Left Ventricular Trabeculation Research Articles

Left Ventricular Trabeculations at Cardiac MRI: Reference Ranges and Association with Cardiovascular Risk Factors in UK Biobank.

Background The extent of left ventricular (LV) trabeculation and its relationship with cardiovascular (CV) risk factors is unclear. Purpose To apply automated segmentation to UK Biobank cardiac MRI scans to (a) assess the association between individual characteristics and CV risk factors and trabeculated LV mass (LVM) and (b) establish normal reference ranges in a selected group of healthy UK Biobank participants. Materials and Methods In this cross-sectional secondary analysis, prospectively collected data from the UK Biobank (2006 to 2010) were retrospectively analyzed. Automated segmentation of trabeculations was performed using a deep learning algorithm. After excluding individuals with known CV diseases, White adults without CV risk factors (reference group) and those with preexisting CV risk factors (hypertension, hyperlipidemia, diabetes mellitus, or smoking) (exposed group) were compared. Multivariable regression models, adjusted for potential confounders (age, sex, and height), were fitted to evaluate the associations between individual characteristics and CV risk factors and trabeculated LVM. Results Of 43 038 participants (mean age, 64 years ± 8 [SD]; 22 360 women), 28 672 individuals (mean age, 66 years ± 7; 14 918 men) were included in the exposed group, and 7384 individuals (mean age, 60 years ± 7; 4729 women) were included in the reference group. Higher body mass index (BMI) (β = 0.66 [95% CI: 0.63, 0.68]; P < .001), hypertension (β = 0.42 [95% CI: 0.36, 0.48]; P < .001), and higher physical activity level (β = 0.15 [95% CI: 0.12, 0.17]; P < .001) were associated with higher trabeculated LVM. In the reference group, the median trabeculated LVM was 6.3 g (IQR, 4.7-8.5 g) for men and 4.6 g (IQR, 3.4-6.0 g) for women. Median trabeculated LVM decreased with age for men from 6.5 g (IQR, 4.8-8.7 g) at age 45-50 years to 5.9 g (IQR, 4.3-7.8 g) at age 71-80 years (P = .03). Conclusion Higher trabeculated LVM was observed with hypertension, higher BMI, and higher physical activity level. Age- and sex-specific reference ranges of trabeculated LVM in a healthy middle-aged White population were established. © RSNA, 2024 Supplemental material is available for this article. See also the editorial by Kawel-Boehm in this issue.

Left Ventricular Trabeculation: Arrhythmogenic and Clinical Significance in Elite Athletes

Left ventricular (LV) trabeculations (LVTs) are common findings in athletes. Limited information exists regarding clinical significance, management, and outcome. The purpose of this study is to examine the prevalence and morphologic characteristics of LVTs in elite athletes, with a focus on clinical correlates and prognostic significance. We enrolled 1,492 Olympic elite athletes of different sports disciplines with electrocardiogram, echocardiogram, and exercise stress test. Individuals with a definite diagnosis of LV noncompaction (LVNC) were excluded; we focused on athletes with LVTs not meeting the criteria for LVNC. Four hundred thirty-five (29.1%) athletes presented with LVTs, which were more frequent in male athletes (62.1% vs 53.5%, P=.002) and Black athletes compared with Caucasian (7.1% vs 2.4%, P<.0001) and endurance athletes (P=.0005). No differences were found with relation to either the site or extent of trabeculations. Endurance athletes showed a higher proportion of LVTs and larger LV volumes (end-diastolic and end-systolic, respectively, 91.5±19.8mL vs 79.3±29.9mL, P=.002; and 33.1±10mL vs 28.6±11.7mL, P=.007) and diastolic pattern with higher E wave (P=.01) and e' septal velocities (P=.02). Ventricular arrhythmias were found in 14% of LVTs versus 11.6% of athletes without LVTs (P=.22). Neither the location nor the LVTs' extension were correlated to ventricular arrhythmias. At 52±32months of follow-up, no differences in arrhythmic burden were observed (11.1% in LVT athletes vs 10.2%, P=.51). Left ventricular trabeculations are quite common in athletes, mostly male, Black, and endurance, likely as the expression of adaptive remodeling. In the absence of associated clinical abnormalities, such as LV systolic and diastolic impairment, electrocardiogram repolarization abnormalities, or family evidence of cardiomyopathy, athletes with LVTs have benign clinical significance and should not require further investigation.

