00539045)
Left ventricular (LV) thrombus is an important complication of acute myocardial infarction (MI) that impacts embolic event risk and anticoagulant therapy. Echocardiograms (echo) are widely used to assess post-MI LV structure and function but can be limited for LV thrombus in the context of poor image quality or advanced LV remodeling (1,2). Delayed enhancement (DE) cardiac magnetic resonance (CMR) identifies thrombus based on avascular tissue properties, an approach shown to markedly improve detection of thrombus (1–5). However, widespread use of DE-CMR as an initial screening modality for thrombus would entail significant costs and be clinically prohibited for a substantial number of post-MI patients.
Improved understanding of post-MI thrombus in the current era is critical for optimization of diagnostic testing strategies. Advances in MI management, including prompt and effective coronary reperfusion, have yielded improvements in LV function and remodeling. Widespread use of antiplatelet agents may potentiate the benefits of reperfusion, thereby lessening the likelihood of LV thrombus. However, the risk for thrombus still persists, especially for patients with infarctions in high-risk regions such as the LV apex. Uncertainty regarding the current prevalence and pathophysiology of thrombus limits the ability to develop practical and effective imaging strategies for the millions of post-MI patients at risk for LV thrombus and its complications.
The present study used a tailored multimodality imaging protocol (including state-of-the-art echo and CMR) to examine post-MI LV thrombus. The goals of the study were: 1) to determine the prevalence and predictors of thrombus; 2) to assess the diagnostic performance of optimized current testing strategies (noncontrast and contrast echo) to a reference standard of DE-CMR tissue characterization; and 3) to develop an effective testing algorithm, predicated on routine noncontrast echo findings, to identify post-MI patients warranting further testing for LV thrombus via DE-CMR.
The population comprised patients with acute MI enrolled in a prospective study focused on LV thrombus. Patients were eligible for inclusion if admitted with acute ST-segment elevation MI (≥1.0 mm in at least 2 contiguous electrocardiogram [ECG] leads). Patients with contraindications to CMR (e.g., glomerular filtration rate <30 ml/min/1.73 m2, ferromagnetic implants, New York Heart Association functional class IV) or taking warfarin (at the time of CMR) were excluded; no patients were excluded based on MI treatment. Patients were approached for study participation using a random selection algorithm targeted for maximum recruitment of 1 patient per week. Participants were similar to nonparticipants with respect to infarct-related artery and MI treatment strategy (both p = NS). Comprehensive clinical data were collected at the time of MI, including cardiac risk factors, coronary artery disease history, and medications. Coronary angiograms were reviewed for infarct culprit vessel.
The present study was conducted at Weill Cornell Medical College with approval of the institutional review board. Participants provided written informed consent for study participation.
Imaging was performed at a target of 30 days (minimum 7 days) after MI. In accordance with the research protocol, CMR and echo were performed within 24 h by dedicated technologists. Testing included the following: 1) noncontrast echo; 2) contrast echo; 3) cine-CMR; and 4) DE-CMR. To identify factors predicting incremental utility of tailored imaging for thrombus, a contrast echo was performed in all patients (without clinical contraindication) irrespective of image quality or findings of noncontrast echo. Similarly, DE-CMR testing included dedicated imaging using a previously validated long inversion time (long TI) pulse sequence tailored to null LV thrombus (1,2,6).
Cardiac magnetic resonance
CMR was performed using 1.5-T scanners (GE Healthcare, Waukesha, Wisconsin). Cine-CMR used a steady-state free precession pulse sequence. Gadolinium was subsequently administered (0.2 mmol/kg), and DE-CMR was performed 10 to 30 min thereafter using an inversion recovery pulse sequence. Cine-CMR and DE-CMR images were obtained in matching short- and long-axis planes. Contiguous short-axis images were acquired from the level of the mitral annulus through the apex. Long-axis images were acquired in 2-, 3-, and 4-chamber orientations. DE-CMR included standard (TI 250 to 350 ms) imaging for MI, and long TI (TI 600 ms) imaging for dedicated identification of LV thrombus; both were acquired using segmented imaging. Standard and long TI DE-CMR were acquired in matching LV long-axis orientations at equivalent spatial resolution (mean in-plane 1.9 × 1.4 mm).
