The Effects of Amlodipine on Left Ventricular Mass and Diastolic Function in Concentric and Eccentric Left Ventricular Hypertrophy

BACKGROUND: The effects of the antihypertensive therapy with amlodipine (5-10 mg/day) on left ventricular mass and diastolic function were examined in 30 mild to moderate essential hypertensive patients who have left ventricular hypertrophy (LVH) and diastolic dysfunction. METHODS AND RESULTS: Each patient's left ventricular mass was measured, and left ventricular diastolic function was assessed by echocardiographic Doppler examination at entry, and at 3 and 6 months after the initiation of the treatment. Amlodipine reduced both blood pressure (from 164 +/- 14/104 +/- 6 mmHg to 134 +/- 9/83 +/- 4 mmHg) and left ventricular mass index (from 160 +/- 30 g/m(2) to 137 +/- 26 g/m(2)) significantly at 3 months and both parameters maintained at these levels for 6 months. When the patients were classified according to the type of the LVH, a significant regression in left ventricular mass index was seen only in the patients who had concentric LVH was a relative wall thickness >/=0.44 (n = 16), but not in the eccentric LVH group (n = 14), although both groups were not significantly different from each other regarding the basal hemodynamic parameters, baseline left ventricular mass index and the decrease in blood pressure in response to amlodipine treatment. The mitral inflow E/A ratio did not show any significant change in either group. CONCLUSIONS: Amlodipine produced significant regression in LVH only in the patients with concentric LVH, but not those with eccentric LVH, while it did not change the diastolic dysfunction. Therefore, the type of LVH seems to be an important feature in determining the effects of antihypertensive treatment on left ventricular mass index.     

Enhanced cardiac production of matrix metalloproteinase-2 and -9 and its attenuation associated with pravastatin treatment in patients with acute myocardial infarction

Previous experimental studies have demonstrated that MMPs (matrix metalloproteinases) contribute to LV (left ventricular) remodelling. We hypothesized that cardiac MMPs are activated in patients with AMI (acute myocardial infarction) and, if so, MMP production may be attenuated by statins (3-hydroxy-3-methylglutaryl-CoA reductase inhibitors) through their cardiovascular protective actions. We studied 30 patients, ten control patients with stable angina pectoris and 20 patients with AMI, in whom LV catheterization at the chronic stage was performed 22+/-12 days (value is mean+/-S.D.) after the onset of AMI. Blood samples were collected from the CS (coronary sinus) and a peripheral artery. In patients with AMI, the levels of MMP-2 and MMP-9 were significantly (P<0.05) higher in the CS than the peripheral artery (MMP-2, 853+/-199 compared with 716+/-127 ng/ml; MMP-9, 165+/-129 compared with 98+/-82 ng/ml), whereas no significant differences were observed in the patients with angina pectoris. The CS-arterial concentration gradients of MMP-2 and MMP-9 correlated positively with BNP (brain natriuretic peptide) levels (MMP-2, R=0.68, P<0.01; MMP-9, R=0.59, P<0.05) and LV end-diastolic volume index (MMP-2, R=0.70, P<0.01; MMP-9, R=0.70, P<0.01). When patients with AMI treated with 10 mg of pravastatin or without (n=10 in each group) were compared, this statin therapy significantly (P<0.05) decreased the CS-arterial concentration gradients of MMP-2 (69+/-43 compared with 213+/-185 ng/ml) and MMP-9 (14+/-27 compared with 119+/-84 ng/ml). In conclusion, the enhanced production of cardiac MMP-2 and MMP-9 is associated with LV enlargement and elevated BNP levels in patients with AMI. A pleiotropic effect of statins appears to be associated with the modulation of cardiac MMP activation, which may be potentially beneficial in the attenuation of post-infarction LV remodelling.     

Systolic and diastolic heart failure are associated with different plasma levels of B-type natriuretic peptide

Previous studies have found that plasma B-type natriuretic peptide (BNP) is elevated during left ventricular systolic or diastolic dysfunction. It is unclear whether the ventricular systolic and diastolic function is associated with different levels of plasma BNP. Plasma BNP was measured in 149 heart failure patients by a rapid point-of-care assay. The patients were divided into left ventricular diastolic dysfunction (n = 48), left ventricular systolic dysfunction (n = 62) and right ventricular systolic dysfunction group (n = 39). The mean BNP level in the left ventricular diastolic dysfunction, left ventricular systolic dysfunction and right ventricular systolic dysfunction was 115 +/- 80 pg/ml, 516 +/- 445 pg/ml and 345 +/- 184 pg/ml, respectively (p < 0.05). We concluded that ventricular systolic and diastolic dysfunction increases plasma BNP levels to a different extent. Left and right ventricular systolic dysfunction is associated with a higher level of plasma BNP than left ventricular diastolic dysfunction.     

