Hypertrophy In Essential Hypertension Research Articles

Correlation of vitamin D3 and serum calcium level with left ventricular hypertrophy patients.

Extra cellular fluid (ECF) Ca++ performs vital functions such as blood clotting, cardiac muscle contraction, second messenger for hormone and neurotransmitter release. Total Ionized serum Ca++ is 4.65 to 5.25 mg/dl Ionized Ca++ performs vital physiological functions such as maintenance of plasma membrane integrity. Objectives: The present study is the first research being reporting on the association of LVH (left ventricular hypertrophy) due to essential hypertension with serum vitamin D3 and serum calcium levels. Study Design: Cross Sectional Research. Setting: Medicine/Cardiology department, Peoples Medical University Hospital, Nawabshah. Period: 1st January 2017 to 30th June 2017. Material & Methods: To assess the correlation of 25-hydroxycholecalciferol and serum calcium with left ventricular hypertrophy in essential hypertension. The thickness of inter ventricular septum (IVS) and posterior wall (PWT) on echocardiography were used to categorize LVH into mild, moderate and severe. Results: Male predominated in the present study. Male to female ratio was 1.65:1. Male and female comprised 62.33% and 37.67% respectively. Chi square value (X2-value) was 14.7 with significant p-value. Mean +SD of 25-hydroxycholecalciferol in mild moderate and severe LVH were noted as 30+7.8, 24.7+7.7 and 14.9+6.1 ng/dl respectively. Mean +SD of serum calcium in mild moderate and severe LVH were noted as 9.20+0.51, 8.93+0.72 and 8.678+0.44 mg/dl respectively. Conclusion: In subjects with left ventricular hypertrophy in essential hypertension the serum levels of vitamin D and calcium were low. There was a negative correlation with left ventricular hypertrophy and serum vitamin D and serum calcium. Thus it could be concluded that in subjects with left ventricular hypertrophy the low levels of serum vitamin D could be an independent modifiable risk factor.

Galectin-3 as the marker of hypertrophy and myocardial dysfunction in males with essential hypertension, carriers of polymorphic genes of angiotensin ii type 1 receptor

One of the main etiological causes of development of heart failure is essential hypertension. The diagnosis of heart failure is usually made on the basis of comprehensive analysis of medical history, sonographic and biochemical examination. Normal ejection fraction does not exclude dyspnea of cardiac origin. Objective: to determine the role of galectin-3 as a marker of structural and functional changes of the myocardium in males with essential hypertension and CHF, carriers of polymorphic AT1R genes, residents of Podillya region of Ukraine. In this contingent, the surveyed were studied сoncentrations of galectin-3 and brain natriuretic peptide (BNP), parameters of central and systemic hemodynamics in carriers of polymorphic variants of angiotensin II type 1 receptor gene (АТ1R) - individuals with no cardiovascular pathology (n=79), male patients with II-III degree essential hypertension (EH) and hypertrophy of the myocardium (n=62), and essential hypertension (n=50) complicated by chronic heart failure (CHF), residents of Podillya region of Ukraine, were studied. Genotyping of АТ1R gene was performed using polymerase chain reaction. Galectin-3 and brain natriuretic peptide levels were determined by enzyme immunoassay. Structural and functional parameters of myocardium were assessed by ultrasound using the apparatus “RADMIR ULTIMARA”. Statistical analysis of the results obtained was done on personal computer using standard statistical package Statistica 10.0. The data are represented as mean values (M) and standard deviations (±m). Carriers of C allele of angiotensin II type 1 receptor gene were found to be dominating among the males with essential hypertension and resultant myocardial hypertrophy. Concentrations of galectin-3 and brain natriuretic peptide were significantly higher in men with essential hypertension and essential hypertension associated with chronic heart failure, as compared to those with no cardiovascular diseases, as well as the carriers of C allele of angiotensin II type 1 receptor gene. It was found that concentrations of study biomarkers were higher in individuals with severe and eccentric left ventricular hypertrophy, as well as in those with decreased ejection fraction of the left ventricle. Therefore, those biomarkers can be used in complex diagnosis of left ventricular hypertrophy in essential hypertension and the development of chronic heart failure in such patients.

