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IntroductionDifferentiating hypertensive heart disease (HHD) from hypertrophic cardiomyopathy (HCM) is crucial yet challenging due to overlapping clinical and morphological features. Recent studies have explored the use of various cardiac magnetic resonance (CMR) parameters to distinguish between these conditions, but findings have remained inconclusive. This study aims to identify which CMR parameters effectively discriminate between HHD and HCM and to investigate their underlying pathophysiological mechanisms through a meta-analysis.MethodsThe researchers conducted a systematic and comprehensive search for all studies that used CMR to discriminate between HHD and HCM and calculated the Hedges'g effect size for each of the included studies, which were then pooled using a random-effects model and tested for the effects of potential influencing variables through subgroup and regression analyses.ResultsIn this review, 26 studies encompassing 1,349 HHD and 1,581 HCM cases were included for meta-analysis. Analysis revealed that HHD showed a significant lower in T1 mapping (g = −0.469, P

BackgroundHypertensive heart disease (HHD) is a major global public health issue resulting from hypertension-induced end-organ damage. The aim of this study was to examine the global impact, risk factors, and age-period-cohort (APC) model of HHD from 1990 to 2019.MethodsData from the 2019 Global Burden of Disease were used to assess age-adjusted HHD prevalence, disability-adjusted life years (DALYs), mortality rates, and contributions of HHD risk factors with 95% uncertainty intervals (UIs). APC models were used to analyze global age, period, and cohort mortality trends for HHD.ResultsIn 2019, 18.6 million prevalent HHD cases led to 1.16 million fatalities and 21.51 million DALYs. Age-adjusted rates were 233.8 (95%UI = 170.5–312.9) per 100,000 individuals for prevalence, 15.2 (11.2–16.7) for mortality, and 268.2 (204.6–298.1) for DALYs. Regionally, the Cook Islands (703.1), Jordan (561.6), and Kuwait (514.9) had the highest age-standardized incidence of HHD in 2019. There were significant increases in HHD prevalence in Andean Latin America (16.7%), western sub-Saharan Africa (5.6%), and eastern sub-Saharan Africa (4.6%). Mortality rate varied widely among countries. Risk factors like elevated systolic blood pressure and high body mass index significant influenced DALY rates, especially in females. The APC model revealed an association between mortality rates and age, with a decreasing mortality risk over time and improved survival rates for a later birth cohort.ConclusionsDespite the reduction in prevalence, HHD remains a significant public health issue, particularly in nations with low sociodemographic indices. To alleviate the impact of HHD, prevention efforts should concentrate on the management of hypertension, weight loss, and lifestyle improvement.

BackgroundDiffuse interstitial myocardial fibrosis is a key common pathological manifestation in hypertensive heart disease (HHD) progressing to heart failure (HF). Angiotensin receptor–neprilysin inhibitors (ARNi), now a front-line treatment for HF, confer benefits independent of blood pressure, signifying a multifactorial mode of action beyond hemodynamic regulation. We aim to test the hypothesis that compared with angiotensin II receptor blockade (ARB) alone, ARNi is more effective in regressing diffuse interstitial myocardial fibrosis in HHD.MethodsRole of ARNi in Ventricular Remodeling in Hypertensive LVH (REVERSE-LVH) is a prospective, randomized, open-label, blinded endpoint (PROBE) clinical trial. Adults with hypertension and left ventricular hypertrophy (LVH) according to Asian sex- and age-specific thresholds on cardiovascular magnetic resonance (CMR) imaging are randomized to treatment with either sacubitril/valsartan (an ARNi) or valsartan (an ARB) in 1:1 ratio for a duration of 52 weeks, at the end of which a repeat CMR is performed to assess differential changes from baseline between the two groups. The primary endpoint is the change in CMR-derived diffuse interstitial fibrosis volume. Secondary endpoints include changes in CMR-derived left ventricular mass, volumes, and functional parameters. Serum samples are collected and stored to assess the effects of ARNi, compared with ARB, on circulating biomarkers of cardiac remodeling. The endpoints will be analyzed with reference to the corresponding baseline parameters to evaluate the therapeutic effect of sacubitril/valsartan vs. valsartan.DiscussionREVERSE-LVH will examine the anti-fibrotic potential of sacubitril/valsartan and will offer mechanistic insights into the clinical benefits of sacubitril/valsartan in hypertension in relation to cardiac remodeling. Advancing the knowledge of the pathophysiology of HHD will consolidate effective risk stratification and personalized treatment through a multimodal manner integrating complementary CMR and biomarkers into the conventional care approach.Clinical Trial Registration: ClinicalTrials.gov, identifier, NCT03553810.