The changing morphology of the ventricular walls of mouse and human with increasing gestation.

That the highly trabeculated ventricular walls of the developing embryos transform to the arrangement during the fetal stages, when the mural architecture is dominated by the thickness of the compact myocardium, has been explained by the coalescence of trabeculations, often erroneously described as 'compaction'. Recent data, however, support differential rates of growth of the trabecular and compact layers as the major driver of change. Here, these processes were assessed quantitatively and visualized in standardized views. We used a larger dataset than has previously been available of mouse hearts, covering the period from embryonic day 10.5 to postnatal day 3, supported by images from human hearts. The volume of the trabecular layer increased throughout development, in contrast to what would be expected had there been 'compaction'. During the transition from embryonic to fetal life, the rapid growth of the compact layer diminished the proportion of trabeculations. Similarly, great expansion of the central cavity reduced the proportion of the total cavity made up of intertrabecular recesses. Illustrations of the hearts with the median value of left ventricular trabeculation confirm a pronounced growth of the compact wall, with prominence of the central cavity. This corresponds, in morphological terms, to a reduction in the extent of the trabecular layer. Similar observations were made in the human hearts. We conclude that it is a period of comparatively slow growth of the trabecular layer, rather than so-called compaction, that is the major determinant of the changing morphology of the ventricular walls of both mouse and human hearts.

Kiosk 8R-FA-05 - Excessive Left Ventricular Trabeculation in Olympic Athletes: Is It a Matter of Ventricular Function?

Kiosk 8R-FA-05 - Excessive Left Ventricular Trabeculation in Olympic Athletes: Is It a Matter of Ventricular Function?

Fractal analysis: Left ventricular trabecular complexity cardiac MRI adds independent risks for heart failure with preserved ejection fraction in participants with end-stage renal disease

PurposeTo measure left ventricular (LV) trabecular complexity by fractal dimension (FD) in patients with end-stage renal disease (ESRD), and assess whether FD was an independent risk factor for heart failure with preserved ejection fraction (HFpEF), or a significant predictor for adverse outcome in this population. MethodsThe study retrospectively enrolled 104 participants with ESRD who underwent 3.0 T cardiac magnetic resonance imaging (MRI) from June 2018 to November 2020. LV trabeculation was quantified with fractal analysis of short-axis cine slices to estimate the FD. Logistic regression analyses were used to evaluate FD and cardiac MRI parameters and to find independent risk predictors. Cox proportional hazard regression was used to investigate the association between FD and MACE. ResultsLV FD was higher in in the HFpEF group than those in the non-HFpEF group, with the greatest difference near the base of the ventricle. Age, minimum left atrial volume index, and LV mean basal FD were independent predictors for HFpEF in patients with ESRD. Combining the mean basal FD with typical predictive factors resulted in a C-index (0.902 vs 0.921), which was not significantly higher. Same improvements were found for net reclassification improvement [0.642; 95% confidence interval (CI), 0.254–1.029] and integrated discrimination index (0.026; 95% CI, 0.008–0.061). Participants with a LV global FD above the cutoff value (1.278) had higher risks of MACE in ESRD patients. ConclusionsLV trabecular complexity measured by FD was an independent risk factor for HFpEF, and a significant predictor for MACE among patients with ESRD.

Physical Activity and Cardiac Morphologic Adaptations.

