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Quantification of Left Ventricular Noncompaction and Trabecular Delayed Hyperenhancement with Cardiac MRI: Correlation with Clinical Severity

Jonathan D. Dodd1,2,3, Godtfred Holmvang4, Udo Hoffmann1,2, Maros Ferencik1,2, Suhny Abbara1,2, Thomas J. Brady1,2 and Ricardo C. Cury1,2

1 Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114.
2 Cardiac MR–PET-CT Program, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114.
3 Present address: Department of Radiology, St. Vincent's University Hospital, Elm Park, Dublin 4, Ireland.
4 Division of Cardiology, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114.


Figure 1
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  		Fig. 1A —Cardiac MRI in 44-year-old woman with left ventricular noncompaction and severe clinical disease. See also Figures S1D and S1E, cine loops, in supplemental data online at www.ajronline.org. Two-chamber steady-state free precession (SSFP) cine image shows left ventricular noncompaction (arrows) at mid and apical levels.

 

Figure 2
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  		Fig. 1B —Cardiac MRI in 44-year-old woman with left ventricular noncompaction and severe clinical disease. See also Figures S1D and S1E, cine loops, in supplemental data online at www.ajronline.org. Delayed contrast-enhanced two-chamber image shows trabecular hyperenhancement (straight arrow). Note that even in segments with normal compacted-to-noncompacted myocardium ratio, there is trabecular hyperenhancement (curved arrow).

 

Figure 3
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  		Fig. 1C —Cardiac MRI in 44-year-old woman with left ventricular noncompaction and severe clinical disease. See also Figures S1D and S1E, cine loops, in supplemental data online at www.ajronline.org. Delayed contrast-enhanced short-axis image shows characteristic dotlike pattern of hyperenhancement within thickened trabeculae (arrows).

 

Figure 4
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  		Fig. 2 —Graph shows severity of left ventricular noncompaction for all clinical stages of disease groups. Significant increases were seen at mid and apical levels among four clinical groups (controls, mild, moderate, and severe left ventricular noncompaction). NS = not significant.

 

Figure 5
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  		Fig. 3 —Graph shows extent of left ventricular noncompaction for all clinical stages of disease groups. Significant increases were seen at mid and apical levels among four clinical groups (controls, mild, moderate, and severe left ventricular noncompaction). No myocardial segment showed left ventricular noncompaction in any clinical group at basal level. No patient in control group showed left ventricular noncompaction at mid or apical level. NS = not significant.

 

Figure 6
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  		Fig. 4 —Graph shows degree of trabecular delayed hyperenhancement for all clinical stages of disease groups among four clinical groups (controls, mild, moderate, and severe left ventricular noncompaction). Significant increases were seen at mid and apical levels among four clinical groups. NS = not significant.

 

Figure 7
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  		Fig. 5 —Graph shows amount of trabecular delayed hyperenhancement for clinical severity groups among four clinical groups (controls, mild, moderate, and severe left ventricular noncompaction). Significant increases were seen at apical level, predominantly in moderate and severe clinical severity groups. NS = not significant.

 

Figure 8
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  		Fig. 6 —Graph shows univariate correlation between degree and amount of trabecular delayed hyperenhancement and ejection fraction. {square} = degree of trabecular delayed hyperenhancement, {diamondsuit} = amount of trabecular delayed hyperenhancement.

 

Figure 9
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  		Fig. 7 —Graph shows relationship between regional segmental functional analysis and degree of trabecular delayed hyperenhancement. Significant correlations were seen at mid (p < 0.003) and apical (p < 0.05) levels.

 

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