Left ventricular trabeculae: quantification in different cardiac diseases and impact on left ventricular morphological and functional parameters assessed with cardiac magnetic resonance

Fernández-Golfín, Covadonga; Pachón, Marta; Corros, Cecília; Bustos, Ana; Cabeza, Beatriz; Ferreirós, Joaquı́n; Isla, Leopoldo Pérez de; Macaya, Carlos; Zamorano, José

doi:10.2459/jcm.0b013e32832e1c60

Cited by 30 publications

(16 citation statements)

References 12 publications

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“…Full voxel analysis closely mimics MP, which partitions myocardium and cavity in a binary manner, with trabeculae included in LVM when contiguous in shape or of similar signal intensity to surrounding LV myocardium. 4,7,8,16 Figures 1B and 1C provide an illustration of partial voxel content as quantified by the segmentation algorithm.…”

Section: Methodsmentioning

confidence: 99%

Improved Left Ventricular Mass Quantification With Partial Voxel Interpolation

Codella

Lee

Fieno

et al. 2012

Circ: Cardiovascular Imaging

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Background CMR typically quantifies LV mass (LVM) via manual planimetry (MP), but this approach is time consuming and does not account for partial voxel components - myocardium admixed with blood in a single voxel. Automated segmentation (AS) can account for partial voxels, but this has not been used for LVM quantification. This study used automated CMR segmentation to test the influence of partial voxels on quantification of LVM. Methods and Results LVM was quantified by AS and MP in 126 consecutive patients and 10 laboratory animals undergoing CMR. AS yielded both partial voxel (ASPV) and full voxel (ASFV) measurements. Methods were independently compared to LVM quantified on echocardiography (echo) and an ex-vivo standard of LVM at necropsy. AS quantified LVM in all patients, yielding a 12-fold decrease in processing time vs. MP (0:21±0:04 vs. 4:18±1:02 min; p<0.001). ASFV mass (136±35gm) was slightly lower than MP (139±35; Δ=3±9gm, p<0.001). Both methods yielded similar proportions of patients with LV remodeling (p=0.73) and hypertrophy (p=1.00). Regarding partial voxel segmentation, ASPV yielded higher LVM (159±38gm) than MP (Δ=20±10gm) and ASFV (Δ=23±6gm, both p<0.001), corresponding to relative increases of 14% and 17%. In multivariable analysis, magnitude of difference between ASPV and ASFV correlated with larger voxel size (partial r=0.37, p<0.001) even after controlling for LV chamber volume (r=.28, p=0.002) and total LVM (r=0.19, p=0.03). Among patients, ASPV yielded better agreement with echo (Δ=20±25gm) than did ASFV (Δ=43±24gm) or MP (Δ=40±22gm, both p<0.001). Among laboratory animals, ASPV and ex-vivo results were similar (Δ=1±3gm, p=0.3), whereas ASFV (6±3gm, p<0.001) and MP (4±5gm, p=0.02) yielded small but significant differences with LVM at necropsy. Conclusions Automated segmentation of myocardial partial voxels yields a 14-17% increase in LVM vs. full voxel segmentation, with increased differences correlated with lower spatial resolution. Partial voxel segmentation yields improved CMR agreement with echo and necropsy-verified LVM.

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Section: Methodsmentioning

confidence: 99%

Improved Left Ventricular Mass Quantification With Partial Voxel Interpolation

Codella

Lee

Fieno

et al. 2012

Circ: Cardiovascular Imaging

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“…A recent study supported that nonischemic DCM was more likely to be associated with hypertrabeculation compared with ischemic or DCM from valvular heart defects. 23 Nonetheless, there is clear overlap between HCM and hypertrabeculation. 24 MYH7, ACTC, and TNNT2 have each been implicated as genetic causes of LVNC, and these genetic studies further support a cardiomyopathy continuum of HCM and LVNC.…”

