Hypertensive Ventricular Hypertrophy Research Articles

Computed tomography myocardial perfusion imaging of patients with left ventricular hypertrophy in hypertension: A retrospective study

ABSTRACT Objective Left ventricular hypertrophy (LVH) is a strong predictor of adverse cardiovascular outcomes including heart failure. This study evaluated characteristics and the influencing factors of computed tomography myocardial perfusion imaging (CT-MPI) of patients with LVH in hypertension. Methods A total of 65 patients with stable chest pain and confirmed coronary stenosis <50% by coronary computed tomography angiography (cCTA) from September 2019 to February 2021 were recruited. According to the results of echocardiography, patients were divided into the LVH group (n = 33) and control group (patients without LVH, n = 32). The general data of all study subjects were collected, and the body mass index (BMI) and body surface area (BSA) were calculated. Myocardial blood flow (MBF), myocardial blood volume (MBV), and echocardiographic parameters were recorded. Spearman correlation analyses were conducted to analyze the relationship between MBF, MBV, and echocardiographic parameters. Results The LVH group had significantly higher left ventricular end diastolic distance (LVEDd), septal wall thickness diastole (SWTd), and post wall thickness diastole (PWTd) than the control group, resulting in higher left ventricular mass index (LVMI) (P < .05). The LVH group showed significantly lower MBF than the control group (P < .05), but there was no significant difference in MBV between two groups (P > .05). Spearman correlation analysis demonstrated that MBF was negatively correlated with SWTd and LVMI (P < .05). Conclusions CT-MPI, as a new noninvasive modality to evaluate myocardial perfusion in hypertensive patients, revealed that MBF is reduced in patients with LVH, while MBV remains unchanged. In hypertensive patients, decreased MBF is significantly correlated with increased LVMI.

Comparative Study of Electrocardiographic and Echocardiographic Evidence of Left Ventricular Hypertrophy in Systemic Hypertension

Background and Aims: Hypertension is a common health problem. Left ventricular hypertrophy, a condition in hypertension is a risk factor for myocardial infarction, stroke and heart failure. This study aims to detect left ventricular hypertrophy in hypertensive patients using Electrocardiography and echocardiography. Methods: In this descriptive cross-sectional study; 143 patients of Hypertension from February 2019 to August 2019 were enrolled. They were evaluated for left ventricular hypertrophy using electrocardiography and echocardiography. Sokolow-Lyon and Cornell Voltage electrocardiographic criteria were used and their sensitivities and specificities to detect left ventricular hypertrophy were calculated taking echocardiography as a gold standard method. Results: The mean age of the study population was 58.69 ± 11.33 years. Mean duration of hypertension was 4.72 ±3.2 years. The mean systolic and diastolic blood pressure were 137 ± 15.42 mmHg and 84 ± 10.5 mmHg respectively. Out of 143 study population, 30(21%) of them had left ventricular hypertrophy on electrocardiography as defined by Sokolow-Lyon criteria, and 29(20.3%) had left ventricular hypertrophy on electrocardiography as per Cornell Voltage criteria. On combining both Sokolow-Lyon and Cornell Voltage criteria, 37(25.9%) of the study population had left ventricular hypertrophy on electrocardiography (either as per Sokolow-Lyon or Cornell Voltage criteria). On echocardiography, 62(43.4%) of them were found to have left ventricular hypertrophy. Conclusions: Electrocardiography is a less sensitive tool to diagnose Left Ventricular Hypertrophy in hypertension but its specificity is high (&gt;95%). Investigation of choice to detect Left Ventricular Hypertrophy in hypertensive people is still the echocardiography.