Hypertensive heart disease constitutes functional and structural dysfunction and pathogenesis occurring primarily in the left ventricle, the left atrium and the coronary arteries due to chronic uncontrolled hypertension. Hypertensive heart disease is underreported and the mechanisms underlying its correlates and complications are not well elaborated. In this review, we summarize the current understanding of hypertensive heart disease, we discuss in detail the mechanisms associated with development and complications of hypertensive heart disease especially left ventricular hypertrophy, atrial fibrillation, heart failure and coronary artery disease. We also briefly highlight the role of dietary salt, immunity and genetic predisposition in hypertensive heart disease pathogenesis.

BackgroundLeft ventricular (LV) hypertrophy (LVH) in patients with hypertension is a significant risk factor for cardiovascular mortality and morbidity. However, the prognostic implication of LVH regression after antihypertensive therapy has not been clearly investigated.MethodsPatients who underwent echocardiography at the time of the diagnosis of hypertension and repeated echocardiography at an interval of 6–18 months were retrospectively identified. LVH was defined as LV mass index (LVMI) >115 g/m2 (men) and >95 g/m2 (women). LVH regression was defined as LVH at initial echocardiography with normal geometry or concentric LV remodeling at follow-up echocardiography. Cardiovascular mortality, hospitalization for heart failure (HHF), coronary revascularization, stroke, and aortic events were analyzed according to changes in LVMI and geometry.ResultsOf 1,872 patients, 44.7% (n = 837) had LVH at the time of diagnosis; among these, 30.7% showed LVH regression. The reduction in LVMI was associated with the reduction in BP, especially in those with LVH at baseline. During follow up (median, 50.4 months; interquartile range, 24.9–103.2 months), 68 patients died of cardiovascular causes, 127 had HHF, and 162 had vascular events (coronary revascularization, stroke, and aortic events). Persistent or newly developed LVH during antihypertensive therapy was a significant predictor of cardiovascular mortality and events, especially HHF. On multivariable analysis, women, diabetes, atrial fibrillation, coronary artery disease, larger LVMI and end-diastolic dimension, and less reduction in systolic BP were associated with persistent or newly developed LVH.ConclusionLVH regression in patients with hypertension is associated with a reduction in cardiovascular events and can be used as a prognostic marker.

BackgroundThe differentiation between hypertrophic cardiomyopathy (HCM) and hypertensive heart disease (HHD) is challenging due to similar myocardial hypertrophic phenotype. The purpose of this study is to evaluate the feasibility of cardiovascular magnetic resonance feature tracking (CMR-FT) and late gadolinium enhancement (LGE) to distinguish between HCM and HHD and the potential relationship between myocardial strain and cardiac functional parameters.MethodsOne hundred and seventy subjects (57 HCM, 45 HHD, and 68 controls) underwent 3.0 T CMR, including steady-state free precession cines and LGE images. Global and segmental (basal, mid, and apical) analyses of myocardial radial, circumferential, longitudinal strain, and left ventricular (LV) torsion, as well as global and 16 segments of LGE were assessed. The multivariate analysis was used to predict the diagnostic ability by combining comprehensive myocardial strain parameters and LGE.ResultsGlobal radial strain (GRS), global circumferential strain (GCS), and LV torsion were significantly higher in the HCM group than in the HHD group (GRS, 21.18 ± 7.52 vs. 14.56 ± 7.46%; GCS, −13.34 ± 3.52 vs. −10.11 ± 4.13%; torsion, 1.79 ± 0.69 vs. 1.23 ± 0.65 deg/cm, all P < 0.001). A similar trend was also seen in the corresponding strain rate. As for segmental strain analysis, basal radial strain (BRS), basal circumferential strain (BCS), basal longitudinal strain (BLS), mid-radial strain (MRS), and mid-circumferential strain (MCS) were higher in the HCM group than in the HHD group (all P < 0.001). The receiver operating characteristic (ROC) results showed that the area under the curve (AUC) of LGE in the mid-interventricular septum (mIVS) was the highest among global and segmental LGE analyses. On the multivariate regression analysis, a combined model of LGE (mIVS) with GRS obtained the highest AUC value, which was 0.835 with 88.89% sensitivity and 70.18% specificity, respectively. In addition, for patients with HCM, GRS, GCS, and global longitudinal strain had correlations with LV ejection fraction (LVEF), maximum interventricular septum thickness (IVST max), and left ventricular mass index (LVMi). Torsion was mildly associated with LVEF.ConclusionCMR-FT-derived myocardial strain and torsion provided valuable methods for evaluation of HCM and HHD. In addition, the combination of GRS and LGE (mIVS) achieved the highest diagnostic value.