Transthoracic echoes were performed by experienced sonographers using commercial equipment (Vivid 7 [GE Healthcare] and Acuson SC2000 [Siemens Healthcare, Malvern, Pennsylvania]). Images were acquired in long- and short-axis orientations concordant with the guidelines of the American Society of Echocardiography (7).
After noncontrast imaging, an echo contrast agent (DEFINITY, Lantheus Medical Imaging, North Billerica, Massachusetts) was infused via the diluted bolus technique in accordance with manufacturer guidelines. To acquire noncontrast and contrast echo images in matching orientations, sonographers then repeated imaging.
LV thrombus identification
A thrombus was identified as an LV mass with avascular tissue properties on post-contrast inversion-recovery imaging. Concordant with previous validation studies (1,2,6), selective nulling of avascular tissue (i.e., thrombus) was performed using a TI of 600 ms, such that the thrombus appeared black and was easily identifiable in relation to surrounding high signal intensity regions such as intracavitary blood and LV myocardium (Figure 1). Thrombus was deemed present on DE-CMR if visualized on any long TI image. Thrombi were also scored for location (assigned using an American Heart Association/American College of Cardiology 17-segment model).
Thrombus was diagnosed on echo using established criteria (1,6,8). They were defined as a protuberant or independently mobile mass in the LV cavity distinguishable from papillary muscles, trabeculae, chordal structures, technical artifact, or tangential views of the LV wall (Figure 1).
Echoes were also scored for diagnostic quality using a previously established 9-point scale. The scale comprised separate scores for endocardial definition (1 = poor; 2 = fair; and 3 = excellent), cavity artifacts (1 = present and obscuring full LV assessment; 2 = present but interpretable; and 3 = absent), number of apical views (1 = single orientation and 2 = at least 2 orientations), and number of LV segments imaged (1 = all segments) (1).
Echo and CMR were each interpreted by experienced (American Heart Association/American College of Cardiology level III) physicians (echo: R.B.D.; CMR: J.W.W.) for whom high inter-reader and intrareader reproducibility concerning diagnosis of LV thrombus has been reported (1). Readers were blinded to clinical history and results of other imaging modalities. Cine-CMR and DE-CMR, as well as the noncontrast and contrast echo, were each read independently.
MI was quantified on conventional (TI 250 to 350 ms) DE-CMR. Infarct transmurality was graded on a 5-point scale for each affected LV segment (0 = no hyperenhancement; 1 = 1% to 25%; 2 = 26% to 50%; 3 = 51% to 75%; and 4 = 76% to 100%). Global infarct size (% LV myocardium) was calculated by summing segmental scores and dividing by the total number of regions (9).
Global and regional LV deformation
LV deformation parameters were measured on echo and CMR to identify contractile indices associated with LV thrombus and discern those patients in whom DE-CMR tissue characterization is most warranted.
Global LV geometry and function were quantified on cine-CMR based on planimetry of end-diastolic and end-systolic chamber volumes, which yielded left ventricular ejection fraction (LVEF) and stroke volume. Corresponding echo parameters were quantified based on linear chamber dimensions; measurements were performed in accordance with the American Society of Echocardiography's guidelines as previously applied by our group in population-based research (10,11). Cine-CMR and echo were also scored for LV aneurysm, defined as a dyskinetic bulge interrupting the LV contour in diastole and systole (1,12).
Regional LV deformation was measured using established echo and recently developed cine-CMR methods. For echo, regional wall motion was scored using an American Heart Association/American College of Cardiology 17-segment model, for which segmental contraction was graded as follows: 0 = normal; 1 = mild hypokinesis; 2 = moderate hypokinesis; 3 = severe hypokinesis; 4 = akinesis; and 5 = dyskinesis. Apical LV wall motion scores were calculated on noncontrast and contrast echo by summing segmental scores within the apical LV and true apex (total 5 segments). For cine-CMR, regional deformation was quantified using a validated automated algorithm for volumetric segmentation (13–15). This algorithm measured temporal and geometric deformation patterns at equidistant locations in the basal, mid, and apical LV.
