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Level Set Methods for Cardiac Segmentation in MSCT Images
Published in Ayman El-Baz, Jasjit S. Suri, Level Set Method in Medical Imaging Segmentation, 2019
Ruben Medina, Sebastian Bautista, Villie Morocho, Alexandra La Cruz
An example for a patient with Left Ventricular Hypertrophy (LVH) is shown in Figures 7.23 and 7.24. The patient has a left ventricle mass of 182 grams and a left ventricle mass index of 141 g/m2 in the moderately abnormal range with a Relative Wall Thickness (RWT) index of 0.78 corresponding to concentric hypertrophy. The contours obtained with the automatic segmentation are shown in Figure 7.23. In this case the contours are shown overlaid with the input image in three standard views axial, coronal and sagittal. Even when the contrast is poor for determining the actual external wall contour, the level set based algorithm is able to attain a feasible solution that recovers a ventricle shape that matches the anatomical information provided by this 3-D image. The 3-D representation of the myocardial segmentation is shown in Figure 7.24 where the endocardial shape is overlaid with the shape representing the external wall of the left ventricle. Three views of the segmentation results are shown where the width of the left ventricle wall is clearly larger than the cases shown in Figure 7.22.
Sensor-Enabled 3D Printed Tissue-Mimicking Phantoms: Application in Pre-Procedural Planning for Transcatheter Aortic Valve Replacement
Published in Ayman El-Baz, Jasjit S. Suri, Cardiovascular Imaging and Image Analysis, 2018
Kan Wang, Chuck Zhang, Ben Wang, Mani A Vannan, Zhen Qian
The aortic valve is a heart valve situated between the left ventricle (LV) of the heart and the aorta. It functions like a one-way flow controller that allows blood from the LV to be pumped into the aorta but prevents the backflow of the blood. Aortic stenosis (AS), which is a narrowing of the aortic valve opening, is the most common valvular heart disease in developed countries [1]. Advanced age is a major risk factor of the development of AS. Some congenital heart defects, such as a bicuspid aortic valve, can also cause AS. The progression of AS involves a series of deteriorations of the cardiac function, including an elevated LV systolic pressure, LV concentric hypertrophy, an elevated LV diastolic pressure, and a decreased cardiac output. If untreated, AS patients ultimately develop heart failure.
Cardiovascular System:
Published in Michel R. Labrosse, Cardiovascular Mechanics, 2018
With high blood pressure (hypertension), the afterload effect is increased. The left ventricle must reach a higher pressure before it can push open the aortic valve against the higher aortic pressure. Thus, the isovolumic contraction period may be elongated, and there would be a shorter ejection period. This would result in a decrease in stroke volume that would have to be compensated for by a higher heart rate. Over time, this can lead to heart failure. In response to hypertension, the ventricular muscle may sometimes thicken in an attempt to achieve higher pressures. Usually, this thickening comes at the expense of the lumen size (concentric hypertrophy), and stroke volumes may again be decreased. Heart failure can also develop with an aortic valve stenosis (decreased ejection) or after a myocardial infarction (weakened muscles and decreased ejection).
Left ventricular function and mechanics in backs and forwards elite rugby union players
Published in European Journal of Sport Science, 2023
Charly Fornasier-Santos, Omar Izem, Falah Aboukhoudir, Thomas Rupp, Paul Stridgeon, Grégoire P. Millet, Stéphane Nottin
LV morphological parameters were assessed according to the recommendations of the American Society of Echocardiography (Lang et al., 2005). The inter-ventricular septum and posterior wall thicknesses and LV diameters were assessed using M-mode from the parasternal long-axis view. LV mass (LVM) was estimated according to Lang et al. (Lang et al., 2015) and indexed (LVMi) to BSA. LV hypertrophy was defined as LVMi > 115 g.m-² (Lang et al., 2015). Relative wall thickness (RWT) was calculated as (2 × PWT)/(LV-EDD). The cut-off of 0.42 was defined to differentiate eccentric versus concentric hypertrophy (Lang et al., 2015). The relative septal thickness (RST) was calculated as (2 × septum wall thickness)/(LV end-diastolic diameter) (Grazioli et al., 2016).
Hypertrophic cardiomyopathy or athlete’s heart? A systematic review of novel cardiovascular magnetic resonance imaging parameters
Published in European Journal of Sport Science, 2023
Constantinos Bakogiannis, Dimitrios Mouselimis, Anastasios Tsarouchas, Efstathios Papatheodorou, Vassilios P. Vassilikos, Emmanuel Androulakis
The search for such competent diagnostic modalities is greatly complicated by “athlete’s heart syndrome”. The heart of athletes undergoes a series of alterations to adapt to sustained high workload conditions (George et al., 2012). This structural and functional remodelling leads to adaptive left ventricular hypertrophy (LVH) with enlarged atrial and ventricular cavities (Maestrini, Torlasco, Hughes, & Moon, 2020). The extent of the remodelling depends on the duration and the intensity of training conditions and individually on the blood pressure of each athlete while training (Galderisi et al., 2015; George et al., 2012). The pattern of hypertrophy is associated with the type of training, as concentric hypertrophy is most common in strength sports caused by pressure overload, (Barczuk-Falęcka, Małek, Krysztofiak, Roik, & Brzewski, 2018) while eccentric is mainly spotted in endurance sports due to volume overload (Galderisi et al., 2015; Małek et al., 2019). In mixed type of sports, a mixed type of hypertrophy might develop. Although athlete’s heart conveys no significant risk for the athlete, it overlaps morphologically with high-risk and life-threatening cardiomyopathies including HCM (George et al., 2012).
Cardiac structure and function in resistance-trained and untrained adults: A systematic review and meta-analysis
Published in Journal of Sports Sciences, 2022
Abigail M Saunders, Rebecca L. Jones, Joanna Richards
Of particular interest within this review, may be the finding that resistance-trained athletes showed not only greater wall thickness compared to the untrained individuals but also greater LV chamber dimensions. The consequent suggestion that the greater LVM seen within the RT athletes is a result of both chamber dilation and myocardial thickening does not align with the well-known original research of Morganroth et al. (Morganroth et al., 1975) which first reported the pattern of concentric hypertrophy in this mode of athlete. The absence of concentric hypertrophy in the resistance-trained athletes may be explained by multiple factors including insufficient exposure to a pressure overload due to the small duration of time in each repetition (Utomi et al., 2013); variations in the type or intensity of resistance training undertaken by the athletes (Hackett & Chow, 2013; Pelliccia et al., 1993); or the influence of mixed-mode athletes who may have been described as “resistance-trained” but did not correctly report their levels of aerobic exercise.