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Journal articles on the topic 'Left ventricular trabeculation model'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Sigvardsen, Per E., Andreas Fuchs, Jørgen T. Kühl, Shoaib Afzal, Lars Køber, Børge G. Nordestgaard, and Klaus F. Kofoed. "Left ventricular trabeculation and major adverse cardiovascular events: the Copenhagen General Population Study." European Heart Journal - Cardiovascular Imaging 22, no. 1 (May 9, 2020): 67–74. http://dx.doi.org/10.1093/ehjci/jeaa110.

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Abstract Aims 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. Methods and results 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. Conclusion Increased left ventricular trabeculation is independently associated with an increased rate of major adverse cardiovascular events in the general population.

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2

Breckenridge, Ross A., Robert H. Anderson, and Perry M. Elliott. "Isolated left ventricular non-compaction: the case for abnormal myocardial development." Cardiology in the Young 17, no. 2 (February 26, 2007): 124–29. http://dx.doi.org/10.1017/s1047951107000273.

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Isolated ventricular non-compaction is an increasingly commonly diagnosed myocardial disorder characterised by excessive and prominent trabeculation of the morphologically left, and occasionally the right, ventricle. This is associated with high rates of thromboembolism, cardiac failure, and cardiac arrhythmia. Recent improvements in understanding the embryonic processes underlying ventricular formation have led to the hypothesis that ventricular non-compaction is due to a failure of normal ventriculogenesis, leading to abnormal myocardium which may present clinically many years later. Experimental work in animal models provides several candidate transcription factors and signalling molecules that could, in theory, cause ventricular non-compaction if disrupted.

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3

Hirono, Keiichi, Yukiko Hata, Nariaki Miyao, Mako Okabe, Shinya Takarada, Hideyuki Nakaoka, Keijiro Ibuki, et al. "Left Ventricular Noncompaction and Congenital Heart Disease Increases the Risk of Congestive Heart Failure." Journal of Clinical Medicine 9, no. 3 (March 13, 2020): 785. http://dx.doi.org/10.3390/jcm9030785.

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Background: Left ventricular noncompaction (LVNC) is a hereditary cardiomyopathy that is associated with high morbidity and mortality rates. Recently, LVNC was classified into several phenotypes including congenital heart disease (CHD). However, although LVNC and CHD are frequently observed, the role and clinical significance of genetics in these cardiomyopathies has not been fully evaluated. Therefore, we aimed to evaluate the impact on the perioperative outcomes of children with concomitant LVNC and CHD using next-generation sequencing (NGS). Methods: From May 2000 to August 2018, 53 Japanese probands with LVNC (25 males and 28 females) were enrolled and we screened 182 cardiomyopathy-associated genes in these patients using NGS. Results: The age at diagnosis of the enrolled patients ranged from 0 to 14 years (median: 0.3 months). A total of 23 patients (43.4%) were diagnosed with heart failure, 14 with heart murmur (26.4%), and 6 with cyanosis (11.3%). During the observation period, 31 patients (58.5%) experienced heart failure and 13 (24.5%) developed arrhythmias such as ventricular tachycardia, supraventricular tachycardia, and atrioventricular block. Moreover, 29 patients (54.7%) had ventricular septal defects (VSDs), 17 (32.1%) had atrial septal defects, 10 had patent ductus arteriosus (PDA), and 7 (13.2%) had Ebstein’s anomaly and double outlet right ventricle. Among the included patients, 30 underwent surgery, 19 underwent biventricular repair, and 2 underwent pulmonary artery banding, bilateral pulmonary artery banding, and PDA ligation. Overall, 30 genetic variants were identified in 28 patients with LVNC and CHD. Eight variants were detected in MYH7 and two in TPM1. Echocardiography showed lower ejection fractions and more thickened trabeculations in the left ventricle in patients with LVNC and CHD than in age-matched patients with VSDs. During follow-up, 4 patients died and the condition of 8 worsened postoperatively. The multivariable proportional hazards model showed that heart failure, LV ejection fraction of < 24%, LV end-diastolic diameter z-score of > 8.56, and noncompacted-to-compacted ratio of the left ventricular apex of > 8.33 at the last visit were risk factors for survival. Conclusions: LVNC and CHD are frequently associated with genetic abnormalities. Knowledge of the association between CHD and LVNC is important for the awareness of clinical implications during the preoperative and postoperative periods to identify the populations who are at an increased risk of additional morbidity.

