THE ROLE OF LEFT VENTRICULAR HYPERTROPHY, RS1801253 AND RS1801252 ALLELIC POLYMORPHISMS OF ADRB1 IN ASSESSING THE RISK OF SUDDEN CARDIAC DEATH IN PATIENTS WITH ARTERIAL HYPERTENSION.

OBJECTIVE: The aim: To study the association of left ventricular hypertrophy (LVH) and polymorphisms rs1801253 and rs1801252 of the ADRB1 gene with the risk of sudden cardiac death (SCD). PATIENTS AND METHODS: Materials and methods: The study included 179 patients which underwent clinical investigation, echocardiography, elektrokardiography. The examined were divided into groups with a low (110 people) and high risk (69 people) of SCD. The distribution of allelic polymorphisms was investigated with polymerase chain reaction (PCR). RESULTS: Results: All patients of group with high-risk cardiovascular mortality showed a decrease in heart rate variability (RV) due to an increase in sympathetic activity (p=0.013). Also, in the group of patients with LVH, predictors of sudden cardiac death and arrhythmogenic substrate, were observed. The variability of the allele C1165G rs1801253 of the ADRB1 gene was associated with an increased risk (2.55-fold increase) of SCD and LVH. Also, the associations of polymorphic locus A145G (rs1801252) of the ADRB1 gene proved the presence of a permanent difference for the "risky" allele A in patients with a high risk of SCD. CONCLUSION: Conclusions: It was set the probable association of alleles rs1801253 (C1165G) and rs1801252 (A145G) ADRB1 at the patients with a high risk of SCD compared to the control group.

Left Atrial Strain Imaging by Speckle Tracking Echocardiography: The Supportive Diagnostic Value in Cardiac Amyloidosis and Hypertrophic Cardiomyopathy.

Background: Left atrial (LA) function is crucial for assessing left ventricular filling in various cardiovascular conditions. Cardiac Amyloidosis (CA) is characterized by atrial myopathy and LA function impairment, with diastolic dysfunction up to restrictive filling pattern, leading to progressive heart failure and arrhythmias. This study evaluates LA function and deformation using speckle tracking echocardiography (STE) in patients with CA compared to a cohort of patients with sarcomeric Hypertrophic Cardiomyopathy (HCM) and a control group. Methods: We conducted a retrospective, observational study (from January 2019 to December 2022) including a total of 100 patients: 33 with ATTR-CA, 34 with HCMs, and 33 controls. Clinical evaluation, electrocardiograms, and transthoracic echocardiography were performed. Echocardiogram images were analyzed in post-processing using EchoPac software for LA strain quantification, including LA-reservoir, LA-conduit, and LA-contraction strain. Results: The CA group exhibited significantly impaired LA function compared to HCMs and control groups, with LA-reservoir median values of -9%, LA-conduit -6.7%, and LA-contraction -3%; this impairment was consistent even in the CA subgroup with preserved ejection fraction. LA strain parameters correlated with LV mass index, LA volume index, E/e', and LV-global longitudinal strain and were found to be associated with atrial fibrillation and exertional dyspnea. Conclusions: LA function assessed by STE is significantly impaired in CA patients compared to HCMs patients and healthy controls. These findings highlight the potential supportive role of STE in the early detection and management of the disease.

Direct and indirect effects of fibroblast growth factor 23 on the heart.

Fibroblast growth factor (FGF)23 is a bone-derived phosphotropic hormone that regulates phosphate and mineral homeostasis. Recent studies have provided evidence that a high plasma concentration of FGF23 is associated with cardiac disease, including left ventricular hypertrophy (LVH), heart failure, atrial fibrillation, and cardiac death. Experimental studies have shown that FGF23 activates fibroblast growth factor receptor 4 (FGFR4)/phospholipase Cγ/calcineurin/nuclear factor of activated T-cells signaling in cardiomyocytes and induces cardiac hypertrophy in rodents. Activation of FGFR4 by FGF23 normally requires the co-receptor α-klotho, and klotho-independent signaling occurs only under conditions characterized by extremely high FGF23 concentrations. Recent studies have demonstrated that FGF23 activates the renin-angiotensin-aldosterone system (RAAS) and induces LVH, at least in part as a result of lower vitamin D activation. Moreover, crosstalk between FGF23 and RAAS results in the induction of cardiac hypertrophy and fibrosis. In this review, we summarize the results of studies regarding the relationships between FGF23 and cardiac events, and describe the potential direct and indirect mechanisms whereby FGF23 induces LVH.