The prognostic value of circulating microRNA-29b in left ventricular hypertrophy in patients with hypertension

Objective: To analyze the relationship between the level of microRNA-29b in circulation and left ventricular hypertrophy in hypertensive patients. Methods: A total of 240 subjects from Henan Province People's Hospital from June 2015 to June 2018 were included in the present study. Among them, 160 were hospitalized patients, and were divided into two groups. Patients with simple hypertension and had no left ventricular hypertrophy (80 cases) were in the simple hypertension group (HBP-NLVH), and patients with hypertension combined with left ventricular hypertrophy (80 cases) were in the high blood pressure with left ventricular hypertrophy group (HBP-LVH). Normal control subjects (80 cases) were those with no hypertension and randomly selected from the medical center of Henan Province People's Hospital. Serum microRNA-29b expressions were detected by real time fluorescence quantitative PCR. The thickness of interventricular septum (IVSD) and left ventricular posterior wall thickness (LVPWD) were measured by echocardiography. Results: Compared with the normal control group (1.95±0.79), the relative expression of microRNA-29b in the patients both in the HBP-NLVH group (2.67±0.92) and the HBP-LVH group (5.12±1.23) was up-regulated, and the difference between normal control and patients was statistically significant (P<0.05). In patients, the microRNA-29b level in the HBP-LVH group was significantly higher than that in the HBP-NLVH group (P<0.05). The expression level of microRNA-29b was positively correlated with IVSD (r=0.71, P<0.05) and LVPWD (r=0.74, P<0.05), respectively. The sensitivity and specificity of serum microRNA-29b levels in the diagnosis of left ventricular hypertrophy in hypertension patients were 96.8% and 91.3%, respectively. Conclusion: Serum microRNA-29b level is elevated in hypertensive patients with left ventricular hypertrophy, and is positively correlated with left ventricular hypertrophy. The circulation microRNA-29b might be a useful biomarker with prognostic value in left ventricular hypertrophy in hypertension patients.

Remote Transplantation of Human Adipose‐derived Stem Cells Induces Regression of Cardiac Hypertrophy by Regulating the Macrophage Polarization in Spontaneously Hypertensive Rats

Left ventricular hypertrophy in hypertension has prognostic significance on cardiovascular mortality and morbidity. Cardioprotection by stem cell therapy can be evoked through extracardiac paracrine approaches. Recently, we have shown that butylidenephthalide (BP) improves adipose‐derived stem cell (ADSC) engraftment via attenuated reactive oxygen species (ROS) production. This prompted us to investigate whether remote transplantation of stem cells confers attenuated left ventricular hypertrophy at an established phase of hypertension. Male spontaneously hypertensive rats (SHRs) aged 12 weeks were randomly allocated to receive hamstring injection of vehicle, ADSCs, and BP‐preconditioned ADSCs for 8 weeks. As compared with untreated SHRs, naïve ADSCs decreased the ratio of left ventricular to body weight, cardiomyocyte cell size, and collagen deposition independent of hemodynamic changes. These changes were accompanied by attenuated myocardial ROS production and increased p‐STAT3 levels. At day 3 after implantation into the right hamstring muscle, SHR treated with vehicle was associated with increased myocardial M1 macrophage infiltration, which can be inhibited by either naïve ADSCs or BP‐preconditioned ADSCs. However, compared with naïve ADSCs, BP‐preconditioned ADSCs provided a further decrease of ROS and left ventricular hypertrophy and an increase of local ADSC engraftment, STAT3 phosphorylation, STAT3 activity, STAT3 nuclear translocation, myocardial IL‐10 levels and the percentage of M2 macrophage infiltration. SIN‐1 or 3SI‐201 reversed the effects of BP‐preconditioned ADSCs increase on myocardial IL‐10 levels. Furthermore, SIN‐1 abolished the phosphorylation of STAT3, whereas superoxide levels were not affected following the inhibition of STAT3. Our results highlighted the feasibility of remote transplantation of ADSCs can be considered as an alternative procedure to reverse cardiac hypertrophy. BP‐pretreated ADSCs polarize macrophages into M2 immunoregulatory cells more efficiently than naïve ADSCs via ROS/STAT3 pathway.Support or Funding InformationnilThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Association of clinical and genetic factors with left ventricular hypertrophy in hypertension among the indigenous population Mountain Shoria