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4

Stöllberger, Claudia, and Josef Finsterer. "Trabeculation and left ventricular hypertrabeculation/noncompaction." Journal of the American Society of Echocardiography 17, no. 10 (October 2004): 1120–21. http://dx.doi.org/10.1016/j.echo.2004.06.009.

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5

D’Silva, Andrew. "Physical Activity–Related Left Ventricular Trabeculation." Journal of the American College of Cardiology 77, no. 5 (February 2021): 662–63. http://dx.doi.org/10.1016/j.jacc.2020.11.054.

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6

Stöllberger, Claudia, Josef Finsterer, Ferdinand Rudolf Waldenberger, Johann Andreas Hainfellner, and Robert Ullrich. "Intramyocardial hematoma mimicking abnormal left ventricular trabeculation." Journal of the American Society of Echocardiography 14, no. 10 (October 2001): 1030–32. http://dx.doi.org/10.1067/mje.2001.115688.

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7

McNally, Elizabeth M., and Amit R. Patel. "Cardiac Magnetic Resonance of Left Ventricular Trabeculation." Circulation: Cardiovascular Imaging 4, no. 2 (March 2011): 84–86. http://dx.doi.org/10.1161/circimaging.110.962472.

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8

Fernández-Golfín, Covadonga, and José Zamorano Gómez. "Left ventricular trabeculation assessment with cardiac magnetic resonance." Journal of Cardiovascular Medicine 11, no. 7 (July 2010): 477. http://dx.doi.org/10.2459/jcm.0b013e32833833bc.

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9

Shieh, Joseph T. C., John L. Jefferies, and Alvin J. Chin. "Disorders of left ventricular trabeculation/compaction or right ventricular wall formation." American Journal of Medical Genetics Part C: Seminars in Medical Genetics 163, no. 3 (July 10, 2013): 141–43. http://dx.doi.org/10.1002/ajmg.c.31370.

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10

Gati, Sabiha, Ahmed Merghani, and Sanjay Sharma. "Increased Left Ventricular Trabeculation Does Not Necessarily Equate to Left Ventricular Noncompaction in Athletes." JAMA Internal Medicine 175, no. 3 (March 1, 2015): 461. http://dx.doi.org/10.1001/jamainternmed.2014.7186.

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11

Peritz, David C., and Eugene H. Chung. "Increased Left Ventricular Trabeculation Does Not Necessarily Equate to Left Ventricular Noncompaction in Athletes." JAMA Internal Medicine 175, no. 7 (July 1, 2015): 1247. http://dx.doi.org/10.1001/jamainternmed.2015.3109.

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12

Woodbridge, Simon P., Nay Aung, Jose M. Paiva, Mihir M. Sanghvi, Filip Zemrak, Kenneth Fung, and Steffen E. Petersen. "Physical activity and left ventricular trabeculation in the UK Biobank community-based cohort study." Heart 105, no. 13 (February 5, 2019): 990–98. http://dx.doi.org/10.1136/heartjnl-2018-314155.

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ObjectiveVigorous physical activity (PA) in highly trained athletes has been associated with heightened left ventricular (LV) trabeculation extent. It has therefore been hypothesised that LV trabeculation extent may participate in exercise-induced physiological cardiac remodelling. Our cross-sectional observational study aimed to ascertain whether there is a ‘dose–response’ relationship between PA and LV trabeculation extent and whether this could be identified at opposite PA extremes.MethodsIn a cohort of 1030 individuals from the community-based UK Biobank study (male/female ratio: 0.84, mean age: 61 years), PA was measured via total metabolic equivalent of task (MET) min/week and 7-day average acceleration, and trabeculation extent via maximal non-compaction/compaction ratio (NC/C) in long-axis images of cardiovascular magnetic resonance studies. The relationship between PA and NC/C was assessed by multivariate regression (adjusting for potential confounders) as well as between demographic, anthropometric and LV phenotypic parameters and NC/C.ResultsThere was no significant linear relationship between PA and NC/C (full adjustment, total MET-min/week: ß=−0.0008, 95% CI −0.039 to –0.037, p=0.97; 7-day average acceleration: ß=−0.047, 95% CI −0.110 to –0.115, p=0.13, per IQR increment in PA), or between extreme PA quintiles (full adjustment, total MET-min/week: ß=−0.026, 95% CI −0.146 to –0.094, p=0.67; 7-day average acceleration: ß=−0.129, 95% CI −0.299 to –0.040, p=0.49), across all adjustment levels. A negative relationship was identified between left ventricular ejection fraction and NC/C, significantly modified by PA (ß difference=−0.006, p=0.03).ConclusionsIn a community-based general population cohort, there was no relationship at, or between, extremes, between PA and NC/C, suggesting that at typical general population PA levels, trabeculation extent is not influenced by PA changes.