伴和不伴左室肥厚高血压患者的组织多普勒特征及其在心功能评价中的价值

目的:应用组织多普勒(DTI)观察伴有和不伴有左室肥厚的高血压患者的组织多普勒特征,探讨DTI在心功能评价中的价值。方法:入选30例高血压患者,分为左室肥厚组(LVH组,15例)与非左室肥厚组(non-LVH组,15例),另选取15例健康人作为对照组,分别行超声多普勒及DTI检查,多普勒超声测量室间隔厚度(IVSd)、左心室后壁厚度(LVPWd)、左心房厚度(LAD),DTI模式测量二尖瓣瓣环心肌收缩峰值速度(Vs)、舒张早期运动速度(Ve)、舒张晚期运动速度(Va)和Ve/Va,以及用猪尾导管直接测量左室舒张末压(LVEDP)。结果:与对照组相比,LVH组和non-LVH组的Ve和Ve/Va显著减小,且LVH组比non-LVH组减小更明显(P<0.05);non-LVH组的Va与对照组相比无明显改变(P>0.05),但LVH组的Va较对照组及non-LVH组显著增大(P<0.05)。Ve/Va与LVPWd及LVEDP呈良好的线性相关。结论:伴有和不伴有左室肥厚的高血压患者均有舒张功能降低,且与左室厚度呈正相关;DTI是评价左室舒张功能的可靠方法。     

Plasma matrix metalloproteinase-3 level is an independent prognostic factor in stable coronary artery disease

BACKGROUND: Recent evidence suggests the important role of matrix metalloproteinases (MMPs) in the progression of atherosclerosis and development of clinical events. We assessed the prognostic value of different plasma MMPs in patients with stable coronary artery disease (CAD). MATERIALS AND METHODS: A total of 165 consecutive nondiabetic patients with angiographically significant CAD (n = 150) or normal coronary angiograms despite exercise-induced myocardial ischemia (cardiac syndrome X, n = 15) and 17 normal subjects were evaluated. In each subject, plasma inflammatory markers including high sensitivity C-reactive protein (hsCRP) and MMP-2, 3 and 9 were measured. In CAD patients, major cardiovascular events including cardiac death, nonfatal myocardial infarction, unscheduled coronary revascularization and hospitalization as a result of unstable angina were prospectively followed up for more than 6 months. RESULTS: Plasma levels of MMPs were significantly higher in CAD patients than in those with cardiac syndrome X and in normal subjects (MMP-2: 914.76 +/- 13.20 vs. 830.79 +/- 31.95 vs. 783.08 +/- 28.40 ng mL(-1), P = 0.002; MMP-3: 129.59 +/- 4.21 vs. 116.86 +/- 8.09 vs. 91.71 +/- 9.55 ng mL(-1), P = 0.011; MMP-9: 31.42 +/- 2.84 vs. 11.40 +/- 5.49 vs. 6.71 +/- 2.89 ng mL(-1), P = 0.006). In CAD patients, there were 48 major cardiovascular events during a mean follow-up period of 17.74 +/- 0.85 months. The numbers of diseased vessels (HR = 2.19, 95% CI 1.20-1.02, P = 0.011), plasma hsCRP (HR = 2.21, 95% CI 1.18-4.11, P = 0.013) and MMP-3 level (HR = 2.46, 95% CI = 1.15-5.28, P = 0.021) were associated with the development of cardiovascular events. However, only the plasma MMP-3 level was an independent predictor of the adverse events in CAD patients (HR = 2.47, 95% CI 1.10-5.54, P = 0.028). CONCLUSIONS: Plasma MMP levels were increased in CAD patients. Plasma MMP-3 level, rather than hsCRP, was an independent prognostic marker for future cardiovascular events, suggesting its potential role in risk stratification and clinical management of stable CAD.     

Hypertensive left ventricular hypertrophy is linked to an enhanced catecholamine response to submaximal exercise.