Introduction: Differentiating hypertensive heart disease (HHD) from hypertrophic cardiomyopathy (HCM) is crucial yet challenging due to overlapping clinical and morphological features. Recent studies have explored the use of various cardiac magnetic resonance (CMR) parameters to distinguish between these conditions, but findings have remained inconclusive. This study aims to identify which CMR parameters effectively discriminate between HHD and HCM and to investigate their underlying pathophysiological mechanisms through a meta-analysis., Methods: The researchers conducted a systematic and comprehensive search for all studies that used CMR to discriminate between HHD and HCM and calculated the Hedges'g effect size for each of the included studies, which were then pooled using a random-effects model and tested for the effects of potential influencing variables through subgroup and regression analyses., Results: In this review, 26 studies encompassing 1,349 HHD and 1,581 HCM cases were included for meta-analysis. Analysis revealed that HHD showed a significant lower in T1 mapping (g = -0.469, P  < 0.001), extracellular volume (g = -0.417, P  = 0.024), left ventricular mass index (g = -0.437, P  < 0.001), and maximal left ventricular wall thickness (g = -2.076, P  < 0.001), alongside a significant higher in end-systolic volume index (g = 0.993, P  < 0.001) and end-diastolic volume index (g = 0.553, P  < 0.001), compared to HCM., Conclusion: This study clearly demonstrates that CMR parameters can effectively differentiate between HHD and HCM. HHD is characterized by significantly lower diffuse interstitial fibrosis and myocardial hypertrophy, along with better-preserved diastolic function but lower systolic function, compared to HCM. The findings highlight the need for standardized CMR protocols, considering the significant influence of MRI machine vendors, post-processing software, and study regions on diagnostic parameters. These insights are crucial for improving diagnostic accuracy and optimizing treatment strategies for patients with HHD and HCM., Systematic Review Registration: https://www.crd.york.ac.uk/prospero/display&#95;record.php?ID=CRD42023470557, PROSPERO (CRD42023470557)., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (© 2024 Zhao, Chen, Qi, Xu, Ren, Li, Zhang and Zhang.)

