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Computers in Biology and Medicine May 2023In our paper, we simulated cardiac hypertrophy with the use of shell elements in parametric and echocardiography-based left ventricle (LV) models. The hypertrophy has an...
In our paper, we simulated cardiac hypertrophy with the use of shell elements in parametric and echocardiography-based left ventricle (LV) models. The hypertrophy has an impact on the change in the wall thickness, displacement field and the overall functioning of the heart. We computed both eccentric and concentric hypertrophy effects and tracked changes in the ventricle shape and wall thickness. Thickening of the wall was developed under the influence of concentric hypertrophy, while the eccentric hypertrophy produces wall thinning. To model passive stresses we used the recently developed material modal based on the Holzapfel experiments. Also, our specific shell composite finite element models for heart mechanics are much smaller and simpler to use with respect to conventional 3D models. Furthermore, the presented modeling approach of the echocardiography-based LV can serve as the basis for practical applications since it relies on the true patient-specific geometry and experimental constitutive relationships. Our model gives an insight into hypertrophy development in realistic heart geometries, and it has the potential to test medical hypotheses regarding hypertrophy evolution in a healthy and heart with a disease, under the influence of different conditions and parameters.
Topics: Humans; Heart Ventricles; Hypertrophy, Left Ventricular; Echocardiography; Cardiomegaly; Heart; Hypertension
PubMed: 36933415
DOI: 10.1016/j.compbiomed.2023.106742 -
Hypertension (Dallas, Tex. : 1979) Jul 2018This longitudinal study aims to characterize longitudinal blood pressure (BP) trajectories from childhood and examine the impact of level-independent childhood BP... (Observational Study)
Observational Study
This longitudinal study aims to characterize longitudinal blood pressure (BP) trajectories from childhood and examine the impact of level-independent childhood BP trajectories on adult left ventricular hypertrophy (LVH) and remodeling patterns. The longitudinal cohort consisted of 1154 adults (787 whites and 367 blacks) who had repeated measurements of BP 4 to 15 times from childhood (4-19 years) to adulthood (20-51 years) and assessment of echocardiographic LV dimensions in adulthood. Model-estimated levels and linear slopes of BP at childhood age points were calculated in 1-year intervals using the growth curve parameters and their first derivatives, respectively. Linear and nonlinear curve parameters of BP showed significant race and sex differences from age 15 years onwards. Adults with LVH had higher long-term BP levels than adults with normal LVM in race-sex groups. Linear and nonlinear slope parameters of BP differed consistently and significantly between LVH and normal groups. Associations of level-independent linear slopes of systolic BP with adult LVH were significantly inverse (odds ratio=0.75-0.82; =0.001-0.015) in preadolescent children of 4 to 9 years but significantly positive (odds ratio=1.29-1.46; =0.001-0.008) in adolescents of 13 to 19 years, adjusting for covariates. These associations were consistent across race-sex groups. Of note, the association of childhood BP linear slopes with concentric LVH was significantly stronger than that with eccentric LVH during the adolescence period of 12 to 19 years. These observations indicate that the impact of BP trajectories on adult LVH and geometric patterns originates in childhood. Adolescence is a crucial period for the development of LVH in later life, which has implications for early prevention.
Topics: Adolescent; Adult; Blood Pressure; Blood Pressure Determination; Child; Child, Preschool; Cross-Sectional Studies; Disease Progression; Echocardiography; Female; Follow-Up Studies; Heart Ventricles; Humans; Hypertension; Hypertrophy, Left Ventricular; Incidence; Male; Middle Aged; New Orleans; Odds Ratio; Retrospective Studies; Risk Factors; Time Factors; Ventricular Remodeling; Young Adult
PubMed: 29785961
DOI: 10.1161/HYPERTENSIONAHA.118.10975 -
Annals of Noninvasive Electrocardiology... May 2017Although left ventricular hypertrophy (LVH) detected by electrocardiography (ECG-LVH) and echocardiography (echo-LVH) independently predict cardiovascular disease...