BACKGROUND: The serial plasma catecholamine response to exercise has not been studied fully in relation to left ventricular hypertrophy (LVH) in patients with hypertension (HT). This study determined whether plasma catecholamine responses to exercise are altered in essential HT in the presence or absence of LVH. MATERIALS AND METHODS: Plasma noradrenaline (NA) and plasma adrenaline (A) were measured at rest, during and after treadmill exercise in 59 hypertensive subjects and 22 age-matched control subjects. Patients were divided into LVH(-) (n = 20) and LVH(+) (n = 39) stratified by left ventricular mass index [LVMI: control subjects, LVH(-), LVH(+): 114 +/- 4, 105 +/- 3, 151 +/- 3 g m-2]. RESULTS: Exercise time (9.9 +/- 0.6, 7.6 +/- 0.7, 7.3 +/- 0.6 min) was shorter in patients with HT. Both systolic and diastolic blood pressures were higher in patients with HT, and no difference was observed between LVH(-) and LVH(+) patients. Resting plasma NA was not different (157 +/- 16, 173 +/- 17, 167 +/- 14 pg mL-1), but plasma NA at stage I (300 +/- 30, 342 +/- 40, 469 +/- 40 pg mL-1) was higher in LVH(+) patients than in LVH(-) patients or control subjects. Plasma A response to exercise was similar among the three groups. There was a positive correlation (r = 0.38, P < 0.001) between LVMI and Deltaplasma NA at stage I in all subjects. CONCLUSIONS: Patients with essential HT with LVH had augmented plasma NA response during submaximal exercise, whereas patients without LVH did not exhibit this augmentation. The positive correlation between LVMI and Deltaplasma NA suggested a possible association between the degree of cardiac hypertrophy and sympathetic activation during exercise.     

Circulating natriuretic peptide concentrations in patients with end-stage renal disease: role of brain natriuretic peptide as a biomarker for ventricular remodeling.

OBJECTIVES: To determine levels of natriuretic peptides (NPs) in patients with end-stage renal disease (ESRD) and to examine the relationship of these cardiovascular peptides to left ventricular hypertrophy (LVH) and to cardiac mortality. PATIENTS AND METHODS: One hundred twelve dialysis patients without clinical evidence of congestive heart failure underwent plasma measurement of NP concentrations and echocardiographic investigation for left ventricular mass index (LVMI). RESULTS: Plasma atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) concentrations correlated positively with LVMI and inversely with left ventricular ejection fraction, whereas C-type NP and Dendroaspis NP levels did not correlate with LVMI. In dialysis patients with LVH (LVMI >125 g/m2), plasma ANP and BNP concentrations were increased compared with those in dialysis patients without LVH (both P<001). In a subset of 15 dialysis patients without LVH or other concomitant diseases, plasma BNP concentrations were not significantly increased compared with those in 35 controls (mean +/- SD, 20.1+/-13.4 vs 13.5+/-9.6 pg/mL; P=.06), demonstrating that the BNP concentration was not increased by renal dysfunction alone. Furthermore, the BNP level was significantly higher in the 16 patients who died from cardiovascular causes compared with survivors (mean +/- SD, 129+/-13 vs 57+/-7 pg/mL; P<.003) and was significantly associated with greater risk of cardiovascular death in Cox regression analysis (P<.001), as was the ANP level (P=.002). CONCLUSIONS: Elevation of the plasma BNP concentration is more specifically related to LVH compared with the other NP levels in patients with ESRD independent of congestive heart failure. Thus, BNP serves as an important plasma biomarker for ventricular hypertrophy in dialysis patients with ESRD.     

Comparison of myocardial tissue Doppler with transmitral flow Doppler in left ventricular hypertrophy

