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DOI:10.2214/AJR.07.2364
AJR 2007; 189:974-980
© American Roentgen Ray Society

Original Research

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.

Received November 29, 2006; accepted after revision May 12, 2007.

 
Address correspondence to J. D. Dodd.


Abstract
Top
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
OBJECTIVE. The purpose of this study was to investigate whether MRI can quantify the severity and extent of left ventricular noncompaction and detect trabecular delayed hyperenhancement and whether doing so can show a relationship with clinical stage of disease.

MATERIALS AND METHODS. In a retrospective blinded study, nine patients with left ventricular noncompaction and 10 control subjects had cardiac MRI studies evaluated for the severity and extent of left ventricular noncompaction and the amount and degree of trabecular delayed hyperenhancement on a myocardial segment basis (16-segment model). Findings were correlated with parameters of clinical stage of disease.

RESULTS. Fifty-seven (39%) myocardial segments showed left ventricular noncompaction whereas 22 (17%) showed trabecular delayed hyperenhancement. Significant differences among clinical severity groups were noted in the severity and extent of left ventricular noncompaction at the mid (p < 0.05 and p < 0.005, respectively) and apical levels (p < 0.003 and p < 0.001, respectively), severity of trabecular delayed hyperenhancement at the mid (p < 0.04) and apical levels (p < 0.02), and amount of trabecular delayed hyperenhancement at the apical level (p < 0.006). The extent of left ventricular noncompaction and the amount and degree of trabecular delayed hyperenhancement correlated significantly with ejection fraction (EF) (r = –0.47, –0.53, –0.53, respectively, p < 0.05). The degree of trabecular delayed hyperenhancement was an independent predictor of EF (R2 = 0.30, p < 0.0001). Significant differences in the severity of trabecular delayed hyperenhancement were detected among patients with mild and those with moderate and severe clinical stage of disease (p < 0.0001).

CONCLUSION. Cardiac MRI shows trabecular delayed hyperenhancement in left ventricular noncompaction. Evaluating the extent and severity of left ventricular noncompaction and trabecular delayed hyperenhancement may improve the ability of the clinician to predict the clinical stage of disease.

Keywords: cardiomyopathy • left ventricle abnormality • left ventricular noncompaction • MRI • trabecular delayed hyperenhancement


Introduction
Top
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
Left ventricular noncompaction syndrome is a rare cardiomyopathy characterized by an increase in the trabeculated, noncompacted myocardium adjacent to compacted myocardium in the left ventricle [1–3]. Clinically, patients present with a spectrum of disease severity ranging from no symptoms to cardiac failure, thromboembolism, cardiac arrhythmias, and sudden death [4, 5].

Traditionally, left ventricular noncompaction is diagnosed by echocardiography when the ratio of noncompacted to compacted myocardium is greater than 2. Echocardiography may not visualize the apical region optimally, leading to underestimation of the degree of left ventricular noncompaction [3]. Cardiac MRI provides a comprehensive depiction of cardiac morphology in any imaging plane. Recent cardiac MRI reports suggest a ratio of noncompacted myocardium to compacted myocardium of > 2.3 yields the highest sensitivity (86%) and specificity (99%) in diagnosis [6].

Jenni et al. [7] studied seven patients with left ventricular noncompaction with pathologic correlation (three heart transplant procedures and four post mortem procedures). Histologic analysis revealed ischemic lesions in the thickened endocardium and thickened trabeculae with accompanying fibrosis. Direct imaging of myocardial fibrosis is possible with the use of an inversion recovery prepared T1-weighted gradient-echo sequence and the extracellular fluid tracer gadopentetate dimeglumine [8]. This technique has been termed "delayed hyperenhancement" and shows nonviable tissue as hyperenhanced or bright. Its accurate delineation of fibrous myocardium has been confirmed with several ex vivo techniques (triphenyltetrazolium chloride and histology) [9].

Such techniques are beginning to be used in left ventricular noncompaction. In a recent study by Ivan et al. [10] using delayed hyperenhancement, MRI in three patients with left ventricular noncompaction revealed areas of subendocardial hyperenhancement. Histologic analysis confirmed subendocardial and trabecular fibroelastosis. We have previously published a case report showing trabecular delayed hyperenhancement on cardiac MRI in a patient with severe left ventricular noncompaction [11]. The hypothesis of the current study was that cardiac MRI may detect trabecular delayed hyperenhancement in a series of patients with left ventricular noncompaction and that the amount and degree of trabecular delayed hyperenhancement might be useful in quantifying the clinical stage of disease. The aims of our study were to quantitatively assess the extent and severity of left ventricular noncompaction using the cardiac segmental anatomy recommended by the American Heart Association [12], quantitatively assess the amount and degree of trabecular delayed hyperenhancement, and evaluate the relationship between left ventricular noncompaction and trabecular delayed hyperenhancement with parameters of the clinical stage of disease.


