Left ventricular hypertrophy is associated with increased sirtuin level in newly diagnosed hypertensive patients

Background: Arterial hypertension is one of the leading causes of mortality and morbidity in general population. Sirtuin 1 (SIRT1) has diverse anti-inflammation, anti-oxidant, and anti-apopytosis effects on endothelium and is associated with endothelial aging and dysfunction. The objective of this study was to evaluate the relation of serum SIRT1 level with left ventricular hypertrophy (LVH) in newly diagnosed hypertensive patients.

Methods: One hundered and twenty-five consecutive, newly diagnosed hypertensive patients were divided into two groups with regard to presence of LVH and compared to 40 healthy control subjects. LVH was determined by transthoracic echocardiography using the cube formula. Serum SIRT1 level was analyzed with enzyme-linked immunosorbent assay.

Results: Serum SIRT1 level was significantly higher in patients with LVH compared to those without LVH (14.3 ± 3.9 ng/ml vs. 7.9 ± 3.6 ng/ml, ?P < 0.001) and healthy control subjects (14.3 ± 3.9 ng/ml vs 6.6 ± 2.0 ng/ml, P < 0.001). Multivariate logistic regression analysis revealed higher serum SIRT1 level independently predicted LVH in hypertensive patients (OR 1.50; 95% CI, 1.30–1.73; P < 0.001). Receiver-operating characteristic curve analysis demonstrated a cutoff value of 9.4 had a sensitivity of 90% and specificity of 74% for the prediction of LVH (AUC 0.885; 95% CI, 0.815–0.935; ?P < 0.0001).

Conclusion: SIRT1 was a powerful biomarker for predicting LVH in hypertensive patients.     

老年高血压病患者血浆内皮素与左室重量和功能关系的研究

目的探讨老年高血压病患者(EH)血浆内皮素(ET)与左室重量和功能的关系。方法采用放射免疫分析法和多昔勒超声心动图技术检测86例EH患者和57例健康对照者血浆ET的浓度及室间隔(IVST)、左室后壁厚度(PWT)、左室心肌重量指数(LVMI)以及左室流入道E峰和A峰比值(E/A)、E峰加速面积(EAA)。结果EH组ET、IVST、PWT、LVMI显著高于对照组(P值均＜0．01),E/A、EAA显著低于对照组(P＜0．01);EH组ET与IVST、LPWT、LVMI之间均存在着显著正相关(P值均＜0．01),ET与E/A、EAA之间均存在着显著负相关(P值均＜0．01)。结论ET可能是引起EH患者左室肥厚及舒张功能不全的原因之一。     

老年高血压病患者血浆内皮素与左室重量和功能关系的研究

目的探讨老年高血压病患者（ＥＨ）血浆内皮素（ＥＴ）与左室重量和功能的关系。方法采用放射免疫分析法和多普勒超声心动图技术检测８６例ＥＨ患者和５７例健康对照者血浆ＥＴ的浓度及室间隔（ＩＶＳＴ）、左室后壁厚度（ＰＷＴ）、左室心肌重量指数（ＬＶＭＩ）以及左室流入道Ｅ峰和Ａ峰比值（Ｅ／Ａ）、Ｅ峰加速面积（ＥＡＡ）。结果ＥＨ组ＥＴ、ＩＶＳＴ、ＰＷＴ、ＬＶＭＩ显著高于对照组（Ｐ值均＜０．０１）,Ｅ／Ａ、ＥＡＡ显著低于对照组（Ｐ＜０．０１）;ＥＨ组ＥＴ与ＩＶＳＴ、ＬＰＷＴ、ＬＶＭＩ之间均存在着显著正相关（Ｐ值均＜０．０１）,ＥＴ与Ｅ／Ａ、ＥＡＡ之间均存在着显著负相关（Ｐ值均＜０．０１）。结论ＥＴ可能是引起ＥＨ患者左室肥厚及舒张功能不全的原因之一。     

Prolonged recovery time in the left precordial leads reflects increased left ventricular mass in the hypertensive patients