BACKGROUND
Although left ventricular hypertrophy (LVH) detected by electrocardiography (ECG-LVH) and echocardiography (echo-LVH) independently predict cardiovascular disease events, it is unclear if ECG-LVH and echo-LVH independently predict atrial fibrillation (AF).
METHODS
This analysis included 4,904 participants (40% male; 85% white) from the Cardiovascular Health Study who were free of baseline AF and major intraventricular conduction delays. ECG-LVH was defined by Minnesota Code Classification from baseline ECG data. Echo-LVH was defined by sex-specific left ventricular mass values >95th sex-specific percentiles. Incident AF events were identified during the annual study ECGs and from hospitalization discharge data. Cox regression was used to compute hazard ratios (HR) and 95% confidence intervals (CI) for the association of ECG-LVH and echo-LVH with incident AF, separately.
RESULTS
ECG-LVH was detected in 224 (4.6%) participants and echo-LVH was present in 231 (4.7%) participants. Over a median follow-up of 11.9 years, a total of 1,430 AF events were detected. In a multivariable Cox model adjusted for age, sex, race, education, income, smoking, systolic blood pressure, diabetes, body mass index, total cholesterol, high-density lipoprotein cholesterol, aspirin, antihypertensive medications, and cardiovascular disease, ECG-LVH (HR = 1.50; 95% CI = 1.18, 1.90) and echo-LVH (HR = 1.39; 95% CI = 1.09, 1.78) were independently associated with AF. When ECG-LVH (HR = 1.47, 95% CI = 1.16, 1.87) and echo-LVH (HR = 1.36, 1.07, 1.75) were included in the same model, both were predictive of incident AF.
CONCLUSION
The association of ECG-LVH with AF is not dependent on left ventricular mass detected by echocardiography, suggesting that abnormalities in cardiac electrophysiology provide a distinct profile in the prediction of AF.
Topics: Aged; Aged, 80 and over; Atrial Fibrillation; Cohort Studies; Electrocardiography; Female; Heart Ventricles; Humans; Hypertrophy, Left Ventricular; Male; Organ Size; Predictive Value of Tests; Prospective Studies; Reproducibility of Results; Risk Factors
PubMed: 28019050
DOI: 10.1111/anec.12419 -
American Journal of Physiology. Heart... Oct 2021Although pulmonary arterial hypertension (PAH) leads to right ventricle (RV) hypertrophy and structural remodeling, the relative contributions of changes in myocardial...
Although pulmonary arterial hypertension (PAH) leads to right ventricle (RV) hypertrophy and structural remodeling, the relative contributions of changes in myocardial geometric and mechanical properties to systolic and diastolic chamber dysfunction and their time courses remain unknown. Using measurements of RV hemodynamic and morphological changes over 10 wk in a male rat model of PAH and a mathematical model of RV mechanics, we discriminated the contributions of RV geometric remodeling and alterations of myocardial material properties to changes in systolic and diastolic chamber function. Significant and rapid RV hypertrophic wall thickening was sufficient to stabilize ejection fraction in response to increased pulmonary arterial pressure by without significant changes in systolic myofilament activation. After , RV end-diastolic pressure increased significantly with no corresponding changes in end-diastolic volume. Significant RV diastolic chamber stiffening by was not explained by RV hypertrophy. Instead, model analysis showed that the increases in RV end-diastolic chamber stiffness were entirely attributable to increased resting myocardial material stiffness that was not associated with significant myocardial fibrosis or changes in myocardial collagen content or type. These findings suggest that whereas systolic volume in this model of RV pressure overload is stabilized by early RV hypertrophy, diastolic dilation is prevented by subsequent resting myocardial stiffening. Using a novel combination of hemodynamic and morphological measurements over 10 wk in a male rat model of PAH and a mathematical model of RV mechanics, we found that compensated systolic function was almost entirely explained by RV hypertrophy, but subsequently altered RV end-diastolic mechanics were primarily explained by passive myocardial stiffening that was not associated with significant collagen extracellular matrix accumulation.