Morphological, functional, and biomechanical progression of LV remodelling in a porcine model of HFpEF.

Heart failure (HF) with preserved ejection fraction (HFpEF) accounts for about half of heart failure cases, but the progression of cardiac biomechanics during pathogenesis is not completely understood. We investigated a published porcine model of HFpEF, generated by progressive constriction of an aortic cuff causing progressive left ventricle (LV) pressure overload, and characterized by hypertrophy, diastolic dysfunction and overt HF with elevated plasma beta natriuretic peptide (BNP). We characterized morphological and functional features and performed image-based finite element modelling over multiple time points, so as to understand how biomechanics evolved with morphological and functional changes during pathogenesis, and to provide data for future growth and remodeling investigations. Results showed that the hypertrophic responses quickly manifested and were effective at preventing an elevation of systolic myocardial stresses, suggesting active compensated remodeling. Consequent to the hypertrophy, diastolic myocardial stresses decreased despite the elevations in diastolic pressures. The left ventricle hypertrophy (LVH) myocardium also exhibited a quick elevation of active tension at the onset of the disease. There was a progressive and significant decrease in myocardial strain, which was more significant in the longitudinal direction. Further, elevated myocardial stiffness and diastolic pressures, which reflected diastolic dysfunction, also manifested, but this was delayed from the onset of the disease. Correlation analysis showed that hypertrophy was closely correlated to systolic pressure, active tension and systolic myocardial stress, suggesting that these factors may play a role in initiating hypertrophy. Myocardial stiffness was weakly correlated to LV pressures and myocardial stresses.

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.

Ventricular-Arterial Uncoupling and Hypertension Mediated Diastolic Dysfunction.

INTRODUCTION: The increase in the pulsatile component of left ventricle afterload is suspected to cause a mismatch between the left ventricle (LV) and the vascular tree. AIM: To demonstrate that ventricular-arterial uncoupling is frequently present in the development of LV hypertrophy (H) and diastolic dysfunction (DD) in hypertension (HBP). METHODS: Observational study, HBP patients with ejection fraction > 54%. Conventional 2D echocardiography and tissue Doppler performed following imaging guidelines. LV end systolic elastance (Ees), the effective arterial elastance (Ea), and ventricular-arterial coupling (VAC) measured by Chen single beat method. RESULTS: 288 patients, mean age 56.3 ± 12.5 years and 168 patients (58.3%) males. Mean LV mass index was 87.2 ± 20.4 grs/m2 and frequency of LVH 20.1% (58 patients). The mean VAC was 0.54 ± 9.23. LV Stroke volume, stroke work and systolic stress were 46.2 ± 10.3 cc/m2, 91.4 ± 22.2 g-min/m2, and 57 ± 14.6 dynes/cm2 in quartile 1, and 33.5 ± 6.6 cc/m2, 65.5 ± 15.2 g-min/m2, and 77.8 ± 17.1 dynes/cm2, in quartile 4, respectively (p < 0.001). Peripheral resistance index was 3349 ± 1072 and 4410 ± 1143 dynes*s/cm-5/m2 quartiles 1 vs. 4 (p < 0.005). The frequency of LVH was 31.9% in quartile 1 and 11.3% in quartile 4 (p < 0.005) and LVH or DD was 37.5% and 12.7%, respectively (p < 0.001). CONCLUSIONS: Stroke volume and stroke work were significantly increased while systolic stress and peripheral resistance index were significantly reduced in patients with worst VAC. Ventricular-arterial uncoupling is mostly caused by an increase in Ees rather than by an elevation of Ea. LVH or DD are more frequent in the worst cases of ventricular-arterial uncoupling.

