Regression of left ventricular hypertrophy by AT1 receptor blockade in renal transplant recipients

AT₁ receptor antagonists control blood pressure (BP) effectively and reduce left ventricular hypertrophy in patients with essential hypertension. Because left ventricular hypertrophy is very common in renal transplant recipients, we examined the cardiovascular effects and the safety profile of the AT₁ receptor antagonist losartan in hypertensive renal transplant recipients. In 20 renal transplant recipients with stable renal graft function 50 mg of losartan was added to the preexisting antihypertensive treatment (no angiotensin-converting enzyme inhibitors) at least 6 months after renal transplantation. Twenty-four–hour ambulatory BP, two-dimensional-guided M-mode echocardiography, and duplex sonography, as well as renal function, red blood cell count, cyclosporine A and FK 506 levels, erythropoetin, and angiotensin II concentration were determined at baseline and after 6 months of therapy. With 24-h ambulatory BP measurement, systolic blood pressure (SBP) was reduced by 7.5 ± 2.4 mm Hg and diastolic blood pressure (DBP) by 4.5 ± 1.8 mm Hg (P < .01 and P < .05, respectively). Posterior, septal, and relative wall thickness decreased by 0.95 ± 0.2 mm, 0.91 ± 0.2 mm and 0.04 ± 0.01 mm, respectively (all P < .001). Left ventricular mass index decreased by 18.1 ± 4.7 g/m² (P < .01). Ejection fraction and midwall fractional fiber shortening as systolic parameters and the relation of passive-to-active diastolic filling of the left ventricle were unaltered. Serum creatinine and cyclosporine A concentration remained stable in all patients. Hemoglobin and hematocrit decreased by 1.0 ± 0.3 g/dL and 3.6% ± 0.9%, respectively (P < .002 and P < .001) without a change in serum erythropoetin level. In renal transplant recipients the AT₁ receptor antagonist losartan reduces left ventricular hypertrophy without altering systolic or diastolic function. It is safe with regard to renal function and immunosuppression, but slightly decreases hemoglobin level.     

ACE inhibitors and regression of left ventricular hypertrophy.

Left ventricular hypertrophy (LVH) is a common condition and a powerful independent risk factor for coronary heart disease, congestive heart failure, and other cardiac morbidity. It is associated with the male sex and advancing age. Its most common cause is hypertension, and many antihypertensive agents induce regression of LVH. Angiotensin-converting enzyme (ACE) inhibitors have been shown to reverse LVH by a mechanism as yet unknown. Reduction in afterload and other hemodynamic abnormalities by reduction of blood pressure is clearly a factor, but ACE inhibitors also block adrenergic action and other sympathetic nervous system influences, and the reduction in angiotensin II produces many effects. By inhibiting this potent vasoconstrictor and suppressing its degradation of the powerful vasodilator bradykinin, and by promoting sodium and water excretion, ACE inhibitors contribute to the restoration of normal ventricular function. Angiotensin II promotes protein synthesis in myocardial myocytes, and blocking this action may arrest the hypertrophic process. To determine the effect of angiotensin II on LVH and normalization of LV function, a study is now underway evaluating the effects of lisinopril, a new lysine analog of enalapril, and a diuretic agent in the treatment of hypertension LVH.     

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.     

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。     

高血压与左心室肥厚

左心室肥厚 ( LVH)是心血管疾病的重要危险因素 ,高血压是 LVH最常见的原因。本文就高血压患者 LVH的诊断方法、致病因素、病理生理、不良后果及药物治疗等问题作介绍     

Regression of left ventricular hypertrophy and improvement of renal hemodynamics in hypertensive patients treated with quinapril

Summary Of 17 patients with mild to moderate essential hypertension, 8 showed echocardiographic evidence of left ventricular hypertrophy. Cardiac and renal function evaluated by glomerular filtration rate (GFR) were studied in all patients before and after 20 weeks of quinapril treatment. Systolic pressure decreased from 174.7±16.7 to 131.7±7.7 mmHg (p<.0001) and diastolic pressure decreased from 101.8±9.8 to 80±4.3 mmHg (p<.0001). Left ventricular mass index decreased in the eight patients with left ventricular hypertrophy (p<.01). Basal values of GFR were lower than normal in 41% of all patients; GFR increased significantly after 20 weeks of treatment (from 96.5±32.3 to 108.6±31.12 ml/min, p<.01); it decreased in only one patient. Patients reported few adverse effects to quinapril, and no important clinical laboratory abnormality was observed. Quinapril not only lowered arterial pressure, but it had a distinct effect on regression of left ventricular hypertrophy and favorable effects on renal function.     

