Association of 1,25 dihydroxyvitamin D with left ventricular hypertrophy and left ventricular diastolic dysfunction in patients with chronic kidney disease.

Left ventricular hypertrophy (LVH) and left ventricular diastolic dysfunction (LVDD) are highly prevalent predictors of cardiovascular disease in individuals with chronic kidney disease (CKD). Vitamin D, particularly 25-hydroxyvitamin D [25(OH)D], deficiency has been reported to be associated with cardiac structure and function in CKD patients. In the current study, we investigated the association between 1,25-dihydroxyvitamin D [1,25(OH)2D], the active form of 25(OH)D, and LVH/LVDD in CKD patients. We enrolled 513 non-dialysis CKD patients. The presence of LVH and LVDD was determined using transthoracic echocardiography. In multivariable analysis, serum 1,25(OH)2D levels, but not serum 25(OH)D, were independently associated with LVH [odds ratio (OR): 0.90, 95% confidential interval (CI): 0.88-0.93, P < 0.001]. Additionally, age, systolic blood pressure, and intact parathyroid hormone levels were independently associated with LVH. Similarly, multivariable analysis demonstrated that serum 1,25(OH)2D levels, but not 25(OH)D levels, were independently associated with LVDD (OR: 0.88, 95% CI: 0.86-0.91, P < 0.001) with systolic blood pressure showing independent association with LVDD. The optimal cut-off values for serum 1,25(OH)2D levels for identifying LVH and LVDD were determined as ≤ 12.7 pg/dl and ≤ 18.1 pg/dl, respectively. Our findings suggest that serum 1,25(OH)2D levels have independent association with LVH and LVDD in CKD patients, underscoring their potential as biomarkers for these conditions in this patient population.

Features of The Dynamics of Profibrotic Markers and Regression of Left Ventricular Hypertrophy After Renal Denervation in Patients With Resistant Hypertension and Stenosing Atherosclerosis of the Coronary Arteries.

AIM: To compare the changes in serum concentrations of matrix metalloproteinases (MMPs) and their tissue inhibitor (TIMP) to the dynamics of blood pressure (BP) and parameters of left ventricular hypertrophy (LVH) 6 months after renal denervation (RD) in patients with resistant arterial hypertension (RAH) and complicated coronary atherosclerosis. MATERIAL AND METHODS: In 22 RAH patients with complicated coronary atherosclerosis (revascularization and/or history of myocardial infarction (MI)), 24-hour BP monitoring, echocardiography, and measurement of blood MMPs and TIMP were performed at baseline and six months after RD. The comparison group consisted of 48 RAH patients without a history of coronary revascularization or MI. RESULTS: In 6 months after RD, BP was decreased comparably in both groups. In the group of complicated atherosclerosis, there were no significant changes in profibrotic markers or LVH parameters. Thus, at baseline and after 6 months, the values of the studied indicators were the following: left ventricular myocardial mass (LVMM) 233.1±48.1 and 243.0±52.0 g, LVMM index 60.6±14.5 and 62.8±10 .9 g/m2.7, proMMP-1 4.9 [2.1; 7.7] and 3.6 [2.0; 9.4]  ng/ml, MMP-2 290.4 [233.1; 352.5] and 352.2 [277.4; 402.9] ng/ml, MMP-9 220.6 [126.9; 476.7] and 263.5 [82.9; 726.2] ng/ml, TIMP-1 395.7 [124.7; 591.4] and 424.2 [118.2; 572.0] ng/ml, respectively. In the comparison group, on the contrary, there was a significant decrease in LVMM from 273.6±83.3 g to 254.1±70.4 g, LVMM index from 67.1±12.3 to 64.0±14.4 g/m2.7, proMMP-1 from 7.2 [3.6; 11.7] to 5.9 [3.5; 10.9] ng/ml, MMP-2 from 328.9 [257.1; 378.1] to 272.8 [230.2; 343.2] ng/ml, MMP-9 from 277.9 [137.0; 524.0] to 85.5 [34.2; 225.9] ng/ml, and the MMP-9/TIMP-1 ratio from 0.80 [0.31; 1.30] to 0.24 [0.07; 0.76]. The BP dynamics in this group was inversely correlated with MMP-2 at 6 months (r=-0.38), and the MMP-9/TIMP-1 ratio was correlated with LVMM and the LVMM index at baseline (r=0.39 and r=0.39) and at 6 months (r=0.37 and r=0.32). The change in TIMP-1 from 543.9 [277.5; 674.1] to 469.8 [289.7; 643.6] ng/ml was not significant (p=0.060). CONCLUSION: In RAH patients with complicated coronary atherosclerosis, the dynamics of profibrotic biomarkers and LVH parameters after RD was absent despite the pronounced antihypertensive effect, probably due to the low reversibility of cardiovascular remodeling processes or more complex regulatory mechanisms of the MMP system.