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13

McGee, Michael, Luke Warner, and Nicholas Collins. "Ebstein’s Anomaly, Left Ventricular Noncompaction, and Sudden Cardiac Death." Case Reports in Cardiology 2015 (2015): 1–3. http://dx.doi.org/10.1155/2015/854236.

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Ebstein’s anomaly is a congenital disorder characterized by apical displacement of the septal leaflet of the tricuspid valve. Ebstein’s anomaly may be seen in association with other cardiac conditions, including patent foramen ovale, atrial septal defect, and left ventricular noncompaction (LVNC). LVNC is characterized by increased trabeculation within the left ventricular apex. Echocardiography is often used to diagnose LVNC; however, magnetic resonance (MR) imaging offers superior characterization of the myocardium. We report a case of sudden cardiac death in a patient with Ebstein’s anomaly with unrecognized LVNC noted on post mortem examination with screening documenting the presence of LVNC in one of the patient’s twin sons.

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14

Papadopoulos, Kyriacos, Petros M. Petrou, and Demos Michaelides. "Left Ventricular Noncompaction Cardiomyopathy Presenting with Heart Failure in a 35-Year-Old Man." Texas Heart Institute Journal 44, no. 4 (August 1, 2017): 260–63. http://dx.doi.org/10.14503/thij-15-5371.

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Isolated ventricular noncompaction, a rare genetic cardiomyopathy, is thought to be caused by the arrest of normal myocardial morphogenesis. It is characterized by prominent, excessive trabeculation in a ventricular wall segment and deep intertrabecular recesses perfused from the ventricular cavity. The condition can present with heart failure, systematic embolic events, and ventricular arrhythmias. Two-dimensional echocardiography is the typical diagnostic method. We report a case of heart failure in a 35-year-old man who presented with palpitations. Two-dimensional echocardiograms revealed left ventricular noncompaction, which markedly improved after standard heart failure therapy.

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15

Stöllberger, Claudia, Josef Finsterer, and Gerhard Blazek. "Isolated Left Ventricular Abnormal Trabeculation Is a Cardiac Manifestation of Neuromuscular Disorders." Cardiology 94, no. 1 (2000): 72–76. http://dx.doi.org/10.1159/000007050.

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16

Finsterer, Josef, Gerhard Blazer, Claudia Stöllberger, Andreas Valentin, and Dimiter Tscholakoff. "Isolated left ventricular abnormal trabeculation in adults is associated with neuromuscular disorders." Clinical Cardiology 22, no. 2 (February 1999): 119–23. http://dx.doi.org/10.1002/clc.4960220212.

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17

André, Florian, Astrid Burger, Dirk Loßnitzer, Sebastian J. Buss, Hassan Abdel-Aty, Evangelos Gianntisis, Henning Steen, and Hugo A. Katus. "Reference values for left and right ventricular trabeculation and non-compacted myocardium." International Journal of Cardiology 185 (April 2015): 240–47. http://dx.doi.org/10.1016/j.ijcard.2015.03.065.

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18

Zhang, Wenjun, Hanying Chen, Xiuxia Qu, Ching-Pin Chang, and Weinian Shou. "Molecular mechanism of ventricular trabeculation/compaction and the pathogenesis of the left ventricular noncompaction cardiomyopathy (LVNC)." American Journal of Medical Genetics Part C: Seminars in Medical Genetics 163, no. 3 (July 10, 2013): 144–56. http://dx.doi.org/10.1002/ajmg.c.31369.

