Three-dimensional alignment of the aggregated myocytes in the normal and hypertrophic murine heart

2009 ◽  
Vol 107 (3) ◽  
pp. 921-927 ◽  
Author(s):  
Boris Schmitt ◽  
Katsiaryna Fedarava ◽  
Jan Falkenberg ◽  
Kai Rothaus ◽  
Narendra K. Bodhey ◽  
...  
Keyword(s):  
Ventricular Hypertrophy ◽  
Diffusion Tensor ◽  
Three Dimensional ◽  
Spatial Arrangement ◽  
Left Ventricular ◽  
Outer Radius ◽  
Myocardial Mass ◽  
3.0 Tesla ◽  
Left Ventricular Chamber ◽  
Hypertrophied Myocardium

Several observations suggest that the transmission of myocardial forces is influenced in part by the spatial arrangement of the myocytes aggregated together within ventricular mass. Our aim was to assess, using diffusion tensor magnetic resonance imaging (DT-MRI), any differences in the three-dimensional arrangement of these myocytes in the normal heart compared with the hypertrophic murine myocardium. We induced ventricular hypertrophy in seven mice by infusion of angiotensin II through a subcutaneous pump, with seven other mice serving as controls. DT-MRI of explanted hearts was performed at 3.0 Tesla. We used the primary eigenvector in each voxel to determine the three-dimensional orientation of aggregated myocytes in respect to their helical angles and their transmural courses (intruding angles). Compared with controls, the hypertrophic hearts showed significant increases in myocardial mass and the outer radius of the left ventricular chamber ( P < 0.05). In both groups, a significant change was noted from positive intruding angles at the base to negative angles at the ventricular apex ( P < 0.01). Compared with controls, the hypertrophied hearts had significantly larger intruding angles of the aggregated myocytes, notably in the apical and basal slices ( P < 0.001). In both groups, the helical angles were greatest in midventricular sections, albeit with significantly smaller angles in the mice with hypertrophied myocardium ( P < 0.01). The use of DT-MRI revealed significant differences in helix and intruding angles of the myocytes in the mice with hypertrophied myocardium.

Abstract 224: A Deep Learning Approach to Left-Ventricular Chamber Quantification for Fully Automated Three Dimensional Strain Analysis in Cardiotoxicity

2020 ◽  
Vol 127 (Suppl_1) ◽  
Author(s):  
Bryant M Baldwin ◽  
Shane Joseph ◽  
Xiaodong Zhong ◽  
Ranya Kakish ◽  
Cherie Revere ◽  
...  
Keyword(s):  
Deep Learning ◽  
Interpolation Method ◽  
Three Dimensional ◽  
Strain Analysis ◽  
Correlation Coefficients ◽  
Semantic Segmentation ◽  
Left Ventricular ◽  
Breast Cancer Patients ◽  
Left Ventricular Chamber ◽  
Longitudinal Strains

This study investigated MRI and semantic segmentation-based deep-learning (SSDL) automation for left-ventricular chamber quantifications (LVCQ) and low longitudinal strain (LLS) determination, thus eliminating user-bias by providing an automated tool to detect cardiotoxicity (CT) in breast cancer patients treated with antineoplastic agents. Displacement Encoding with Stimulated Echoes-based (DENSE) myocardial images from 26 patients were analyzed with the tool’s Convolution Neural Network with underlying Resnet-50 architecture. Quantifications based on the SSDL tool’s output were for LV end-diastolic diameter (LVEDD), ejection fraction (LVEF), and mass (LVM) (see figure for phase sequence). LLS was analyzed with Radial Point Interpolation Method (RPIM) with DENSE phase-based displacements. LVCQs were validated by comparison to measurements obtained with an existing semi-automated vendor tool (VT) and strains by 2 independent users employing Bland-Altman analysis (BAA) and interclass correlation coefficients estimated with Cronbach’s Alpha (C-Alpha) index. F1 score for classification accuracy was 0.92. LVCQs determined by SSDL and VT were 4.6 ± 0.5 vs 4.6 ± 0.7 cm (C-Alpha = 0.93 and BAA = 0.5 ± 0.5 cm) for LVEDD, 58 ± 5 vs 58 ± 6 % (0.90, 1 ± 5%) for LVEF, 119 ± 17 vs 121 ± 14 g (0.93, 5 ± 8 g) for LV mass, while LLS was 14 ± 4 vs 14 ± 3 % (0.86, 0.2 ± 6%). Hence, equivalent LV dimensions, mass and strains measured by VT and DENSE imaging validate our unique automated analytic tool. Longitudinal strains in patients can then be analyzed without user bias to detect abnormalities for the indication of cardiotoxicity and the need for therapeutic intervention even if LVEF is not affected.