Porcine Model of Hypertrophy-Independent Left Ventricular Stiffening via Repetitive Pressure Overload.

Diastolic dysfunction arising from alterations in myocardial structure and/or function is a central component of several cardiovascular disorders, including heart failure with preserved ejection fraction (HFpEF). Basic research aimed at understanding underlying mechanisms contributing to the development of diastolic dysfunction has generally centered upon models of left ventricular (LV) hypertrophy arising from persistent and severe elevations in myocardial afterload (e.g., aortic banding). Mechanisms of hypertrophy-independent diastolic dysfunction, on the other hand, have received less attention, even though overt anatomic LV hypertrophy is absent in many HFpEF patients. Here, we describe the development of a novel porcine model of repetitive pressure overload (RPO) in which chronic, intermittent exposure to transient episodes of hypertension produces an increase in LV stiffness, interstitial fibrosis, cardiomyocyte hypertrophy, and capillary rarefaction without significant changes in LV mass. This model offers important insight into how diastolic dysfunction and HFpEF may develop in the absence of comorbidities, sustained hypertension, or LV hypertrophy, while also providing a useful translational research tool for investigation of novel therapeutic approaches to restore myocardial compliance and improve diastolic function.

Differential associations between abnormal cardiac left ventricular geometry types and cerebral white matter disease.

OBJECTIVES: Reduced cardiac outflow due to left ventricular hypertrophy has been suggested as a potential risk factor for development of cerebral white matter disease. Our study aimed to examine the correlation between left ventricular geometry and white matter disease volume to establish a clearer understanding of their relationship, as it is currently not well-established. METHODS: Consecutive patients from 2016 to 2021 who were ≥18 years and underwent echocardiography, cardiac MRI, and brain MRI within one year were included. Four categories of left ventricular geometry were defined based on left ventricular mass index and relative wall thickness on echocardiography. White matter disease volume was quantified using an automated algorithm applied to axial T2 FLAIR images and compared across left ventricular geometry categories. RESULTS: We identified 112 patients of which 34.8 % had normal left ventricular geometry, 20.5 % had eccentric hypertrophy, 21.4 % had concentric remodeling, and 23.2 % had concentric hypertrophy. White matter disease volume was highest in patients with concentric hypertrophy and concentric remodeling, compared to eccentric hypertrophy and normal morphology with a trend-P value of 0.028. Patients with higher relative wall thickness had higher white matter disease volume (10.73 ± 10.29 cc vs 5.89 ± 6.46 cc, P = 0.003), compared to those with normal relative wall thickness. CONCLUSION: Our results showed that abnormal left ventricular geometry is associated with higher white matter disease burden, particularly among those with abnormal relative wall thickness. Future studies are needed to explore causative relationships and potential therapeutic options that may mediate the adverse left ventricular remodeling and its effect in slowing white matter disease progression.

Cardio-Ankle Vascular Index as a Marker of Left Ventricular Hypertrophy in Treated Hypertensives: Findings From the Pamela Study.

BACKGROUND: Findings regarding the association between Cardio-Ankle Vascular Index (CAVI) and cardiac hypertension-mediated organ damage (HMOD), such as left ventricular hypertrophy (LVH) assessed by echocardiography, in elderly hypertensive patients are scanty. We sought to investigate this issue in the hypertensive fraction of the general population treated with anti-hypertensive drugs enrolled in the Pressioni Monitorate E Loro Associazioni (PAMELA) study. METHODS: The study included 239 out of 562 participants who attended the second and third surveys of the PAMELA study performed after 10 and 25 years from the initial evaluation. Data collection included medical history, anthropometric parameters, office, home, ambulatory blood pressure (BP), blood examinations, echocardiography, and CAVI measurements. RESULTS: In the whole study sample (age 69 ±â€…9 years, 54% males), CAVI was positively correlated with age, office, home, ambulatory systolic BP, LV mass (LVM) index, and negatively associated with body mass index (BMI). In multivariate analysis, CAVI was associated with the LVM index (P < 0.05) independently of major confounders. The participants with LVH exhibited significantly higher CAVI (10.6 ±â€…2.8 vs. 9.2 ±â€…1.8 m/s P < 0.001), larger left atrial diameter, and lower LV ejection fraction values than their counterparts without it. The CAVI value of 9.4 m/s was the best cut-off for prediction of LVH in the whole sample. CONCLUSIONS: Our study provides new evidence of an independent association between CAVI and LVH in treated elderly hypertensive patients and suggests that the use of this metric of arterial stiffness could not only be used to evaluate vascular damage but also to stratify the risk of LVH.