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19

Bernabé, Gregorio, Javier Cuenca, Domingo Giménez, and Josefa González-Carrillo. "A Training Engine for Automatic Quantification of Left Ventricular Trabeculation from Cardiac MRI." Procedia Computer Science 80 (2016): 2246–50. http://dx.doi.org/10.1016/j.procs.2016.05.399.

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20

Gati, S., M. Papadakis, N. Van Niekerk, M. Reed, T. Yeghen, and S. Sharma. "Increased left ventricular trabeculation in individuals with sickle cell anaemia: Physiology or pathology?" International Journal of Cardiology 168, no. 2 (September 2013): 1658–60. http://dx.doi.org/10.1016/j.ijcard.2013.03.039.

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21

Yoo, Shi-Joon, Siew Yen Ho, Philip J. Kilner, Jeong-Wook Seo, and Robert H. Anderson. "Sectional anatomy of the ventricular septal defect in double outlet right ventricle—correlation of magnetic resonance images from autopsied hearts with anatomic sections." Cardiology in the Young 3, no. 2 (April 1993): 118–23. http://dx.doi.org/10.1017/s1047951100001372.

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AbstractA ventricular septal defect is, almost always, an integral part of double outlet right ventricle and has been classified into the subaortic, subpulmonary, doubly committed and non-committed varieties. This study was performed to correlate the cross-sectional imaging characteristics of such ventricular septal defect in double outlet right ventricles using pathological specimens. The extent and the orientation of the outlet septum were the most important in the differentiation of the four varieties of ventricular septal defect. In the subaortic variety, the outlet septum fused with the left anterior margin of the defect, this being marked by the anterior limb of the septomarginal trabeculation. In the subpulmonary variety, the outlet septum fused with the right posterior margin of the defect, this being the posterior limb of the septomarginal trabeculation. The outlet septum was vestigial in case with doubly committed defects. In those with non-committed defects, the defect was not shown in those images or sections which demonstrated the outlet septum.

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22

Bernabé, Gregorio, José D. Casanova, Josefa González-Carrillo, and Juan R. Gimeno-Blanes. "Towards an Enhanced Tool for Quantifying the Degree of LV Hyper-Trabeculation." Journal of Clinical Medicine 10, no. 3 (February 1, 2021): 503. http://dx.doi.org/10.3390/jcm10030503.

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Left ventricular non-compaction (LVNC) is defined by an increase of trabeculations in left ventricular (LV) endomyocardium. Although LVNC can be in isolation, an increase in hypertrabeculation often accompanies genetic cardiomyopathies. Current methods for quantification of LV trabeculae have limitations. Several improvements are proposed and implemented to enhance a software tool to quantify the trabeculae degree in the LV myocardium in an accurate and automatic way for a population of patients with genetic cardiomyopathies (QLVTHCI). The software tool is developed and evaluated for a population of 59 patients (470 end-diastole cardiac magnetic resonance images). This tool produces volumes of the compact sector and the trabecular area, the proportion between these volumes, and the left ventricular and trabeculated masses. Substantial enhancements are obtained over the manual process performed by cardiologists, so saving important diagnosis time. The parallelization of the detection of the external layer is proposed to ensure real-time processing of a patient, obtaining speed-ups from 7.5 to 1500 with regard to QLVTHCI and the manual process used traditionally by cardiologists. Comparing the method proposed with the fractal proposal to differentiate LVNC and non-LVNC patients among 27 subjects with previously diagnosed cardiomyopathies, QLVTHCI presents a full diagnostic accuracy, while the fractal criteria achieve 78%. Moreover, QLTVHCI can be installed and integrated in hospitals on request, whereas the high cost of the license of the fractal method per year of this tool has prevented reproducibility by other medical centers.

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23

Zemrak, Filip, Mark A. Ahlman, Gabriella Captur, Saidi A. Mohiddin, Nadine Kawel-Boehm, Martin R. Prince, James C. Moon, et al. "The Relationship of Left Ventricular Trabeculation to Ventricular Function and Structure Over a 9.5-Year Follow-Up." Journal of the American College of Cardiology 64, no. 19 (November 2014): 1971–80. http://dx.doi.org/10.1016/j.jacc.2014.08.035.