Objective. To determine the association of clinical and genetic factors with the left ventricular hypertrophy among indigenous patients with hypertension living in Mountain Shoria.Design and methods. A clinical-epidemiological study of Mountain Shoria indigenous populations at isolated regions was undertaken. Continuous method surveyed 547 people, consisted of a sample of the adult population (18 years and older). Studied anthropometric data, lipid spectrum of the blood polymorphisms of genes ADRB1 (Ser49Gly, A/G, rs1801252) ADRA2B (I/D), ACE (I/D), eNOS (4a/4b) and MTHFR (C677T, Ala222Val, rs1801133) and their association with left ventricular hypertrophy.Results. The left ventricular hypertrophy in patients with hypertension was detected in 47.3% of the respondents. The odds ratio found among patients with hypertension duration of 5 years with the respondents hypertrophied myocardium 0.5 times lower (38.2%) than people without this disease of the heart - 61.8%, while among those with hypertension long history of more than 10 years, 4.1 times higher: 73.3% vs 26.7%. In a population of Shor hypercholesterolemia and giperbetaholesterinemiya associated with exaggerated myocardial damage. The percentage of smokers in a cohort of patients with hypertensive cardiac disease was (37.8%) and was higher by 2.0 times than in hypertensive patients without left ventricular hypertrophy (22.0%). With the relative risk of hypertension with myocardial damage in a population Shor associated gene ACE I allele. The odds ratio of hypertension to identify patients with cardiac respondents with heterozygous genotype AG ADRB1 gene was 3.0 times higher compared to the surveyed individuals with homozygous genotypes AA and GG.Conclusion. Among Shor risk of hypertension with left ventricular hypertrophy was influenced by factors: prolonged duration of the disease more than 10 years, smoking, hypercholesterolemia, giperbetaholesterinemiya. Installed Association II genotype of ACE gene and gene genotype AG ADRB1s development of left ventricular hypertrophy in patients with arterial hypertension in the population of Shor.

The Human Myotrophin Variant Attenuates MicroRNA-Let-7 Binding Ability but Not Risk of Left Ventricular Hypertrophy in Human Essential Hypertension

Myotrophin, known as a myocardial hypertrophy-inducing factor, is responsible for the initiation of cardiac hypertrophy that transits to heart failure. MicroRNAs are small noncoding RNAs that down-regulate posttranscriptional expression of target molecules. We investigated the role of variants of the microRNA-binding site in myotrophin in affecting its expression and any association with cardiac hypertrophy. Bioinformatics demonstrated that variant rs17168525 was identified to be located in the let-7/miR-98-binding site of myotrophin. We further experimentally test to effects of the identified variant on myotrophin translation using luciferase reporter assay and Western blotting. We found that the C allele of rs17168525 suppressed myotrophin translation by facilitating let-7c binding, but not the T allele. Let-7c overexpression caused a significant decrease in the level of myotrophin protein. Next, we investigated the association of the variant with cardiac hypertrophy in 1614 hypertensive patients, including 552 with left ventricular hypertrophy and 1062 without left ventricular hypertrophy, as well as 591 healthy control subjects from a Han Chinese population. No significant association between the variant rs17168525 and left ventricular hypertrophy in hypertensive patients in a Han Chinese population (P>0.05). In conclusion, our experimental results provide evidence that the T allele of rs17168525 in the 3′-UTR of myotrophin might influence the level of myotrophin protein by interfering with let-7/miR-98 binding.

Left Ventricular Hypertrophy in Hypertension and Nocturnal Blood Pressure.

Left Ventricular Hypertrophy in Hypertension and Nocturnal Blood Pressure.

Mechanisms of Left Ventricular Hypertrophy in Hypertension: More than Just Blood Pressure