Co-simulation of hypertensive left ventricle based on computational fluid dynamics and a closed-loop network model.

OBJECTIVE: Hypertension is one of the most common chronic and cardiovascular diseases, with the largest number of deaths. According to clinical experience, long-term hypertension will cause cardiac hypertrophy and other complications, and heart structure remodeling will significantly change the energy characteristics of the heart chambers, and impair heart function. Research shows that, early hypertension can be diagnosed by the blood flow and energy loss in the left ventricle. Therefore, it is important to choose an appropriate method to simulate and predict the flow domain of this ventricle. METHODS: This study took the left ventricular flow field of patients with hypertensive myocardial hypertrophy as the research object, used MATLAB-SIMULINK to establish a closed-loop network cardiovascular model, provided flow boundary conditions for the computational fluid dynamics (CFD) numerical simulation method, and, finally, completed a co-simulation. RESULTS: This article compared the degree of agreement between the energy loss in different phases of the heart cavity and clinical experimental data and summarized the characteristics of the flow field in patients with hypertensive myocardial hypertrophy. The analysis of three simulation groups (control group, non-left ventricular hypertrophy group, and left ventricular hypertrophy [LVH] group) showed that the vortices in the LVH group were irregular and not fully developed, accompanied by significant energy loss. CONCLUSION: The simulation method used in this study is basically consistent with the clinical data. Myocardial hypertrophy has a significant influence on the blood flow of the left ventricle. Changes in the blood flow make the left ventricular vortex distribution abnormal during the rapid systole and rapid ejection periods, leading to a series of dangerous factors, including increased energy loss and a low cardiac ejection fraction.

Association of deep white matter hyperintensity with left ventricular hypertrophy in acute ischemic stroke.

BACKGROUND AND PURPOSE: White matter hyperintensities (WMHs) are associated with the presence of left ventricular hypertrophy (LVH). It is unclear if periventricular WMH (PV-WMH) and or deep WMH (D-WMH) are associated with LVH. We evaluated the association of PV-WMH and D-WMH with common transthoracic echocardiogram abnormalities, including LVH in acute ischemic stroke. METHODS: PV-WMH and D-WMH were graded on a 0-3 score based on the Fazekas scale. Patients were categorized into clinically significant PV-WMH and D-WMH (score 2-3) and controls (score 0-1). Multivariate logistic regression analysis was performed to determine abnormalities on echocardiogram associated with PV-WMH and D-WMH. RESULTS: Among 272 patients, 137 patients had PV-WMH and 93 patients had D-WMH with a score of 2-3 on Fazekas scale. Compared to controls, patients with PV-WMH (mean age±standard deviation: 60.8±14.4 vs. 73.8±11.2 years) and D-WMH (63.4±14.4 vs. 75.0±11.1 years) were older. Compared to controls, PV-WMH was associated with history of stroke (22 [16%] vs. 37 [27%], p = .03) and valvular calcification (33 [24%] vs. 61 [45%], p = .0005); D-WMH was associated with history of atrial fibrillation (25 [14%] vs. 22 [24%], p = .04), valvular calcification (50 [28%] vs. 44 [47%], p = .001), and LVH (30 [17%] vs. 25 [27%], p = .049). In multivariate analysis, PV-WMH was associated with age (odds ratio [OR] = 1.09; 95% confidence interval [CI] = 1.06-1.12) and stroke history (OR = 2.1; 95% CI = 1.1-4.1), and D-WMH was associated with age (OR = 1.07; 95% CI = 1.05-1.10) and LVH (OR = 2.0; 95% CI = 1.0-4.0). CONCLUSION: LVH is associated with D-WMH but not with PV-WMH. Although valvular calcification is common, it is likely age related than due to WMH.

Cardiac Magnetic Resonance in Hypertensive Heart Disease: Time for a New Chapter.

