Metabolic syndrome is associated with abnormal left ventricular diastolic function independent of left ventricular mass

Aim To characterize the extent to which metabolic syndrome criteriapredict left ventricular (LV) structure and function. Methods and results Metabolic syndrome criteria were assessedin 607 adults with normal LV function. The cohort was groupedaccording to the number of criteria satisfied: (1) Absent (0criteria, n = 110); (2) Pre-Metabolic Syndrome (1–2 criteria,n = 311); and (3) Metabolic Syndrome (3 criteria, n = 186).Echocardiography was used to assess LV structure (LV mass) andsystolic (LVEF, Vs) and diastolic function, by pulse-wave Doppler(E/A ratio) and tissue Doppler imaging (Ve). LV volumes andLVEF were similar between groups. However, LV mass increasedsignificantly and progressively (LVM/Ht^2.7, in g/m^2.7: 34.9± 6.7, 41.0 ± 9.5, 46.3 ± 11.0, P <0.001); LV relaxation decreased progressively (Ve_global', incm/s: 13.5 ± 2.8, 12.1 ± 3.0, 10.5 ± 2.2,P < 0.001) from Absent to Pre-Metabolic Syndrome to MetabolicSyndrome groups, respectively. Multiple variable analyses showedthat diastolic blood pressure, waist circumference, and triglyceridelevels were independent predictors of Ve after adjustment forLV mass. Conclusion Patients with metabolic syndrome have LV diastolicdysfunction independent of LV mass. These functional abnormalitiesmay partially explain the increased cardiovascular morbidityand mortality associated with metabolic syndrome.     

Effects of captopril on left ventricular structure and function in SHR with established hypertension

Summary While antihypertensive therapy is considered to be an important clinical intervention in hypertensive patients, its effects on cardiac structure and function have not been intensely evaluated. In this study we tested the hypotheses that lowering blood pressure (BP) with the angiotensin I-converting enzyme inhibitor captopril, would: 1) normalize left ventricular mass and increase the cardiocyte mitochondria/myofibrils volume (V_mito/V_myo) ratio; and 2) not compromise peak ventricular performance. We treated 16-week-old SHR and WKY with captopril (40–80 mg/kg) and hydrochlorothiazide (500 mg/l) via their drinking water. After six weeks of treatment peak cardiac performance was measured during rapid volume overload. Tissue samples from the left ventricular wall were analyzed by electron microscopy and stereology. Captopril lowered BP in SHR and WKY but had no affect on the left ventricular/body weight ratio. The only intracellular change in treated SHR was an increase in sarcoplasmic volume density. Treated WKY exhibited decreased midmyocardial mitochondrial volume density. At peak cardiac output, acceleration of flow and cardiac index were not affected by treatment. Stroke work at peak cardiac output was decreased in the treated groups due to a decrease in mean arterial pressure. In addition, captopril treatment resulted in a shift of the cardiac output (CO)-left ventricular end diastolic pressure (LVEDP) curves, such that LVEDP at peak cardiac output was approximately 50% less in the treated groups compared to their respective control groups. Although captopril was efficacious in lowering BP, it is suggested that lowering BP with this agent does not, at least within six weeks, lead to a reversal of hypertrophy or to a significant alteration in the volume densities of myofibrils and mitochondria. However, an important effect of this antihypertensive drug which may be of clinical significance, is that it leads to a leftward shift of the CO-LVEDP curve in both hypertensive and normotensive rats.     

Different impact of the metabolic syndrome on left ventricular structure and function in hypertensive men and women