Hypertensive left ventricular hypertrophy (LVH) is considered to be a risk for arrhythmogenicity, but the quantification of the changes in T-wave morphology, as the reflection of repolarization abnormality, has not been fully established. The purpose of this study was to quantify the T-wave changes in the hypertensive patients and to investigate the relationship with the increased left ventricular mass. Standard 12-lead electrocardiogram and echocardiogram were recorded in 90 hypertensive patients. Activation time (AT), activation recovery interval (ARI), and recovery time (RT) were measured in the precordial lead and QT interval in the 12 leads. To compare the left precordial T-wave changes among patients, measurements of ARI and RT in the right precordial negative T wave were excluded. Each parameter excluding AT was corrected with Bazett formula, and then the dispersion was calculated. Left ventricular mass index was determined echocardiographically to select non-LVH group (n=31) and LVH group (n=59). In both groups, AT, ARI, and RT in the left precordial leads were larger compared with those in the right precordial leads. Dispersion of AT was not different between the 2 groups. However, the dispersion of ARI and RT in LVH group was significantly greater than that in non-LVH group. There were correlations between left ventricular mass index and the dispersion of RT (r=0.66, P<.001), ARI (r=0.61, P<.001), and 12-lead QT (r=0.42, P<.001). In patients with LVH, significant prolongation of RT in the left precordial leads was observed, suggesting that this RT change resulted from the nonuniformity of epicardial action potential duration.     

Regression of left ventricular hypertrophy and systolic function in hypertensive patients during long-term treatment with ketanserin

Summary It is now generally accepted that antihypertensive therapy can induce regression of left ventricular hypertrophy (LVH) in hypertensive subjects. However, the influence of LVH reversal on both the systolic and diastolic functions, and particularly the ability of the heart to meet sudden overloads caused by exercise and/or recurrence of hypertension, remain unanswered questions. The long-term effects of ketanserin, a selective serotonin S₂-receptor antagonist with additional alpha₁-adrenergic blocking properties, on LVH and systolic function were studied in 13 untreated subjects (age range 35–55 years) with mild-to-moderate essential hypertension, echocardiographic evidence of LVH, and normal ejection fraction. Blood pressure values and echocardiographic measurements of dimensions, wall thicknesses, and indices of LV mass were determined before and after 3, 6, and 12 months treatment; ejection fractions at rest and during exercise were evaluated by equilibrium multigated radionucleide angiocardiography at baseline and after 12 months of therapy. Mean arterial pressure was significantly reduced from the first month of treatment (p<0.001) and remained well controlled up to the end of the trial. Both posterior and septum wall thicknesses decreased after 3 months of therapy and remained stable throughout the whole study period. LV mass index decreased from a mean ± SD of 187.7±47.6 g/m² to a mean of 157.81±31.63 g/m² (p<0.01) at the third month, reaching greater decreases after 6 months (156.05±31.00 g/m²) and after 12 months (153.21±28.80 g/m²) of treatment. A significant correlation was found between LV mass and posterior wall thickness at the different observation times in the study. Finally, the regression of LVH at the end of therapy was not associated with impairment of systolic function, as assessed by measurements of ejection fraction at rest and during exercise.     

Left ventricular hypertrophy regression and function changes with ketanserin in elderly hypertensives

Summary Ketanserin is a serotonin antagonist with age-related antihypertensive efficacy. Its effects on left ventricular (LV) function and hypertrophy have not been adequately reported. We studied noninvasively 54 elderly hypertensives before and 6 months after ketanserin monotherapy. Mean blood pressure was controlled (174/101 to 145/86 mmHg, p<0.0001) with no heart rate changes. LV dimensions and volumes remained unchanged, as did all LV ejection indices, thus preserving LV output (p=ns). Total peripheral resistances fell (from means of 1986 to 1615 dynes, cm.s^-5, p<0.0001), as did LV systolic wall stresses. Mean LV mass was reduced (248 to 237 g, p<0.0001), mainly due to interventricular septum thinning (11.8 to 11.1 mm, p<0.0001), resulting in a decrease in mean LV cross-sectional area (21.3 to 20.5 cm², p<0.0001) and mass/volume ratio (2.14 to 2.01 p=0.0001). Thus, LV hypertrophy regression did not affect contractility (LV mass index relation to stress/end-systolic volume index, r=–0.558 before and r=–0.564 after ketanserin therapy). It is concluded that ketanserin is an effective antihypertensive agent in the elderly that reduces LV hypertrophy indices and maintains cardiac output, with no concomitant burdening on LV hemodynamics.     