Hypertension is one of the most important cardiovascular risk factors, associated with significant morbidity and mortality. Chronic high blood pressure leads to various structural and functional changes in the myocardium. Different sophisticated imaging methods are developed to properly estimate the severity of the disease and to prevent possible complications. Cardiac magnetic resonance can provide a comprehensive assessment of patients with hypertensive heart disease, including accurate and reproducible measurement of left and right ventricle volumes and function, tissue characterization, and scar quantification. It is important in the proper evaluation of different left ventricle hypertrophy patterns to estimate the presence and severity of myocardial fibrosis, as well as to give more information about the benefits of different therapeutic modalities. Hypertensive heart disease often manifests as a subclinical condition, giving exceptional value to cardiac magnetic resonance as an imaging modality capable to detect subtle changes. In this article, we are giving a comprehensive review of all the possibilities of cardiac magnetic resonance in patients with hypertensive heart disease.

Serum Zinc and Selenium Concentrations in Patients with Hypertrophy and Remodelling of the Left Ventricle Secondary to Arterial Hypertension.

The aim of the study was to assess the relationship between serum selenium and zinc concentrations (Se-S and Zn-S) and the left ventricle geometry in patients suffering from arterial hypertension. A total of 78 people with arterial hypertension (mean age: 53.72 ± 12.74 years) participated in the study. Se-S and Zn-S were determined in all patients. The type of left ventricular remodelling and hypertrophy was determined by the left ventricular mass index (LVMI) and relative wall thickness (RWT) measured by echocardiography. Se-S and Zn-S in the whole group were 89.84 ± 18.75 µg/L and 0.86 ± 0.13 mg/L. Normal left ventricular geometry was found in 28.2% of patients; left ventricular hypertrophy (LVH) in 71.8%, including concentric remodelling in 28.2%, concentric hypertrophy in 29.5%, and eccentric hypertrophy in 14.1%. LVH was statistically significantly more frequent in patients with Se-S < median compared to patients with Se-S ≥ median (87.2% vs. 56.4%, p < 0.05), as well as in patients with Zn-S < median compared to patients with Zn-S ≥ median (83.8% vs. 60.9%, p < 0.05). In hypertensive patients, older age, higher LDL cholesterol, higher fasting glucose, lower Se-S, and lower Zn-S were independently associated with LVH. In conclusion, in hypertensive patients, left ventricular hypertrophy may be associated with low levels of selenium and zinc in the serum.

Association of Maternal Gestational Weight Gain With Left Ventricle Geometry and Function in Offspring at 4 Years of Age: A Prospective Birth Cohort Study.

Background: Maternal gestational weight gain (GWG) may be associated with cardiovascular diseases in the offspring from childhood to adulthood. We aimed to investigate the association between maternal GWG and the left ventricle (LV) geometry and function in the offspring, and explore the influence of the intrauterine environment on early childhood cardiac change. Methods: Data of 981 mother-offspring pairs from the Shanghai Birth Cohort was used. Maternal pre-pregnancy weight and height, weight in the first trimester (≤ 12 weeks), and before delivery were measured. The echocardiography, blood pressure, and anthropometry assessment were evaluated in the offspring at 4 years of age. Results: Interventricular septal thickness during diastole had a significantly positive correlation with total GWG [ß = 0.009, (0.001, 0.017)]. In the second and third trimesters, LV mass index [ß = 0.149, (0.015,0.282)], interventricular septal thickness in systole [ß = 0.027, (0.011,0.043)], and in diastole [ß = 0.014, (0.005,0.023)] were positively associated with GWG. The risks of eccentric [OR = 1.115, (1.232, 1.010)] and concentric hypertrophy [OR = 1.133, (1.259,1.018)] increased with the elevation of maternal GWG. Conclusions: This study suggested that the excessive maternal GWG was associated with the thickening of the interventricular septum in the offspring, especially during the second and third trimesters. Excessive GWG in the second and third trimesters was a risk factor for LV eccentric and concentric hypertrophy in the offspring.