氯沙坦对高血压左室肥厚血清脑钠肽的影响

目的探讨氯沙坦对高血压左室肥厚(LVH)患者血清脑钠肽(BNP)水平的影响及其意义。方法选取高血压LVH患者44例,随机分为治疗组和对照组各22例,治疗组服用氯沙坦20周,对照组不给氯沙坦,治疗前后血清BNP浓度以电化学发光法测定,左室重量指数(LVM I)用超声心动图测定。结果高血压LVH患者氯沙坦治疗后LVM I和血清BNP水平分别从(151.54±33.01)g/m3与(174.30±146.95)ng/L降为(134.36±22.71)g/m3与(110.31±83.06)ng/L(P均<0.05),两者治疗前后均呈显著正相关,r分别为0.8和0.75(P均<0.001),血清BNP水平下降的患者LVM I从(147.16±32.97)g/m3降为(131.15±23.48)g/m3(P<0.01)。结论氯沙坦能逆转高血压LVH及降低血清BNP水平,BNP可能可作为高血压治疗后LVH是否逆转的参考指标之一。     

Symmetric and asymmetric left ventricular hypertrophy in patients with end-stage renal failure on long-term hemodialysis

Background: Patients with end-stage renal disease on regular hemodialysis have an increased prevalence of left ventricular (LV) hypertrophy that is associated with morbidity and mortality. Asymmetric septal hypertrophy and impairment of LV outflow can occur in these patients and may contribute to adverse outcomes. More insight into the prevalence, extent, geometry, and promoting factors of LV hypertrophy is important. Methods: An unselected group of 62 patients (31 women), aged 55 ± 14 years, on maintenance hemodialysis was investigated by Doppler echocardiography. Eight patients with valvular heart disease were excluded from further analysis. We assessed prevalence of LV hypertrophy and asymmetric septal hypertrophy, as well as parameters of LV geometry and LV filling and outflow dynamics. Results: Prevalence of LV hypertrophy was 65%. Patients were analyzed according to LV mass and geometry. Mean LV mass index was normal (105 ± 17 g/m²) in Group 1 without LV hypertrophy (n = 19); it was markedly elevated in Group 2 (symmetric hypertrophy, n = 22) and Group 3 (asymmetric hypertrophy with systolic anterior movement of mitral valve, n = 7), and highest (191 ± 54 g/m²) in Group 4 (asymmetric hypertrophy without systolic anterior movement of mitral valve, n = 6, p < 0.001). Age, body mass index, and duration of hypertension were associated with LV hypertrophy and asymmetric septal hypertrophy (p = 0.01). Group 3 with systolic anterior motion of mitral valve had the smallest end-diastolic LV diameters (p = 0.02); increased heart rates, and increased ejection velocities in the LV outflow tract (p = 0.03, and p = 0.005, respectively, vs. Groups 1,2, and 4) which pointed to an impairment of LV outflow. Conclusions: Symmetric LV hypertrophy and asymmetric septal hypertrophy are frequent in patients on maintenance hemodialysis. Predictors for LV hypertrophy were age and body mass index, and, particularly for asymmetric septal hypertrophy, age and hypertension duration. Volume withdrawal during hemodialysis may lead to symptomatic hypotension due to dynamic obstruction in some patients with severe asymmetric septal hypertrophy.     

Regression of left ventricular mass in systemic hypertension.

The importance of treatment in systemic hypertension and cardiovascular morbidity and mortality has been established. Although systemic hypertension is the most important factor in the pathogenesis of left ventricular hypertrophy, other factors such as catecholamines and renin-angiotensin system may be involved. Increased left ventricular mass causes reduction in coronary reserve and may lead to acute ischemic events. Equally efficacious antihypertensive agents may have diverse effects on left ventricular hypertrophy and left ventricular function. New tomographic techniques with improved spatial resolution are emerging in the evaluation of left ventricular mass and may therefore provide better assessment of changes in left ventricular mass. With improved measures of left ventricular mass the question as to whether regression of left ventricular mass provides an additional benefit beyond control of blood pressure in hypertensive individuals may be finally answered.     