Chronic and intense exercise programs lead to cardiac adaptations, followed by increased left ventricular wall thickness and cavity diameter, at times meeting the criteria for left ventricular hypertrophy (LVH), commonly referred to as "athlete's heart". Recent studies have also reported that extremely vigorous exercise practices have been associated with heightened left ventricular trabeculation extent, fulfilling noncompaction cardiomyopathy criteria, as part of exercise-induced structural adaptation. These changes are specific to the exercise type, intensity, duration, and volume and workload demands imposed on the myocardium. They are considered physiologic adaptations not associated with a negative prognosis. Conversely, hypertrophic cardiac adaptations resulting from chronic elevations in blood pressure (BP) or chronic volume overload due to valvular regurgitation, lead to compromised cardiac function, increased cardiovascular events, and even death. In younger athletes, hypertrophic cardiomyopathy (HCM) is the usual cause of non-traumatic, exercise-triggered sudden cardiac death. Thus, an extended cardiac examination should be performed, to differentiate between HCM and non-pathological exercise-related LVH or athlete's heart. The exercise-related cardiac structural and functional adaptations are normal physiologic responses designed to accommodate the increased workload imposed by exercise. Thus, we propose that such adaptations are defined as "eutrophic" hypertrophy and that LVH is reserved for pathologic cardiac adaptations. Systolic BP during daily activities may be the strongest predictor of cardiac adaptations. The metabolic demand of most daily activities is approximately 3-5 metabolic equivalents (METs) (1 MET = 3.5 mL of kg of body weight per minute). This is similar to the metabolic demand of treadmill exercise at the first stage of the Bruce protocol. Some evidence supports that an exercise systolic BP response 150 mmHg at the end of that stage is a strong predictor of left ventricular hypertrophy, as this BP reflects the hemodynamic burden of most daily physical tasks. Aerobic training of moderate intensity lowers resting and exercise systolic BP at absolute workloads, leading to a lower hemodynamic burden during daily activities, and ultimately reducing the stimulus for LVH. This mechanism explains the significant LVH regression addressed by aerobic exercise intervention clinical studies.

Abstract 12506: Assessment of the Left Ventricular Trabeculation Phenotype Contributes to Risk Stratification in Hypertrophic Cardiomyopathy Patients

Aims: To investigate clinical values associated with the “left ventricular (LV) trabeculation phenotype” that did not meet the diagnostic criteria of LV noncompaction (LVNC) in hypertrophic cardiomyopathy (HCM). Hypothesis: The presence of left ventricular trabeculation phenotype was associated with a poor prognosis in HCM patients. Genetic factors contributed to this particular phenotype. Methods: A total of 940 HCM patients were recruited. The primary endpoint was cardiovascular death; the secondary endpoints were sudden cardiac death (SCD) and all-cause death. The LV trabeculation phenotype was assessed by cardiac magnetic resonance. Baseline and survival analyses regarding the LV trabeculation phenotype were conducted in general HCM patients and obstructive subset. A combination model was constructed by adding the LV trabeculation phenotype to the HCM risk-SCD model. The whole exome sequencing was used for genetic analysis. Results: The LV trabeculation phenotype was recognized in 34.5% HCM patients and was mostly observed at the apex and free wall. Patients with the LV trabeculation phenotype were younger, had a higher prevalence of family history of SCD and more frequent presence of late gadolinium enhancement. Cox proportional hazards regression analysis showed that the LV trabeculation phenotype increased the risk of cardiovascular death (P=0.031), SCD (P=0.008), and all-cause death (P=0.047) in obstructive HCM patients. Furthermore, the LV trabeculation phenotype-combined model improved risk stratification for SCD. The genetic analysis showed that DTNA variants were more frequently identified in patients with the LV trabeculation phenotype. Conclusions: The LV trabeculation phenotype contributes to risk stratification in obstructive HCM, thus this parameter should be assessed in obstructive HCM patients even if the degree of trabeculation does not fulfil the LVNC criteria. DTNA mutation underlies the cause of this phenotype.