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24

Gati, S., N. Van Niekerk, M. Reed, A. Cox, A. Zaidi, S. Ghani, N. Sheikh, M. Papadakis, T. Tula, and S. Sharma. "156 THE PREVALENCE OF INCREASED LEFT VENTRICULAR TRABECULATION IN INDIVIDUALS WITH SICKLE CELL ANAEMIA?" Heart 99, suppl 2 (May 2013): A91.2—A92. http://dx.doi.org/10.1136/heartjnl-2013-304019.156.

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25

Aleksova, Natasha, and Filio Billia. "Excessive Left Ventricular Trabeculation: New Evidence Points to Pathological Significance in a Previously Murky Area." Canadian Journal of Cardiology 36, no. 4 (April 2020): 462–63. http://dx.doi.org/10.1016/j.cjca.2019.10.026.

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26

Gati, Sabiha, Navin Chandra, Rachel Louise Bennett, Matt Reed, Gaelle Kervio, Vasileios F. Panoulas, Saqib Ghani, et al. "Increased left ventricular trabeculation in highly trained athletes: do we need more stringent criteria for the diagnosis of left ventricular non-compaction in athletes?" Heart 99, no. 6 (February 7, 2013): 401–8. http://dx.doi.org/10.1136/heartjnl-2012-303418.

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27

Naumova, Anna V., Gregory Kicska, Kiana Pimentel, Lauren E. Neidig, Hiroshi Tsuchida, Kenta Nakamura, and Charles E. Murry. "Quantitative Analyses of the Left Ventricle Volume and Cardiac Function in Normal and Infarcted Yucatan Minipigs." Journal of Imaging 7, no. 7 (July 1, 2021): 107. http://dx.doi.org/10.3390/jimaging7070107.

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(1) Background: The accuracy of the left ventricular volume (LVV) and contractility measurements with cardiac magnetic resonance imaging (CMRI) is decreased if the papillary muscles are abnormally enlarged, such as in hypertrophic cardiomyopathy in human patients or in pig models of human diseases. The purpose of this work was to establish the best method of LVV quantification with CMRI in pigs. (2) Methods: The LVV in 29 Yucatan minipig hearts was measured using two different techniques: the “standard method”, which uses smooth contouring along the endocardial surface and adds the papillary volume to the ventricular cavity volume, and the “detailed method”, which traces the papillary muscles and trabeculations and adds them to the ventricular mass. (3) Results: Papillary muscles add 21% to the LV mass in normal and infarcted hearts of Yucatan minipigs. The inclusion or exclusion of these from the CMRI analysis significantly affected the study results. In the normal pig hearts, the biggest differences were found in measurements of the LVV, ejection fraction (EF), LV mass and indices derived from the LV mass (p < 0.001). The EF measurement in the normal pig heart was 11% higher with the detailed method, and 19% higher in the infarcted pig hearts (p < 0.0001). The detailed method of endocardium tracing with CMRI closely represented the LV mass measured ex vivo. (4) Conclusions: The detailed method, which accounts for the large volume of the papillary muscles in the pig heart, provides better accuracy and interobserver consistency in the assessment of LV mass and ejection fraction, and might therefore be preferable for these analyses.

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de Boer, Bouke A., Jean-François Le Garrec, Vincent M. Christoffels, Sigolène M. Meilhac, and Jan M. Ruijter. "Integrating multi-scale knowledge on cardiac development into a computational model of ventricular trabeculation." Wiley Interdisciplinary Reviews: Systems Biology and Medicine 6, no. 6 (October 6, 2014): 389–97. http://dx.doi.org/10.1002/wsbm.1285.

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29

Bentatou, Z., M. Finas, P. Habert, F. Kober, M. Guye, S. Bricq, A. Lalande, et al. "Distribution of left ventricular trabeculation across age and gender in 140 healthy Caucasian subjects on MR imaging." Diagnostic and Interventional Imaging 99, no. 11 (November 2018): 689–98. http://dx.doi.org/10.1016/j.diii.2018.08.014.

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Im, JunYong, and Dong Su Kim. "Cardiac Papillary Fibroelastoma in Left Ventricular Trabeculation as a Potential Cause of Cerebral Infarction: A Case Report." Journal of the Korean Society of Radiology 82, no. 4 (2021): 988. http://dx.doi.org/10.3348/jksr.2020.0107.

