Detection of Left Ventricular Thrombus by Delayed-Enhancement Cardiovascular Magnetic ResonancePrevalence and Markers in Patients With Systolic Dysfunction
Jonathan W. Weinsaft, MD*, ,
Han W. Kim, MD*, ,
Dipan J. Shah, MD*, ,
Igor Klem, MD*, ,
Anna Lisa Crowley, MD*, ,
Rhoda Brosnan, MD*, ,
Olga G. James, MD*, ,
Manesh R. Patel, MD*, ,
John Heitner, MD*, ,
Michele Parker, MS, RN*,
Eric J. Velazquez, MD ,
Charles Steenbergen, MD, PhD ,
Robert M. Judd, PhD*, and
Raymond J. Kim, MD*, ,*
* Duke Cardiovascular Magnetic Resonance Center, Duke University Medical Center, Durham, North Carolina
Department of Medicine, Duke University Medical Center, Durham, North Carolina
Department of Pathology, Duke University Medical Center, Durham, North Carolina
Nashville Cardiovascular Magnetic Resonance Institute, Brentwood, Tennessee.

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Figure 1 DE-CMR Compared With Cine-CMR for Identification of Pathology-Verified Thrombus
(A) Typical images from a patient with concordant findings by DE-CMR and cine-CMR. Both techniques show an intracavitary thrombus within the LV apex (4-chamber views). Pathology (hematoxylin and eosin stain, low power) confirmed the presence of thrombus with organizing features, including prominent collagen and fibrin content. (B) Typical images from a patient with discordant findings by DE-CMR and cine-CMR. DE-CMR demonstrates a large mural thrombus adherent to a left ventricular inferior wall aneurysm, whereas cine-CMR shows no evidence of thrombus (midventricular short-axis views). Thrombus was verified by pathology (gross examination [overlay] and histopathology [inset, Masson trichrome stain]). Both patient examples show that thrombus may have an etched appearance with a black border and a central gray zone on standard inversion time (TI) DE-CMR, whereas it appears homogeneously black on long-TI imaging. See text for details. Thrombus denoted by yellow arrows. CMR = cardiac magnetic resonance; DE-CMR = delayed-enhancement cardiovascular magnetic resonance; LA = left atrium; LV = left ventricle; LVA = left ventricular aneurysm; Myo = myocardium.
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Figure 2 Validation of DE-CMR During Clinical Follow-Up
Stratification of patients with 6-month follow-up according to presence or absence of thrombus by DE-CMR yielded over a 7-fold difference in study end points (TIA, CVA, or pathology-verified thrombus) between groups (15.1% vs. 2.1%). Further stratification based on cine-CMR did not improve differentiation of patients. Details regarding the 8 patients who were DE-CMR–positive for thrombus and had clinical event or pathology confirmation are shown in the corresponding table (bottom). CVA = cerebrovascular accident; TIA = transient ischemic attack; other abbreviations as in Figure 1.
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Figure 3 Thrombus Prevalence According to Etiology and Severity of Myopathic Dysfunction
Thrombus prevalence (bar graph, left) was over 5-fold higher among patients with ischemic cardiomyopathy as compared with those with nonischemic cardiomyopathy (9.2% vs. 1.7%) despite nearly identical left ventricular ejection fraction. When each group was stratified according to ejection fraction (line graph, right), prevalence was higher in patients with ischemic disease for every ejection fraction group.
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Figure 4 Utility of Clinical, Functional, and Scar Markers for Thrombus
(A) Components of clinical, LV ejection fraction, and LV scar inclusive multivariable models for thrombus presence. (B) Adding LV ejection fraction and then LV scar results in an improved model. (C) The synergistic nature of considering both myocardial contraction and scarring as markers for thrombus presence. See text for details. LV = left ventricular.
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