A2808 Association between serum uric acid and left ventricular hypertrophy in essential hypertension

A2808 Association between serum uric acid and left ventricular hypertrophy in essential hypertension

Galectin-3 as a potential marker of myocardial hypertrophy in essential hypertension in individuals with polymorphic AT1R genotypes

Background: The potential use of plasma galectin-3 level as a of myocardial changes in the development of hypertrophy in males with essential hypertension (EH), carriers of polymorphic variants of II type 1 receptor gene, was studied. The level of brain peptide (BNP), as well as the parameters of central and systemic, and structural and functional parameters of the heart in carriers of polymorphic variants of II type 1 receptor gene, were studied as reference.
 Methods: The study included 79 individuals with no signs of cardiovascular disease, and 62 males with stage II EH, aged 40-60, who were residents of Ukraine. All patients were treated at the Military Medical Clinical Center of Central Region of Air Forces of Ukraine and Vinnytsia Regional Specialized Clinical Hospital of Radiation Protection of the Ministry of Health of Ukraine, from December 2013 to June 2015. The patients were studied during their treatment at the in-patient department. Anesthetic, clinical and laboratory findings, and measures were entered into a special chart. Biochemical analyses were done upon admission of the patients to the hospital. Immunologic, and instrumental methods of examination were used as well. Statistical analyses of the results obtained were done on a personal computer using standard statistical package STATISTICA 10. Microsoft Excel was used for primary preparations of tables and intermediate calculations.
 Results: In patients with EH and myocardial hypertrophy, the C allele of angiotensin II type 1 receptor gene was found to be dominating. They had higher levels of both galectin-3 and BNP. The threshold levels of galectin-3 and BNP for screening diagnosis of EH with myocardial hypertrophy in males (who were residents of the Podillya region of Ukraine) were evaluated.

PS 17-54 EFFECTS OF CILNIDIPINE VERSUS ATENOLOL ON LEFT VENTRICULAR DIASTOLIC FUNCTION AND HYPERTROPHY IN ESSENTIAL HYPERTENSION - CANDLE TRIAL

Objective: Effects of Cilnidipine versus Atenolol on Left Ventricular Diastolic Function and Hypertrophy in Essential Hypertension (CANDLE) study was designed as a prospective, randomized, double-blind, parallel-group to test whether cilnidipine achieves greater left ventricular (LV) mass reduction and improves LV diastolic function than does atenolol. Design and method: Seventy-two patients with uncomplicated essential hypertension and increased LV mass index at screening echocardiography (55 ± 2 years; 59% male; BP 157 ± 4/99 ± 3 mmHg) were enrolled and were randomly assigned and forced-titrated to 20 mg/d cilnidipine or 100 mg of atenolol treatment for 36 weeks. Echocardiography, 24-hours ambulatory blood pressure monitoring, biochemical studies including N-terminal pro-B-type natriuretic peptide and 24-hours urine protein and microalbumin were measured at baseline and after 36-weeks therapy. Results: Clinical examination and blinded echocardiogram in a per-protocol analysis of 28 cilnidipine-treated and 26 atenolol-treated patients revealed similar reductions in systolic/diastolic pressure (−16.5/8.9 versus −23.9/14.8 mmHg, both P > 0.05) and LV mass index (−21.4 versus −19.5 g/m2, both P > 0.05). No significant between-treatment difference was detected in population subsets defined by monotherapy treatment, sex, age, or severity of baseline hypertrophy. Similarly, there was no between-treatment difference in change in biochemical parameters. As we expected, cilnidipine-treated group showed lesser reduction on night-time heart rate (−2.4 versus −5.6 %, p = 0.021) rather than atenolol-treated group. Interestingly, cilnidipine-treated group showed reduction on left atrial (LA) volume index but on the contrary, atenolol-treated group showed more enlarged LA after treatment (−5.1 versus 7.3 %, p = 0.035). Conclusions: Both cilnidipine and atenolol similarly and effectively reduced blood pressure and LV mass index. However, only cilnidipine reduced LA volume index, whereas atenolol increased. Cilnidipine may provide more beneficial effect on the management in essential hypertension with diastolic dysfunction.