Role of metabolomics in identifying cardiac hypertrophy: an overview of the past 20 years of development and future perspective.

Cardiac hypertrophy (CH) is an augmentation of either the right ventricular or the left ventricular mass in order to compensate for the increase of work load on the heart. Metabolic abnormalities lead to histological changes of cardiac myocytes and turn into CH. The molecular mechanisms that lead to initiate CH have been of widespread concern, hence the development of the new field of research, metabolomics: one 'omics' approach that can reveal comprehensive information of the paradigm shift of metabolic pathways network in contrast to individual enzymatic reaction-based metabolites, have attempted and until now only 19 studies have been conducted using experimental animal and human specimens. Nuclear magnetic resonance spectroscopy and mass spectrometry-based metabolomics studies have found that CH is a metabolic disease and is mainly linked to the harmonic imbalance of glycolysis, citric acid cycle, amino acids and lipid metabolism. The current review will summarise the main outcomes of the above mentioned 19 studies that have expanded our understanding of the molecular mechanisms that may lead to CH and eventually to heart failure.

Sex-Specific Association of Left Ventricular Hypertrophy With Rheumatoid Arthritis.

Objectives: Clinical expression of rheumatoid arthritis (RA) varies by gender, but whether cardiovascular disease (CVD) is gender related in RA is unknown. Left ventricular (LV) hypertrophy (LVH) is a hallmark of CVD in RA patients. We investigated whether the association of LVH with RA is gender driven. Methods: Consecutive outpatients with established RA underwent echocardiography with measurement of LVH at baseline and one follow-up. All participants had no prior history of CVD or diabetes mellitus. We assessed CVD risk factors associated with LVH at follow-up, including sex, age, arterial blood pressure, and body mass index (BMI). We also evaluated inflammatory markers, autoimmunity, disease activity, and the use of RA medications as predictors of LVH. Results: We recruited 145 RA patients (121 females, 83%) and reassessed them after a median (interquartile range) of 36 months (24-50). At baseline, women were more dyslipidemic but otherwise had fewer CVD risk factors than men, including less prevalent smoking habit and hypertension, and smaller waist circumference. At follow-up, we detected LVH in 42/145 (44%) RA patients. LV mass significantly increased only in women. In multiple Cox regression analysis, women with RA had the strongest association with LVH, independently from the presence of CVD risk factors (OR, 6.56; 95% CI, 1.34-30.96) or RA-specific characteristics (OR, 5.14; 95% CI, 1.24-21.34). BMI was also significantly and independently associated with LVH. Conclusion: Among established RA patients, women carry the highest predisposition for LVH.

Valor diagnóstico del índice de Sokolow-Lyon en la hipertrofia ventricular izquierda

RESUMEN Introducción: La hipertrofia de ventrículo izquierdo constituye un gran problema entre los pacientes con hipertensión arterial a nivel mundial, además se relaciona con diversas enfermedades, las cuales pueden ser fatales. Objetivo: Evaluar el rendimiento diagnóstico del índice de Sokolow-Lyon en derivaciones precordiales para la hipertrofia de ventrículo izquierdo. Método: Se realizó un estudio de medios diagnósticos de tipo observacional, analítico y transversal. Se estudiaron 122 pacientes ingresados en los servicios de Medicina Interna, Nefrología y Neurología del Hospital Militar Carlos J. Finlay (La Habana, Cuba) de enero del 2017 a marzo del 2019, a los cuales se les realizó ecocardiograma y electrocardiograma. Resultados: Existió un predominio de la población mayor de 45 años (77,9%), del sexo masculino (59,8%) y con hipertensión arterial (77,0%). Se realizó una descripción cualitativa del índice electrocardiográfico de Sokolow-Lyon para precordiales en el total de casos estudiados y se encontró una prevalencia de hipertrofia ventricular izquierda de 71,3%. Este criterio de voltaje presentó una alta especificidad (83%), alto valor predictivos positivo (85%) y una razón de verosimilitud (likelihood ratio) positiva de 2,28. Conclusiones: En pacientes hospitalizados, donde la prevalencia de hipertensión arterial es elevada, el criterio de Sokolow-Lyon presentó alta utilidad diagnóstica para la hipertrofia de ventrículo izquierdo, así como para confirmar los casos que verdaderamente la padecían.