Metabolic syndrome (MS) is increasingly recognized as an important cardiovascular risk factor in hypertension, but its influence on left ventricular (LV) mass and function in the 2 genders has not been specifically addressed. Among 618 nondiabetic, untreated hypertensive subjects, echocardiographically detected LV mass was significantly greater in subjects with MS. A significant interaction was observed between sex and the MS (P<0.003 for the multiplicative interaction term). Compared with women without the MS, those with the syndrome had a 24% greater LV mass (49.5+/-12 versus 40.0+/-10 g x m(-2.7); P<0.001), whereas the difference was only 9% in men (50.3+/-12 versus 46.1+/-10 g x m(-2.7); P=0.003). A greater prevalence of LV hypertrophy was found in women (37% versus 14%; P<0.001) but not in men (39% versus 29%; P=0.09) with the MS. After adjustment for the effect of age, body mass index, 24-hour systolic blood pressure, and several confounders, the MS was independently associated with a greater LV mass index in women (regression coefficient, 4.80; P<0.001) but not in men. Women with the MS also had a greater LV relative wall thickness (0.42+/-0.07 versus 0.39+/-0.07; P=0.004) and a depressed afterload-corrected midwall fractional shortening (94.0+/-12% versus 101.0+/-13%; P<0.001) than women without the syndrome, whereas no differences emerged in men. We conclude that, in untreated hypertension, MS has a different impact on LV hypertrophy and function in men and women. The effect of MS is more pronounced in women and is partly independent from the effect of several hemodynamic and nonhemodynamic determinants of LV mass.     

原发性高血压左室质量适宜和过高对左室结构和功能的影响

目的 :利用左室质量比值 (%PLM )将左室重构分为左室质量适宜 (aLVM )、左室质量过高 (iLVM )和左室质量不足 ,观察并比较aLVM和iLVM的心脏结构和功能特点。方法 :对 187例原发性高血压 (EH)患者进行超声心动图检查 ,测量其心脏结构和功能。结果 :aLVM、iLVM和左室质量不足的分布分别占 4 8.1%、4 8.7%和 3.2 %。与aLVM相比 ,iLVM的主动脉根部内径、左房内径、左室质量和相对室壁厚度更高 (P <0 .0 5 ) ;心排血量、心搏量、左室射血分数、左室短轴缩短率和舒张早期充盈峰速度E峰 /舒张晚期充盈峰速度A峰比值更低 (P <0 .0 5 ) ;总外周血管阻力更高 (P <0 .0 5 )。结论 :与aLVM相比 ,iLVM的心脏结构和功能特点提示它是左室重构发展的进一步阶段。     

Aortic elastic properties and left ventricular diastolic function in white-coat hypertensive individuals

OBJECTIVES: Although white-coat hypertension may be present in 25% or more of hypertensive individuals, its prognostic significance and predisposition to end organ damage is unknown. To evaluate whether white-coat hypertension is associated with end organ damage, we compared prognostically relevant measures of target-organ damage among 35 individuals with white-coat hypertension and age and sex-matched groups of sustained hypertension and normotensive individuals classified by clinical and 24-h ambulatory blood pressures. METHODS: We evaluated left ventricular diastolic function and aortic elastic properties of 35 individuals with white-coat hypertension, 50 patients with sustained hypertension, and 35 normotensive healthy volunteers using transthoracic Doppler echocardiography. None of the study participants with sustained hypertension and white-coat hypertension, who were newly diagnosed and never treated, had any systemic disease or coronary risk factor except hypertension. RESULTS: Age, sex, and body mass indexes were similar among the three groups. Left ventricular diastolic function was more significantly impaired in the sustained hypertension and white-coat hypertension groups than in the control group, but it was not significantly different between the white-coat hypertension and sustained hypertension groups. Aortic distensibility was significantly lower, and aortic stiffness index was significantly higher in the sustained hypertension group than in the white-coat hypertension and control groups. Furthermore, aortic elastic properties were slightly impaired in the white-coat hypertension group compared with those in the control group. We also found a significant correlation between aortic elastic properties and left ventricular diastolic function. CONCLUSIONS: White-coat hypertension may alter left ventricular diastolic function and aortic elastic properties. These alterations, however, might not be as remarkable as those caused by sustained hypertension. In this respect, individuals with white-coat hypertension are not at such a risk for end organ damage as patients with sustained hypertension.     