Association Between Elevated Body Mass Index and Cardiac Organ Damage in Children and Adolescents: Evidence and Mechanisms.

INTRODUCTION: Although a number of pathophysiological aspects of childhood obesity have been reported, few information are available on obesity-related cardiac organ damage. AIM: The present study was aimed at assessing the impact of anthropometric, blood pressure (BP) and metabolic variable on cardiac structure and function in youth. METHODS: In 78 subjects aged 5-16 years attending the outpatient clinic of cardiovascular risk (Valencia, Spain) anthropometric and metabolic variables, clinic and ambulatory BP and echocardiographic parameters were assessed. Subjects were also classified according to the presence of insulin resistance. RESULTS: Subjects mean age (± SD) amounted to 12.03 ± 2.4 years and males to 53.8%. Ten subjects were normoweight, 11 overweight, 39 obese, and 18 severely obese. No significant difference in office and ambulatory BP was detected among different bodyweight groups. A significant direct correlation was observed between left ventricular mass index (LVMI) and obesity markers [body mass index (BMI): r = 0.38, waist circumference (WC): r = 0.46, P < 0.04 for both]. Left ventricular hypertrophy, relative wall thickness and left atrial diameter were significantly related to BMI and WC. In contrast, office and ambulatory BP were unrelated to other variables, and differences in LVMI among different BP phenotypes were not significant. When partitioning the population by insulin resistance, LVMI, adjusted for confounders, was significantly greater in the insulin-resistant group. CONCLUSIONS: In children and adolescents characterized by different body weight patterns, weight factors "per se" and the related insulin resistance state appear to represent the main determinants of LVMI and left ventricular hypertrophy, independently on BP values and BP phenotypes.

Gender Differences in Cardiac Organ Damage in Arterial Hypertension: Assessing the Role of Drug Nonadherence.

INTRODUCTION: Cardiac organ damage like left ventricular (LV) hypertrophy and left atrial (LA) enlargement is more prevalent in women than men with hypertension, but the mechanisms underlying this gender difference remain unclear. METHODS: We tested the association of drug nonadherence with the presence of LV hypertrophy and LA enlargement by echocardiography in 186 women and 337 men with uncontrolled hypertension defined as daytime systolic blood pressure (BP) ≥ 135mmHg despite the prescription of at least two antihypertensive drugs. Drug adherence was assessed by measurements of serum drug concentrations interpreted by an experienced pharmacologist. Aldosterone-renin-ratio (ARR) was measured on actual medication. RESULTS: Women had a higher prevalence of LV hypertrophy (46% vs. 33%) and LA enlargement (79% vs 65%, both p < 0.05) than men, while drug nonadherence (8% vs. 9%, p > 0.514) did not differ. Women were older and had lower serum renin concentration and higher ARR than men, while 24-h systolic BP (141 ± 9 mmHg vs. 142 ± 9 mmHg), and the prevalences of obesity (43% vs. 50%) did not differ (all p > 0.10). In multivariable analyses, female gender was independently associated with a two-fold increased risk of LV hypertrophy (OR 2.01[95% CI 1.30-3.10], p = 0.002) and LA enlargement (OR 1.90 [95% CI 1.17-3.10], p = 0.010), while no association with drug nonadherence was found. Higher ARR was independently associated with LV hypertrophy in men only (OR 2.12 [95% CI 1.12-4.00] p = 0.02). CONCLUSIONS: Among patients with uncontrolled hypertension, the higher prevalence of LV hypertrophy and LA enlargement in women was not explained by differences in drug nonadherence. REGISTRATION: URL:  https://www. CLINICALTRIALS: gov ; Unique identifier: NCT03209154.

Large animal models of pressure overload-induced cardiac left ventricular hypertrophy to study remodelling of the human heart with aortic stenosis.