Topics: Animals; Biomechanical Phenomena; Diastole; Disease Models, Animal; Fibrosis; Heart Ventricles; Hypertrophy, Right Ventricular; Male; Models, Cardiovascular; Myocardium; Pulmonary Arterial Hypertension; Rats, Sprague-Dawley; Systole; Time Factors; Ventricular Dysfunction, Right; Ventricular Function, Right; Ventricular Remodeling; Rats
PubMed: 34448637
DOI: 10.1152/ajpheart.00046.2021 -
Nutrients Jul 2022Osteoprotegerin (OPG) is a molecule which belongs to the tumor necrosis factor receptor superfamily. OPG concentration is elevated in patients with left ventricle...
Serum Osteoprotegerin Is an Independent Marker of Left Ventricular Hypertrophy, Systolic and Diastolic Dysfunction of the Left Ventricle and the Presence of Pericardial Fluid in Chronic Kidney Disease Patients.
BACKGROUND
Osteoprotegerin (OPG) is a molecule which belongs to the tumor necrosis factor receptor superfamily. OPG concentration is elevated in patients with left ventricle hypertrophy, heart failure and acute myocardial infarction. OPG concentrations rise in chronic kidney disease (CKD). The aim of this study was to investigate the association between OPG concentrations and cardiovascular complications, such as left ventricle hypertrophy, systolic and diastolic dysfunction of left ventricle and dysfunction of right ventricle in chronic kidney disease patients not treated with dialysis. The relation between OPG and the amount of pericardial fluid was also examined.
METHODS
One hundred and one men with CKD stage 3-5 not treated with dialysis were included in the study. Overhydration, body fat mass and lean body mass were measured using bioimpedance spectroscopy (BIS). Echocardiography was performed to evaluate the amount of pericardial fluid and to measure the thickness of the interventricular septum (IVS), systolic and diastolic function of left ventricle, as well as systolic function of right ventricle.
RESULTS
We observed a significant positive association between OPG and the thickness of the interventricular septum, the size of the left atrium (LA) and the presence of pericardial fluid. A negative relationship was observed between OPG and ejection fraction (EF).
CONCLUSIONS
Our results suggest that OPG can be an independent marker of left ventricular hypertrophy, systolic and diastolic dysfunction of left ventricle and the presence of pericardial fluid in chronic kidney disease patients.
Topics: Heart Failure; Heart Ventricles; Humans; Hypertrophy, Left Ventricular; Male; Osteoprotegerin; Pericardial Fluid; Renal Dialysis; Renal Insufficiency, Chronic; Ventricular Dysfunction, Left
PubMed: 35889849
DOI: 10.3390/nu14142893 -
JACC. Cardiovascular Imaging Nov 2015
Topics: Heart Ventricles; Humans; Hypertension; Hypertrophy, Left Ventricular; Ventricular Function, Left; Ventricular Remodeling
PubMed: 26563856
DOI: 10.1016/j.jcmg.2015.08.012 -
Annals of Biomedical Engineering May 2021Critical aortic stenosis (AS) of the fetal heart causes a drastic change in the cardiac biomechanical environment. Consequently, a substantial proportion of such cases...