代谢综合征对老年高血压患者左心室重量和功能的影响

目的探讨代谢综合征(MS)对老年高血压患者左心室重量和功能的影响。方法选择老年高血压患者513例,根据诊断分为高血压非MS组(266例)和高血压合并MS组(247例)。采用超声心动图测定左心室结构相关参数,计算左心室重量指数(LVMI),并测定左心室舒张早期二尖瓣最大血流速度(E)、舒张晚期二尖瓣最大血流速度(A),计算E/A值和LVEF。结果与高血压非MS组比较,高血压合并MS组LVMI和左心室肥厚率明显升高,E/A明显降低(P<0.05,P<0.01);与单纯高血压比较,合并2项组分和合并3项组分患者左心室肥厚率明显增加(17.1%υs 30.9%υs 37.5%,P<0.05);分别以LVMI、E/A为因变量进行多元线性逐步回归分析,以MS及其他因变量相关因素为自变量,MS与LVMI相关(R~2=0.306,P<0.05);以MS各个组分及其他因变量相关因素为自变量时,收缩压、体重指数、空腹胰岛素与LVMI相关(R~2=0.419,P<0.05),收缩压、体重指数与E/A相关(R~2=0.303,P<0.05)。结论 MS与老年高血压患者的左心室重量增加有关,合并MS者左心室舒张功能受损。     

伊贝沙坦对高血压左室肥厚患者的左室结构的影响

目的 研究伊贝沙坦对高血压左室肥厚（LVH）患者的左室结构的影响。方法 60例原发性高血压左室肥厚患者随机分为2组：治疗组每天口服伊贝沙坦150mg，对照组每天口服氨氯地平5mg。平均12个月，观察用药后血压、左室结构的变化。结果 用药后2组收缩压（SBP）和舒张压（DBP）均显著降低（P〈0．01）；室间隔厚度（IVST）及左室后壁厚度（LYPWT）均变薄（P〈0．01），左室重量指数（LYMI）明显减少（P〈0．01），对照组各项指标无明显变化（P〈0．05）。结论 对原发性高血压左室肥厚的患者，长期应用伊贝沙坦具有良好降压效果，同时还可逆转LVH，改善患者预后。     

Left ventricular hypertrophy in athletes and hypertensive patients

Systemic hypertension and physical exercise are both associated with cardiac adaptations. The impact is most prominent on the left side of the heart, which hypertrophies leading to left ventricular hypertrophy. This article reviews structural and functional cardiac changes seen in hypertensive and athlete's hearts.     

Discrepancy between increased left ventricular mass and "normal" QRS voltage is associated with decreased connexin 43 expression in early stage of left ventricular hypertrophy in spontaneously hypertensive rats

Background and Purpose

On the basis of our previous results of animal and human studies, we assume that the discrepancies between increased left ventricular mass (LVM) and electrocardiographic (ECG) findings not exceeding the upper normal limits in left ventricular hypertrophy (LVH) are conditioned by the electrical remodeling of hypertrophied myocardium. We assumed that these discrepancies observed in the early stage of LVH in spontaneously hypertensive rats (SHR) are associated with a decreased expression of connexin 43.

Methods

Standard 12-lead ECG was recorded in 20-week-old male SHR and age-matched and sex-matched normotensive Wistar rats (Institute of Experimental Pharmacology SAV, Dobra Voda, Slovakia). The approximated maximum QRS spatial vector magnitude (QRSmax) was calculated from leads V₂, aVF, and V₅. Left ventricular mass was weighed, and the specific potential (SP) of myocardium was calculated as the QRSmax-to-LVM ratio. Left ventricular protein levels of connexin 43 were analyzed with sodium dodecyl sulfate-polyacrylamide gel electrophoresis and Western blotting.

Results

The LVM values were significantly higher in SHR than in normotensive controls (0.96 ± 0.03 g and 0.680 ± 0.07 g, respectively; P < .001). The QRSmax values in SHR did not follow the increase either in systolic blood pressure or in LVM. The SP values in SHR were significantly lower than those in control rats (0.92 ± 0.11 mV/g and 1.358 ± 0.06 mV/g, respectively; P < .01). A 37% decrease in connexin 43 level was observed in SHR.