Comparisons between groups with or without thrombus were made using the Student t test (expressed as mean ± SD) for normally distributed continuous variables. Non-normally distributed variables (median [interquartile range]) were compared via the Mann-Whitney U test. Categorical variables were compared using chi-square tests or, when <5 expected outcomes per cell, the Fisher exact test was used. Univariate and multivariate logistic regression analyses were used to test associations between echo variables and thrombus. Statistical calculations were performed using SPSS version 22.0 (IBM SPSS Statistics, IBM Corporation, Armonk, New York). Receiver-operating characteristic (ROC) analysis was used to evaluate the diagnostic performance of echo parameters for thrombus detection; comparison between ROC curves was performed using the DeLong test with pROC, a statistical package for R (16,17). A 2-sided p value <0.05 was considered indicative of statistical significance.
The population comprised 201 patients who underwent a multimodality imaging protocol after acute ST-segment elevation MI. Imaging was performed 28 ± 6 days post-MI; echo and CMR were obtained within 24 h. No embolic events or acute coronary syndromes occurred during the interval between MI and imaging.
LV thrombus was present on DE-CMR in 8% (n = 17) of the population. Nearly all (94%) thrombi occurred in the context of a left anterior descending (LAD) infarct-related artery. The sole patient with a thrombus in whom left circumflex artery was the angiography-assigned culprit vessel had concomitant LAD obstruction and findings consistent with LAD injury, as evidenced by apical contractile dysfunction on echo and corresponding Q waves on ECG.
As shown in Table 1, patients with LV thrombus did not differ from those without thrombus in terms of age, sex, or risk factors for coronary artery disease (all p = NS). Difference in thrombus prevalence between patients treated with primary percutaneous coronary intervention compared with thrombolytic agents did not achieve statistical significance (6% vs. 13%; p = 0.21). Infarct size and chest pain after percutaneous coronary intervention duration were greater (both p ≤ 0.01) among patients with thrombus; 41% of affected patients underwent revascularization within a narrow (8-h) time period. Consistent with this finding, although LVEF was lower (p < 0.001), echo demonstrated that only 12% of patients with thrombus had advanced systolic dysfunction (EF ≤ 30%) and only 18% had an LV aneurysm. Results were similar with cine-CMR, which demonstrated advanced LV dysfunction in 12% and LV aneurysm in only 24% of patients with thrombus.
Regional LV deformation
In all cases, thrombus was located within or adjacent to the LV apex. Consistent with this finding, LV functional parameters measured in levels from the basal to mid to apical LV demonstrated stepwise increases in magnitude of contractile dysfunction between patients with, compared with those without, thrombus. Table 2 details results of cine-CMR analysis using regional volumetric quantification in 3 equidistant (short-axis) planes in the basal, mid, and apical LV. In the basal LV, volumetric (ejection fraction [EF], peak ejection rate) and temporal (time to peak ejection rate) contractile indices were similar between patients with and without thrombus (all p = NS). Parallel analysis of the mid–LV demonstrated moderately lower EF and stroke volume among patients with thrombus (both p < 0.05). In the apical LV, differences were greater with respect to all volumetric and temporal contractile indices, which differed significantly between patients with and without thrombus (p < 0.005). Cine-CMR yielded similar results when analysis was restricted to patients with LAD infarction, among whom regional contractility was progressively impaired from the basal to apical LV.