Impact of alcohol intake on the relationships of uric acid with blood pressure and cardiac hypertrophy in essential hypertension

BackgroundHyperuricemia, which is frequently associated with hypertension, can be caused by alcohol intake. To date, limited data have shown the link between alcohol intake and hyperuricemic hypertension. MethodsWe retrospectively examined the influence of alcohol intake on the relationship between the uric acid level and blood pressure or cardio-metabolic parameters in 171 untreated non-failing hypertensive patients (mean 59.3±10.7 years).Cross-sectional analysis was separately performed in regular alcohol drinkers (more than 25g/day ethanol, n=74, 82.4% men) and non-drinkers (n=97, 33.0% men). ResultsDiastolic blood pressure was significantly higher in drinkers than in non-drinkers (101.6±11.5mmHg vs. 96.8±8.2mmHg, p<0.01). Estimated glomerular filtration rate (80.4±14.7mL/min/1.73m2 vs. 80.0±17.8mL/min/1.73m2) and body mass index (BMI, 24.7±4.4kg/m2 vs. 24.8±4.2kg/m2) were similar in the two groups. In the drinker group, the uric acid level (mean 6.3±1.7mg/dL) was positively correlated with both systolic and diastolic blood pressures (r=0.270/p=0.020 and r=0.354/p=0.0020, respectively), and with the markers of cardiac hypertrophy, including electrocardiographic voltage (V1S+V5R, r=0.244/p=0.042) and echocardiographic left ventricular mass index (r=0.270/p=0.026). These correlations were also observed in the male drinker sub-group. In the non-drinkers, the uric acid level (mean 5.0±1.4mg/dL) was positively correlated with BMI (r=0.369/p=0.0002) but not with blood pressure or the markers of cardiac hypertrophy. ConclusionsThe results suggest that the role of uric acid in blood pressure might differ between hypertensive drinkers and non-drinkers. In regular alcohol drinkers, there was a positive association of uric acid level with blood pressure and the severity of cardiac hypertrophy. In non-regular drinkers, an increased uric acid level is likely to be closely associated with increased BMI.

Left ventricular hypertrophy and arterial stiffness in essential hypertension.

The aim of this study was to evaluate the association between an increase in arterial stiffness and the development of left ventricular hypertrophy in essential hypertension patients. One hundred forty essential hypertension patients were included in the study. Patients were divided into two groups based on echocardiographic measurements; with left ventricular hypertrophy (n=70) and without left ventricular hypertrophy (n=70). The criterion for hypertrophy was accepted as an intraventricular septum and posterior wall thickness in diastole of 11 mm or above. Aortic stiffness values of the patients groups were measured noninvasively by arteriography through the brachial artery. Pulse wave velocity (PWV) measurements were used as indicators of arterial stiffness. When compared to the group without left ventricular hypertrophy, elevated systolic blood pressure, mean blood pressure, and pulse pressure were located in the left ventricular hypertrophy group at a significant level (p > 0.01). A statistically significant difference was not observed in the diastolic blood pressure and pulse measurements of the groups. Pulse wave velocity, the indicator of arterial stiffness, was elevated to a significant degree in the left ventricular hypertrophy group (p > 0.01). While a positive correlation was found between pulse wave velocity and left ventricle mass index, microalbuminuria, high sensitive C-reactive protein (Hs-CRP), and left ventricle end-diastolic volume, a negative correlation was found between pulse wave propagation velocity and left ventricle E/A. In conclusion, pulse wave analysis is a valuable method for predicting cardiac hypertrophy in essential hypertension (Tab. 6, Ref. 25).