We sought to determine the most useful echocardiographic measurements for assessment of diastolic function in patients with left ventricular hypertrophy (LVH) and normal systolic function. We compared myocardial Doppler velocities of the basal inferoposterior wall with mitral inflow pulsed wave Doppler velocities in 11 healthy volunteers (age, 36 +/- 6 years), 25 patients (age, 64 +/- 14 years) without LVH, and 37 patients (age, 67 +/- 14 years) with LVH and otherwise normal echocardiograms. The discriminatory measurements were myocardial A-wave duration (120 +/- 18 versus 98 +/- 20 and 92 +/- 12 ms, P <.0001), myocardial isovolumetric relaxation time (124 +/- 45 versus 95 +/- 48 and 78 +/- 25 ms, P =.0035), mitral A-wave velocity (0.98 +/- 0.37 versus 0.73 +/- 0.28 m/s and 0.61 +/- 0.22 m/s, P =.009), and mitral E-wave deceleration time (257 +/- 93 versus 201 +/- 85 ms and 184 +/- 83 ms, P =.015), which were significantly increased, and myocardial E-wave velocity (0.84 +/- 0.04 m/s versus 0.13 +/- 0.03 m/s and 0.14 +/- 0.03 m/s, P <.0001), which was significantly decreased, in patients with LVH compared with patients without LVH and normal volunteers, respectively. Left ventricular posterior wall thickness correlated with myocardial isovolumetric relaxation time (r = 0.52, P <.0001) and myocardial A-wave duration (r = 0.59, P <.0001), negatively with myocardial E wave (r = -0.43, P <.0001), and showed no correlation with mitral inflow parameters except mitral inflow A wave (r = 0.43, P =.002). On multivariate analysis using these variables, myocardial isovolumetric relaxation time (P =.0014) and A-wave duration (P =.001) were the only 2 variables that correlated with posterior wall thickness (multiple R = 0.71). In the presence of LVH and preserved left ventricular systolic function, myocardial relaxation time and velocities are more sensitive than mitral Doppler inflow parameters in detecting abnormal left ventricular relaxation.     

多普勒组织成像对高血压左心室肥厚患者左心室舒张功能的评价

目的 应用多普勒组织成像（DTI）技术评价高血压左心室肥厚患者左心室舒张功能，并与二尖瓣血流频谱作对比。方法 研究对象为35例临床与超声诊断的高血压左心室肥厚患者（高心组）和20例正常人（对照组）。采用心尖四腔观，选取室间隔中段，左室侧壁中段，二尖瓣环-室间隔交界处、二尖瓣环一侧壁交界处为取样点，分别显示各部位组织的运动情况，并测量心肌收缩峰速度（Vs）、心肌舒张早期峰值速度（Ve）、舒张晚期峰值速度（VA）及VE与VA比值（VE/VA）。常规测量二尖瓣血流频谱，与DTI参数作对比。结果 与对照组相比，高心组室间隔中段，侧壁中段、二尖瓣环VE、VE/VA均显著下降，各部位VE/VA均与二尖瓣血流频谱E/A之间存在高度相关性；DTI对高血压左心室肥厚患者左心室舒张功能异常的诊断灵敏度高于二尖瓣血流频谱。结论 DTI技术可以定量评价高血压左心室肥厚患者的左心室舒张功能，并且比常规脉冲波多普勒二尖瓣血流参数更加敏感。     

Regression of left ventricular hypertrophy and control of hypertension in the spontaneously hypertensive rat (SHR): oxprenolol versus hydrochlorothiazide

The control of hypertension with antihypertensive agents, in the spontaneously hypertensive rats (SHR) can result in regression of established cardiac hypertrophy. This study compared the effects of therapy with oxprenolol (Ox) and with hydrochlorothiazide (Htz) for (1) regression of established left ventricular hypertrophy (LVH) and (2) blood pressure control. Three groups of SHR and 3 comparable groups of Wistar-Kyoto (WKY) rats, matched for age, sex and body wt, were treated with tap water (Gp I), 60-200 mg hydrochlorothiazide kg-1 day-1 (Gp II) and 15-500 mg oxprenolol kg-1 day-1 (Gp III) for 13 weeks. Systolic and diastolic blood pressures (SBP, DBP mmHg), left ventricular wt/body wt ratio (LVwt/Bwt mg g-1) and left ventricular wall thickness (LVWT mm) were recorded. Oxprenolol lowered both systolic (mean +/- S.E. mmHg, 130 +/- 7 vs 189 +/- 8; P less than 0.01) and diastolic blood pressures (mean +/- S.E. mmHg, 104 +/- 6 vs 159 +/- 6; P less than 0.001) and caused regression of left ventricular hypertrophy (mean +/- S.E. mg g-1, 2.91 +/- 0.06 vs 3.10 +/- 0.09; P less than 0.05). In contrast, hydrochlorothiazide did not control blood pressure (mean +/- S.E. mmHg, 183 +/- 5 vs 189 +/- 6 and 152 +/- 5 vs 156 +/- 6), but it did cause regression of left ventricular hypertrophy (mean +/- S.E. mg g-1, 2.67 +/- 0.03 vs 3.10 +/- 0.09; P less than 0.01). Left ventricular wall thickness, measured in the mid-ventricular region, was significantly reduced only by hydrochlorothiazide (mean +/- S.E. mm, 2.76 +/- 0.06 vs 3.21 +/- 0.01; P less than 0.05). These results suggest that regression of left ventricular hypertrophy can occur with or without control of hypertension in the SHR.     