Echo analysis (performed via standard visual assessment) paralleled those of the quantitative cine-CMR. As shown in Table 3, regional wall motion scores in the basal LV were similar between patients with and without LV thrombus (p = NS). In the mid–LV, there was a 3-fold difference in median (interquartile range) wall motion score (9.0 [4.0 to 12.0] vs. 3.0 [0 to 7.0]), and in the apical LV, a 6-fold difference (16.0 [10.5 to 18.5] vs. 2.5 [0.0 to 8.8]) between patients with and without thrombus. Echo results were similar when analyzed based on contrast-enhanced wall motion scores and, as with cine-CMR, when restricted to patients with LAD infarction.
Both echo-evidenced apical wall motion score (odds ratio [OR]: 1.29 per point [95% confidence interval (CI): 1.16 to 1.44]; p < 0.001) and LV aneurysm (OR: 12.93 [95% CI: 2.39 to 70.08]; p = 0.003) were associated with DE-CMR–proven LV thrombus in univariate logistic regression. However, multivariate regression demonstrated apical wall motion score (OR: 1.28 per point [95% CI: 1.15 to 1.43]; p < 0.001) was associated with thrombus after controlling for aneurysm (OR: 1.96 [95% CI: 0.31 to 12.44]; p = 0.48) (chi-square model = 35.54; p < 0.001).
Table 4 presents the diagnostic performance results of the noncontrast and contrast echo, as well as cine-CMR, compared with the reference DE-CMR. Importantly, dedicated noncontrast echo provided high specificity (98%), which was near equivalent to that of the contrast echo (99%). However, despite the fact that all of the examinations were tailored for LV thrombus evaluation, noncontrast echo yielded limited sensitivity (35%), which remained suboptimal with the use of contrast echo (64%). Figures 1 and 2 provide representative examples of echo performance, including incremental utility of contrast echo (Figure 1B), as well as DE-CMR–evidenced thrombus missed by both echo techniques (Figure 2).
Echo image quality was evaluated to determine whether technical factors varied in relation to performance of each approach. Table 5 compares the prevalence of optimally scored echo image quality (including endocardial definition and absence of LV cavity artifacts) between echo interpreted concordantly or discordantly with DE-CMR. Noncontrast echoes interpreted concordantly with DE-CMR more commonly had optimal overall image quality than did those discordant with DE-CMR (p = 0.01), paralleled by a higher prevalence of excellent endocardial definition (p = 0.008) and absence of cavity artifacts (p = 0.007). For contrast echo, diagnostic performance did not vary in relation to image quality, which was similar between exams concordant and discordant with DE-CMR (p = 1.00).
Echo functional parameters as a gatekeeper for DE-CMR
LV functional parameters on echo were tested to determine whether they could effectively stratify those patients in need of further evaluation for thrombus via DE-CMR. Figure 3 provides ROC curves for noncontrast echo-derived EF and apical wall motion. As shown, apical wall motion score on noncontrast echo yielded improved overall performance compared with EF on the basis of area under the curve (p = 0.01). Apical wall motion score on contrast echo also yielded excellent performance (area under the curve 0.89 ± 0.44) in relation to DE-CMR–evidenced thrombus.
Table 6 reports the diagnostic performance of the noncontrast and contrast echo using apical wall motion partitions necessary to provide perfect sensitivity (100% negative predictive value) for DE-CMR–evidenced thrombus together with maximal specificity. As shown, a noncontrast wall motion score ≥5 would have enabled all patients with thrombus to be appropriately referred for DE-CMR, while avoiding unnecessary additional testing (via DE-CMR) in more than one-half of the study population (56% [112 of 201]). A slightly higher partition for contrast echo (≥7) would have enabled identification of all patients with LV thrombus, while avoiding further testing via DE-CMR in a higher proportion of patients (63% [120 of 190]).
The data were further stratified on the basis of angiography-evidenced infarct-related artery. The positive predictive value of the echo-based apical wall motion score was approximately 4-fold higher among patients with LAD culprit vessel MI (23%) versus those with right coronary artery or left circumflex artery (6%) culprit vessels, paralleling a higher prevalence of thrombus (15% vs. 1%).