Pathologic cardiac hypertrophy is a common consequence of many cardiovascular diseases, including aortic stenosis (AS). AS is known to increase the pressure load of the left ventricle, causing a compensative response of the cardiac muscle, which progressively will lead to dilation and heart failure. At a cellular level, this corresponds to a considerable increase in the size of cardiomyocytes, known as cardiomyocyte hypertrophy, while their proliferation capacity is attenuated upon the first developmental stages. Cardiomyocytes, in order to cope with the increased workload (overload), suffer alterations in their morphology, nuclear content, energy metabolism, intracellular homeostatic mechanisms, contractile activity, and cell death mechanisms. Moreover, modifications in the cardiomyocyte niche, involving inflammation, immune infiltration, fibrosis, and angiogenesis, contribute to the subsequent events of a pathologic hypertrophic response. Considering the emerging need for a better understanding of the condition and treatment improvement, as the only available treatment option of AS consists of surgical interventions at a late stage of the disease, when the cardiac muscle state is irreversible, large animal models have been developed to mimic the human condition, to the greatest extend. Smaller animal models lack physiological, cellular and molecular mechanisms that sufficiently resemblance humans and in vitro techniques yet fail to provide adequate complexity. Animals, such as the ferret (Mustello purtorius furo), lapine (rabbit, Oryctolagus cunigulus), feline (cat, Felis catus), canine (dog, Canis lupus familiaris), ovine (sheep, Ovis aries), and porcine (pig, Sus scrofa), have contributed to research by elucidating implicated cellular and molecular mechanisms of the condition. Essential discoveries of each model are reported and discussed briefly in this review. Results of large animal experimentation could further be interpreted aiming at prevention of the disease progress or, alternatively, at regression of the implicated pathologic mechanisms to a physiologic state. This review summarizes the important aspects of the pathophysiology of LV hypertrophy and the applied surgical large animal models that currently better mimic the condition.

Age-dependent implications of left ventricular hypertrophy regression in patients with hypertension.

Left ventricular hypertrophy (LVH) is a significant risk factor for cardiovascular mortality and morbidity in patients with hypertension. However, the effect of age on LVH regression or persistence and its differential prognostic value remain unclear. Therefore, we investigated the clinical implications of LVH regression in 1847 patients with hypertension and echocardiography data (at baseline and during antihypertensive treatment at an interval of 6-18 months) according to age. LVH was defined as a left ventricular mass index (LVMI) > 115 g/m2 and >95 g/m2 in men and women, respectively. LVH prevalence at baseline was not different according to age (age < 65 years: 42.6%; age ≥65 years: 45.7%; p = 0.187), but LVH regression was more frequently observed in the younger group (36.4% vs. 27.5%; p = 0.008). Spline curves and multiple linear regression analysis showed a significant relationship between reductions in systolic blood pressure and LVMI in the younger group (ß = 0.425; p < 0.001), but not the elderly group (ß = 0.044; p = 0.308). LVH regression was associated with a lower risk of the study outcome (composite of cardiovascular death and hospitalization for heart failure) regardless of age. In conclusion, the association between the reduction in blood pressure and LVH regression was prominent in patients with age < 65 years, but not in those with age ≥65 years. However, an association between LVH regression and lower risk of cardiovascular death and hospitalization for heart failure was observed regardless of patient age, suggesting the prognostic value of the LVH regression not only in the younger patients but also in elderly patients.

Renal Denervation Reduces Blood Pressure and Improves Cardiac Function: Results from a 12-Month Study.

Background: Previous studies showed that a decline in BP can reverse pressure-overloaded left ventricular hypertrophy in the long term. Whether this structural remodeling and improved cardiac function were due to reduced BP levels or sympathetic tone is unclear. The aim of this study was to evaluate the efficacy of renal denervation (RDN) on cardiac function and left ventricular hypertrophy in patients diagnosed with resistant hypertension with systolic and diastolic dysfunction. Methods: Thirteen patients diagnosed with resistant hypertension underwent bilateral RDN (RDN group), and 13 patients were selected as the control group (drug group) who received regular antihypertensive drugs for the first time. Demographic analysis and hematologic tests were performed to determine renal function as well as BNP levels. Echocardiogram was performed at baseline and 12 months after RDN. Results: All the baseline characteristics are comparable in two groups. Both RDN and drug regiments resulted in significant reduction from baseline in SBP/DBP at 12-month follow-up (all P values < 0.01), and the decline due to two interventions showed no statistically significant difference (F = 1.64, P = 0.213 and F = 0.124, P = 0.853 for SBP and DBP, respectively). RDN significantly reduced mean LV mass index (LVMI) from 151.43 ± 46.91 g/m2 to 136.02 ± 37.76 g/m2 (P = 0.038) and ejection fraction (LVEF) increased from 57.15 ± 5.49% at baseline to 59.54 ± 4.18% at 12 months (P = 0.039). No similar changes were detected in the drug group (P values, 0.90 for EF and 0.38 for LVMI). Renal parameters including BUN, Cr, UA, and eGFR at baseline, 3 months, and 12 months showed no marked difference (P = 0.497, 0.223, 0.862, 0.075, respectively). Conclusions: Our findings show that in addition to hypertension and its progression, elevated sympathetic hyperactivity is related to left ventricular hypertrophy and cardiac function.