Hypertension is associated with a constellation of cardiac structural and functional changes, including increased left ventricular (LV) mass, and LV systolic and diastolic dysfunction. (1) Of the several adverse changes in cardiovascular morphology and function that occur in association with hypertension, LV hypertrophy is an established and independent prognostic factor for major cardiovascular events, including sudden cardiac death, acute myocardial infarction, stroke, and congestive heart failure. (2-6) Furthermore, there is a wealth of literature which demonstrates that decrease of LV mass in hypertensive patients results in improved survival rates. (7) Pathological changes of the left ventricle during long-term exposure to chronic pressure overload include an increase in the size of the cardiomyocyte, alterations in the extracellular matrix with accumulation of fibrosis, and abnormalities of the intramyocardial coronary vasculature, including medial hypertrophy and perivascular fibrosis (8) (Figure). However, given the detrimental contribution of LV hypertrophy to survival and cardiovascular events, most attention has also been focused on other mechanisms which may explain the risk associated with LV hypertrophy, and on the beneficial effects of anti-hypertensive pharmacological treatment. (1, 9-11) The mechanisms responsible for progression to hypertrophy include not only a mere response to the mechanical stress from elevated blood pressure (BP), but also the influence of neurohormones, growth factors, and cytokines. (1,12) Specifically, among factors promoting the progression of LV pathological remodeling, secretion and production of vasoactive peptides (such as angiotensin II, endothelin-1 and norepinephrine) are increased during the process and play critical roles in the hypertrophic response to systemic hypertension. (1) Oxidative stress, heat shock proteins, calcineurin, and some kinases are also involved in the hypertrophic process. (13)

Left Ventricular Hypertrophy and Insulin Resistance in Adults from an Urban Community in the Gambia: Cross-Sectional Study

ObjectiveTo determine the association between left ventricular hypertrophy and insulin resistance in Gambians.DesignCross-sectional study.SettingOutpatient clinics of Royal Victoria Teaching Hospital and Medical Research Council Laboratories in Banjul.ParticipantsThree hundred and sixteen consecutive patients were enrolled from outpatient clinics. The data of 275 participants (89 males) were included in the analysis with a mean (± standard deviation) age of 53.7 (±11.9) years.InterventionsA questionnaire was filled and anthropometric measurements were taken. 2-D guided M-mode echocardiography, standard 12-1ead electrocardiogram, fasting insulin and the oral glucose tolerance test were performed.Main Outcome MeasuresThe Penn formula was used to determine the left ventricular mass index, 125 g/m2 in males and 110 g/m2 in females as the cut-off for left ventricular hypertrophy. Using the fasting insulin and fasting glucose levels, the insulin resistance was estimated by the homeostatic model assessment formula. Logistic regression analysis was used to determine the association between left ventricular hypertrophy and insulin resistance.ResultsThe mean Penn left ventricular mass index was 119.5 (±54.3) and the prevalence of Penn left ventricular mass index left ventricular hypertrophy was 41%. The mean fasting glucose was 5.6 (±2.5) mmol/l, fasting insulin was 6.39 (±5.49) μU/ml and insulin resistance was 1.58 (±1.45). There was no association between Penn left ventricular mass index left ventricular hypertrophy and log of insulin resistance in univariate (OR = 0.98, 95% CI = 0.80 – 1.19, p = 0.819) and multivariate logistic regression (OR = 0.93, 95% CI = 0.76–1.15, p = 0.516) analysis.ConclusionNo association was found in this study between left ventricular hypertrophy and insulin resistance in Gambians and this does not support the suggestion that insulin is an independent determinant of left ventricular hypertrophy in hypertensives.

Vitamin D is independently related to left ventricular hypertrophy in hypertensive patients, whereas effect of parathyroid hormone on left ventricular mass is mediated by blood pressure

Objective: Vitamin D and parathyroid hormone (PTH) may affect structure and function of left ventricle in patients with kidney disease. The aim of this study was to investigate associations of serum 25-hydroxyvitamin D (25(OH)D) and PTH concentrations with left ventricular hypertrophy in hypertensive patients. Methods: We examined 41 patients with essential hypertension (M/F 15/26, mean age=62.3±4.5 yrs), 32 of whom (81%) were receiving antihypertensive treatment. ABPM monitors (SpaceLabs 90207) were programmed to obtain measurements each 15 min. during the day (6.00-22.00) and each 30 min. nighttime. Anthropometric data were collected with standardized protocol. Two-dimensionally guided M-mode echocardiography (VIVID 7 GE Pro) was performed to measure left ventricular structure. Left ventricular mass index (LVMI) was calculated as LVM divided by body surface area. Serum 25(OH)D and intact PTH concentrations were measured. In our analyses we adjusted for covariables. Results: Based on the results of the echocardiographic examination, the study group was divided into patients with LVH (LVH+, n=19) and those without LVH (LVH-, n=22). No statistically significant difference was found between the two groups in terms of basic characteristics. The average 25(OH)D level was lower in LVH+ patients as compared to LVH- participants (18.7±8.9 vs. 31.6±9.4 ng/ml, p = 0.01), both in unadjusted and adjusted analyses. In unadjusted analysis, the average PTH level of LVH+ patients was higher than LVH- patients (85.3±14.2 vs. 56.9±30.8 pg/mL, P =0.03). However, in multivariate model, additional adjustment for 24-h systolic BP, this association was non-significant (p=0.12). Conclusion: Our results suggest that vitamin D deficiency could be related to development of left ventricular hypertrophy in hypertension. Left ventricular hyperthorphy is associated with higher parathyroid hormone, however the effect is mediated by blood pressure.