ABSTRACT Introduction: Left ventricular hypertrophy is a major problem among patients with high blood pressure worldwide; it is also related to various entities, which can be fatal. Objective: To evaluate the diagnostic performance of the Sokolow-Lyon index in precordial leads for left ventricular hypertrophy. Method: An observational, analytical and cross-sectional study of diagnostic means was carried out. One hundred and twenty-two patients admitted to the Departments of Internal Medicine, Nephrology and Neurology of the Hospital Militar Carlos J. Finlay (Havana, Cuba) were studied from January 2017 to March 2019, who underwent echocardiography and electrocardiogram. Results: There was a predominance of the population over 45 years old (77.9%), males (59.8%) and with high blood pressure (77.0%). A qualitative description of the Sokolow-Lyon electrocardiographic index for precordial leads was performed in the total number of the studied cases, and a prevalence of 71.3% of left ventricular hypertrophy was found. This voltage criterion showed high specificity (83%), high positive predictive values ​​(85%) and positive likelihood ratio at 2.28. Conclusions: In admitted patients, where the prevalence of high blood pressure is elevated, the Sokolow-Lyon criterion presented high diagnostic usefulness for left ventricular hypertrophy as well as to confirm the cases that actually present it.

Antagonistic modulation of SIK1 and SIK2 isoforms in high blood pressure and cardiac hypertrophy triggered by high-salt intake.

Salt-inducible kinases (SIKs) represent a subfamily of AMPK family kinases. SIK1 has been shown to act as a mediator during the cellular adaptation to variations in intracellular sodium in a variety of cell types. SIK2, as an isoform of the SIK family, modulates various biological functions and acts as a signal transmitter in various pathways. To evaluate the role of both SIK1 and SIK2 isoforms in blood pressure (BP), body fluid regulation and cardiac hypertrophy development, we made use of constitutive sik1-/- (SIK1-KO), sik2-/- (SIK2-KO), double sik1-/-sik2-/- (double SIK1*2-KO) knockout and wild-type (WT) mice challenged to a standard (0.3% NaCl) or chronic high-salt (HS, 8% NaCl) diet intake for 12 weeks.Mice, under a standard diet intake, had similar and normal BP. On a chronic HS intake, SIK1-KO and double SIK1*2-KO mice showed increased BP, but not WT and SIK2-KO mice. A chronic HS intake led to the development of cardiac left ventricle hypertrophy (LVH) in normotensive WT and hypertensive SIK1-KO mice, but not in SIK2-KO mice. Double SIK1*2-KO mice under standard diet intake show normal BP but an increased LV mass. Remarkably, in response to a dietary stress condition, there is an increase in BP but LVH remained unchanged in double SIK1*2-KO mice.In summary, SIK1 isoform is required for maintaining normal BP in response to HS intake. LVH triggered by HS intake requires SIK2 isoform and is independent of high BP.

Glycogen storage cardiomyopathy (PRKAG2): diagnostic findings of standard and advanced echocardiography techniques.