P320 LEFT DOMINANT ARRHYTHMOGENIC CARDIOMYOPATHY: HOW TO STRATIFY THE ARRHYTHMIC RISK? EARLY ONSET CLINICAL CASE

Abstract Introduction Arrhythmogenic cardiomyopathy (ACM) is a genetic disease characterized by the progressive replacement of myocardiocytes by fibroadipose tissue that becomes a susbstrate for ventricular arrhythmias with risk of sudden cardiac death. Arrhythmogenic cardiomyopathy can manifest itself through three different phenotypes: the classic phenotype, the most frequent, involving only the right ventricle, the biventricular variant with possible right or left dominance and the rare variant involving only the left ventricle. We present a case of left ventricular arrhythmogenic cardiomyopathy. Case Report 16–year–old male patient in complete physical well–being, with no significant medical history and a negative family history of heart disease and/or sudden cardiac death (Fig. 1). He practiced competitive sports for years with periodic medical–sports visits. In 2017, ventricular extrasystole was detected on the electrocardiogram, for which he performed cardiological investigations. On electrocardiogram: sinus rhythm with QRS fragmented into DIII and aVL and negative T waves from V4 to V6 (Fig. 2). On transthoracic echocardiography, evidence of normal cavity dimensions, ejection fraction at lower normal limits (42%) and left ventricular trabeculation, in the absence of significant valvulopathy. He then performed a cardiac MRI that showed: left ventricle moderately dilated and hypokinetic with widespread alterations of myocardial signal secondary to fibroadipose replacement phenomena, configuring a picture of left ventricular dilation and dysfunction referable to arrhythmogenic left ventricular cardiomyopathy (Fig. 3). The patient was also subjected to genetic analysis aimed at searching for mutations of genes involved in arrhythmic heart disease, which was negative. In light of the absence of conclusive scientific evidence on the implantation of a defribrillator in primary prevention in clinical–instrumental cases such as the present, the risk of infection and the risk of inappropriate discharges, it was proposed the implantation of a loop–recorder in order to monitor and record any arrhythmic events, starting beta–blocker therapy. The possibility of continuing competitive physical activity was therefore denied. Conclusions Currently, guidelines on ACM and diagnostic criteria focus mainly on the right variant, so there are no clear indications to stratify arrhythmic risk in left ventricular ACM.

A Systematic Review of Ebstein’s Anomaly with Left Ventricular Noncompaction

Traditional definitions of Ebstein’s anomaly (EA) and left ventricular noncompaction (LVNC), two rare congenital heart defects (CHDs), confine disease to either the right or left heart, respectively. Around 15–29% of patients with EA, which has a prevalence of 1 in 20,000 live births, commonly manifest with LVNC. While individual EA or LVNC literature is extensive, relatively little discussion is devoted to the joint appearance of EA and LVNC (EA/LVNC), which poses a higher risk of poor clinical outcomes. We queried PubMed, Medline, and Web of Science for all peer-reviewed publications from inception to February 2022 that discuss EA/LVNC and found 58 unique articles written in English. Here, we summarize and extrapolate commonalities in clinical and genetic understanding of EA/LVNC to date. We additionally postulate involvement of shared developmental pathways that may lead to this combined disease. Anatomical variation in EA/LVNC encompasses characteristics of both CHDs, including tricuspid valve displacement, right heart dilatation, and left ventricular trabeculation, and dictates clinical presentation in both age and severity. Disease treatment is non-specific, ranging from symptomatic management to invasive surgery. Apart from a few variant associations, mainly in sarcomeric genes MYH7 and TPM1, the genetic etiology and pathogenesis of EA/LVNC remain largely unknown.

Impact of Right Ventricular Trabeculation on Right Ventricular Function in Patients With Left Ventricular Non-compaction Phenotype.

Right ventricular (RV) involvement in left ventricular (LV) non-compaction (LVNC) remains unknown. We aimed to describe the RV volumetric, functional, and strain characteristics and clinical features of patients with LVNC phenotype and good LV ejection fraction (EF) using cardiac magnetic resonance to characterize RV trabeculation in LVNC and to study the relationships of RV and LV trabeculation with RV volume and function. This retrospective study included 100 Caucasian patients with LVNC phenotype and good LV-EF and 100 age- and sex-matched healthy controls. Patients were further divided into two subgroups according to RV indexed trabecular mass [RV-TMi; patients with RV hypertrabeculation (RV-HT) vs. patients with normal RV trabeculation (RV-NT)]. We measured the LV and RV volumetric, functional, and TMi values using threshold-based postprocessing software and the RV and LV strain values using feature tracking and collected the patients' LVNC-related clinical features. Patients had higher RV volumes, lower RV-EF, and worse RV strain values than controls. A total of 22% of patients had RV-TMi values above the reference range; furthermore, RV-HT patients had higher RV and LV volumes, lower RV- and LV-EF, and worse RV strain values than RV-NT patients. We identified a strong positive correlation between RV- and LV-TMi and between RV-TMi and RV volumes and a significant inverse relationship of both RV- and LV-TMi with RV function. The prevalence of LVNC-related clinical features was similar in the RV-HT and RV-NT groups. These results suggest that some patients with LVNC phenotype might have RV non-compaction with subclinical RV dysfunction and without more severe clinical features.