Hemodynamic Mechanism of Ventricular Hypertrophy in Hypertension

Arterial hemodynamic assessments with technique of spectral analysis can obtain complete hemodynamic parameters including steady and pulsatile components. The steady parameters include arterial pressure (AP), heart rate, cardiac output, stroke volume and total peripheral resistance (TPR). Parameters of pulsatile hemodynamics are characteristic impedance (Zc), arterial compliance (Cm) and pulse wave reflection (Pb) etc. Studies of ventricular hypertrophy (VH) and arterial hemodynamics have disclosed several important findings. Hypertension in spontaneously hypertensive rat (SHR) and human subjects causes functional abnormalities in the resistance and Windkessel vessels. The extent of VH in SHR and hypertensive subjects was not correlated with AP and TPR, but positively correlated with pulsatile hemodynamic factors such as Zc and Pb. Many antihypertensive and vasodilators were capable of reducing the AP, but did not improve the VH. We have also investigated the effects of vasodilatory agents such as nifedipine (a calcium channel blocker), propranol (a non-selective β-adrenergic blocker) and atenol (a selective β-adrenergic inhibitor) on the arterial hemodynamics and VH. In addition, the effects of acute and chronic nitric oxide (NO) deprivation with Nω-nitro-L-arginine methyl ester (L-NAME) on the arterial hemodynamics and VH were evaluated. We compared the endothelium-dependent and -independent vasodilation to acetylcholine, sodium nitroprusside and S-nitroso-N-acetylpenicillanine and the endothelium-dependent or -independent vasoconstriction to norepinephrine and phenylephrine between SHR and normotensive Wistar Kyoto strain. In SHR with long-term administration of L-NAME, VH was associated with decreases in left ventricular cGMP and nitrate/nitrite accompanying increase in collagen content. Coadministration of NO precursor L-arginine improved the VH and fibrosis. In VH caused by long-term L-NAME, the LW/BW ratio, total number, numerical density and size of cardiomyocytes were correlated well with both steady and pulsatile hemodymanics. Aortic stiffness has significant impact on the cardiovascular risks. We simulated aortic stiffness by applying silicon gel embedding of the abdominal and/or thoracic aorta. Aortic stiffness did not affect the blood pressure and the steady hemodynamics. It caused VH associated with increases in the pulsatile hemodynamics. The extent of VH (LVW/BW, total number, numerical density, size of cardiomyocytes and collagen volume fraction) was correlated with the pulsatile hemodynamics (impedance, pulse wave velocity and wave reflection). The finding further supports the contention that blood pressure is not the determinant of VH. The ventricular afterload is the major cause of VH. The hemodynamic consequences of ovariectomy (Ovx), menopause and estrogen replacement were investigated. Ovx increased body weight, LVW/BW ratio, Zc and Pb, but decreased Cm. These changes were reversed by estrogen replacement. For steady hemodynamics, Ovx did not much alter the systolic, mean and diastolic pressure. The pulse pressure was slightly elevated. There was large increase in TPR. Again, these changes were reversed by estrogen supplement. The implication of these findings was that menopause tends to exert vasoconstrictory effects on the resistance and Windkessel vessels. On the contrary, estrogen possesses a vasodilatory influence on the systemic vessels.