AIMS: Describe the findings obtained using standard echocardiography (Echo) and deformation indices (2D and 3D speckle tracking strain) in patients (Pts) with PRKAG2 cardiomyopathy. Seek to identify any peculiar characteristics and possible strain patterns that may distinguish this condition from other causes of left ventricular hypertrophy (LVH). METHODS AND RESULTS: Thirty Pts with genetically proven PRKAG2 (R302Q and H401Q), 16 (53.3%) male, mean age 39.1± 15.4 years old, were examined using standard, speckle tracking (STE), and 3D Echo. Pacemaker (PM) had been implanted in 12 (40%) Pts with a mean age of 38.1 ± 13 years. Hypertrophy was found in varying degrees in 18 (86%) Pts. Seven Pts (24%) presented 3D ejection fraction (EF) below normal limits. Diastolic function was abnormal in 17 (63%) Pts. Global longitudinal strain (GLS) on 2D measured -16.4% ± 5.3%. GLS measured -13.2% ± 4.8%, global radial strain 40.8% ± 13.8%, global circumferential strain (GCS) -16.1% ± 4.4%, and global area strain -26.1% ± 6.7% by 3D Echo offline analyses. Pts with PM presented lower EF and GCS compared with those without PM. EF/GLS measured 3.65 ± 1.00. In the bull's eye map, a strain pattern similar to stripes in 18 (60%) Pts was identified, which might be a differentiating signal among LVH. CONCLUSION: Echocardiography is a valuable tool in detecting diffuse and focal myocardial abnormalities in PRKAG2 cardiomyopathy. The deformation indices are especially revealing because they may help distinguish this rare infiltrative disease, thereby favouring early diagnosis, enhanced treatment, and improved outcome.

Is Masked Hypertension an underlying Cause of Unexplained Left Ventricle Hypertrophy?

OBJECTIVES: Unexplained left ventricular hypertrophy (ULVH) is defined as increased wall thickness in the absence of conditions that predispose to hypertrophy. The aim of this study was to evaluate the rate of masked hypertension in patient with unexplained left ventricle hypertrophy. METHOD: A total of 120 consecutive unexplained left ventricle hypertrophy patients without overt hypertension and diabetes and 121 healthy control subjects were included in the study. After a complete medical history and laboratory examination, patients' height, weight, waist circumference heart rate, and office blood pressure were recorded. All subjects underwent ambulatory blood pressure monitoring, and transthoracic echocardiography. RESULTS: Mean age were similar between patients with ULVH and controls. There was no significant difference in total cholesterol, HDL, LDL cholesterol and triglyceride levels, left ventricle ejection fraction, between the groups. Prevalence of Masked hypertension was significantly higher in patients with ULVH than controls (28.3% vs 6.6%, p < .001). Left ventricular mass index (141.9 ± 16.8 g/cm2 vs. 67.3 ± 10.3 g/cm2, p < .001) was significantly higher in masked hypertensive patients with ULVH compared to normotensive ULVH and control subjects. CONCLUSION: In this study, we found high prevalence of masked hypertension in ULVH patients. Patients with ULVH should be screened by ABPM to detect possible masked hypertension.

Renal sympathetic denervation attenuates left ventricle hypertrophy in spontaneously hypertensive rats by suppressing the Raf/MEK/ERK signaling pathway.

OBJECTIVE: To explore the effect of renal sympathetic denervation (RSD) on left ventricle hypertrophy and the Raf/MEK/ERK signaling pathway in spontaneously hypertensive rats (SHRs). METHODS: SHRs were divided into SHR, SHR + Sham, SHR + RSD and SHR + U0126 groups, with WKY rats as the baseline controls. The blood pressure of rats was observed, while myocardial fibrosis was evaluated through Masson staining. Thereafter, real-time quantitative polymerase chain reaction (qRT-PCR) was carried out to determine the levels of myocardial-hypertrophy-related markers, and Western blotting was used to measure the activity of the Raf/MEK/ERK signaling pathway. RESULTS: In comparison with the WKY group, significant increases were observed in the systolic pressure and diastolic pressure of rats from the other four groups at different time points after surgery. In addition, rats in these groups had obvious increases in LVMI, renal NE and IVSd and decreases in LVEDd, LVEF and LVFS. In addition, the CVF of myocardial tissues was increased, with the upregulation of ANP, BNP and ß-MHC and the downregulation of α-MHC. For the activity of the Raf/MEK/ERK signaling pathway, the levels of p-Raf/Raf, p-MEK/MEK and p-ERK1/2/ERK1/2 were all remarkably elevated (all P < .05). Further comparison with the SHR group showed that the above indexes in the rats were significantly improved in the RSD group and SHR + U0126 group (all P < .05). CONCLUSION: RSD may decrease blood pressure, mitigate hypertension-induced left ventricle hypertrophy and improve cardiac function efficiently in SHRs via the suppression of the Raf/MEK/ERK signaling pathway.