Persistent resistant hypertension during long term follow-up is related with lack of regression of left ventricular hypertrophy in essential hypertensives

Persistent resistant hypertension during long term follow-up is related with lack of regression of left ventricular hypertrophy in essential hypertensives

Age related prevalence of severe left ventricular hypertrophy in essential hypertension: Echocardiographic findings from the ETODH study

Aim. We sought to investigate the prevalence and correlates of severe left ventricular hypertrophy (LVH) in relation to age in a large cohort of essential hypertensives referred to a single outpatient hypertension clinic. Methods. A total of 3752 (mean age 53±13 years, 53% men) untreated (29.5%) and treated hypertensive patients categorized in three age groups (I: 18–40 years; II: 41–64 years; III: ≥65 years) were considered for this analysis. All patients underwent extensive investigations searching for target organ damage. LVH, defined as LV mass ≥49/45 g/m2.7 in men/women, respectively, was graded as mild, moderate and severe according to Lang's report. Results. LVH prevalence was 29.4% in group I, 48.2% in group II and 63.6% in group III. Overall, more than one fourth of patients with LVH had a severely increased LV mass index; the likelihood of having severe LVH was two- and four-fold higher in elderly hypertensives than in their middle-aged and young counterparts, respectively. Increasing age and LVH degree were both associated with a greater prevalence of concentric LV geometry as well as of extra-cardiac organ damage (i.e. carotid intima-media thickness). Conclusions. LVH is a highly prevalent organ damage in essential hypertensives, particularly in the elderly, who exhibited a more severe increase of LV mass index, higher relative wall thickness and extra-cardiac organ damage compared with young and middle-aged sub-groups. Our findings suggest that the assessment of cardiovascular risk by grading LVH rather than simply defining the presence/absence of this cardiac phenotype could improve therapeutic strategies in the hypertensive population, particularly in the elderly.

Low serum 25-hydroxyvitamin D levels are associated with left ventricular hypertrophy in essential hypertension

Background and aimLow serum 25-hydroxyvitamin D [25(OH)D] levels may have an important role in predisposing to hypertension and myocardial disease. We investigated the relationship between 25(OH)D and left ventricular (LV) structure and function, assessed by echocardiography, in a series of patients with essential hypertension (EH). Methods and resultsSixty-two newly diagnosed never-treated patients (32 male/30 female), aged 18–65 years, with grade 1–2 hypertension, no diabetes, no obesity, no hyperlipidemia, and no cardiopulmonary, renal, or hepatic disease, were studied. Twenty-four healthy normotensive sex-, age-, BMI-matched subjects served as controls. Hypertensive patients with 25(OH)D deficiency, defined as serum 25(OH)D levels <50 nmol/L, had higher prevalence of LV hypertrophy (LVH) than their 25(OH)D-sufficient counterparts (57.1 vs 17.6%, P = 0.02); no differences between the two groups were found in blood pressure levels as well as in other biochemical and hormone parameters. There was an inverse correlation between LV mass index and 25(OH)D levels (r = –0.366, P < 0.003) and a direct correlation between LV mass index and BMI (r = 0.333, P < 0.006) in the entire hypertensive population. The two variables remained independently associated with LVH at multivariable logistic regression analysis (OR 1.05, P < 0.005 and OR 1.25, P = 0.03, respectively). Prevalence of 25(OH)D deficiency was similar in EH patients and controls (45.1 vs 41.6%, P = 0.89), whereas no correlation between echocardiographic parameters and hormone levels was found. ConclusionsIn the absence of major cardiovascular risk factors, 25(OH)D deficiency is a frequent finding in EH patients and is independently associated with LVH.