高血压左心室肥厚及药物逆转

本文收集并分析了近10年,尤其是近5年来国内外有关这一领域的研究文献,概括并总结了高血压左心室肥厚的概念、形成机制及其药物逆转,这些药物包括ACE抑制剂,CCB1,β-阻滞剂,α-阻滞剂。     

Renal involvement and left ventricular hypertrophy are novel risk factors for morbidity and mortality in diabetes mellitus

Diabetes mellitus and its complications are major causes of morbidity and mortality. Traditionally hypertension and poor diabetic control have been considered to be major risk factors for the development of cardiac involvement. This review will examine two novel risk factors, namely renal involvement and left ventricular hypertrophy. Renal involvement is manifested by increased excretion of protein in the urine and/or decreasing renal function. Several large studies have shown that both these factors are significant risk factors for cardiac involvement and increased mortality both in diabetic and non-diabetic subjects. There is strong evidence to suggest an association between renal and cardiac involvement. Cardiac hypertrophy is an important risk factor for the development of cardiac involvement. It is generally assumed that ventricular hypertrophy is a result of hypertension. However, it has been shown to be associated with metabolic disorders such as central obesity, diabetes mellitus and hypercholesterolemia, even in the absence of hypertension. The prevalence of ventricular hypertrophy is increased in patients with diabetes mellitus, especially in the presence of renal involvement. Diabetic patients with renal involvement and cardiac hypertrophy have also been shown to have an increased risk for developing cardiac complications and having an increased mortality rate. Thus these two risk factors are important in the prognosis of the diabetic patient. Follow-up of the diabetic patient should include careful examination for the presence of proteinuria, reduced renal function and left ventricular hypertrophy in the hope that treatment of these factors may reduce morbidity and mortality.     

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.     

Prevalence and factors associated with left ventricular remodeling in renal artery stenosis

The objective of this study is to evaluate the prevalence, geometric patterns, and factors associated with left ventricular remodeling in patients with renal artery stenosis (RAS). Demographic, clinical, and echocardiographic data were assessed in 77 patients with RAS prior to endovascular stenting. The left ventricular mass index (LVMI) and relative wall thickness were calculated using American Society of Echocardiography (ASE) recommendations. Patients were classified based on LVMI and relative wall thickness into four ventricular remodeling patterns: normal geometry, concentric remodeling (CR), concentric hypertrophy (CH), and eccentric hypertrophy (EH). Logistic regression was done to investigate the determinants of the different ventricular remodeling patterns. Mean LVMI and relative wall thickness were 118 ± 40 g/m² and 0.45 ± 0.1. Left ventricular hypertrophy was observed in 65%. CH was the most prevalent geometric pattern of remodeling (normal, 16.9%; CR, 18.2%; CH, 40%; EH, 24.6%). Thirty (39%) patients had an abnormal LV systolic function (ejection fraction <55%), with 14 (46%) of them having eccentric hypertrophy. Independent predictor of EH was glomerular filtration rate (odds ratio [OR], 0.943; confidence interval [CI], 0.899–0.989; P = .01). Systolic elevation of blood pressure (OR, 1.030; CI, 1.003–1.058; P = .03) was associated with CH, and elevated diastolic blood pressure was associated with CR (OR, 0.927; CI, 0.867–0.992; P = .02). Patients with RAS have a high prevalence of left ventricular remodeling and LVH. Even though CH was the most prevalent pattern of left ventricular remodeling, EH was commonplace and was associated with renal dysfunction and heart failure.     

心电图电压标准诊断左室肥大价值的研究

目的 评价临床上最常用的几项心电图电压标准诊断左室肥大（LVH）的价值及性别差异。方法 选择1999—2003年我院体检及住院患者499例，依据超声心动图测定的左室重量指数（LVMI）分为正常组（男210饲，女83例）和左室肥大组（男126例，女80例）。计算各项电压标准诊断左室肥大的敏感性、特异性和准确率，并比较各项电压标准诊断左室肥大的性别差异。结果 各项电压标准诊断左室肥大的特异性均〉95％,在单项指标中，Rvs〉2．5my标准的敏感性和准确率分别为62．8％和85．1％，明显高于Rvs及RaVL电压标准。在复合指标中，Comell指数和Sokolow指数诊断左室肥大的敏感性和准确率明显高于R4＋Sm指标。男、女性采用相同的电压阈值，其诊断性能存在明显性别差异。结论 Cornell指数、Sokolow指数及Rv5电压标准是诊断左宣肥大较好的指标。男、女性采用不同的电压阈值标准，可望进一步改善目前心电图诊断左室肥大的性能。     

替米沙坦改善原发性高血压病患者心肌肥厚及早期肾功能失调

目的:评估替米沙坦在高血压病靶器官损害中的保护作用。方法:轻中度原发性高血压病左室肥厚患者60例服用替米沙坦40～80mg/d,共26周,服药前后行超声心动图,观察舒张末期室间隔厚度（IVST）,舒张末期左心室后壁厚度（LVPWT）及A/E比值的变化;并计算左室心肌质量指数（LVMI）的改变;同时放射免疫分析法测量血β2微球蛋白（β2MG）、尿β2MG含量。结果:替米沙坦能有效降低血压,降压有效率为72%,治疗后LVMI降低（146±12vs123±10）（P<0.01）,A/E值改善（P<0.05）,血、尿β2MG水平降低。结论:替米沙坦在降低血压同时能够有效地保护心肾功能。     