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Samson, Françoise, Nicolas Bonnet, Michèle Heimburger, Catherine Rücker-Martin, Dimitri O. Levitsky, Guy M. Mazmanian, Jean-Jacques Mercadier, and Alain Serraf. "Left Ventricular Alterations in a Model of Fetal Left Ventricular Overload." Pediatric Research 48, no. 1 (July 2000): 43–49. http://dx.doi.org/10.1203/00006450-200007000-00010.

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32

Miao, Lianjie, Jingjing Li, Jian Li, Yangyang Lu, David Shieh, Joseph E. Mazurkiewicz, Margarida Barroso, et al. "Cardiomyocyte orientation modulated by the Numb family proteins–N-cadherin axis is essential for ventricular wall morphogenesis." Proceedings of the National Academy of Sciences 116, no. 31 (July 12, 2019): 15560–69. http://dx.doi.org/10.1073/pnas.1904684116.

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The roles of cellular orientation during trabecular and ventricular wall morphogenesis are unknown, and so are the underlying mechanisms that regulate cellular orientation. Myocardial-specific Numb and Numblike double-knockout (MDKO) hearts display a variety of defects, including in cellular orientation, patterns of mitotic spindle orientation, trabeculation, and ventricular compaction. Furthermore, Numb- and Numblike-null cardiomyocytes exhibit cellular behaviors distinct from those of control cells during trabecular morphogenesis based on single-cell lineage tracing. We investigated how Numb regulates cellular orientation and behaviors and determined that N-cadherin levels and membrane localization are reduced in MDKO hearts. To determine how Numb regulates N-cadherin membrane localization, we generated an mCherry:Numb knockin line and found that Numb localized to diverse endocytic organelles but mainly to the recycling endosome. Consistent with this localization, cardiomyocytes in MDKO did not display defects in N-cadherin internalization but rather in postendocytic recycling to the plasma membrane. Furthermore, N-cadherin overexpression via a mosaic model partially rescued the defects in cellular orientation and trabeculation of MDKO hearts. Our study unravels a phenomenon that cardiomyocytes display spatiotemporal cellular orientation during ventricular wall morphogenesis, and its disruption leads to abnormal trabecular and ventricular wall morphogenesis. Furthermore, we established a mechanism by which Numb modulates cellular orientation and consequently trabecular and ventricular wall morphogenesis by regulating N-cadherin recycling to the plasma membrane.

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G. Almeida, Ana. "Comment on “The relationship of left ventricular trabeculation to ventricular function and structure over a 9.5 year follow-up. The MESA study“." Revista Portuguesa de Cardiologia (English Edition) 34, no. 2 (February 2015): 147–49. http://dx.doi.org/10.1016/j.repce.2015.02.003.

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Douglas, K., D. Graham, W. Crawford, MW McBride, and AF Dominiczak. "LEFT VENTRICULAR FUNCTION IN A MODEL OF LEFT VENTRICULAR HYPERTROPHY: 4C.02." Journal of Hypertension 28 (June 2010): e213. http://dx.doi.org/10.1097/01.hjh.0000378854.46256.4f.

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Marchal, P., O. Lairez, T. Cognet, V. Chabbert, P. Barrier, M. Berry, S. Mejean, et al. "Relationship between left ventricular sphericity and trabeculation indexes in patients with dilated cardiomyopathy: a cardiac magnetic resonance study." European Heart Journal - Cardiovascular Imaging 14, no. 9 (May 3, 2013): 914–20. http://dx.doi.org/10.1093/ehjci/jet064.

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Millner, Russell W. J., Jessica M. Mann, Ian Pearson, and John R. Pepper. "Experimental model of left ventricular failure." Annals of Thoracic Surgery 52, no. 1 (July 1991): 78–83. http://dx.doi.org/10.1016/0003-4975(91)91424-t.

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37

Kawamura, Takayuki, Masakazu Yasuda, Mana Okune, Kazuyoshi Kakehi, Yoshinori Kagioka, Takashi Nakamura, Shunichi Miyazaki, and Yoshitaka Iwanaga. "Increased Left Ventricular Trabeculation Is Associated With Increased B-Type Natriuretic Peptide Levels and Impaired Outcomes in Nonischemic Cardiomyopathy." Canadian Journal of Cardiology 36, no. 4 (April 2020): 518–26. http://dx.doi.org/10.1016/j.cjca.2019.09.012.