Echocardiographic left ventricular hypertrophy and geometry in Chinese chronic hemodialysis patients: the prevalence and determinants.

BACKGROUND: To investigate the prevalence of left ventricular hypertrophy (LVH) and explore left ventricular geometry in maintenance hemodialysis (MHD) patients, and to explore the risk factors of LVH which is an important predictor of cardiovascular events. METHODS: The subjects were patients who are on MHD for more than 3 months in Peking University People's Hospital from March 2015 to February 2017. Demographic and clinical data were retrospectively collected. Left ventricular mass was measured by echocardiography. LVH is defined by Left ventricular mass index (LVMI) > 115 g/m2 for men and > 95 g/m2 in women. LVMI and relative wall thickness were used to determine left ventricular geometry. Logistic regression was used to analyze the risk factors of LVH. RESULTS: Altogether, 131 patients including 77 males were enrolled. The median age was 60 (47, 69) years, with a median dialysis vintage of 48 (18, 104) months. There were 80 patients with LVH, the prevalence rate was 61.1%, and 66.3% of them were moderate to severe LVH. We found that (1) most of the patients were concentric hypertrophy; (2) one-third of the patients were concentric remodeling; (3) only 4 cases with normal geometry. The pre-dialysis serum sodium level and time average pre-dialysis systolic blood pressure (SBP) were independent risk factors of LVH. CONCLUSION: LVH is prevalent in MHD patients. Concentric hypertrophy and concentric remodeling are the most common geometric patterns. Attention should be paid to long-term pre-dialysis SBP management and pre-dialysis sodium control as they might be potentially modifiable risk factors for LVH.

Relationship of a new anthropometric index with left ventricular hypertrophy in hypertensive patients among the Han Chinese.

BACKGROUND: This study aimed to assess the relationship of a new anthropometric index with left ventricular hypertrophy (LVH) in hypertensive patients among the Han Chinese. METHODS: The study is a community-based cross-sectional study that included 4639 patients with hypertension and integrated clinical and echocardiographic data. Left ventricular (LV) mass was measured by transthoracic echocardiography. LVH was diagnosed by using the criteria of left ventricular mass indexed (LVMI) over 49.2 g/m2.7 for men and 46.7 g/m2.7 for women. Quartiles of a body shape index (ABSI), body roundness index (BRI), waist circumference (WC), and body mass index (BMI) were used regarding LVH prevalence. The logistic regression model was used to determine the odds ratio (OR) and 95% confidence intervals (CI) of the new anthropometric index and LVH. Receiver operating characteristic (ROC) curve analysis was used to evaluate the predictive ability of the obesity indices for LVH risk. RESULTS: The prevalence of LVH increased across quartiles for ABSI, BRI, BMI, and WC. Comparing the lowest with the highest quartile, adjusted OR (95% CI) for LVH were significantly different for BRI 3.86 (3.12-4.77), BMI 3.54 (2.90-4.31), and WC 2.29 (1.88-2.78). No association was observed for ABSI. According to ROC analysis, the area under the curve (AUC) of BRI was (AUC: 0.653, 95% CI 0.637-0.669), BMI (AUC: 0.628, 95% CI 0.612-0.644), WC (AUC: 0.576, 95% CI 0.559-0.593), ABSI (AUC: 0.499, 95% CI 0.482-0.516). CONCLUSIONS: This study shows that LVH prevalence increased per quartile across the Han Chinese population with hypertension for ABSI, BRI, BMI, and WC. There is a significant association between BRI and LVH in hypertensive people, while ABSI was not. BRI showed potential for use as an alternative obesity measure in the assessment of LVH.

O-ring-induced transverse aortic constriction (OTAC) is a new simple method to develop cardiac hypertrophy and heart failure in mice.