Protective effect of the 1742(C/G) polymorphism of human cardiotrophin-1 against left ventricular hypertrophy in essential hypertension

Experimental and clinical evidence supports a role of cardiotrophin-1 (CT-1) in the development of hypertensive left ventricular hypertrophy (LVH). The goal of this study was to investigate the relationship between human CT-1 genetic background and LVH in essential hypertension. A total of 900 individuals were genotyped for the 1742(C/G) polymorphism of the human CT-1 gene. Serum CT-1 levels were assessed by ELISA in 681 individuals. Left ventricular parameters were determined by two-dimensional echocardiography in 297 individuals. The prevalence of the GG genotype of the 1742(C/G) polymorphism was reduced in essential hypertension (8.4% in normotensive individuals, 4.9% in hypertensive patients, P = 0.046 versus CC/CG individuals) and in LVH (11.5% in nonhypertrophic normotensive individuals, 12.2% in nonhypertrophic hypertensive patients, 2.6% in hypertensive patients with LVH, P = 0.008 versus CC/CG individuals). Apart from this, GG individuals presented lower serum concentration of CT-1 (GG, 147.1 ± 10.5 fmol/ml; CC/CG, 187.1 ± 4.8 fmol/ml; P = 0.036) and left ventricular mass index (GG, 91 ± 6 g/m; CC/CG, 119 ± 3 g/m; P = 0.002). Multivariate analyses showed that the 1742(C/G) polymorphism was a significant determinant of both left ventricular mass index and serum CT-1, after adjusting for confounding factors. Finally, in-vitro studies supported the functionality of the 1742(C/G) polymorphism. Our results indicate that the 1742(C/G) polymorphism of the human CT-1 gene is associated with LVH in hypertension and that the GG genotype may have a protective role. It is suggested that CT-1 is one of the mediators of this association.

E0026 Association between the M235T, T174M polymorphism of the angiotensinogen gene and left ventricular hypertrophy in essential hypertension in Kazakans

ObjectiveTo investigate whether the M235T, T174M polymorphisms of the angiotensinogen gene were associated with left ventricular hypertrophy (LVH) in Xinjiang Kazakans with essential hypertension.Methods86 patients with essential hypertension and left...

Prevalence and clinical correlates of right ventricular hypertrophy in essential hypertension

Right ventricular hypertrophy (RVH) has been reported to be a component of cardiac damage in systemic hypertension; this evidence, however, is based on small studies and major determinants of biventricular hypertrophy are still undefined. Thus, the prevalence and clinical correlates of RVH have been investigated in essential hypertension. A total of 330 untreated and treated uncomplicated essential hypertensives consecutively attending a hospital out-patient hypertension clinic were considered for the analysis. All individuals underwent a quantitative echocardiographic examination as well as extensive clinical and laboratory investigations. RVH was defined by an anterior RV wall thickness equal or higher than 3.1/3.0 mm/m2 in men and women, respectively, and left ventricular hypertrophy (LVH) by LV mass index equal or higher than 51/47g/m2.7 in men and women, respectively. Overall, 114 (34.5%) patients fulfilled the criteria for LVH and 111 (33.6%) for RVH; normal cardiac morphology was observed in 164 patients (49.6%), isolated RVH in 52 (15.7%), isolated LVH in 55 (16.6%) and bi-ventricular hypertrophy in 59 (17.8%). In a logistic regression analysis, modifiable risk factors such as abdominal obesity (OR 3.41, CI 1.73-6.74, P = 0.0004), LV mid-wall fractional shortening (OR 2.48, CI 1.26-4.85, P = 0.008), fasting blood glucose (OR 2.47, CI 1.25-4.89, P = 0.009) and systolic blood pressure (OR 2.39, CI 1.19-4.82, P = 0.014) were the major independent correlates of biventricular hypertrophy. RVH is commonly found in systemic hypertension and is associated with LVH (i.e., biventricular hypertrophy) in approximately one-fifth of the patients seen in a specialist setting. The clinical correlates of biventricular hypertrophy suggest that this phenotype is associated with a profile of very high cardiovascular risk.