Materials and Methods
Top
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
Patient Group
The hospital institutional review board approved this study and informed consent was not required. Between 2002 and 2006, nine patients underwent cardiac MRI with a diagnosis suggestive of left ventricular noncompaction on the basis of clinical and echocardiographic findings. Clinical stage of disease was derived from previous studies that have evaluated the clinical presentation and long-term follow-up in patients with left ventricular noncompaction [5, 13]. Patients were excluded if they had a history of coronary artery disease or myocardial infarction. A group of 10 control subjects was included who had normal global and regional left ventricular function and no evidence of myocardial delayed hyperenhancement on cardiac MRI.

In the current study, shortness of breath was defined according to the New York Heart Association (NYHA) functional classification [14]. All patients underwent echocardiography; left ventricular EF < 55% was regarded as abnormal. We stratified patients as having a mild stage of disease if they had no or minimal dyspnea (NYHA ≥ I), normal EF < 55%, and no history of arrhythmias or thromboembolism; a moderate stage of disease if they had dyspnea (NYHA 0 or I), abnormal EF < 55% but no evidence of arrhythmias or thromboembolism; and a severe stage of disease if they had dyspnea (NYHA ≥ I), abnormal EF < 55, and Holter monitor evidence of arrhythmia such as atrial fibrillation or ventricular tachycardia [5, 13].

MR Imaging Protocol
All subjects were examined on a 1.5-T magnet (Signa CV/i, GE Healthcare) using an eight-element phased-array cardiac coil for signal reception. Left ventricular function was obtained with cine images using a steady-state free precession (SSFP) technique (TR/TE, 3.5/1.4; matrix, 192 x 192; field of view, 34 x 34 cm; slice thickness, 8 mm) obtained in two-chamber, four-chamber, and short-axis planes. In addition, in six patients SSFP radial long-axis views were obtained with the axis placed in the center of the left ventricular cavity at the mid level and 12–16 slices acquired with imaging parameters similar to those of the preceding cine sequences.

After baseline imaging, a bolus injection of 0.2 mmol/kg of gadopentetate dimeglumine was administered using an infusion pump at 3 mL/s followed by a 20-mL saline flush. Between 10 and 12 minutes later, delayed hyperenhancement MRI was performed using an inversion recovery prepared gated fast gradient-echo pulse sequence [15]. We acquired multiple sequences with varying inversion time (TI) values and then selected the images with the most appropriate TI. Delayed hyperenhancement images were acquired to optimally show normal myocardium and trabeculae (dark) and regions of delayed hyperenhancement within the myocardium and trabeculae (bright) with proper selection of the TI. Imaging parameters were as follows: 7.1/3.1; matrix, 256 x 192; flip angle, 20°; inversion pulse, 180°; and TI between 150 and 300 milliseconds.

Analysis for Left Ventricular Noncompaction
A cardiac MRI fellowship-trained cardiac radiologist interpreted the images blinded to the diagnosis and clinical severity in all cases. For the purposes of this study, the extent of left ventricular noncompaction was taken to indicate the number of cardiac segments showing left ventricular noncompaction, and the severity of left ventricular noncompaction was taken to indicate the ratio of noncompacted to compacted myocardium for a given myocardial segment. Segmental analysis was evaluated using a standard 17-segment cardiac model as defined by the American Heart Association/American College of Cardiology (AHA/ACC) for standardized myocardial segmentation [12]. The apex (segment 17) was excluded from analysis because it is normally thin and may lead to false-positive interpretations.

Cine short-axis images for calculation of ejection fraction (EF), end-diastolic volume (EDV), end-systolic volume (ESV), and myocardial mass were evaluated using Simpson's method (MassPlus, Medis, Inc.). Ventricular wall motion abnormalities were defined as normal, mild to moderate hypokinesia, severe hypokinesia, akinesia, or dyskinesia by wall thickening > 30%, 10–29%, < 10%, absent, or no appreciable wall thickening with systolic movement away from the center of the left ventricular segments, respectively [16]. Regional wall motion was scored on a 5-point system: 1 = normal, 2 = mild to moderate hypokinesia, 3 = severe hypokinesia, 4 = akinesia, 5 = dyskinesia) [17]. Distribution of noncompacted to compacted myocardium was quantitatively analyzed by measuring the thickness in millimeters of noncompacted and compacted myocardium in all 16 segments using the acquired cine SSFP sequences. Noncompaction was defined as a ratio of noncompacted to compacted myocardium > 2.3 at end-diastole [6].