Serum aldosterone effect on left ventricular structure and diastolic function in essential hypertension

Aldosterone has hypertrophic and profibrotic effects on the heart. This study aims to determine the relationship between serum aldosterone concentration (SAC) and aldosterone-to-renin ratio (ARR) with left ventricular (LV) geometry and diastolic function in essential hypertension (EH). We investigated 213 EH patients (50.3 ± 12.6 years; 57.7% male). SAC, ARR measurements, and echocardiographic analysis were performed for participants. Overall, stepwise multiple regression analysis showed significant associations between SAC and interventricular septum, LV posterior wall thickness, LV amass, LV mass index, e′ velocity, a′ velocity, and E/e′ ratio after adjustment of potentially confounding covariates. When patients were divided into three SAC tertiles, multivariate-adjusted analysis of covariance (ANCOVA) demonstrated a significant increase in LV mass (P ˂ 0.001), LV mass index (P ˂ 0.001), relative wall thickness (P = 0.003), interventricular septum (P = 0.001), LV posterior wall thickness (P = 0.001) and E/e′ ratio (P ˂ 0.001), but a decrease in e′ velocity (P = 0.002) from the first to third tertile of SAC. In logistic regression analysis, increased SAC was independently associated with concentric LV hypertrophy [OR: 1.21, 95% CI: 1.11–1.33, P ˂ 0.001]. No significant associations were found between ARR and echocardiographic parameters of LV structure or diastolic function. In conclusion, SAC, but not ARR, is independently associated with echocardiographic indices of LV structure and diastolic function and is also related to concentric LV hypertrophy. Our findings suggest that aldosterone's pro-hypertrophic and myocardial fibrosis effects contribute to alterations in LV structure and diastolic function in EH beyond blood pressure.     

高血压病左房结构及左室舒张功能的超声心动图改变

高血压是最常见的心血管疾病,可引起严重的心、脑、肾并发症,是脑卒中、冠状动脉粥样硬化性心脏病的主要危险因素。研究表明,高血压病患者出现左室舒张功能障碍早于收缩功能障碍。对无症状高血压患者,通过超声心动图检查早期发现其舒张功能改变,及时采取预防措施,对防止高血压病进展具有一定的意义。     

Aortic distensibility and left ventricular structure and function in isolated systolic hypertension

Aortic mechanical properties were assessed in a group of elderlysubjects with untreated isolated systolic hypertension usingtwo-dimensional echocardiography. Echocardiographic (two-dimensionaland Doppler) assessment of left ventricular structure and functionwas also made. Ten subjects (mean age 71.7 ± 1.9 years,20% male, mean clinic blood pressure 163.6/79.2 ± 1.2/2.0mmHg) were compared with 16 normotensive subjects of similarage (69.4 ± 1.6 years, 38% male, mean clinic blood pressure129.8/78.2 ± 3.2/2.9 mmHg). Aortic distensibility atthe level of the transverse aortic arch was signficantly reducedamong subjects with isolated systolic hypertension. The thicknessof the interventricular septum was approximately 20% greaterin the hypertensive subjects (P < 0.01) and the average wallthickness to radius ratio was increased by 30%. Patterns oftransmitral diastolic flow were also different in subjects withisolated systolic hypertension. Deceleration time was significantlygreater (P < 0.01) and the ratio of early to late transmitraldiastolic peak flow velocities was significantly less in thehypertensive (P < 0.05) than in the normotensive group. Leftventricular systolic function was well preserved. These findingsare consistent with the suggestion that isolated systolic hypertensionrepresents a state of increased aortic stiffness which may contributeto the development of left ventricular hvpertrophy. Whetherthis increase in aortic stiffness is the cause or effect ofthe elevated systolic blood pressure remains unresolved.     

Effects of indapamide on left ventricular mass and function in systemic hypertension with left ventricular hypertrophy