Background: Hypertensive heart disease (HHD) is a major global public health issue resulting from hypertension-induced end-organ damage. The aim of this study was to examine the global impact, risk factors, and age-period-cohort (APC) model of HHD from 1990 to 2019., Methods: Data from the 2019 Global Burden of Disease were used to assess age-adjusted HHD prevalence, disability-adjusted life years (DALYs), mortality rates, and contributions of HHD risk factors with 95% uncertainty intervals (UIs). APC models were used to analyze global age, period, and cohort mortality trends for HHD., Results: In 2019, 18.6 million prevalent HHD cases led to 1.16 million fatalities and 21.51 million DALYs. Age-adjusted rates were 233.8 (95%UI = 170.5-312.9) per 100,000 individuals for prevalence, 15.2 (11.2-16.7) for mortality, and 268.2 (204.6-298.1) for DALYs. Regionally, the Cook Islands (703.1), Jordan (561.6), and Kuwait (514.9) had the highest age-standardized incidence of HHD in 2019. There were significant increases in HHD prevalence in Andean Latin America (16.7%), western sub-Saharan Africa (5.6%), and eastern sub-Saharan Africa (4.6%). Mortality rate varied widely among countries. Risk factors like elevated systolic blood pressure and high body mass index significant influenced DALY rates, especially in females. The APC model revealed an association between mortality rates and age, with a decreasing mortality risk over time and improved survival rates for a later birth cohort., Conclusions: Despite the reduction in prevalence, HHD remains a significant public health issue, particularly in nations with low sociodemographic indices. To alleviate the impact of HHD, prevention efforts should concentrate on the management of hypertension, weight loss, and lifestyle improvement., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (© 2024 Gao, Chen, Yan and Bao.)

Aim: The aim of the work was to study the circulating microRNA-133a levels in blood plasma of patients with arterial hypertension (AH), hypertensive heart disease (HHD), and left ventricular (LV) diastolic dysfunction (DD).Materials and Methods: A total of 48 patients with grade 2–3 AH and HHD at the age of 52.23 ± 7.26 (23 patients had LV DD [main group] and 25 patients had normal LV diastolic function [comparison group]) and 21 practically healthy individuals of comparable gender and age were examined. Diagnosis of AH and HHD was carried out according to the 2018 ESC/ESH recommendations. LV DD was determined according to the 2016 ASE/EACVI recommendations. Plasma microRNA-133a level was obtained by polymerase chain reaction using the CFX96 Touch System (BioRad), ≪TaqMan microRNA Assay≫ and ≪TaqMan® Universal PCR Master Mix≫ reagent kits (Thermo Fisher Scientific, USA).Results: We have found that in patients from the main and comparison groups plasma microRNA-133a levels were significantly lower than in practically healthy individuals (0.094 [0.067, 0.147]) and (0.182 [0.102, 0.301]) vs. (0.382 [0.198,0.474]), p = 0.002 and p = 0.04, respectively. In all this among patients with AH, HHD, and LV DD, plasma microRNA-133a levels were significantly lower than in patients with AH, HHD, and normal diastolic function (p = 0.03). In the main and comparison groups there was a statistically significant negative relationship between plasma microRNA-133a level and left ventricular mass index (LVMI) (R = −0.40, p = 0.003 and R = −0.35, p = 0.04, respectively).Conclusions: The findings suggest the significant role of decreased microRNA-133a levels in blood plasma of patients with AH in the pathogenesis and development of both HHD and LV DD.

Background: Diffuse interstitial myocardial fibrosis is a key common pathological manifestation in hypertensive heart disease (HHD) progressing to heart failure (HF). Angiotensin receptor-neprilysin inhibitors (ARNi), now a front-line treatment for HF, confer benefits independent of blood pressure, signifying a multifactorial mode of action beyond hemodynamic regulation. We aim to test the hypothesis that compared with angiotensin II receptor blockade (ARB) alone, ARNi is more effective in regressing diffuse interstitial myocardial fibrosis in HHD., Methods: Role of ARNi in Ventricular Remodeling in Hypertensive LVH (REVERSE-LVH) is a prospective, randomized, open-label, blinded endpoint (PROBE) clinical trial. Adults with hypertension and left ventricular hypertrophy (LVH) according to Asian sex- and age-specific thresholds on cardiovascular magnetic resonance (CMR) imaging are randomized to treatment with either sacubitril/valsartan (an ARNi) or valsartan (an ARB) in 1:1 ratio for a duration of 52 weeks, at the end of which a repeat CMR is performed to assess differential changes from baseline between the two groups. The primary endpoint is the change in CMR-derived diffuse interstitial fibrosis volume. Secondary endpoints include changes in CMR-derived left ventricular mass, volumes, and functional parameters. Serum samples are collected and stored to assess the effects of ARNi, compared with ARB, on circulating biomarkers of cardiac remodeling. The endpoints will be analyzed with reference to the corresponding baseline parameters to evaluate the therapeutic effect of sacubitril/valsartan vs. valsartan., Discussion: REVERSE-LVH will examine the anti-fibrotic potential of sacubitril/valsartan and will offer mechanistic insights into the clinical benefits of sacubitril/valsartan in hypertension in relation to cardiac remodeling. Advancing the knowledge of the pathophysiology of HHD will consolidate effective risk stratification and personalized treatment through a multimodal manner integrating complementary CMR and biomarkers into the conventional care approach. Clinical Trial Registration : ClinicalTrials.gov, identifier, NCT03553810., Competing Interests: JB is a consultant to Abbott, American Regent, Amgen, Applied Therapeutic, AstraZeneca, Bayer, Boehringer Ingelheim, Bristol Myers Squibb, Cardiac Dimension, Cardior, CVRx, Cytokinetics, Edwards, Element Science, Innolife, Impulse Dynamics, Imbria, Inventiva, Lexicon, Lilly, LivaNova, Janssen, Medtronics, Merck, Occlutech, Novartis, Novo Nordisk, Pfizer, Pharmacosmos, Pharmain, Roche, Sequana, SQ Innovation, and Vifor. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (© 2023 Lee, Zheng, Toh, Pua, Bryant, Lee, Cook, Butler, Díez, Richards, Le and Chin.)