The association of growth differentiation factor-15 with left ventricular hypertrophy in hypertensive patients.

Growth differentiation factor-15 (GDF-15) has been identified as an endogenous anti-hypertrophy effect. However, the association of plasma GDF-15 levels with left ventricular hypertrophy (LVH) in hypertension is poorly understood. We investigate the effect of plasma GDF-15 levels on left ventricular hypertrophy (LVH) in hypertension. We measured the plasma levels of GDF-15 in 299 untreated hypertensive patients which consisted of 99 with LVH and 200 without LVH using immunoradiometric assay. All subjects were examined by the ultrasonic cardiograph to determine Left ventricular (LV) internal diameters, septal thickness, and posterior wall thickness. The associations of GDF-15 with left ventricular mass index (LVMI), LV end-systolic and –diastolic diameters, LV wall thickness, and LV ejection fraction were evaluated. We found that plasma GDF-15 levels in hypertensive patients with LVH [median 1101, 25th–75th percentiles (879–1344) ng/L] were higher than that in hypertensive patients without LVH [median 516, 25th–75th percentiles (344–640) ng/L] (P<0.001). After adjustment for traditional covariates, plasma GDF-15 levels were independently related to LVMI (R2 = 0.53; β = 0.624, P<0.001), LV interventricular septal thickness (R2 = 0.23; β = 0.087, P<0.01) and LV posterior wall thickness (R2 = 0.26; β = 0.103, P<0.05). Our cross-sectional data on a hospital-based sample indicate that plasma GDF-15 levels are associated with LVH in hypertensive patients.

Gender differences of voltage electrocardiographic criteria of left ventricular hypertrophy in hypertensive individuals living in the North

Objective. To estimate the changes of voltage electrocardiographic criteria of the left ventricular hypertrophy in arterial hypertension in subjects of different gender. Design and methods. The study included 94 hypertensive patients (55 males, 39 females). Mean age was 51 ± 6 years. Based on gender and the presence of left ventricular hypertrophy patients were divided into four groups. Results. There were significant differences of indices of Sokolow-Lyon and Cornell in males with I and II stages of arterial hypertension (р = 0,012 and р = 0,017, respectively). The same differences were found in females with I and II stages of arterial hypertension (р = 0,037 and р = 0,001, respectively). Specificity was 92 % for both indices, and the sensitivity was 26 % for Sokolow-Lyon index, and 39 % for Cornell index. In women sensitivity was 0 and 72 % for Sokolow-Lyon and Cornell indices, respectively, and specificity was more than 90 % for both criteria. Conclusion. Gender differences should be considered when voltage electrocardiographic criteria of the left ventricular hypertrophy are assessed in hypertensive patients.

Would corrected QT dispersion predict left ventricular hypertrophy in hypertensive patients?

Aims. We explored whether QT corrected dispersion (QTcD) can identify left ventricular hypertrophy (LVH) in hypertensives. Methods. We enrolled 100 hypertensive patients (study group) and 30 normotensive subjects (control group). Echocardiography was performed to measure left ventricular mass and left ventricular mass index. Electrocardiogram was performed to measure QTcD. Results. LVH was present in 42 patients (42%) of the study group, none among controls. Hypertensive patients had significantly greater indices of LVH and QTcD compared with controls (p < 0.001 for all). Similarly, among hypertensive patients, those with LVH had a significantly greater QTcD compared with those without (p < 0.001). Pearson's correlation coefficient test demonstrated strongly positive correlations between QTcD and the indices of LVH (p < 0.001 for all). Analysis of the receiver operating characteristic curves identified 60 ms as the optimal cut-off value of QTcD that best predicts LVH in hypertensives. Using this value, QTcD was able to predict LVH with a sensitivity of 92.9% and specificity 98.2%. Conclusions. QTcD is significantly increased in hypertensive patients with LVH compared with those without, being strongly correlated with the indices of LVH. A QTcD cut-off value of 60 ms predicted LVH in hypertensive patients with a high sensitivity and specificity.