Abstract 13454: Cardiac Abnormalities in a Large Student Athletes Screening Cohort in Central Texas

Introduction: Sudden cardiac death (SCD) in the young is a rare but devastating event. Pre-participation evaluation is required prior to competitive sports. The Texas Adolescent Athlete Heart Screening Registry (TAAHSR) performs screening events including history, ECG and limited echocardiogram (ECHO). Hypothesis: Cardiac abnormalities are identified in athlete screening and challenges exist in long-term follow up. Methods: The TAAHSR database of 4309 participants between 2013-2020 was analyzed and follow up data obtained from phone and electronic medical records. Screening results were classified as: I - no abnormality (abnl) identified, II - abnl identified and further evaluation but no activity restriction recommended, level III - abnl identified and further evaluation with activity restriction recommended if concern for SCD. Results: Of 4309 participants, 218 (5%) screened positive on either ECG, ECHO, or both. ECG abnl were seen in 117/4309 (2.7%) level II and 23/4309 level III (0.5%). ECHO abnl were seen in 73/4309 (1.7%) level II and 13/4307 (0.3%) level III. The most frequent abnl in 218 positive screenings included: ECG - right ventricular hypertrophy (27, 12%), right bundle branch block (26, 12%), T-wave abnormalities (23, 10%), left ventricular hypertrophy (22, 10%), left axis deviation (17, 8%), Wolff-Parkinson-White (8, 4%); ECHO - bicuspid aortic valve (15, 7%), mitral valve prolapse (9, 4%), increased left ventricular trabeculations (9, 4%). The most frequent positive history in the cohort (218) was family history of heart disease (56, 25%), racing or skipped beats (30, 14%), chest pain after exercise (28, 13%), family history of SCD before age 50 (21, 10%). Follow up data was obtained, to date, in 130/218 (60%) positive screening participants and 72/130 (55%) had the suspected diagnosis confirmed. Of 130, 42 (32%) were reached and are alive at median follow up of 5.3 years. Conclusions: Our data shows 3.2% ECG and 2% ECHO positive screening for suspected cardiovascular abnl. Screening results may improve with better utilization of ECG criteria in athletes and lower referral based on ECHO findings that may represent normal pattern in certain populations. Follow up remains a challenge to determine long term outcomes of athlete screening.

Left ventricular noncompaction: the importance of identifying high-risk patients within the scope of left ventricular hypertrabeculation

Abstract Introduction Prominent left ventricular (LV) trabeculation is frequently encountered, however LV noncompaction (LVNC) criteria are not always fulfilled. The clinical and prognostic significance of these findings remains unclear. Objectives To characterize the patients (P) with echocardiographic suspicion of LVNC and to assess clinical outcomes. Methods Retrospective single-centre study that included all echocardiograms between January 2018 and June 2020 perceiving LV hypertrabeculation. The cohort underwent diagnostic assessment for LVNC by Chin and Jenni criteria. Baseline characteristics were evaluated. Composite endpoint of cardiovascular death, heart failure (HF) hospitalization, ventricular arrythmias (VA) and nonfatal stroke was considered. Results 51P, 75% male, mean age 50±18 years. 35P (69%) had associated heart conditions, of which 57% had other known cardiomyopathy (mainly dilated cardiomyopathy), 14% congenital, 26% ischemic and 3% valvular heart disease. 2P were in postpartum period and 1P was an athlete. Family history of cardiomyopathy was present in 8P (16%). 12P underwent genetic testing, with TTN and MYH7 mutations being the most frequently detected. Prior clinical HF was reported in 53%, previous stroke in 14%, and non-sustained and sustained VA in 24% and 4%, respectively. Mean NYHA classification was 1.8±0.7, with 31% being asymptomatic. The prevalence of LVNC by Chin criteria was 31% and by Jenni criteria was 55%. 32P (63%) met at least one LVNC criteria. This group was younger (45±18 vs 59±15, p=0.004), had higher NT-proBNP levels (3644±2819 vs 389±640, p=0.048) and QRS fragmentation (59% vs 21%, p=0.027). Significantly higher LV end-diastolic volume (84 (41) vs 64 (28)ml/m2, p=0.008) and end-systolic volume (51 (37) vs 35 (20)ml/m2, p=0.004), along with lower LV ejection fraction (39±12 vs 49±13%, p=0.009) and global longitudinal strain (−11±5 vs −17±4%, p=0.003) were noticed. P who met LVNC criteria also had higher number of affected LV segments (6.4±1.8 vs 4.2±1.6, p&amp;lt;0.001). Over a mean follow-up of 18±9 months, the incidence of composite endpoint was 35%. Univariate Cox analysis showed a significant association between the presence of LVNC criteria and adverse outcomes (HR: 5.108, 95% CI: 1.682–11.236, p=0.030) (Fig. 1). Conclusion LV hypertrabeculation can be encountered in a variety of clinical scenarios and often overlaps with other heart diseases. P satisfying criteria for LVNC had more impairment in LV performance and worse clinical outcomes. Funding Acknowledgement Type of funding sources: None. Figure 1