This study provides new data concerning the performance of current imaging strategies, as well as utility of a novel approach (predicated on a routine echo) for post-MI LV thrombus. There were several key findings. First, LV thrombus remains an important diagnostic issue in the current reperfusion era. Among the broad post-MI population studied, thrombus was present in 8% of all patients, including 15% of those with LAD infarction. Second, although generally associated with adverse remodeling, markedly depressed EF (≤30%) on echo occurred in only 12% of patients with thrombus, and only 18% had an LV aneurysm. Third, despite tailored imaging with uniform contrast administration, echo remained limited as a solitary strategy for post-MI thrombus. Noncontrast echo yielded a diagnostic sensitivity of 35% compared with the reference DE-CMR. Although use of contrast improved echo image quality and sensitivity (64%), one-third of DE-CMR–evidenced thrombi were missed. Fourth, thrombus was strongly associated with regional LV dysfunction involving the apical LV. Altered patterns of volumetric and temporal contractility quantified by state-of-the-art cine-CMR segmentation were paralleled by echo assessment using routine visual wall motion scores. Echo-based wall motion partitions (selected to provide perfect sensitivity and optimized specificity) would have enabled all patients with thrombus to be appropriately referred for DE-CMR, while avoiding unnecessary additional testing (via DE-CMR) in more than one-half (56% to 63%) of the population.
Our results extend previous research showing that DE-CMR improved LV thrombus detection compared with an echo (1–5). Despite this advantage, CMR remain an impractical means of screening for thrombus in the approximately 500,000 Americans who sustain MI annually (18). In addition to CMR’s substantial costs, neither the equipment nor expertise required for CMR is widely available. Beyond technical considerations, the repeated breath-holds, supine positioning, and closed space environment typically required for CMR make this modality impractical for a substantial number of post-MI patients. Echo is inexpensive, widely available, and portable, thus facilitating its use as a screening tool for even critically ill patients. Our findings indicate that noncontrast echo can be used to effectively stratify those post-MI patients with the highest likelihood for thrombus, thereby allowing more sensitive evaluation via DE-CMR tissue characterization to be appropriately applied in high-risk cohorts while avoiding further testing in the majority of post-MI patients.
Our observed strong association between LAD infarction and LV thrombus is consistent with echo studies conducted before widespread changes in post-MI revascularization. For example, among 8,326 participants in the GISSI-3 study, thrombus was 5-fold more common with anterior wall MI (11.5% vs. 2.3%) (19). Based on this marked differential prevalence, it is tempting to use infarct-related artery as a primary means of stratifying those patients in whom dedicated thrombus imaging (contrast echo and/or DE-CMR) is most warranted. Applied clinically, our data indicate that if a contrast echo were to be performed in all patients with LAD infarction, and apical wall motion score was used to stratify those in need of further testing, approximately 95% of all thrombi would be identified with use of DE-CMR in only about 20% of all post-MI patients. Conversely, our study results, as well as previous research, indicate that there is a small, albeit lesser, risk for thrombus among patients with non-LAD infarction; this fact should not be minimized in light of thrombus-associated risk for embolic events (6). Notably, in the 1 case of thrombus with non-LAD culprit vessel MI, adjunctive testing via ECG and echo demonstrated evidence of apical injury. In this context, further studies are warranted to determine whether cost-effective tools such as ECG can augment echo-evidenced apical dysfunction, so as to better identify patients in whom DE-CMR yields greatest incremental utility (over conventional post-MI testing) for LV thrombus.
The majority of previous CMR studies that have examined LV thrombus were conducted in mixed cohorts or in patients with chronic heart failure (1,2,4–6). To the best of our knowledge, only 1 study used CMR to examine LV thrombus in an exclusively post-MI cohort (5). However, DE-CMR and cine-CMR were interpreted together, regional LV contractility was not quantified, and thrombus location was not reported, thereby resulting in knowledge gaps regarding imaging and pathophysiology of post-MI thrombus. Although DE-CMR has been used to study thrombus in patients with systolic dysfunction (2–4), our study found that substantial differences exist regarding thrombus in the post-MI setting compared with the chronic heart failure setting. Regarding distribution, all thrombi in this post-MI cohort were apical in location. In our previous study of patients with systolic dysfunction, the prevalence of thrombus was similar (7%) to the current study (8%), but 20% were nonapical in location (within the basal or mid–LV) (6). Similarly, among heart failure patients undergoing LV reconstruction surgery, Srichai et al. (4) reported that 29% of thrombi were located outside the LV apex. Possible reasons for differences in thrombus distribution relate to variability in LV remodeling and/or contractile dysfunction between patients with chronic heart failure versus those with acute MI.