Analysis of Trabecular Delayed Hyperenhancement
For the purposes of this study, the amount of trabecular delayed hyperenhancement indicated the number of cardiac segments exhibiting trabecular delayed hyperenhancement. The degree of trabecular hyperenhancement was measured by placing a region of interest (ROI) in the trabeculae and a second ROI in the middle myocardium of the corresponding myocardial segment at the same ventricular level. This was performed for each of the 16 segments, and the ratio of trabecular to myocardial signal was calculated. We defined trabecular delayed hyperenhancement as present when the ratio of trabecular to corresponding myocardial signal intensity was ≥ 3.

Statistical Analysis
All data are presented as mean ± SD. Data were analyzed per myocardial segment. Comparison among multiple groups was performed with Kruskal-Wallis analysis of variance. To compare individual groups at each ventricular level, the Scheffe post hoc test was used. Univariate correlations were performed with the Spearman's rank correlation test. Stepwise multiple regression analysis with EF as the dependent variable and age, sex, extent and severity of left ventricular noncompaction, and amount and degree of trabecular delayed hyperenhancement as independent variables was used to evaluate the relationship among left ventricular dysfunction, left ventricular noncompaction, and trabecular delayed hyperenhancement. A p value < 0.05 was considered statistically significant.


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).

 

Results
Top
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
Baseline Characteristics
Baseline characteristics are given in Table 1. One patient with left ventricular noncompaction did not undergo hyperenhancement sequences for technical reasons. Of the two patients with a mild clinical stage of disease, one had very mild shortness of breath (NYHA 0) and complained of intermittent palpitations, and the other patient had more progressive shortness of breath (NYHA II); both patients had a normal EF. Of the four patients with a moderate clinical stage of disease, one presented with palpitations and had an EF of 49%; one had atypical chest pain and an EF of 23%; one complained of shortness of breath and had an EF of 27%; and one had shortness of breath, chest pain, and an EF of 53%. Of the three patients with a severe clinical stage of disease (Fig. 1A, 1B, 1C, including cine loops Figs. S1D and S1E available at www.ajronline.org) all presented with shortness of breath, abnormal EF, and Holter recordings showing evidence of either atrial fibrillation or ventricular tachycardia. In the left ventricular noncompaction group, 57 (39%) of 144 segments fulfilled the definition for left ventricular noncompaction compared with no segments in the control group; 22 (17%) of 128 segments showed trabecular delayed hyperenhancement. No patient in the control group showed trabecular delayed hyperenhancement.


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  		TABLE 1: Comparison of Control Group and Patients with Left Ventricular Noncompaction

 

Extent and Severity of Left Ventricular Noncompaction
For severity of left ventricular noncompaction there were statistically significant differences in the anterior, anterolateral, and inferolateral segments (Kruskal-Wallis; p < 0.02, p <0.03, and p < 0.01, respectively) among all clinical stage groups at the mid level and for all segments at the apical level (p < 0.004) (Fig. 2). For extent of left ventricular noncompaction, there were statistically significant differences in the anterior, anterolateral, inferolateral, and inferior segments (p < 0.002, p < 0.01, p < 0.02, and p < 0.008, respectively) among all clinical stage groups at the mid level and for all segments at the apical level (p < 0.001) (Fig. 3).


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.

 
Amount and Degree of Trabecular Delayed Hyperenhancement
For degree of trabecular delayed hyperenhancement, there were statistically significant differences among all clinical stage groups at the mid level in the inferior segment (Kruskal-Wallis, p < 0.02) and the anterior, lateral, and septal segments at the apical level (p < 0.02, p < 0.01, and p < 0.04, respectively) (Fig. 4). For the amount of trabecular delayed hyperenhancement, there were statistically significant differences among all clinical stage groups at the basal level in the anterior and inferolateral segments (p < 0.01), inferior segment at the mid level, and all segments at the apical level (p < 0.03) (Fig. 5).


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.

