Background: early diagnosis of left ventricular mass (LVM) inappropriateness and left ventricular hypertrophy (LVH) can result in preventing diastolic left ventricular dysfunction and its related morbidity and mortality. This study was performed to determine if diastolic dysfunction is associated with LVH and inappropriate LVM.Materials and Methods: one hundred and twenty five uncomplicated hypertension from Isfahan Healthy Heart Program underwent two-dimensional echocardiography. Inappropriate LVM was defined as an LVM index greater than 88 g/m2 of body-surface area in women and greater than 102 g/m2 in men. LVH-defined septal and posterior wall thickness greater than 0/9 cm in women and greater than 1 cm in men, respectively. Echocardiographic parameters, including early diastolic peak velocity (E) /late diastolic peak velocity (A), deceleration time (DT), and E/early mitral annulus velocity (E') were measured.Results: the mean systolic and diastolic blood pressure at the patients’ admission day were 142.87 ± 18.12 and 88.45 ± 9.18 mmHg, respectively. Totally, 21.7% of subjects had inappropriate LV mass that moderate and severe abnormal LV mass was revealed in 5.6% and 5.6%, respectively. The mean of age and BMI was significantly higher in patients with moderate left ventricular hypertrophy (P<0.05). Adjusted by age, gender, BMI, and systolic and diastolic blood pressures, both E/A ratio and deceleration time were higher in those with the severer ventricular hypertrophy. Subjects with severe showed significantly higher BMI 33.7 ± 3.7 (P< 0.001). There was a slight difference between the grade of diastolic dysfunction and the severity of inappropriate LV mass (P=0.065). But no significant difference was found between E/A, E/E', and deceleration time and the level of inappropriate LV mass (P>0.05). Spearman’s Rank test was used to test the correlation between diastolic dysfunction and LV mass (P=0.025).Conclusion: LVH is correlated with the severity of diastolic dysfunction manifested by the E/A value and deceleration time, but inappropriate LVM can slightly predict diastolic dysfunction severity in uncomplicated hypertension.

Background: Cardiovascular disease (CVD) is one of the leading causes of mortality among kidney transplant (KTx) recipients. Left ventricular hypertrophy (LVH) is a known important risk factor for CVD in KTx recipients. The current study aimed at evaluating the association of LVH with hypertension, carotid intima media thickness (CIMT), and serum biomarkers. Methods: The current cross sectional study included KTx recipients; ambulatory blood pressure monitoring, echocardiography, and CIMT measurement were performed. In addition to standard laboratory investigations, high sensitivity C-reactive protein (CRP) and serum homocysteine were measured. Results: A total of 30 KTx recipients (20 male, 10 female, mean age: 44. 53 13. 59 years) were enrolled. One-third had diabetes and 73. 3% hypertension. Their mean systolic and diastolic blood pressure (BP) was 132. 0 14. 4 and 77. 8 11. 3mmHg, respectively. BP was well controlled, albeit with more antihypertensive agents of 1. 5 (interquartile range (IQR): 0-4). Their baseline serum creatinine and eGFR were 108. 3 (IQR: 66-319)  M/L and 69. 8  20. 8 mL/min/1. 73 m2, respectively. Seven patients had LVH and predominantly had diabetes, a higher pulse pressure, and elevated serum homocysteine. Predictors of left ventricular mass index (LVMI) were the incidence of diabetes, higher pulse pressure, serum homocysteine, and the number of antihypertensive agents prescribed. On multivariate analysis, diabetes and pulse pressure were the main predictors of left ventricular mass index. Conclusions: LVH is common in patients with KTx, especially in the ones with diabetes. Serum homocysteine is a surrogate marker for LVH.

Cardiovascular diseases are the major cause of death in industrialized countries. Recent attempts in computational modeling of the human heart in normal and diseased conditions made it possible to find a way to predict the behavior and test the cures virtually with less harm for the human body. Ventricular hypertrophy that occurs in response to blood pressure and volume overload in ventricles can change its property and function and finally lead to heart failure. In this research, concentric left ventricular hypertrophy of the human heart was modeled in silico. The left ventricle (LV) model was implemented into the commercial nonlinear finite elements (FE) software ABAQUS/STANDARD through the user-defined subroutine UMAT based on continuum mechanics. We tried to determine the fibers distribution with more accuracy and considered the fibers and sheets dispersion in the anisotropic hyperelastic growing model. When the ventricular pressure and the resultant wall stress increased, the sheet growth multiplier started to increase from the endocardium to the epicardium and the ventricular wall became thicker. Residual stresses were observed in the model after unloading. Sheet growth multiplier changes versus stress showed that sheet growth multiplier increased dramatically near the maximum pressure while the stress remained almost constant.