高血压左室肥厚及构型与室性心律失常的关系

为探讨高血压左室肥厚(LVH)及不同构型与室性心律失常的关系,对320例有或无左室肥厚(LVH)高血压患者进行超声心动图、24h动态心电图检测.结果表明:LVH为105例,检出率为32.8%.复杂性室性心律失常的发生率在有无LVH组间有显著性差异(P<0.05),LVH程度与复杂性室性心律失常级别有密切的关系(r=0.57,p<0.05),LVH不同构型之间复杂性室性心律失常的发生率存在显著差异(p<0.05),不对称性LVH发生率较高.因此,对于肥厚程度较重、不对称LVH的高血压患者要给予高度重视.     

Effects of ketanserin of left ventricular hypertrophy in hypertensive patients

Summary Ketanserin, a serotonergic S₂-receptor antagonist, was used in a prospective study in nine hypertensive patients with ECG criteria of left ventricular hypertrophy (LVH). Echocardiographic measurement with M mode was made after 1 month of placebo, and after 3, 6, and 12 months of ketanserin treatment as monotherapy at a mean dose of 31 mg bid. Ketanserin treatment decreased mean left ventricular mass by 9.3% at 3 months (not significant), by 15.3% at 6 months (p < 0.008), and by 26.2% at 12 months (p < 0.02), with a tendency towards improvement in left ventricular ejection fraction, which was not statistically significant. The study showed a sustained effect upon regression of LVH in hypertensives, with preservation of left ventricular function.     

胸前导联最大QRS波振幅诊断左室肥厚的研究

目的通过验证如下两项基本假设提出心电图(ECC)诊断左室肥厚(LVH)的新指标:①胸导联最大QRS振幅(Vmax)应该比某一特定导联的R或S波能更好地反映左室心肌重量(LVM);②体重/身高比值(WT/HT)可近似地代替左室中心到胸壁距离的平方而用以校正胸导联QRS振幅。方法将76例高血压患者常规12导联心电图与M型超声心动图左室心肌重量(LVM)及左室心肌重量指数(LVMI)进行分析比较。结果Vmax是与心室重量指数(LVMI)相关最密切的心电图指标(r=0.545,p<0.001)。Vmax乘以WT/HT后,与心室重量指数(LVMI)的相关系数由r=0.442提高到r=0.659(p<0.05)。结论①胸导联最大QRS振幅可能取代常规的电压指标,作为心电图左室肥厚的诊断新指标;②Vmax乘以WT/HT可进一步提高其诊断效能。     

Comparison of electrocardiographic versus echocardiographic detection of left ventricular mass changes over time and evaluation of new onset left ventricular hypertrophy

We assessed the value of 3 electrocardiographic (EKG) voltage criteria in detecting variations of left ventricular mass (LVM) over time, taking echocardiographic (ECHO) LVM as reference, in the Pressioni Arteriose Monitorate E Loro Associazioni study. In 927 subjects (age 47 ± 13 years on entry, 49.9% men) an ECHO evaluation of LVM and EKG suitable for measurement of EKG-LVH criteria (Sokolow-Lyon voltage, Cornell voltage and R-wave voltage in aVL) were available at baseline and at a 2^nd evaluation performed 10 years later. Δ (delta) LVM, Δ LVMI, and Δ EKG parameters values were calculated from 2^nd evaluation to baseline. The sensitivity of the EKG criteria in the diagnosis of LVH, poor at baseline, becomes even worse after 10 years, reaching very low values. Only the sensitivity of R-wave amplitude exhibited slight increase over time but with unsatisfactory absolute values. Despite the prevalence of ECHO-LVH at the 2^nd evaluation was threefold increased compared to baseline (29.3% and 33.7% for LVM indexed to BSA and height^2.7, respectively), the prevalence of EKG-LVH was unchanged when evaluated by Sokolow-Lyon criteria, significantly reduced when assessed by Cornell voltage index, while significantly increased using R-wave voltage in aVL criteria. Despite an ECHO-LVM increase over the time, mean EKG changes were of opposite sign, except for R-wave amplitude in aVL. Our study highlights the discrepancy between ECHO and EKG in monitoring LVM changes over the time, especially for Sokolow-Lyon and Cornell voltage. Thus, EKG is an unsuitable method for the longitudinal evaluation of LVM variations.