Conclusions

The QRS voltage did not follow the increase in the LVM in 20-week-old SHR, and the values of connexin 43 were lower in SHR than in normotensive controls. We believe that the discrepant findings between ECG voltage and LVM can be caused by the electrical remodeling in the early stages of LVH.     

老年高血压左室肥厚患者的室性心律失常与心肌缺血

目的　了解老年原发性高血压左室肥厚患者的室性心律失常、心肌缺血的特点及两者的关系。方法　 90例老年 (≥ 6 0岁 )高血压患者经超声心动图测定左室质量指数 (LVMI) ,分为左室肥厚 (A组 )和非左室肥厚 (B组 )。经2 4h动态心电图测定 2 4h室性早搏总数 (VPCs)、Lown’s分级、ST段压低程度、持续时间及 2 4h发作次数。结果　A组室性心律失常的发生率明显增加 (P <0 .0 5 ) ,室性早搏 :75 %比 5 4% ,Lown’s 3～ 4级 :2 6 %比 4%。A组发作性ST段压低的发生率高 ,缺血持续时间长 (5 0 %比 15 % ,P <0 .0 5 )。所有缺血发作均为无症状性。室性心律失常与心肌缺血的昼夜节律变化基本相同。结论　无冠心病临床证据的老年原发性高血压左室肥厚患者的室性心律失常及心肌缺血的发生率增加 ,两者的昼夜节律变化基本相同     

Diastolic left ventricular function after renal transplantation in patients with normal and hypertrophied myocardium

While diastolic left ventricular (LV) dysfunction is frequent and associated with cardiovascular complications in end-stage renal disease treated with dialysis, controversial information exists on diastolic LV function after renal transplantation. Therefore, Doppler echocardiographic parameters of LV diastolic filling were analyzed in 17 transplanted patients with normal LV mass (< 150 g/m2; mean: 128 +/- 17 g/m2) and 24 transplanted patients with LV hypertrophy (> 150 g/m2; mean: 197 +/- 36 g/m2) and compared with 28 normal controls without and 11 controls with LV hypertrophy. Mean age (normal vs. increased LV mass: 46 +/- 13 vs. 48 +/- 11 years; p = NS) and transplantation duration (60 +/- 35 vs. 50 +/- 37 months; p = NS) were comparable between renal patients, while systolic blood pressure (136 +/- 12 vs. 149 +/- 14 mmHg; p < 0.02) and serum creatinine (1.55 +/- 0.45 vs. 1.98 +/- 0.76 mg/dl; p < 0.05) were higher in patients with than without LV hypertrophy. In transplanted patients with LV hypertrophy, peak early/atrial filling velocity ratios were decreased (1.17 +/- 0.34 vs. 0.94 +/- 0.34; p < 0.05), mean atrial filling fractions were increased (37 +/- 7% vs. 42 +/- 7%; p < 0.05), and isovolumic relaxation periods were prolonged (86 +/- 23 vs. 106 +/- 26 ms; p < 0.02) compared with transplanted patients with normal LV mass. The frequency of pathologic peak early/atrial filling velocity ratios (12 vs. 42%; p < 0.05), atrial filling fractions (12 vs. 25%; p = NS) and isovolumic relaxation periods (6 vs. 29%; p = NS) was higher in transplanted patients with than without LV hypertrophy. Individual ratios of peak early/atrial filling velocity were inversely correlated with age in transplanted patients with normal LV mass (p < 0.002), and atrial filling fractions were correlated with LV mass index in transplanted patients with LV hypertrophy (p < 0.01). Diastolic LV function was comparable in both groups of transplanted patients with their corresponding non-renal controls. It is concluded that, in transplanted patients, diastolic LV filling is comparable to nonrenal controls; it is age-dependent in patients with normal LV mass and mass-dependent in those with LV hypertrophy.     