Critical aortic stenosis (AS) of the fetal heart causes a drastic change in the cardiac biomechanical environment. Consequently, a substantial proportion of such cases will lead to a single-ventricular birth outcome. However, the biomechanics of the disease is not well understood. To address this, we performed Finite Element (FE) modelling of the healthy fetal left ventricle (LV) based on patient-specific 4D ultrasound imaging, and simulated various disease features observed in clinical fetal AS to understand their biomechanical impact. These features included aortic stenosis, mitral regurgitation (MR) and LV hypertrophy, reduced contractility, and increased myocardial stiffness. AS was found to elevate LV pressures and myocardial stresses, and depending on severity, can drastically decrease stroke volume and myocardial strains. These effects are moderated by MR. AS alone did not lead to MR velocities above 3 m/s unless LV hypertrophy was included, suggesting that hypertrophy may be involved in clinical cases with high MR velocities. LV hypertrophy substantially elevated LV pressure, valve flow velocities and stroke volume, while reducing LV contractility resulted in diminished LV pressure, stroke volume and wall strains. Typical extent of hypertrophy during fetal AS in the clinic, however, led to excessive LV pressure and valve velocity in the FE model, suggesting that reduced contractility is typically associated with hypertrophy. Increased LV passive stiffness, which might represent fibroelastosis, was found to have minimal impact on LV pressures, stroke volume, and wall strain. This suggested that fibroelastosis could be a by-product of the disease progression and does not significantly impede cardiac function. Our study demonstrates that FE modelling is a valuable tool for elucidating the biomechanics of congenital heart disease and can calculate parameters which are difficult to measure, such as intraventricular pressure and myocardial stresses.
Topics: Aortic Valve Stenosis; Biomechanical Phenomena; Cardiomyopathies; Fetal Heart; Finite Element Analysis; Heart Ventricles; Humans; Hypertrophy, Left Ventricular; Models, Cardiovascular; Ultrasonography; Ventricular Function, Left
PubMed: 33175989
DOI: 10.1007/s10439-020-02683-x -
Journal of the American Heart... Feb 2019Background Sustained pressure overload leads to changes in cardiac metabolism, function, and structure. Both time course and causal relationships between these changes...
Background Sustained pressure overload leads to changes in cardiac metabolism, function, and structure. Both time course and causal relationships between these changes are not fully understood. Therefore, we studied spontaneously hypertensive rats (SHR) during early hypertension development and compared them to control Wistar Kyoto rats. Methods and Results We serially evaluated myocardial glucose uptake rates (Ki) with dynamic 2-[F] fluoro-2-deoxy-D-glucose positron emission tomography, and ejection fraction and left ventricular mass to body weight ratios with cardiac magnetic resonance imaging in vivo, determined glucose uptake and oxidation rates in isolated perfused hearts, and analyzed metabolites, mammalian target of rapamycin activity and endoplasmic reticulum stress in dissected hearts. When compared with Wistar Kyoto rats, SHR demonstrated increased glucose uptake rates (Ki) in vivo, and reduced ejection fraction as early as 2 months of age when hypertension was established. Isolated perfused SHR hearts showed increased glucose uptake and oxidation rates starting at 1 month. Cardiac metabolite analysis at 2 months of age revealed elevated pyruvate, fatty acyl- and branched chain amino acid-derived carnitines, oxidative stress, and inflammation. Mammalian target of rapamycin activity increased in SHR beginning at 2 months. Left ventricular mass to body weight ratios and endoplasmic reticulum stress were elevated in 5 month-old SHR. Conclusions Thus, in a genetic hypertension model, chronic cardiac pressure overload promptly leads to increased myocardial glucose uptake and oxidation, and to metabolite abnormalities. These coincide with, or precede, cardiac dysfunction while left ventricular hypertrophy develops only later. Myocardial metabolic changes may thus serve as early diagnostic markers for hypertension-induced left ventricular hypertrophy.
Topics: Animals; Blood Pressure; Disease Models, Animal; Disease Progression; Heart Ventricles; Hypertension; Hypertrophy, Left Ventricular; Male; Myocardium; Oxidative Stress; Positron-Emission Tomography; Rats; Rats, Inbred SHR; Rats, Inbred WKY; Tomography, X-Ray Computed; Ventricular Function, Left
PubMed: 30764689
DOI: 10.1161/JAHA.118.010926 -
Clinical Science (London, England :... Mar 2018T-cell infiltration and the subsequent increased intracardial chronic inflammation play crucial roles in the development of cardiac hypertrophy and heart failure (HF)....