 

Intergroup Comparison Among Clinical Stages of Disease for Left Ventricular Noncompaction and Trabecular Delayed Enhancement
For extent of left ventricular noncompaction, at the basal ventricular level, no significant differences were found among clinical stage groups; at the midventricular level, significant differences were found among the severe clinical stage group and all other clinical stage groups; at the apical ventricular level, no significant differences were found among any clinical stage groups. For severity of left ventricular noncompaction, at the basal ventricular level, significant differences were found among the mild and severe clinical stage groups; at the midventricular level, significant differences were found among the severe clinical stage group and all other clinical stage groups; at the apical ventricular level, no significant differences were found among any clinical groups with left ventricular noncompaction.

For degree of trabecular delayed hyperenhancement, at the basal ventricular level, significant differences were found between the severe clinical stage group and all other clinical stage groups; at the midventricular level, significant differences were found among the control and mild stage groups compared with the moderate and severe stage groups. At the apical level, no significant differences were found among clinical stage groups. For amount of trabecular delayed hyperenhancement, at the basal ventricular level, significant differences were found between the severe clinical stage group and all other clinical stage groups; at the midventricular level, significant differences were found among the severe clinical group and the control and mild clinical stage groups; no significant difference was detected among the moderate and severe clinical stage groups; at the apical ventricular level, significant differences were found among the moderate and severe clinical stage groups and all other clinical stage groups.


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.

 
Correlation Analysis
On univariate analysis, amount and degree of trabecular delayed hyperenhancement and extent of left ventricular noncompaction correlated significantly with EF (r = –0.53, –0.53, and –0.47, respectively, p < 0.05) (Table 2, Fig. 6). Regional wall motion abnormality correlated significantly with the severity and extent of left ventricular noncompaction at the mid level (p < 0.001 and p < 0.01, respectively). Regional wall motion abnormalities also correlated significantly with the amount and degree of trabecular delayed hyperenhancement at the mid (p < 0.003 and p < 0.03, respectively) and apical levels (p < 0.05 and p < 0.001, respectively) (Fig. 7). Stepwise linear regression analysis revealed the amount of trabecular delayed hyperenhancement to be the only independent predictor of EF (R2 = 0.30, p < 0.05).


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  		TABLE 2: Univariate Correlation Among Trabecular Delayed Hyperenhancement, Left Ventricular Noncompaction, and Left Ventricular Function

 


Discussion
Top
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
In this study we quantified the extent and severity of left ventricular noncompaction and the amount and degree of trabecular delayed hyperenhancement on cardiac MRI in a series of patients with left ventricular noncompaction and correlated these with parameters of clinical stage of disease. We found many significant differences in quantitative parameters of left ventricular noncompaction and trabecular delayed hyperenhancement among patients with different clinical stages of disease. Using delayed hyperenhancement MRI sequences added important additional information to the evaluation of left ventricular noncompaction.

Several ventricular levels showed abnormalities in the amount and degree of trabecular delayed hyperenhancement but not in the extent or severity of left ventricular noncompaction. For example, for the degree of trabecular delayed hyperenhancement at the basal ventricular level, significant differences were found among the severe clinical stage group and any of the other clinical stage groups, whereas no differences in the extent of left ventricular noncompaction were found among any of the clinical groups. For the amount of trabecular delayed hyperenhancement at the apical ventricular level, significant differences were found among the moderate and severe clinical stage groups and all other clinical stage groups compared with no significant differences in extent or severity of left ventricular noncompaction.

Furthermore, stepwise linear regression analysis revealed the amount of trabecular delayed hyperenhancement to be the only independent predictor of EF (R2 = 0.30, p < 0.05). The most likely explanation for this finding is that several myocardial segments showed trabecular delayed hyperenhancement with a normal ratio of compacted to noncompacted myocardium, which was unexpected. This was found mostly in patients with clinically severe stages of disease and suggests that in patients with left ventricular noncompaction, even in segments that do not meet the morphologic criteria for left ventricular noncompaction, ischemic trabecular foci may coexist.

It has been suggested that increasing severity of trabecular fibrosis may affect inotropic function [5], and our results would also support this concept. Delayed enhanced cardiac MRI was used by Ivan et al. [10] in a study of three patients with left ventricular noncompaction who underwent heart transplantation. Interestingly, delayed hyperenhancement was detected in a subendocardial distribution in two of three patients. Histologic examination revealed spongy myocardium with focal fibroelastosis, fibrointimal proliferation, and thickening of the endocardial lining. That distribution differs from our findings in which delayed hyperenhancement had a characteristic dotlike appearance within the trabeculae of noncompacted myocardium. The patients in the study by Ivan et al. may have had more severe disease than those in our study (two patients were awaiting transplantation and required bridging with a biventricular assist device). It may be that fibroelastosis progresses from trabecular to subendocardial endocardium with progressively severe disease. It is also possible that technical differences in our study, such as higher matrix resolution and use of double-dose gadolinium, may have resulted in better depiction of fibrosis within the trabeculae, although we cannot confirm this because few MRI technical parameters were included in the study by Ivan et al. Such differences in enhancement pattern highlight the poorly understood pathophysiologic mechanisms leading to left ventricular noncompaction and its clinical manifestations.