Left and right ventricular structural changes in obese hypertensives

Aim. Obesity is known to be independently related to left ventricular (LV) hypertrophy (LVH); however, in human hypertension the association of obesity with right ventricular hypertrophy (RVH) is still unsettled. We investigated the relationship of obesity with RVH and biventricular hypertrophy in essential hypertension. Methods. A cohort of untreated and treated uncomplicated essential hypertensives consecutively attending a hospital outpatient hypertension clinic, categorized in three groups according to body mass index (BMI) thresholds (<25, 25–29.9 and ≥30 kg/m2) was considered for the present analysis. RVH was defined by an anterior RV wall thickness equal or higher than 3.1/3.0 mm/m2 in men and women, respectively, and LVH by LV mass index (LVMI) equal or higher than 51 and 47 g/m2.7 in men and women, respectively. Results. A total of 124 patients (37.6%) had normal BMI, 151 patients (45.7%) were overweight and 55 (16.7%) obese. Prevalence rates of biventricular hypertrophy (i.e. LVMI>51 and 47 g/m2.7 and RVWT>3.1 and 3.0 mm) in the three groups were 7.3%, 21.2% and 32.7%, respectively. In a multivariate analysis, BMI (OR=3.58, 95% CI 1.82–7.03, p=0.0002), was the most important correlate of biventricular hypertrophy. Conclusions. Our findings extend previous data on the impact of obesity on cardiac structure by showing that this phenotype is strongly associated with biventricular hypertrophy.

Metabolic syndrome and biventricular hypertrophy in essential hypertension

The hypertrophyof the right ventricle is not because of pressureoverload, and therefore non-haemodynamic factors,such as angiotensin II, aldosterone, insulin, thesympathetic nervous system and endothelin may beinvolved in this process.The contribution of non-haemodynamic factors tothe development of cardiac hypertrophy may alsoexplain why in several studies it has been shown thatthe increase in left ventricular mass precededhypertension. For example, we followed 500 younghealthy Israeli air force aviators, who underwentechocardiography at the start of their military servicefor an average period of 7.5±3.0 years.

Metabolic syndrome and biventricular hypertrophy in essential hypertension

The metabolic syndrome (MS) is associated with structural and functional alterations of the left ventricle (LV); no evidence is available on the impact of the MS on the right ventricle (RV). To assess whether MS, as defined by the ATP III report, is associated with biventricular hypertrophy, a total of 286 hypertensive subjects (mean age 58.7+/-12.2 years) attending our outpatient clinic underwent the following procedures: (1) physical examination and standard clinic blood pressure (BP) measurement; (2) routine laboratory investigations; (3) M-mode, two-dimensional and Doppler echocardiography. LV hypertrophy (LVH) was defined by LM mass index>or=51/47 g m(-2.7) in men and women, respectively. Right-sided chambers were measured in parasternal long axis at the outflow tract and subcostal view; RV hypertrophy (RVH) was defined by anterior RV wall thickness>or=6.0/5.5 mm in men and women, respectively. Filling velocities of both ventricles were assessed by pulsed Doppler echocardiography. Structural cardiac alterations were more pronounced in hypertensive men and women with MS than in their non-MS counterparts and involved both ventricles as shown by the differences in continuous variables as well as in prevalence rates of LVH (58 and 48% vs 28 and 30%, respectively, P<0.01) and RVH (48 and 54% vs 25 and 35%, respectively, P<0.01). Both LV and RV filling in MS hypertensives were more dependent on the atrial systole. Our study shows that in human hypertension, structural and functional cardiac changes induced by MS are not limited to the LV but also involve the right one.