Left ventricular hypertrophy (LVH) is frequently associated with hypertension and constitutes a major cardiovascular risk factor, the reduction of which should be considered when initiating antihypertensive therapy. To assess the effects of indapamide on LVH, 18 hypertensive patients were included in the study (11 men and 7 women, age 53.6 +/- 2.9 years, mean +/- standard deviation) whose supine diastolic blood pressure was greater than 95 mm Hg without (n = 11) or with (n = 7:6 beta blockers, 1 calcium antagonist) antihypertensive therapy. All presented with LVH, echocardiographically defined by a left ventricular mass index greater than 110 g/m2. After a 2-week preinclusion period, all patients received indapamide, 2.5 mg/day, for a period of 6 months. Physical examination including blood pressure measurement was performed on selection (M-1/2), before (M0), and after 1 (M1), 3 (M3) and 6 (M6) months of indapamide treatment, and echocardiography was performed at M0 and M6. Quality of life was evaluated by means of questionnaires completed by the patient and the physician, and a visual analog scale was completed by the patient at M-1/2, M0 and M6. All clinical parameters remained stable during the 2-week preinclusion period. Indapamide administration induced a highly significant reduction in both supine systolic and diastolic blood pressures from 173.9 +/- 2.9/100.5 +/- 1.2 mm Hg at M0 to 150.9 +/- 1.9/90.5 +/- 1.3 mm Hg at M1 (p less than 0.001), and 145.0 +/- 1.7/86.0 +/- 1.5 mm Hg at M6 (p less than 0.001). Similar favorable effects were observed in the upright position.(ABSTRACT TRUNCATED AT 250 WORDS)     

二维斑点追踪技术评价白大衣高血压患者左心房功能

目的采用二维斑点追踪技术评价白大衣高血压(white-coat hypertension,WCH)患者左心房功能。方法选取辽宁中医药大学附属第二医院诊断为WCH的患者59例作为WCH组,健康体检者48例作为对照组。所有受试者均进行诊室血压和动态血压测量。运用常规超声心动图评价左心室舒张和收缩功能。运用二维斑点追踪技术测量左心房储备期纵向应变及应变率(LASr,LASRr),通道期纵向应变及应变率(LAScd,LASRcd)和收缩期纵向应变及应变率(LASct,LASRct),分别评价左心房储备功能、通道功能和泵功能。结果 WCH组诊室收缩压和诊室舒张压均高于对照组(t=12.34、15.36,P <0.05);而两组之间动态血压平均值差异无统计学意义(P> 0.05)。WCH组Mitral e'小于对照组,而Mitral E/e'大于对照组(t=6.52、6.76、8.35、8.61,P <0.05);两组之间左心室射血分数(LVEF)差异无统计学意义(P> 0.05)。WCH组LAScd和LASRct小于对照组(t=4.08、2.84,P<0.05),LASct和LASRcd大于对照组(t=4.14、6.10,P<0.05);两组之间LASr和LASRr差异无统计学意义(P> 0.05)。WCH患者诊室收缩压和舒张压与LAScd和LASRct呈负相关(r=-0.21～-0.36,P <0.05),与LASRcd和LASct呈正相关(r=0.27～0.34,P <0.05)。结论 WCH患者左心房通道功能减低,而左心房泵功能增强,左心房功能与诊室血压密切相关。     

老年高血压伴左室肥厚对左心功能的影响

目的 :探讨老年高血压伴左室肥厚对心功能的影响。方法 :应用核素心血池扫描的方法 ,对老年高血压伴左室肥厚和无左室肥厚的患者 ,进行了左室射血分数 (LVEF)、左室高峰射血率 (PER)、左室高峰充盈率(PFR)、1/ 3充盈分数 (1/ 3FF)及相角程 (PA)的测定 ,并进行比较。结果 :伴左室肥厚的患者PFR、1/ 3FF明显低于无左室肥厚的患者 ,PA明显高于无左室肥厚的患者。结论 :老年高血压伴左室肥厚对心功能的影响 ,主要表现为对舒张功能的影响 ;左室肥厚导致的心室肌纤维化、顺应性下降和运动协调性异常 ,是影响舒张功能的重要原因     