Left ventricular characteristics of noncompaction phenotype patients with good ejection fraction measured with cardiac magnetic resonance.

We describe left ventricular (LV) volumes, myocardial and trabeculated muscle mass and strains with Cardiac magnetic resonance of a large cohort (n=81) who fulfilled the morphologic criteria of left ventricular noncompaction (LVNC) and had good ejection fraction (EF >55%) and compare them with healthy controls (n=81). Male and female patients were compared to matched controls and to each other. We also investigated the LV trabeculated muscle mass cutoff in male and female patients with LVNC. 81 participants with LVNC and 81 healthy controls were included. Male and female patients were compared to matched controls and to each other. We also investigated the left ventricular trabeculated muscle mass cut-off in male and female LVNC patients. The LV parameters of the LVNC population were normal, but they had significantly higher volumes, myocardial and trabeculated muscle mass, and a significantly smaller EF than the controls. Similar differences were observed after stratifying by sex. The optimal LV trabeculated muscle mass cutoffs were 25.8 g/m2 in men (area under the curve: 0.81) and 19.0 g/m2 in women (area under the curve: 0.87). The patients had normal global strains but a significantly worse global circumferential strain (patients vs controls: -29.9±4.9 vs. -35.8±4.7%, p<0.05) and significantly higher circumferential mechanical dispersion than the controls (patients vs. controls: 7.6±4.2 vs. 6.1±2.8%; p<0.05). No disease-related strain differences were noted between men and women. The LV functional and strain characteristics of the LVNC cohort differed significantly from those of healthy participants; this might be caused by increased LV trabeculation, and its clinical relevance might be questionable. The LV trabeculated muscle mass was very different between men and women; thus, the use of sex-specific morphologic diagnostic criteria should be considered.

Right ventricular non-compaction: myth or reality?

Abstract Funding Acknowledgements Type of funding sources: None. Noncompaction cardiomyopathy (NCMP) is characterized by excessive left ventricular (LV) trabeculation. The involvement of the right ventricle (RV) is still questionable, furthermore, the normal range for RV trabeculation is undefined. Our aim was to describe the RV functional and strain values of patients with NCMP with preserved LV ejection fraction (EF) using cardiac MRI and to compare these parameters with healthy control subjects, furthermore, we aimed to define the normal range for RV trabeculation. We included 81 NCMP patients with good LV-EF (mean age: 37.0 ± 14 years; EF: 69.4 ± 13.2%) and without comorbidities. Their parameters were compared to an age and sex matched control group (mean age: 37.2 ± 13.7 years; EF: 77.2 ± 15.0%). MR examinations were performed with 1,5T Philips Achieva and Siemens Aera devices. The Medis Suite software was used for post-processing analysis, the MedCalc software for statistics, p &amp;lt; 0.05 was considered statistically significant. The RV trabecular mass index (RV-TRABi) was significantly greater and the RV-EF significantly smaller in the NCMP group compared with the controls (NCMP vs. control; TRABi: 20.6 ± 7.0 vs. 16.9 ± 4.2 g/m2; RV-EF: 62.8 ± 5.5 vs. 64.5 ± 4.5%; p &amp;lt; 0.05). As for the RV global longitudinal strain (GLS) the results were close to significant (NCMP vs. control: -25.1 ± 4.0 vs. -26.4 ± 4.3%; p = 0.05). We defined the normal range of RV-TRABi with a lower limit of 8.2 g/m2 (90% confidence interval (CI): 6.8-9.5) and the upper limit of 22.1 g/m2 (90% CI: 23.6-26.5). 27.2% of the NCMP patients exceeded the upper limit of RV-TRABi. The described differences in the RV-EF, RV-TRABi and RV-GLS draws attention to the possibility of the involvement of RV in patients with NCMP. Further follow-up studies would be necessary to evaluate the clinical importance of these alterations.