Actual aspects of pathogenesis and treatment of asymmetric left ventricular hypertrophy in essential hypertension

Actual aspects of pathogenesis and treatment of asymmetric left ventricular hypertrophy in essential hypertension

Promise of Low-Density Lipoprotein–Lowering Therapy for Primary and Secondary Prevention

One of the foremost medical advances of the past 2 decades has been proof that elevated low-density lipoprotein (LDL) is a cause of atherosclerotic cardiovascular disease (ASCVD) and that lowering of LDL levels will reduce risk for ASCVD.1,2 The application of this knowledge in clinical and public health arenas offers the opportunity to greatly reduce morbidity and mortality from ASCVD. This article outlines the rationale underlying this opportunity. Response by Superko and King p 573 Although several major risk factors for ASCVD exist, the realization that elevated plasma LDL is the driving force of atherogenesis highlights the possibilities for prevention. Many studies in laboratory animals have shown that high serum cholesterol levels induce atherosclerotic lesions resembling those found in humans.1 Similarly, humans with severe forms of hypercholesterolemia commonly exhibit premature atherosclerotic disease. Epidemiological studies reveal a strong association between serum cholesterol levels and ASCVD prevalence3; moreover, in populations in which cholesterol levels are low, ASCVD is correspondingly low even when other risk factors are common.4 The latter observation has recently been confirmed through genetic epidemiology; in those persons who carry a mutation causing low cholesterol levels over a lifetime, ASCVD is virtually absent even in the presence of other risk factors.5 Finally, many recent clinical trials have documented that LDL-lowering therapy reduces risk for ASCVD.6 All told, these several lines of evidence indicate that a lifetime of low LDL levels lowers risk for ASCVD by up to 80% to 90% compared with the general population of the United States,5 whereas intensive LDL-lowering therapy even in the presence of advanced atherosclerotic disease reduces risk for major ASCVD events by 40% to 50%.6–8 However, the latter response leaves 50% to 60% of risk untouched; this has called been residual risk. Because of the …

C-Reactive Protein and Incident Left Ventricular Hypertrophy in Essential Hypertension

Elevated C-reactive protein (CRP) levels have been associated with increased cardiovascular risk in hypertensive adults. The aim of this study was to determine whether plasma CRP level is more predictive of left ventricular hypertrophy (LVH) than is ambulatory blood pressure (BP) in hypertensive children. Baseline and 12-month follow-up measures of BP, body mass index (BMI), low-density lipoprotein/high density lipoprotein cholesterol, left ventricular mass (LVM), and CRP data collected from 48 newly diagnosed, untreated hypertensive children were analyzed. CRP was measured by a highly sensitive nephelometric method. Left ventricular mass index (LVMI) was calculated as LVM/height2.7, and LVH was defined as LVMI>38.6 g/m2.7 being the cut-point for the 95th percentile found in healthy children. Average systolic BP (SBP), diastolic BP (DBP), SBP index, and DBP index were calculated. All patients received hydrochlorothiazide therapy in combination with angiotensin converting enzyme inhibitor treatment. Five patients also had angiotensin receptor blocker therapy to reach the target BP (<95th percentile corrected for age and gender). In a multiple regression analysis, LMVI was correlated with CRP, BMI, SBP, and SBP index. CRP alone explained 77% of the variance of LVMI, whereas BMI, SBP, and SBP index explained only 1.3, 0.3, and 0.4% of the variance, respectively. CRP was also the most significant correlate of follow-up LVH. In conclusion, elevated CRP level is significantly associated with LVH in children with essential hypertension. BP reduction with renin-angiotensin system blocker and hydrochlorothiazide therapy reduces LVH while lowering CRP level.

Ultrasonic changes and clinical observation of enalapril and indapamide to reverse left ventricular hypertrophy in essential hypertension

目的 观察依那普利和吲达帕胺对原发性高血压伴左心室肥厚(LVH)的逆转作用.方法 将136例原发性高血压患者随机分为治疗组(n=68)和对照组(n=68),治疗组给予依那普利和吲达帕胺;对照组给予吲达帕胺.分别于服药前及服药6个月后测量血压,观察24 h动态血压、心电图、超声心动图改变.结果 两组治疗后收缩压及舒张压均较治疗前有明显降低(P＜0.01),心功能指标较治疗前明显改善(P＜0.05),高血压伴LVH有明显的逆转作用(P＜0.05～0.01).结论 依那普利和吲达帕胺均有逆转LVH作用,两者联合应用在逆转LVH方面优于单独使用吲达帕胺。