Hypertensive heart disease constitutes functional and structural dysfunction and pathogenesis occurring primarily in the left ventricle, the left atrium and the coronary arteries due to chronic uncontrolled hypertension. Hypertensive heart disease is underreported and the mechanisms underlying its correlates and complications are not well elaborated. In this review, we summarize the current understanding of hypertensive heart disease, we discuss in detail the mechanisms associated with development and complications of hypertensive heart disease especially left ventricular hypertrophy, atrial fibrillation, heart failure and coronary artery disease. We also briefly highlight the role of dietary salt, immunity and genetic predisposition in hypertensive heart disease pathogenesis., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (© 2023 Masenga and Kirabo.)

Background: Left ventricular (LV) hypertrophy (LVH) in patients with hypertension is a significant risk factor for cardiovascular mortality and morbidity. However, the prognostic implication of LVH regression after antihypertensive therapy has not been clearly investigated., Methods: Patients who underwent echocardiography at the time of the diagnosis of hypertension and repeated echocardiography at an interval of 6-18 months were retrospectively identified. LVH was defined as LV mass index (LVMI) >115 g/m 2 (men) and >95 g/m 2 (women). LVH regression was defined as LVH at initial echocardiography with normal geometry or concentric LV remodeling at follow-up echocardiography. Cardiovascular mortality, hospitalization for heart failure (HHF), coronary revascularization, stroke, and aortic events were analyzed according to changes in LVMI and geometry., Results: Of 1,872 patients, 44.7% ( n = 837) had LVH at the time of diagnosis; among these, 30.7% showed LVH regression. The reduction in LVMI was associated with the reduction in BP, especially in those with LVH at baseline. During follow up (median, 50.4 months; interquartile range, 24.9-103.2 months), 68 patients died of cardiovascular causes, 127 had HHF, and 162 had vascular events (coronary revascularization, stroke, and aortic events). Persistent or newly developed LVH during antihypertensive therapy was a significant predictor of cardiovascular mortality and events, especially HHF. On multivariable analysis, women, diabetes, atrial fibrillation, coronary artery disease, larger LVMI and end-diastolic dimension, and less reduction in systolic BP were associated with persistent or newly developed LVH., Conclusion: LVH regression in patients with hypertension is associated with a reduction in cardiovascular events and can be used as a prognostic marker., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Kim, Hwang, Choi, Yoon and Cho.)