Decreased adrenergic response in hypertensive patients without left ventricular hypertrophy

To analyze the adrenergic responses and to compare them between hypertensive patients with and without left ventricular hypertrophy (LVH), left ventricular (LV) fractional shortening (FS) and end-systolic wall stress (ESS) were measured by echocardiography and the inotropic response to the infusion of isoproterenol (0.02 μg/kg/min for 5 min) was studied in 25 hypertensive patients without LVH [H(-)] and 30 hypertensive patients with LVH [H(+)]. LVH was determined by echocardiography. Age, gender, heart rate, systolic and diastolic blood pressures, LV end-systolic and end-diastolic diameters, and FS were matched between the groups. The tests were performed before introduction of antihypertensi ve treatment or 4 weeks after its discontinuation. ESS showed a significant inverse linear relation with FS in all the subjects before isoproterenol infusion. The inotropic response to isoproterenol was measured as the increase of FS corrected for the decrease of ESS (ΔFS/-ΔESS), that is, the slope of the change of the relation between FS and ESS. The change in ΔFS/-ΔESS was significantly smaller (0.49 ± 0.15 cm²/g, mean ± SD) in H(?) than in H(+) patients (1.01 ± 0.57 cm²/g) (p < 0.001). It is concluded that, compared with the H(+) group, adrenergic response is depressed in H (?) patients. This depression might be etioloically related to the phenomenon that LVH did not develop in the H(?) group in spite of the same level of pressure load as in the H(+) group.     

Aging and left ventricular mass and function in people with end-stage renal disease

OBJECTIVES: To identify the main age‐related factors responsible for cardiomyopathy in people with end‐stage renal disease (ESRD). DESIGN: Cross‐sectional. SETTING: Dialysis unit. PARTICIPANTS: Two hundred fifty‐four individuals undergoing chronic dialysis. MEASUREMENTS: Left ventricular (LV) systolic function (assessed according to midwall fractional shortening (mwFS)) and LV mass index (LVMI). RESULTS: At echocardiography, 196 (77%) participants displayed LV hypertrophy (LVH) and 123 (48%) had LV systolic dysfunction. On univariate analysis, age was related directly to LVMI (correlation coefficient (r)=0.33, P<.001) and inversely to mwFS (r=?0.23, P<.001) and a 10‐year increase in age was associated with 4.2‐g/m^2.7 greater LVMI and 0.5% lower mwFS. Albumin, pulse pressure, cardiovascular comorbidities, and C‐reactive protein were age‐related risk factors for LVMI and mwFS, whereas hemoglobin was an age‐dependent risk factor only for LVMI and heart rate and diabetes mellitus only for mwFS. After adjusting for age‐related risk factors, the predictive value of age for cardiomyopathy was substantially less (–67%) and the age‐dependent variability in LVMI and mwFS was much attenuated (?61%), and neither was significant. CONCLUSION: This study suggests that in people with ESRD, the relationship between age and cardiomyopathy is largely dependent on age‐related risk factors and that interventions focused on modifiable risk factors linked to age (e.g., malnutrition and inflammation) could attenuate the detrimental effect of aging on cardiovascular risk in the dialysis population.     

Left ventricular mass changes with nicardipine therapy in essential hypertension

Summary Eighteen hypertensive patients (13 males, 5 females; age 48±13; diastolic blood pressure >95 mmHg), either previously untreated or who had been off treatment for more than 3 months, underwent M-mode echocardiography before (DO) and after (D90) 3 months of nicardipine therapy (60–90 mg/day). All echocardiograms were read blind, and left ventricular mass (LVM) was calculated (Devereaux's formula). Blood pressure was significantly reduced after 3 months from 167±15/102±8 mmHg on DO to 152±16/92±mmHg on D90 (p<0.001). The reduction in LVM was not significant: 266±95 g on DO, 247±78 g on D90. There was a trend to a higher (although nonsignificant) LVM reduction in patients with left ventricular hypertrophy at entry (–11%, n=11) than in patients without left ventricular hypertrophy (–2%), n=7).     

Left atrial conduit function for left ventricular filling dynamics in patients with myocardial infarction

This study observed the left atrial function in determining filling dynamics of the left ventricle in patients with myocardial infarction. The study consisted of eight control subjects and ten patients with myocardial infarction. The left ventricular filling volume is considered to be composed of the left atrial passive emptying, active emptying, and conduit volumes. The change of left ventricular filling volume was correlated with that of conduit volume (r = .87, P < .01). However, the change of left ventricular filling volume did not have any correlation to those of left atrial passive emptying and active emptying volumes. These results suggested that the left atrial conduit function was important in determining filling dynamics of the left ventricle.     