Deep Learning-based Automated Segmentation of Left Ventricular Trabeculations and Myocardium on Cardiac MR Images: A Feasibility Study.

To develop and evaluate a complete deep learning pipeline that allows fully automated end-diastolic left ventricle (LV) cardiac MRI segmentation, including trabeculations and automatic quality control of the predicted segmentation. This multicenter retrospective study includes training, validation, and testing datasets of 272, 27, and 150 cardiac MR images, respectively, collected between 2012 and 2018. The reference standard was the manual segmentation of four LV anatomic structures performed on end-diastolic short-axis cine cardiac MRI: LV trabeculations, LV myocardium, LV papillary muscles, and the LV blood cavity. The automatic pipeline was composed of five steps with a DenseNet architecture. Intraobserver agreement, interobserver agreement, and interaction time were recorded. The analysis includes the correlation between the manual and automated segmentation, a reproducibility comparison, and Bland-Altman plots. The automated method achieved mean Dice coefficients of 0.96 ± 0.01 (standard deviation) for LV blood cavity, 0.89 ± 0.03 for LV myocardium, and 0.62 ± 0.08 for LV trabeculation (mean absolute error, 3.63 g ± 3.4). Automatic quantification of LV end-diastolic volume, LV myocardium mass, LV trabeculation, and trabeculation mass-to-total myocardial mass (TMM) ratio showed a significant correlation with the manual measures (r = 0.99, 0.99, 0.90, and 0.83, respectively; all P < .01). On a subset of 48 patients, the mean Dice value for LV trabeculation was 0.63 ± 0.10 or higher compared with the human interobserver (0.44 ± 0.09; P < .01) and intraobserver measures (0.58 ± 0.09; P < .01). Automatic quantification of the trabeculation mass-to-TMM ratio had a higher correlation (0.92) compared with the intra- and interobserver measures (0.74 and 0.39, respectively; both P < .01). Automated deep learning framework can achieve reproducible and quality-controlled segmentation of cardiac trabeculations, outperforming inter- and intraobserver analyses.Supplemental material is available for this article.© RSNA, 2020.

Left ventricular non-compaction cardiomyopathy: how many needles in the haystack?

### Learning objectives Left ventricular non-compaction cardiomyopathy (LVNC) remains a subject of unsettled debate between those who perceive it to be a primary genetic cardiomyopathy1 and those who believe excessive...

Left Ventricular Hypertrabeculation Is Not Associated With Cardiovascular Morbity or Mortality: Insights From the Eurocmr Registry.

Aim: Left ventricular non-compaction (LVNC) is perceived as a rare high-risk cardiomyopathy characterized by excess left ventricular (LV) trabeculation. However, there is increasing evidence contesting the clinical significance of LV hyper-trabeculation and the existence of LVNC as a distinct cardiomyopathy. The aim of this study is to assess the association of LV trabeculation extent with cardiovascular morbidity and all-cause mortality in patients undergoing clinical cardiac magnetic resonance (CMR) scans across 57 European centers from the EuroCMR registry.Methods and Results: We studied 822 randomly selected cases from the EuroCMR registry. Image acquisition was according to international guidelines. We manually segmented images for LV chamber quantification and measurement of LV trabeculation (as per Petersen criteria). We report the association between LV trabeculation extent and important cardiovascular morbidities (stroke, atrial fibrillation, heart failure) and all-cause mortality prospectively recorded over 404 ± 82 days of follow-up. Maximal non-compaction to compaction ratio (NC/C) was mean (standard deviation) 1.81 ± 0.67, from these, 17% were above the threshold for hyper-trabeculation (NC/C > 2.3). LV trabeculation extent was not associated with increased risk of the defined outcomes (morbidities, mortality, LV CMR indices) in the whole cohort, or in sub-analyses of individuals without ischaemic heart disease, or those with NC/C > 2.3.Conclusion: Among 882 patients undergoing clinical CMR, excess LV trabeculation was not associated with a range of important cardiovascular morbidities or all-cause mortality over ~12 months of prospective follow-up. These findings suggest that LV hyper-trabeculation alone is not an indicator for worse cardiovascular prognosis.