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38

Masso, Anthony H., Carlo Uribe, James T. Willerson, Benjamin Y. Cheong, and Barry R. Davis. "Left Ventricular Noncompaction Detected by Cardiac Magnetic Resonance Screening: A Reexamination of Diagnostic Criteria." Texas Heart Institute Journal 47, no. 3 (June 1, 2020): 183–93. http://dx.doi.org/10.14503/thij-19-7157.

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In a previous cross-sectional screening study of 5,169 middle and high school students (mean age, 13.1 ± 1.78 yr) in which we estimated the prevalence of high-risk cardiovascular conditions associated with sudden cardiac death, we incidentally detected by cardiac magnetic resonance (CMR) 959 cases (18.6%) of left ventricular noncompaction (LVNC) that met the Petersen diagnostic criterion (noncompaction:compaction ratio >2.3). Short-axis CMR images were available for 511 of these cases (the Short-Axis Study Set). To determine how many of those cases were truly abnormal, we analyzed the short-axis images in terms of LV structural and functional variables and applied 3 published diagnostic criteria besides the Petersen criterion to our findings. The estimated prevalences were 17.5% based on trabeculated LV mass (Jacquier criterion), 7.4% based on trabeculated LV volume (Choi criterion), and 1.3% based on trabeculated LV mass and distribution (Grothoff criterion). Absent longitudinal clinical outcomes data or accepted diagnostic standards, our analysis of the screening data from the Short-Axis Study Set did not definitively differentiate normal from pathologic cases. However, it does suggest that many of the cases might be normal anatomic variants. It also suggests that cases marked by pathologically excessive LV trabeculation, even if asymptomatic, might involve unsustainable physiologic disadvantages that increase the risk of LV dysfunction, pathologic remodeling, arrhythmias, or mural thrombi. These disadvantages may escape detection, particularly in children developing from prepubescence through adolescence. Longitudinal follow-up of suspected LVNC cases to ascertain their natural history and clinical outcome is warranted.

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39

Ootaki, Yoshio, Hirotsugu Yamada, Masao Daimon, Keiji Kamohara, Zoran Popović, David Van Wagoner, Yuanna Cheng, and Kiyotaka Fukamachi. "An Experimental Rabbit Model for Off-Pump Left Ventricular Reconstruction Following Left Ventricular Aneurysm." Heart Surgery Forum 9, no. 5 (October 1, 2006): E786—E791. http://dx.doi.org/10.1532/hsf98.20061035.

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40

WOODARD, JOHN C., DAVID J. FARRAR, EDNA CHOW, WILLIAM P. SANTAMORE, DANIEL BURKHOFF, and J. DONALD HILL. "Computer Model of Ventricular Interaction During Left Ventricular Circulatory Support." ASAIO Transactions 35, no. 3 (July 1989): 439–41. http://dx.doi.org/10.1097/00002216-198907000-00086.

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41

WOODARD, JOHN C., DAVID J. FARRAR, EDNA CHOW, WILLIAM P. SANTAMORE, DANIEL BURKHOFF, and J. DONALD HILL. "Computer Model of Ventricular Interaction During Left Ventricular Circulatory Support." ASAIO Transactions 35, no. 3 (July 1989): 439–41. http://dx.doi.org/10.1097/00002480-198907000-00086.

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42

Gati, S., K. Melchiorre, M. Papadakis, N. Sheikh, S. Ghani, A. Zaidi, B. Thllaganathan, and S. Sharma. "155 INCREASED LEFT VENTRICULAR TRABECULATION IN AFRO-CARIBBEAN INDIVIDUALS: AN INHERITED CARDIOMYOPATHY OR A PHYSIOLOGICAL RESPONSE TO INCREASED CARDIAC PRELOAD." Heart 99, suppl 2 (May 2013): A91.1—A91. http://dx.doi.org/10.1136/heartjnl-2013-304019.155.