Background: The differentiation between hypertrophic cardiomyopathy (HCM) and hypertensive heart disease (HHD) is challenging due to similar myocardial hypertrophic phenotype. The purpose of this study is to evaluate the feasibility of cardiovascular magnetic resonance feature tracking (CMR-FT) and late gadolinium enhancement (LGE) to distinguish between HCM and HHD and the potential relationship between myocardial strain and cardiac functional parameters., Methods: One hundred and seventy subjects (57 HCM, 45 HHD, and 68 controls) underwent 3.0 T CMR, including steady-state free precession cines and LGE images. Global and segmental (basal, mid, and apical) analyses of myocardial radial, circumferential, longitudinal strain, and left ventricular (LV) torsion, as well as global and 16 segments of LGE were assessed. The multivariate analysis was used to predict the diagnostic ability by combining comprehensive myocardial strain parameters and LGE., Results: Global radial strain (GRS), global circumferential strain (GCS), and LV torsion were significantly higher in the HCM group than in the HHD group (GRS, 21.18 ± 7.52 vs. 14.56 ± 7.46%; GCS, -13.34 ± 3.52 vs. -10.11 ± 4.13%; torsion, 1.79 ± 0.69 vs. 1.23 ± 0.65 deg/cm, all P < 0.001). A similar trend was also seen in the corresponding strain rate. As for segmental strain analysis, basal radial strain (BRS), basal circumferential strain (BCS), basal longitudinal strain (BLS), mid-radial strain (MRS), and mid-circumferential strain (MCS) were higher in the HCM group than in the HHD group (all P < 0.001). The receiver operating characteristic (ROC) results showed that the area under the curve (AUC) of LGE in the mid-interventricular septum (mIVS) was the highest among global and segmental LGE analyses. On the multivariate regression analysis, a combined model of LGE (mIVS) with GRS obtained the highest AUC value, which was 0.835 with 88.89% sensitivity and 70.18% specificity, respectively. In addition, for patients with HCM, GRS, GCS, and global longitudinal strain had correlations with LV ejection fraction (LVEF), maximum interventricular septum thickness (IVST max), and left ventricular mass index (LVMi). Torsion was mildly associated with LVEF., Conclusion: CMR-FT-derived myocardial strain and torsion provided valuable methods for evaluation of HCM and HHD. In addition, the combination of GRS and LGE (mIVS) achieved the highest diagnostic value., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Liu, Li, Zhao, Wang, Wu, Gu, Xu, Li, Tian, Cui, Wang and Yu.)

Aim: The aim of the work was to study the circulating microRNA-133a levels in blood plasma of patients with arterial hypertension (AH), hypertensive heart disease (HHD), and left ventricular (LV) diastolic dysfunction (DD). Materials and Methods: A total of 48 patients with grade 2-3 AH and HHD at the age of 52.23 ± 7.26 (23 patients had LV DD [main group] and 25 patients had normal LV diastolic function [comparison group]) and 21 practically healthy individuals of comparable gender and age were examined. Diagnosis of AH and HHD was carried out according to the 2018 ESC/ESH recommendations. LV DD was determined according to the 2016 ASE/EACVI recommendations. Plasma microRNA-133a level was obtained by polymerase chain reaction using the CFX96 Touch System (BioRad), ≪TaqMan microRNA Assay≫ and ≪TaqMan® Universal PCR Master Mix≫ reagent kits (Thermo Fisher Scientific, USA). Results: We have found that in patients from the main and comparison groups plasma microRNA-133a levels were significantly lower than in practically healthy individuals (0.094 [0.067, 0.147]) and (0.182 [0.102, 0.301]) vs. (0.382 [0.198,0.474]), p = 0.002 and p = 0.04, respectively. In all this among patients with AH, HHD, and LV DD, plasma microRNA-133a levels were significantly lower than in patients with AH, HHD, and normal diastolic function ( p = 0.03). In the main and comparison groups there was a statistically significant negative relationship between plasma microRNA-133a level and left ventricular mass index (LVMI) ( R = -0.40, p = 0.003 and R = -0.35, p = 0.04, respectively). Conclusions: The findings suggest the significant role of decreased microRNA-133a levels in blood plasma of patients with AH in the pathogenesis and development of both HHD and LV DD., (Copyright © 2020 Koval, Snihurska, Yushko, Mysnychenko, Penkova, Lytvynova, Berezin and Lytvynov.)