That the extent and severity of left ventricular noncompaction correlated with global left ventricular dysfunction corroborates previous echocardiographic studies of left ventricular noncompaction [4, 7]. A distinct advantage of MRI is the ability to depict fibrosis with contrast-enhanced delayed imaging. In our study, the extent and severity of left ventricular noncompaction did not correlate as strongly with EF as did the amount and degree of trabecular delayed hyperenhancement. Jenni et al. [7] showed ischemic lesions and fibrosis within the thickened trabeculae of the noncompacted myocardium in seven patients with left ventricular noncompaction. Histologically, the amount of such fibrosis varied considerably, supporting our observation that trabecular delayed hyperenhancement was distributed heterogeneously through the noncompacted myocardial layer.

In the absence of MRI delayed hyperenhancement sequences, therefore, the degree of fibrotic and possibly dysfunctional cardiac segments may be underestimated on routine cardiac MRI protocols because certain segments with a normal ratio of compacted to noncompacted myocardium may contain trabecular fibrosis. Thus, depiction of trabecular delayed hyperenhancement appears to improve the correlation between MRI and progressive clinical stages of disease in comparison with routine MRI protocols.

Quantifying the severity and extent of left ventricular noncompaction was also important. We found the greatest difference among patients with different clinical stages of disease was at the midventricular level. Evidence of left ventricular noncompaction at the midventricular level suggests the presence of more severe clinical disease. Evidence of left ventricular noncompaction at the apical level is not a useful discriminator because all patients in our series, even those with a mild clinical stage of disease, showed apical left ventricular noncompaction.

Six patients had radial long-axis SSFP sequences of the left ventricle in addition to traditional cardiac MRI two-chamber, four-chamber, and short-axis views. Imaging techniques primarily using short-axis planes to diagnose left ventricular noncompaction can potentially overestimate the extent and severity of left ventricular noncompaction, particularly at the apical region, which is also the most commonly affected [6]. For example, in the study by Ivan et al. [10], 2D echocardiography failed to diagnose left ventricular noncompaction in all three patients. An advantage of cardiac MRI is its ability to prescribe imaging planes in any obliquity. Prescribing radial long-axis projections ensures that each slice passes through the center of the ventricle, minimizing the potential to overestimate the ratio of compacted to noncompacted myocardium. Although a formal comparison of different imaging planes was not the primary focus of this study, nevertheless, we found radial long-axis projections most useful and suggest these to be the optimal imaging planes for cardiac MRI evaluation of left ventricular noncompaction.

A limitation of our study was the small number of patients. Left ventricular noncompaction is a rare cardiomyopathy that has yet to be comprehensively classified [18]. A related point is the small number of myocardial segments with severe regional wall motion abnormalities. Segments exhibiting dyskinesis lacked trabecular delayed hyperenhancement, which does not support our hypothesis. However, only five out of a potential 128 segments showed dyskinesis. Cardiac MRI studies with larger numbers of patients with left ventricular noncompaction are needed to elucidate further the relationship between left ventricular noncompaction and ventricular dysfunction. A very mild increased signal related to residual contrast material within the left ventricular cavity may be seen in healthy subjects and should not be confused with the marked dotlike pattern of trabecular delayed hyperenhancement in left ventricular noncompaction. We used a ratio for including a segment as showing trabecular delayed hyperenhancement of ≥ 3, which was arbitrarily chosen; this should not invalidate our findings because the control group had the same criteria applied. However, it would be of interest to validate this ratio in a larger group of patients with left ventricular noncompaction and to evaluate it as a differentiating feature from other types of cardiomyopathies in future studies.

In conclusion, cardiac MRI delayed hyperenhancement sequences can show trabecular delayed hyperenhancement. Some trabeculae show delayed hyperenhancement despite having a normal compacted-to-noncompacted myocardial ratio, suggesting that left ventricular noncompaction may be a more diffuse disease process than previously suspected. The use of delayed hyperenhancement sequences improves the correlation between cardiac MRI and the parameters of clinical stage of disease.


References
Top
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

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