原发性高血压伴阻塞性睡眠呼吸暂停低通气综合征对左心室结构的影响

目的:研究原发性高血压(EH)伴阻塞性睡眠呼吸暂停低通气综合征(OSAHS)与左心室结构改变的关系,并分析其可能的影响因素。方法:随机抽取2007年10月至2010年11月,在北京安贞医院高血压科住院的男性,年龄30～60岁,EH患者282例,进行夜间多导睡眠监测,并对其一般资料、生化指标、超声心动图检查结果进行分析,比较EH+OSAHS与EH患者间左心室结构的差异,观察其影响因素。结果:①EH+OSAHS组体质量指数、空腹及餐后2 h血糖均高于EH组,差异有统计学意义(均P<0.05);EH+OSAHS组血总胆固醇、三酯甘油、低密度脂蛋白、尿酸均高于EH组,EH+OSAHS组计算的肾小球滤过率低于EH组,差异无统计学意义(P>0.05)。②EH+OSAHS组的左心室舒张末期内径、室间隔厚度、左心室后壁厚度、左心室质量指数均高于EH组,差异有统计学意义(均P<0.05);EH+OSAHS组左心室肥厚(LVH)的患病率明显高于EH组(41.0%vs.27.3%)。③Logistic回归分析表明:与左心室肥厚发生相关的危险因素为OSAHS(OR=1.827,95%CI=1.006～3.220,P=0.048)、高血压病程(OR=2.122,95%CI=1.185～3.982,P=0.012)、血压分级(OR=3.797,95%CI=2.447～5.893,P=0.000)。结论:与EH相比,EH+OSAHS左心室构型改变更加严重;其危险因素可能为OS-AHS、高血压病程、血压分级。     

老年高血压病人左室肥厚与左室舒张功能的关系

目的：研究老年高血压病人左室肥厚与左室舒张功能各参数的关系,探讨在老年人左室肥厚对左室舒张功能的影响。方法：用彩色多普勒超声心动图测量101例老年高血压病人左心室结构及舒张功能参数。结果：101例高血压病人中,左室肥厚组（48例）的左房内径指数（LADI）、等容舒张时间（IVRT）、舒张期二尖瓣E波减速时间（EDT）显著大于左室正常组（53例,P〈0．05～〈0．01）．多元逐步回归分析发现,左室质量指数（LVMI）与左房射血分数（LAEF）、LADI、IVRT和EDT有明显的相关关系（r分别为0．213,0．251．0．450．0．338．P〈0．05～0．001）结论：老年高血压病人的左室增厚可进一步降低左室舒张功能。     

The effects of simvastatin on left ventricular hypertrophy and left ventricular function in patients with essential hypertension

This study is to evaluate the effects of Simvastatin on left ventricular hypertrophy and left ventricular function in patients with essential hypertension. Untreated or noncompliance with drug treatment patients with simple essential hypertension were treated with a therapy on the basis of using Telmisartan to decrease blood pressure (BP). There were 237 patients who had essential hypertension combined with left ventricular hypertrophy as diagnosed by echocardiography, taken after their BPs were decreased to meet the values of the standard normal. Among them, there were only 41 out of the original 237 patients, 17.3%, who had simple essential hypertension combined with left ventricular hypertrophy without any other co-existing disease. They were the patients selected for this study. All patients were randomly, indiscriminately divided into two groups: one was the control group (Group T), treated with the Telmisartan-based monotherapy; the other was the target group (Group TS), treated with the Telmisartan-based plus simvastatin therapy. The changes of left ventricular hypertrophy and left ventricular function were rediagnosed by echocardiography after 1 year. The results we obtained from this study were as follows: (i) The average BPs at the beginning of the study, of simple essential hypertension combined with left ventricular hypertrophy, were high levels (systolic blood pressure (SBP) 189.21 ± 19.91 mm Hg, diastolic blood pressure 101.40 ± 16.92 mm Hg). (ii) The Telmisartan-based plus simvastatin therapy was significantly effective in lowering the SBP (128.26 ± 9.33 mm Hg vs. 139.22 ± 16.34 mm Hg). (iii) After the 1-year treatment, the parameters of left ventricular hypertrophy in both groups were improved. Compared to group T, there were no differences in the characteristics of the subjects, including interventricular septum, left ventricular mass, left ventricular mass index, ejection fraction, left atrium inner diameter at baseline. The patients' interventricular septum (Group TS 10.30 ± 1.80 mm vs. Group T 10.99 ± 1.68 mm, P < .05), LVM (Group TS 177.43 ± 65.40 g vs. Group T 181.28 ± 65.09 g, P < .05), and LVMI (Group TS 100.97 ± 37.33 g/m(2) vs. Group T 106.54 ± 27.95 g/m(2), P < .05), all dropped more prominently (P < .05) in group TS; the ejection fraction rose more remarkably in group TS (Group TS: 57.50 ± 16.41% to 65.43 ± 11.60%, P < .01 while showing no change in Group T); the left ventricular hypertrophy reversed more significantly and the left ventricular systolic function improved more. (iv) The left atrium inner diameter of Group TS decreased (P < .01), the ratio of E/A, which indicates the left ventricular diastolic function, continued to drop further, showing no change to the trend of left ventricular diastolic function declination. Patients who have hypertension with left ventricular hypertrophy usually suffer other accompanying diseases at the same time. Telmisartan-based plus Simvastatin treatment can significantly reduce SBP, reverse left ventricular hypertrophy, improve the left ventricular systolic function, but it has no effect on reversing the left ventricular diastolic function. This experiment indicated that Simvastatin can reverse left ventricular hypertrophy and improve left systolic function.     