Left ventricular muscle mass and diastolic function in patients with essential hypertension under long-term clonidine monotherapy

To determine whether alterations of left ventricular (LV) structure are associated with improved LV function under chronic clonidine monotherapy (300-450 g/day) of essential hypertension, 11 male patients (age range 47-61 years) were followed for 5.4 +/- 0.9 months using echocardiography and Doppler echocardiography. Blood pressure decreased from a mean of 168/105 to 150/96 mmHg (p less than 0.01), heart rate remained unchanged (73 +/- 10 vs. 71 +/- 10 beats/min). LV muscle mass decreased from 350 +/- 73 to 297 +/- 56 g (p less than 0.02), LV volume/muscle mass ratio increased from 0.58 +/- 0.13 to 0.69 +/- 0.12 ml/g (p less than 0.005). Ejection time increased from 276 +/- 17 to 296 +/- 17 ms (p less than 0.01), whereas no significant change was found for pre-ejection period, ejection fraction, cardiac index and LV dimensions. Doppler analysis revealed improved isovolumic relaxation time (116 +/- 17 vs. 84 +/- 28 ms; p less than 0.05), but no change in isovolumic contraction duration, maximal inflow velocities, time-velocity integrals and their duration, rate of acceleration and deceleration of early and atrial filling, and of their ratios. It is concluded that no reliable improvement in diastolic or systolic LV function is observed in chronic clonidine monotherapy of essential hypertension despite a normalization of blood pressure and a regression of LV hypertrophy.     

Left ventricular dysfunction in hypertensive patients with Type 2 diabetes mellitus.

AIMS: To characterize left ventricular function in hypertensive patients with Type 2 diabetes and normal ejection fraction, and to relate these findings to pathogenic factors and clinical risk markers. METHODS: We examined 70 hypertensive patients with Type 2 diabetes mellitus with ejection fraction > 0.55 and fractional shortening > 0.25, all without any cardiac symptoms. Thirty-five non-diabetic subjects served as control subjects. Left ventricular longitudinal function was examined by tissue Doppler derived myocardial strain rate and peak systolic velocities. RESULTS: Hypertensive patients with diabetes had a significantly higher systolic strain rate (-1.1 +/- 0.3 s(-1) vs. -1.6 +/- 0.3 s(-1), P < 0.001) and lower systolic peak velocities (3.3 +/- 1.0 vs. 5.6 +/- 1.0 cm/s, P < 0.001) compared with control subjects. Myocardial systolic strain rate correlated significantly to left ventricular mass (r = 0.40, P < 0.01) and to both HbA1c (r = 0.43, P < 0.01), and fructosamine (r = 0.40, P < 0.01), but was not related to serum levels of carboxymethyllysine, albuminuria, blood pressure (dipping/non-dipping), or oral hypoglycaemic therapy. Patients with diastolic dysfunction had significantly higher levels of urine albumin [21.0 (5-2500) mg/l, vs. 9.5 (1-360), P < 0.01], heart rate (78 +/- 13 vs. 67 +/- 10 b.p.m., P < 0.005), and seated diastolic blood pressure (85 +/- 6 vs. 81 +/- 7 mmHg, P < 0.05) and non-dipping diastolic blood pressure was more frequent. CONCLUSIONS: Long axis left ventricular systolic function was significantly decreased in hypertensive patients with Type 2 diabetes mellitus, and is associated with hyperglycaemia and left ventricular hypertrophy. Diastolic dysfunction was closely related to increased diastolic blood pressure, non-dipping and increased urinary albumin excretion.     

高血压病左室肥大Q-T离散度异常与室性心律失常的关系

观察180例高血压病患者的Q-T离散度(Q-Td),左室肥大组及左室正常组Q-Td分别为67.31±13.57和38.8±8.55ms(P<0.001),左室肥大组室性心律失常检出率为92.5%,其中复杂性者为64.2%,室速为23.9%,该组中Q-Td>60ms 3项检出率均高于<60ms及左室正常组中Q-Td>60ms者,复杂性室性心律失常及室速有显著性差异(P<0.001).提示高血压左室肥大Q-Td增加与室性心律失常尤其是复杂性室性心律失常及室速有一定关系,结合左室重量指数(LVMI)和Q-Td可作为评估高血压病患者预后的参考指标.