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43

Hanna, J., S. McKenzie, D. Platts, M. Brown, G. Javorsky, A. McCann, P. Larsen, W. Strugnell, and C. Hamilton-Craig. "Six Year Follow Up and Outcome of Cardiac Magnetic Resonance Detected Left Ventricular Trabeculation Without Non-compaction in Dilated Cardiomyopathy." Heart, Lung and Circulation 21 (January 2012): S224. http://dx.doi.org/10.1016/j.hlc.2012.05.553.

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44

Waterford, Robert R., Joseph R. Van Camp, Marsha A. Gallagher, Michael T. Anderson, Steven F. Bolling, and Louis A. Brunsting. "Adjustable Model of Chronic Left Ventricular Dysfunction." Annals of Thoracic Surgery 64, no. 6 (December 1997): 1682–85. http://dx.doi.org/10.1016/s0003-4975(97)01019-9.

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45

Markovitz, Lawrence J., Edward B. Savage, Mark B. Ratcliffe, Joseph E. Bavaria, Gerhard Kreiner, Renato V. Iozzo, W. Clark Hargrove, Daniel K. Bogen, and L. Henry Edmunds. "Large animal model of left ventricular aneurysm." Annals of Thoracic Surgery 48, no. 6 (December 1989): 838–45. http://dx.doi.org/10.1016/0003-4975(89)90682-6.

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46

Letsou, George V., Thomas D. Pate, Jeffrey R. Gohean, Mark Kurusz, Raul G. Longoria, Larry Kaiser, and Richard W. Smalling. "Improved left ventricular unloading and circulatory support with synchronized pulsatile left ventricular assistance compared with continuous-flow left ventricular assistance in an acute porcine left ventricular failure model." Journal of Thoracic and Cardiovascular Surgery 140, no. 5 (November 2010): 1181–88. http://dx.doi.org/10.1016/j.jtcvs.2010.03.043.

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47

Sankova, Barbora, Jakub Machalek, and David Sedmera. "Effects of mechanical loading on early conduction system differentiation in the chick." American Journal of Physiology-Heart and Circulatory Physiology 298, no. 5 (May 2010): H1571—H1576. http://dx.doi.org/10.1152/ajpheart.00721.2009.

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Abstract:

The primary ring, a horseshoe-shaped structure situated between the left and right ventricle and connected superiorly to the atrioventricular canal, is the first specialized fast ventricular conduction pathway in the embryonic heart. It has been first defined immunohistochemically and is characterized as a region of slow myocyte proliferation. Recent studies have shown that it participates in spreading the ventricular electrical activation during stages preceding ventricular septation in the mouse, chick, and rat. Here we demonstrate its presence using optical mapping in chicks between embryonic days (ED) 3–5. We then tested the effects of hemodynamic unloading in the organ culture system upon its functionality. In ED3 hearts cultured without hemodynamic loading for 24 h, we observed a significant decrease in the percentage activated through the primary ring conduction pathway. A morphological examination revealed arrested growth, collapse, and elongation of the outflow tract and disorganized trabeculation. A similar reversal toward more primitive activation patterns was observed with culture between ED4 and ED5. This phenotype was completely rescued with the artificial loading of the ventricles with a droplet of silicone oil. We conclude that an appropriate loading is required during the early phases of the conduction system formation and maturation.

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Krupnick, A. S., D. Kreisel, W. Y. Szeto, S. H. Popma, and B. R. Rosengard. "A murine model of left ventricular tissue engineering." Journal of Heart and Lung Transplantation 20, no. 2 (February 2001): 197–98. http://dx.doi.org/10.1016/s1053-2498(00)00417-4.

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49

Sun, Ying, Mazen Beshara, Richard J. Lucariello, and Salvatore A. Chiaramida. "Computer model for left ventricular pressure-volume loops." Journal of the American College of Cardiology 27, no. 2 (February 1996): 247. http://dx.doi.org/10.1016/s0735-1097(96)81868-7.

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50

Abe, Hiroyuki, Satoru Goto, Teruo Kimura, Hidetsugu Kushibiki, and Shigeru Arai. "Left Ventricular Model Taking Account of Residual Stress." Transactions of the Japan Society of Mechanical Engineers Series A 60, no. 578 (1994): 2452–58. http://dx.doi.org/10.1299/kikaia.60.2452.

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