氯沙坦对原发性高血压患者左室结构和功能及升主动脉弹性的影响

目的 :应用超声心动图评价血管紧张素Ⅱ 1型受体拮抗剂氯沙坦对原发性高血压 (EH)患者左室结构和功能及升主动脉弹性的影响。方法 :分别于氯沙坦服用前和服用 3个月后 ,对 2 6例轻至中度EH患者进行超声心动图检查。结果 :服用氯沙坦 3个月后 ,血压从 (14 8± 13) / (95± 9) (1mmHg =0 .133kPa)下降到 (138±12 ) / (88± 8)mmHg (均 P <0 .0 1) ;升主动脉弹性显著增加 ,显示为Ep指数从 (44 .2± 5 7.9)下降到 (19.9±14 .9)N/cm2 (P 0 .0 5 )和 β指数从2 7.4± 32 .9下降到 13.3± 9.9(P 0 .0 5 )。氯沙坦治疗后Ep指数和 β指数百分变化率与舒张压百分变化率之间存在显著相关性 (Ep指数 ,r =0 .4 0 ,P <0 .0 5 ;β指数 ,r =0 .5 5 ,P <0 .0 1) ;E/A比值 (1.2 0± 0 .32 )明显高于服用前 (1.0 7± 0 .31,P <0 .0 1) ,E峰减速时间从 (185± 32 )下降到 (16 4± 2 9)ms(P <0 .0 1) ;左室重量从 (2 2 0± 5 3)减低为 (194± 5 3)g(P <0 .0 1)。结论 :氯沙坦的降压作用与左室舒张功能的改善和升主动脉弹性增加有关 ,并且氯沙坦具有消退左室肥厚的作用     

Aldosterone and left ventricular hypertrophy in Afro-Caribbean subjects with low renin hypertension

BACKGROUND: Activity of the renin-angiotensin-aldosterone system is thought to play a major role in determining blood pressure (BP) and target organ damage such as left ventricular hypertrophy. In Afro-Caribbean subjects, however, hypertension tends to be more severe despite lower plasma renin activity. We investigated whether this might be due to a different relation between aldosterone and renin in Afro-Caribbean compared to white subjects. METHODS: Plasma aldosterone and renin activity were assessed in the morning after 15 min seated in 383 hypertensive subjects of Afro-Caribbean or white ethnicity (61% Afro-Caribbean, 83% on treatment) attending a hypertension clinic in London, UK. Left ventricular mass index (LVMI) was assessed by echocardiography in 276 subjects. RESULTS: Plasma renin activity was lower in Afro-Caribbean compared to white subjects (0.4 [0.3-1.0] v 1.4 [0.5-3.4] ng/mL/h, medians [interquartile range], P < .0001). Despite this, aldosterone was higher in Afro-Caribbean compared to white subjects (8.0 [6.1-12.6] v 7.4 [2.3-17.1] ng/dL, medians [interquartile range], P < .01). The LVMI corrected for sex and BP was higher in Afro-Caribbean than in white subjects. In Afro-Caribbean but not in white subjects LVMI was independently correlated with plasma aldosterone (standardized regression coefficient, beta= 0.25, P < .001). CONCLUSIONS: In Afro-Caribbean hypertensive subjects in London, plasma aldosterone is elevated despite lower renin and may contribute to increased severity of hypertension and left ventricular hypertrophy in Afro-Caribbean compared to white subjects.