Exercise-induced left ventricular trabeculation- what’s the evidence?

Exercise-induced left ventricular trabeculation- what’s the evidence?

Prevalence and significance of isolated left ventricular non-compaction phenotype in normal black Africans using echocardiography

BackgroundSeveral large, prospective screening studies of predominantly Caucasian patients have suggested that hypertrabeculation may not necessarily be pathologic unless there is concomitant left ventricular (LV) dysfunction, LV dilatation, history of arrhythmia, family history, or characteristic gene mutations. This conundrum may be magnified in blacks, in whom hypertrabeculation and LV hypertrophy is more common. We therefore investigated the frequency of hypertrabeculation/isolated LV noncompaction (ILVNC) phenotype in normal black Africans and evaluated LV function using sensitive measures of deformation and twist.MethodsTwo hundred and fifty-three volunteers were recruited and evaluated according to strict inclusion and exclusion criteria. Their mean age was 36.3 ± 12.2 years.ResultsTrabeculations were found in 12 (4.74%) participants. Three (1.2%) subjects had ≥ 4 LV trabeculations. The LV apex was the most common anatomical site for the location of trabeculations. Subjects with trabeculations were more likely to be males of a younger age, and had greater LV end-diastolic and end-systolic parameters and lateral e’. However, 0.8% of the population fulfilled the Stollberger criteria, and none fulfilled the Jenni, Milwaukee, or Baragwanath criteria. All subjects in this study had normal rotation patterns with no differences in rotational parameters or net twist.ConclusionsTrabeculations may be found as a normal variant in black Africans. Assessing trabeculations alone may infer ILVNC; however, utilizing the more comprehensive ILVNC criteria enables differentiation of a possible LVNC phenotype. Normal individuals with hypertrabeculation have normal LV function and normal rotation patterns, with no differences in rotational parameters or net twist.

Left ventricular trabeculation and major adverse cardiovascular events: the Copenhagen General Population Study

Prominent left ventricular trabeculations is a phenotypic trait observed in cardiovascular diseases. In the general population, the extent of left ventricular trabeculations is highly variable, yet it is unknown whether increased trabeculation is associated with adverse outcome. Left ventricular trabeculated mass (g/m2) was measured with contrast-enhanced cardiac computed tomography in 10 097 individuals from the Copenhagen General Population Study. The primary endpoint was a composite of major adverse cardiovascular events and defined as death, heart failure, myocardial infarction, or stroke. The secondary endpoints were the individual components of the primary endpoint. Cox regression models were adjusted for clinical parameters, medical history, electrocardiographic parameters, and cardiac chamber sizes. The mean trabeculated mass was 19.1 g/m2 (standard deviation 4.9 g/m2). During a median follow-up of 4.0 years (interquartile range 1.5-6.7), 710 major adverse cardiovascular events occurred in 619 individuals. Individuals with a left ventricular trabeculated mass in the highest quartile had a hazard ratio for major adverse cardiovascular events of 1.64 [95% confidence interval (CI) 1.30-2.08; P < 0.001] compared to those in the lowest quartile. Corresponding hazard ratios were 2.08 (95% CI 1.38-3.14; P < 0.001) for death, 2.63 (95% CI 1.61-4.31; P < 0.001) for heart failure, 1.08 (95% CI 0.56-2.08; P = 0.82) for myocardial infarction, and 1.07 (95% CI 0.72-1.57; P = 0.74) for stroke. Increased left ventricular trabeculation is independently associated with an increased rate of major adverse cardiovascular events in the general population.