Blood Pressure Control and Left Ventricular Hypertrophy in Long-Term Capd and Hemodialysis Patients: A Cross-Sectional Study

2003 ◽  
Vol 23 (6) ◽  
pp. 563-567 ◽  
Author(s):  
Ali Ihsan Günal ◽  
Erdogan Ilkay ◽  
Ercan Kirciman ◽  
Ilgin Karaca ◽  
Ayhan Dogukan ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Left Ventricular Hypertrophy ◽  
Wall Thickness ◽  
Left Atrial ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Volume Control ◽  
Left Ventricular Chamber ◽  
Significant Difference

Background It is still not clear whether hypertension and left ventricular hypertrophy (LVH) are more common in continuous ambulatory peritoneal dialysis (CAPD) than in hemodialysis (HD) patients. Methods To examine this subject, the indices of cardiac performance were compared between 50 HD and 34 CAPD patients. Patients were further divided into two subgroups [long-term (L) CAPD and L-HD] according to dialysis modality and duration of dialysis (more than 60 months’ duration). Results The blood pressure and cardiothoracic index of CAPD patients did not differ from HD patients. On average, the left atrial index was 2 mm/m2 higher in HD patients than in CAPD patients. Left ventricular chamber sizes, wall thickness, and left ventricular mass index (LVMI) in patients on CAPD were similar to those of HD patients. Isovolumic relaxation time (IVRT) of CAPD patients was insignificantly less than that of HD patients (101 ± 22 and 115 ± 27 msec respectively). There was no significant difference between the two subgroups (L-HD and L-CAPD) in blood pressure, left atrial diameter, left ventricular chamber size, wall thickness, LVMI, ejection fraction, or IVRT. Conclusion If normovolemia and normotension are obtained by strict volume control without using antihypertensive drugs, the effects of the two modalities of chronic dialysis treatment (HD and CAPD) on cardiac structure and function are not different from each other.

Effect of heart rate on myocardial blood flow in dogs with left ventricular hypertrophy

1980 ◽  
Vol 239 (5) ◽  
pp. H621-H627
Author(s):  
T. R. Vrobel ◽  
W. S. Ring ◽  
R. W. Anderson ◽  
R. W. Emery ◽  
R. J. Bache
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Left Ventricular Hypertrophy ◽  
Myocardial Blood Flow ◽  
Ventricular Hypertrophy ◽  
Lateral Wall ◽  
Left Ventricular ◽  
Myocardial Mass ◽  
Previous Suggestion ◽  
Heart Rates

Because of the previous suggestion that subendocardial perfusion may be inadequate in the hypertrophied heart, this study was carried out to examine the response of transmural myocardial blood flow to pacing induced tachycardia in dogs with chronic left ventricular hypertrophy. Myocardial hypertrophy, produced by banding the ascending aorta of puppies at 5-6 wk of age, resulted in an 87% average increase in relative left ventricular mass compared with the control dogs. Myocardial blood flow was examined during ventricular pacing at heart rates of 100, 200, and 250 beats/min using radionuclide-labeled microspheres. Mean blood flow per unit myocardial mass was similar in the two groups of dogs at a heart rate of 100 beats/min and increased regularly during pacing in both groups of animals. Increasing heart rates did not change the transmural pattern of myocardial blood flow in the normal dogs, but in the animals with left ventricular hypertrophy pacing at 250 beats/min resulted in a significant redistribution of perfusion away from the subendocardium, with the ratio of subendocardial/subepicardial blood flow falling from 1.03 +/- 0.08 at 100 beats/min to 0.83 +/0 0.06 at 250 beats/min (P < 0.01). This redistribution of blood flow away from the subendocardium was especially marked in the regions encompassing the papillary muscles and the intervening left ventricular lateral wall.