T-cell infiltration and the subsequent increased intracardial chronic inflammation play crucial roles in the development of cardiac hypertrophy and heart failure (HF). A77 1726, the active metabolite of leflunomide, has been reported to have powerful anti-inflammatory and T cell-inhibiting properties. However, the effect of A77 1726 on cardiac hypertrophy remains completely unknown. Herein, we found that A77 1726 treatment attenuated pressure overload or angiotensin II (Ang II)-induced cardiac hypertrophy , as well as agonist-induced hypertrophic response of cardiomyocytes In addition, we showed that A77 1726 administration prevented induction of cardiac fibrosis by inhibiting cardiac fibroblast (CF) transformation into myofibroblast. Surprisingly, we found that the protective effect of A77 1726 was not dependent on its T lymphocyte-inhibiting property. A77 1726 suppressed the activation of protein kinase B (AKT) signaling pathway, and overexpression of constitutively active AKT completely abolished A77 1726-mediated cardioprotective effects and Pretreatment with siRNA targetting (si ) blunted the protective effect elicited by A77 1726 More importantly, A77 1726 was capable of blocking pre-established cardiac hypertrophy in mice. In conclusion, A77 1726 attenuated cardiac hypertrophy and cardiac fibrosis via inhibiting FYN/AKT signaling pathway.
Topics: Animals; Cell Differentiation; Cells, Cultured; Disease Models, Animal; Fibroblasts; Fibrosis; Heart Ventricles; Hypertrophy, Left Ventricular; Leflunomide; Male; Mice, Inbred C57BL; Myofibroblasts; Phosphorylation; Protein Kinase Inhibitors; Proto-Oncogene Proteins c-akt; Proto-Oncogene Proteins c-fyn; Rats; Signal Transduction; Ventricular Function, Left; Ventricular Remodeling
PubMed: 29540538
DOI: 10.1042/CS20180160 -
American Journal of Respiratory Cell... Mar 2021Monoamine oxidases (MAOs), a class of enzymes bound to the outer mitochondrial membrane, are important sources of reactive oxygen species. Increased MAO-A activity in...
Monoamine oxidases (MAOs), a class of enzymes bound to the outer mitochondrial membrane, are important sources of reactive oxygen species. Increased MAO-A activity in endothelial cells and cardiomyocytes contributes to vascular dysfunction and progression of left heart failure. We hypothesized that inhibition of MAO-A can be used to treat pulmonary arterial hypertension (PAH) and right ventricular (RV) failure. MAO-A levels in lung and RV samples from patients with PAH were compared with levels in samples from donors without PAH. Experimental PAH was induced in male Sprague-Dawley rats by using Sugen 5416 and hypoxia (SuHx), and RV failure was induced in male Wistar rats by using pulmonary trunk banding (PTB). Animals were randomized to receive either saline or the MAO-A inhibitor clorgyline at 10 mg/kg. Echocardiography and RV catheterization were performed, and heart and lung tissues were collected for further analysis. We found increased MAO-A expression in the pulmonary vasculature of patients with PAH and in experimental experimental PAH induced by SuHx. Cardiac MAO-A expression and activity was increased in SuHx- and PTB-induced RV failure. Clorgyline treatment reduced RV afterload and pulmonary vascular remodeling in SuHx rats through reduced pulmonary vascular proliferation and oxidative stress. Moreover, clorgyline improved RV stiffness and relaxation and reversed RV hypertrophy in SuHx rats. In PTB rats, clorgyline had no direct clorgyline had no direct effect on the right ventricle effect. Our study reveals the role of MAO-A in the progression of PAH. Collectively, these findings indicated that MAO-A may be involved in pulmonary vascular remodeling and consecutive RV failure.
Topics: Animals; Clorgyline; Disease Models, Animal; Disease Progression; Heart Ventricles; Humans; Hypertrophy, Right Ventricular; Indoles; Monoamine Oxidase; Oxidative Stress; Pulmonary Arterial Hypertension; Pulmonary Artery; Pyrroles; Rats; Vascular Remodeling; Vascular Stiffness; Vasodilation
PubMed: 33264068
DOI: 10.1165/rcmb.2020-0105OC