Cardiac hypertrophic risk markers of left ventricle and left atrium in chronic heart failure due to aortic and mitral valve disease.

BACKGROUND: Chronic valvular heart disease leads to systolic dysfunction and left atrial enlargement that ultimately results in heart failure. PURPOSE: To investigate prognostic importance of Echocardiography and plasma natriuretic peptide levels that increase as a compensatory response and can be used as predictive markers for cardiac hypertrophy. MATERIAL AND METHODS: The patients were divided into three groups: 51 with left ventricle hypertrophy due to aortic valve disease; 126 with left atrial enlargement due to mitral valve dysfunction; and 76 with both conditions. Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) plasma levels were measured in all three respective groups showing dilated cardiomyopathy. RESULTS: The mean left ventricular end-diastolic dimension at 64.3 ± 1.6 mm (P < 0.00) and left atrial dimension at 58.3 ± 3.7 mm (P < 0.00) were significantly high. However, patients with both conditions showed significantly high values for left ventricular end-diastolic dimension (63.3 ± 3 mm, P < 0.00) and left atrial dimension (54.9 ± 4 mm, P < 0.00) when compared with controls. A significant positive correlation was found between plasma natriuretic peptides levels and dilated cardiomyopathy. The mean values of ANP were 173 ± 46.6 pg/mL (P < 0.00), 140.4 ± 42.4 pg/mL (P < 0.00), and 295.1 ± 67.5 pg/mL (P < 0.00), significantly high in all three respective disease groups. The levels of BNP were also significantly high at 189 ± 44.5 pg/mL (P < 0.00), 166.6 ± 36.6 pg/mL (P < 0.00), and 323 ± 69.1 pg/mL (P < 0.00) in the disease groups with left ventricular hypertrophy, left atrial enlargement, and the disease group showing both characteristics, respectively. CONCLUSION: Significant positive associations were found between left ventricle hypertrophy and left atrial enlargement with ANP and BNP.

The effect of intensive hemodialysis on LVH regression and blood pressure control in ESRD patients.

INTRODUCTION: Cardiovascular diseases are considered the major cause of death in dialysis patients with end-stage renal disease (ESRD). Recently, intensive hemodialysis has increasingly used and replaced conventional hemodialysis. The present study aimed to evaluate the effect of intensive hemodialysis on LVH regression and blood pressure control. METHODS: The present study is self-control, pre- and post-intervention clinical trial on hemodialysis ESRD patients with hypertension (52.5% female with a mean age of 55.55 ± 12.96), who were admitted to Imam Khomeini Hospitals, Golestan Ahvaz in 1396. All patients underwent intensive hemodialysis treatment 4 times a week for 2 months. 2-D color Doppler echocardiography was performed for all patients before the intervention and following 2 months of intensive hemodialysis. The results of chest echocardiographic were used to determine left ventricular thickness. RESULTS: In this study, 40 patients with hypertension were studied. The results of this study showed a significant decrease (P < 0.0001) in the levels of LVH, SBP, DBP and mean BP after intervention in ESRD patients. The level of LVH was decreased from 15.42 ± 1.67 mmHg to 13.86 ± 1.39 mmHg, SBP from 161.50 ± 12.16 mmHg to 141.12 ± 8.87 mmHg, DBP from 25.25 ± 5.15 mmHg to 81/75 ± 2.89 mmHg, and mean BP from 114.66 ± 6.82 mmHg to 101/54 ± 3.98 mmHg. CONCLUSION: Based on the results, it can be concluded that intensive hemodialysis resulted in improved LVH regression and blood pressure control, and fewer requirements for blood pressure-lowering medications.