scholarly journals Operative Myocardial protection in patients with Left Ventricular Hypertrophy: The Role of systemic Hypothermia

2011 ◽  
Vol 4 ◽  
pp. OJCS.S6937
Author(s):  
Tamer Elghobary ◽  
Idris M. Ali ◽  
Ahmad F. Ahmad
Keyword(s):  
Body Temperature ◽  
Myocardial Protection ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Group I ◽  
Hypertrophied Myocardium ◽  
Systemic Hypothermia ◽  
Group Ii ◽  
The Ideal

Objectives Myocardial hypertrophy represents a great challenge in cardiac surgery. Several strategies have been described to protect the hypertrophied myocardium during cardiopulmonary bypass, and aortic clamping, yet the ideal strategy has not been identified. This study investigates the use of moderate systemic hypothermia (MSH) as an adjuvant method to protect the hypertrophied myocardium in patients undergoing aortic valve replacement (AVR). Methods Twenty eight patients undergoing AVR were divided into two groups, (Group I) received continuous cold 5–8 °C retrograde blood cardioplegia (CRBC) and their body temperature was cooled down to 23–26 °C. (Group II) also received CRBC but their body temperature was kept at 32–34 °C. Results No operative morality (30 days) was noted in both groups. Postoperative reduction in ejection fraction (EF) was seen in nine patients of group I and in twelve patients of group II ( P < 0.05). The need for multiple inotropes was more in group II (eight patients) than in group I (two patients) ( P < 0.001). IABP was needed in three patients of group II and non in group I ( P < 0.01). Conclusion Moderate systemic hypothermia might have a role in protecting hypertrophied myocardium in patients undergoing AVR.

Altered β-adrenergic signal transduction in nonfailing hypertrophied myocytes from Dahl salt-sensitive rats

2000 ◽  
Vol 279 (5) ◽  
pp. H2502-H2508 ◽  
Author(s):  
Kohzo Nagata ◽  
Catherine Communal ◽  
Chee C. Lim ◽  
Mohit Jain ◽  
Thomas M. Suter ◽  
...  
Keyword(s):  
Ventricular Hypertrophy ◽  
Physiological Role ◽  
Cellular Level ◽  
Left Ventricular ◽  
Cell Shortening ◽  
Hypertrophied Myocardium ◽  
Intracellular Ca ◽  
Myocyte Contractility ◽  
Dose Dependent

Desensitization of the β-adrenergic receptor (β-AR) response is well documented in hypertrophied hearts. We investigated whether β-AR desensitization is also present at the cellular level in hypertrophied myocardium, as well as the physiological role of inhibitory G (Gi) proteins and the L-type Ca2+channel in mediating β-AR desensitization. Left ventricular (LV) myocytes were isolated from hypertrophied hearts of hypertensive Dahl salt-sensitive (DS) rats and nonhypertrophied hearts of normotensive salt-resistant (DR) rats. Cells were paced at a rate of 300 beats/min at 37°C, and myocyte contractility and intracellular Ca2+concentration ([Ca2+]i) were simultaneously measured. In response to increasing concentrations of isoproterenol, DR myocytes displayed a dose-dependent augmentation of cell shortening and the [Ca2+]i transient amplitude, whereas hypertrophied DS myocytes had a blunted response of both cell shortening and the [Ca2+]i transient amplitude. Interestingly, inhibition of Gi proteins did not restore β-AR desensitization in DS myocytes. The responses to increases in extracellular Ca2+ and an L-type Ca2+ channel agonist were also similar in both DS and DR myocytes. Isoproterenol-stimulated adenylyl cyclase activity, however, was blunted in hypertrophied myocytes. We concluded that compensated ventricular hypertrophy results in a blunted contractile response to β-AR stimulation, which is present at the cellular level and independent of alterations in inhibitory G proteins and the L-type Ca2+ channel.

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