The α2C-Del322–325 adrenoceptor polymorphism and the occurrence of left ventricular hypertrophy in hypertensives

Objectives. Sympathetic activation has a role in the development of left ventricular hypertrophy (LVH). The presynaptic α2C-adrenoceptor inhibits the release of norepinephrine from sympathetic nerve terminals in the heart. A deletion polymorphism in the α2C-adrenoceptor (α2CDel322–325) generates a hypofunctional α2C-adrenoceptor, which may result in chronic adrenergic signalling. This study aimed to investigate whether the α2CDel322–325 polymorphism was associated with an increased prevalence of LVH in patients with systemic hypertension. Methods. Left ventricular mass was measured in 205 patients with systemic hypertension and 60 normal volunteers using a 1.5-T Philips MRI system. Genotyping was performed using a restriction fragment length polymorphism assay. Results. No significant difference was observed between the distribution of the α2CDel322–325 genotypes in hypertensive patients with LVH compared with those without LVH. Adjusting for confounding variables the odds ratio (OR) of being ins/del for the α2CDel322–325 and having LVH was 0.49 (95% CI 0.14–1.69, p = 0.256). Conclusions. These observations suggest that there is little evidence for an association between α2CDel322–325 polymorphism and an increased prevalence of LVH in patients with systemic hypertension.

Left ventricular hypertrophy in hypertensive patients with different ambulatory monitoring daily pattern

The aim of the present study was to try to identify which parameters of blood pressure (BP) ambulatory monitoring are better related to the presence of left ventricular hypertrophy in hypertensives. Fifty-six ambulatory hypertensive patients were investigated. Patients were subdivided into two groups of comparable casual and twenty-four-hour ambulatory pressure but with different nighttime decrements of the mean BP (respectively>10%, n=29, and ≤10%, n=27). When all the patients were considered, no significant correlation between left ventricular mass index (LVMI) and casual pressure values was found. On the contrary significant relationships between LVMI and systolic ambulatory twenty-four-hour (p<0.01), daytime (p<0.01), and nighttime (p<0.001) pressures, but not with diastolic pressures, were found. The interventricular septum (P<0.03) and the LVMI (P<0.03) respectively measured and calculated by echocardiography, were significantly larger in patients with limited pressure fall at nighttime. The extent of BP fall at nighttime assessed by ambulatory monitoring seems, therefore, to permit identification of hypertensive patients at higher cardiovascular risk.

Prevalence and severity of echocardiographic left ventricular hypertrophy in hypertensive patients in clinical practice

Background and aim. The prevalence of left ventricular hypertrophy (LVH) in human hypertension has been mostly documented in population-based samples and selected hypertensive cohorts. Rather scant data are available from clinical practice. Thus, we examined the prevalence of LVH in a large group of hypertensive patients referred by general practitioners to a routine echocardiographic examination. Methods. A total of 2249 hypertensive subjects (mean age 62 years, 52.3% men, 84.5% treated) referred by their practitioners to 17 outpatient echocardiographic laboratories across Italy for detection of hypertensive early cardiac damage were included in the study. LVH was defined as left ventricular mass (A) ≥ 225/163 g, (B) ≥ 116/96 g/m2, (C) ≥ 49/45 g/m2.7 in men/women, respectively; LVH was graded as mild, moderate and severe according to Lang's report. Results. Overall, patients with LVH were 58%, 58% and 65% by criteria A, B and C, respectively. LVH was mild in 33% (A), 36% (B) and 29% (C), moderate in 31% (A), 28% (B) and 27% (C), and severe in 36% (A), 36% (B) and 44% (C). Conclusions. Data provided by this multicentre nationwide survey support the view that, despite therapeutic interventions, LVH remains a highly frequent phenotype in human hypertension and that severe LVH is present in a large fraction of hypertensives.