It is important to note that LV thrombus can occur in the absence of severely impaired LVEF, as evidenced by the fact that 8% of all patients had thrombus but only 2% had LVEF ≤30%. This finding may relate to the fact that apical dysfunction can be profound despite preserved global LV function. Regarding spatial distribution, our cine-CMR results shed light on mechanisms responsible for apical thrombus. Regional contractile parameters increased in magnitude between patients with and without thrombus, and the magnitude of difference increased with progression from the basal to apical LV. Consistent with this finding, previous studies using animal models have shown LAD infarction to acutely alter apical blood flow (20). It is possible that regional differences in contractile function, combined with prothrombotic alterations induced by myocardial necrosis, may explain the link between MI and apical thrombus. Notably, our results show that differences in contractile function related to thrombus are discernable on both advanced cine-CMR and routine echo analyses. Further studies are warranted to test whether quantitative assessment of apical blood flow (combined with measures of infarct distribution) can further stratify risk for thrombus, thereby facilitating targeted strategies to detect or prevent LV thrombus.
One limitation concerns the fact that our sample size (particularly the small number of positive cases in this single-center cohort) prohibits comprehensive multivariate analysis concerning LV thrombus. Importantly, the prevalence of post-MI LV thrombus in our study (8%) is similar to previous multicenter CMR data (8.8%) (5), supportive of the notion that our findings are broadly reflective of post-MI LV thrombus in the current era. It is also important to recognize that imaging for this study was performed at a target of 1 month post-MI, a time point selected based on previous echo data (21). More recent CMR research has shown that LV thrombus can be present early post-MI and self-resolve thereafter (5). It is certainly possible that some patients in our cohort could have had LV thrombus that resolved by 1 month after MI.
Our findings show that LV thrombus remains an important consideration in post-MI patients, and they can occur even in the absence of aneurysm or advanced LV dysfunction. Although DE-CMR tissue characterization yields improved detection of post-MI thrombus, echo, analyzed in a routine manner for apical wall motion, can be used as an effective stratification tool to identify patients in whom thrombus assessment via DE-CMR is most warranted.
COMPETENCY IN MEDICAL KNOWLEDGE: Among a broad cohort of patients with acute MI, LV thrombus were present on DE-CMR in 8%, were strongly related to LAD infarction, and often occurred in the absence of LV aneurysm. Although echo yielded limited diagnostic performance for LV thrombus, apical wall motion score as assessed via echo effectively stratified need for further testing for thrombus via DE-CMR.
TRANSLATIONAL OUTLOOK: Additional studies are needed to further validate current findings in larger multicenter cohorts, as well as to compare DE-CMR thrombus detection with echo-based apical wall motion score for thromboembolic risk stratification after an acute MI.
This work was partially funded through a research grant provided by Lantheus Medical Imaging (echo contrast product manufacturer). Dr. Weinsaft was supported by a Doris Duke Clinical Scientist Development Award, National Institutes of Health grant K23 HL102249-01, and Lantheus Medical Imaging. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Abbreviations and Acronyms
- confidence interval
- cardiac magnetic resonance
- ejection fraction
- left anterior descending
- left ventricular
- left ventricular ejection fraction
- myocardial infarction
- odds ratio
- receiver-operating characteristic
- inversion time
- Received March 20, 2015.
- Revision received June 9, 2015.
- Accepted June 18, 2015.
- American College of Cardiology Foundation
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