Suture-based transverse aortic constriction (TAC) in mice is one of the most frequently used experimental models for cardiac pressure overload-induced heart failure. However, the incidence of heart failure in the conventional TAC depends on the operator's skill. To optimize and simplify this method, we proposed O-ring-induced transverse aortic constriction (OTAC) in mice. C57BL/6J mice were subjected to OTAC, in which an o-ring was applied to the transverse aorta (between the brachiocephalic artery and the left common carotid artery) and tied with a triple knot. We used different inner diameters of o-rings were 0.50 and 0.45 mm. Pressure overload by OTAC promoted left ventricular (LV) hypertrophy. OTAC also increased lung weight, indicating severe pulmonary congestion. Echocardiographic findings revealed that both OTAC groups developed LV hypertrophy within one week after the procedure and gradually reduced LV fractional shortening. In addition, significant elevations in gene expression related to heart failure, LV hypertrophy, and LV fibrosis were observed in the LV of OTAC mice. We demonstrated the OTAC method, which is a simple and effective cardiac pressure overload method in mice. This method will efficiently help us understand heart failure (HF) mechanisms with reduced LV ejection fraction (HFrEF) and cardiac hypertrophy.

Inhibiting cardiac myeloperoxidase alleviates the relaxation defect in hypertrophic cardiomyocytes.

AIMS: Hypertrophic cardiomyopathy (HCM) is characterized by cardiomyocyte hypertrophy and disarray, and myocardial stiffness due to interstitial fibrosis, which result in impaired left ventricular filling and diastolic dysfunction. The latter manifests as exercise intolerance, angina, and dyspnoea. There is currently no specific treatment for improving diastolic function in HCM. Here, we investigated whether myeloperoxidase (MPO) is expressed in cardiomyocytes and provides a novel therapeutic target for alleviating diastolic dysfunction in HCM. METHODS AND RESULTS: Human cardiomyocytes derived from control-induced pluripotent stem cells (iPSC-CMs) were shown to express MPO, with MPO levels being increased in iPSC-CMs generated from two HCM patients harbouring sarcomeric mutations in the MYBPC3 and MYH7 genes. The presence of cardiomyocyte MPO was associated with higher chlorination and peroxidation activity, increased levels of 3-chlorotyrosine-modified cardiac myosin binding protein-C (MYBPC3), attenuated phosphorylation of MYBPC3 at Ser-282, perturbed calcium signalling, and impaired cardiomyocyte relaxation. Interestingly, treatment with the MPO inhibitor, AZD5904, reduced 3-chlorotyrosine-modified MYBPC3 levels, restored MYBPC3 phosphorylation, and alleviated the calcium signalling and relaxation defects. Finally, we found that MPO protein was expressed in healthy adult murine and human cardiomyocytes, and MPO levels were increased in diseased hearts with left ventricular hypertrophy. CONCLUSION: This study demonstrates that MPO inhibition alleviates the relaxation defect in hypertrophic iPSC-CMs through MYBPC3 phosphorylation. These findings highlight cardiomyocyte MPO as a novel therapeutic target for improving myocardial relaxation associated with HCM, a treatment strategy which can be readily investigated in the clinical setting, given that MPO inhibitors are already available for clinical testing.

Association of central arterial blood pressure and left ventricular hypertrophy in patients with chronic kidney disease.

AIMS: In the general population, central arterial blood pressure has proved to be more closely related to left ventricular hypertrophy (LVH) than brachial arterial blood pressure. We aimed to investigate whether this relationship was true in patients with chronic kidney disease (CKD). METHODS: In this retrospective study, we reviewed the medical records of 289 adult patients with CKD from the Zhejiang Provincial People's Hospital in Zhejiang, China. Demographic, echocardiographic and brachial and central blood pressure parameters were retrieved from medical records. Central blood pressure was measured using the SphygmoCor® CvMS (AtCor, Australia) device and its corresponding software. Multivariate logistic regression analyses were performed to identify independent predictors of LVH. Receiver operating characteristic curves were used to determine the ability of central and brachial blood pressure to predict LVH. RESULTS: The left ventricular mass index was positively associated with both central and brachial blood pressures. However, multiple logistic regression analysis demonstrated that a central pulse pressure (CPP) ≥ 58 mm Hg was an independent risk factor for LVH (OR = 5.597, 95%CI 2.363-13.259, p < .001). Brachial pulse pressure is not superior to CPP in predicting LVH (area under the curve [AUC] = 0.695, 95%CI 0.634-0.756, p < .001 vs. AUC = 0.687, 95%CI: 0.626-0.748, p < .001, respectively; p = .4824). CONCLUSION: Our results suggested that, similarly to the general population, CPP is a better parameter for predicting the occurrence of LVH in patients with CKD.