Nocturnal nondipping and left ventricular hypertrophy in hypertension: an updated review

The classification of hypertensive subjects according to circadian blood pressure (BP) variations (i.e., dipping vs nondipping) is a useful means for reliable individual risk stratification and effective therapeutic decision-making. Increasing evidence, although not univocal, suggests that a reduced nocturnal BP fall relates to an excess of cardiovascular complications. The association between nondipping status with left ventricular hypertrophy (LVH) and its therapeutic implications are still debated; in this article we examined the studies published in the last decade on this controversial issue. The studies identified by a PubMed search were eligible for the analysis if they fulfilled the following criteria: full articles in English, published from 1 January 2000 to 31 December 2009, and inclusion of adult or elderly subjects. According to these criteria, 26 studies encompassing 3877 participants have been selected. A total of 17 studies for a total of 2497 subjects were positive for a link between nondipping and LVH, whereas the remaining nine studies were negative. Notably, three studies that accurately defined the nondipping status on the basis of two consistent ambulatory blood pressure monitoring sessions over a short time interval showed a significant association of this pattern with LVH; this suggests that a persisting nondipping pattern is associated with a more pronounced cardiac involvement. Preliminary data support the view that nondipping may be reverted to dipping by chronotherapy and by diuretics in salt-sensitive patients. Whether restoring the normal nocturnal BP dip in hypertensives with LVH regresses cardiac damage at present remains an untested hypothesis.

Lack of Association Between Common Endothelial Nitric Oxide Synthase Gene Haplotypes and Left Ventricular Hypertrophy in Hypertension

The endothelial nitric oxide synthase (NOS3) gene has been implicated in the pathogenesis of hypertension-related left ventricular hypertrophy (LVH). Candidate-gene studies have examined the role of NOS3 variation, but reported results are inconsistent. In this study, we investigated the association of three clinically relevant polymorphisms (promoter T786C, intronic 4a/b, and nonsynonymous G894T) in a case-control sample of 230 ethnically homogeneous (Caucasians) patients with essential hypertension, with (n = 64) and without (n = 166) clinically diagnosed LVH. Haplotype analysis was also performed. In single-marker analyses, no significant associations with LVH were detected by univariate and multivariate regression models. In the haplotype-based association analysis, no common haplotype was associated with the development of LVH. A rare haplotype consisting of the three mutant alleles (C-a-T*) was found to be present only in patients with LVH (3.4%) and not in control hypertensive patients. Despite the biological rationale for the involvement of the NOS3 gene in LVH, no evidence for a major role of common NOS3 haplotypic variation was found. Considering the totality of available evidence, single-gene analyses of the NOS3 gene have not uncovered detectable genetic effects, and pathway-based analyses that examine interactions of multiple loci may be more informative about the complex genetic etiology of LVH.

Risk Reduction After Regression of Echocardiographic Left Ventricular Hypertrophy in Hypertension: A Meta-Analysis

The prognostic relevance of echocardiographic left ventricular hypertrophy (LVH) regression in hypertension is uncertain. The aim of this study was to perform an updated meta-analysis about the impact of LVH regression on the occurrence of cardiovascular events in hypertensive patients. We searched for studies on echocardiographic LVH regression and prognosis in hypertension that compared patients with or without LVH regression or groups including subjects with or without LVH regression and reported adjusted hazard ratio (HR) for calculating the overall effect size. Five studies were identified (3,149 patients, mean age range 48-66 years, 58% men). Follow-up echocardiography was performed after a mean period ranging from 1 to 5 years. Entire follow-up duration ranged from 3 to 9 years. Globally, 333 cardiovascular events occurred. Three whole studies and subgroups of two others were included in the meta-analysis, comprising 2,449 patients, 1,900 (78%) with baseline LVH and 969 (51%) with LVH regression, who experienced 304 events. The overall adjusted HR of total cardiovascular events was 0.54, 95% confidence interval (CI) 0.35-0.84, P = 0.007, for LVH regression/persistent normal left ventricular (LV) mass vs. LVH persistence/LVH development. Heterogeneity was found between studies. Higher baseline prevalence of comorbid conditions and Japanese ethnicity seemed to be associated with lower benefit from LVH regression. This meta-analysis indicates that regression of echocardiographic LVH in hypertension, even after adjustment for various confounders, is associated with reduction of cardiovascular events. However, future studies are needed to evaluate whether LVH regression is of benefit for all hypertensive patients and ethnic groups.