Section: Sarcomere Mutations In Lvnc Hcm and Dcmmentioning

confidence: 99%

Sarcomere Mutations in Cardiomyopathy With Left Ventricular Hypertrabeculation

Dellefave

Pytel

Mewborn

et al. 2009

Circ Cardiovasc Genet

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Background-Mutations in the genes encoding sarcomere proteins have been associated with both hypertrophic and dilated cardiomyopathy. Recently, mutations in myosin heavy chain (MYH7), cardiac actin (ACTC), and troponin T (TNNT2) were associated with left ventricular noncompaction, a form of cardiomyopathy characterized with hypertrabeculation that may also include reduced function of the left ventricle. Methods and Results-We used clinically available genetic testing on 3 cases referred for evaluation of left ventricular dysfunction and noncompaction of the left ventricle and found that all 3 individuals carried sarcomere mutations. The first patient presented with neonatal heart failure and was referred for left ventricular noncompaction cardiomyopathy. Genetic testing found 2 different mutations in MYBPC3 in trans. The first mutation, 3776delA, Q1259fs, rendered a frame shift at 1259 of cardiac myosin-binding protein C and the second mutation was L1200P. The frameshift mutation was also found in this mother who displayed mild echocardiographic features of cardiomyopathy, with only subtle increase in trabeculation and an absence of hypertrophy. A second pediatric patient presented with heart failure and was found to carry a de novo MYH7 R369Q mutation. The third case was an adult patient with dilated cardiomyopathy referred for ventricular hypertrabeculation. This patient had a family history of congestive heart failure, including pediatric onset cardiomyopathy where 3 individuals in the family were found to have the MYH7 mutation R1250W. Conclusion-Genetic testing should be considered for cardiomyopathy with hypertrabeculation. (Circ Cardiovasc Genet.2009;2:442-449.)

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“…They proposed a value of 20% as a threshold for distinguishing LVNC from DCM. Fernndez-Golfin et al studied the same method on a larger cohort of ischemic heart disease, DCM, valvular heart disease, and left ventricular hypertrophy patients, and normal subjects [17] . They found relatively higher values in their patients (17.2±4.9 in normal subjects, 23.3±6 in DCM patients).…”

Section: Discussionmentioning

confidence: 99%

507 A Novel Method for Quantification of Left Ventricular Hypertrabeculation/Noncompaction Using Two-Dimensional Echocardiography

Jamei

Sayadpoor

Kocharian³

et al. 2012

Archives of Disease in Childhood

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AbstractsDesign 27 infants and children with CHD (10 with VSD, 8 with ASD, 9 PDA) without heart failure, before and 12 months or more after surgical or catheter intervention. Eighty normal children served as controls. Results At presentation, age = (35.6 +/-26 months),patients were significantly shorter, height SDS (HtSDS)(−1.6 +/-1.1) and had lower BMI (15.1 +/-2.5) compared to normal controls (HtSDS = 0.25 +/-0.3, BMI = (16.4 +/-1.5). One year or more after catheter or surgical treatment the HtSDS and BMI increased significantly in patients to -0.55 +/-0.9 and 15.9 +/-1.5 respectively. Circulating concentrations of IGF-I increased from 46.8 +/-29 mcg/L before to 77.3 +/-47.6 mcg/L after intervention. The HtSDS after treatment was correlated with the IGF-I concentration (r = 0.804, P<0.001). The change in the HtSDS after intervention was correlated significantly with BMI (r=0.594, p<0.001). The shunt size was correlated negatively with BMI before intervention (r = − 0.35, P<0.01) and with HtSDS (r = -0.461, p<0.05). Conclusions These data denoted that early surgical interference and good weight gain have beneficial effect on postoperative growth spurt. The accelerated linear growth after intervention appears to be mediated through activation of the GH/IGF-I system.

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Left ventricular trabeculae: quantification in different cardiac diseases and impact on left ventricular morphological and functional parameters assessed with cardiac magnetic resonance

Cited by 30 publications

References 12 publications

Improved Left Ventricular Mass Quantification With Partial Voxel Interpolation

Improved Left Ventricular Mass Quantification With Partial Voxel Interpolation

Sarcomere Mutations in Cardiomyopathy With Left Ventricular Hypertrabeculation

507 A Novel Method for Quantification of Left Ventricular Hypertrabeculation/Noncompaction Using Two-Dimensional Echocardiography

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