伴和不伴左室肥厚高血压患者的组织多普勒特征及意义

目的 应用组织多普勒（DTI）观察伴有和不伴有左室肥厚的高血压患者的组织多普勒特征，探讨DTI在心功能评价中的价值。方法 入选30例高血压患者，分为左室肥厚组（LVH）15例与非左室肥厚组（non-LVH）15例,另选取15例健康人作为对照组，分别行超声多普勒及DTI检查，多普勒超声测量室间隔厚度（IVSd）、左心室后壁厚度（LVPWd）、左心房厚度（LAD），DTI模式测量二尖瓣环舒张早期运动速度（Ve）、舒张晚期运动速度（Va）和Ve/Va,以及用猪尾导管直接测量左室舒张末压(LVEDP)。结果 与对照组相比，高血压组的Ve和Ve/Va显著减小，且LVH组比non-LVH组减小更明显(P<0.05)；non-LVH组的Va与对照组相比无明显改变(P>0.05)，但LVH组的Va较对照组及non-LVH组显著增大(P<0.05)。Ve/Va与左室厚度及LVEDP呈良好的线性相关。 结论 伴有和不伴有左室肥厚的高血压患者均有舒张功能降低，且与左室厚度呈正相关；DTI是评价左室舒张功能的可靠方法。     

氯沙坦对高血压左室肥厚和左室舒张功能的作用

目的：观察氯沙坦对高血压左室肥厚及左室舒张功能的作用。方法：对符合WHO关于高血压诊断标准的68例原发性高血压合并左室肥厚患，服用氯沙坦治疗，用多普勒彩超超声心动图测定治疗前后左室肥厚指标，左室舒张及收缩功能指标。结果：治疗后室间隔厚度，左室后壁厚度，左室心肌重量．左室心肌重量／左室容量均明显减少．舒张早期流速峰值明显增大，舒张晚期流速下降．两比值下降．左室射血分数无变化。结论：氯沙坦可有效逆转高血压患左室肥厚，改善左室舒张功能。     

高血压病患者左室舒张功能的研究

目的 研究高血压病患者左室舒张功能的变化。方法 二维超声检测高血压组72例(左室肥厚35例、非肥厚组37例)、对照组30例的左房大小、室间隔厚度(IVST)、左室后壁厚度，多普勒测定二尖瓣血流频谱及左室等容舒张时间(IVRT)。结果 高血压组与对照组比较：左房明显扩大，室间隔及左室后壁明显增厚，E峰、Ei显著减小，A峰、Ai显著增高，WRT显著延长。高血压组中，左室肥厚组与非肥厚组比较：肥厚组左房扩大，室间隔及左室后壁增厚，E峰、Ei减小，A峰、Ai增高，IVRT延长均较非肥厚组明显。结论 高血压病患者存在左室舒张功能异常，左室肥厚者舒张功能的损害更为严重。     

Effect of 24-week treatment with telmisartan on myocardial structure and function: relationship to insertion/deletion polymorphism of the angiotensin-converting enzyme gene

The aim of the present study was to assess the effect of treatment with the angiotensin II receptor blocker telmisartan for 24 weeks on myocardial structure and function in patients with essential hypertension, and the relationship between this effect and the structural polymorphism of the angiotensin-converting enzyme (ACE) gene. Thirty-five patients with essential hypertension and left ventricular hypertrophy (LVH) without other associated morbidity were included in an open-label, non-comparative study. The patients were treated with telmisartan 40-80 mg once daily. In the final analysis, there were 29 patients who received the full course of treatment and were evaluated echocardiographically before and after treatment by the same blinded investigator, and myocardial structure and function were analysed. The myocardial mass of the left ventricle was determined in M-mode. Assessment of diastolic function of transmitral blood flow was performed using pulsed Doppler echocardiography. All patients were genotyped for insertion/deletion (I/D) polymorphism of the ACE gene. Telmisartan produced a significant reduction in left ventricular mass index from 140.4 +/- 48.6 to 128.7 +/- 40.6 g/m2 that was accompanied by an improvement in characteristics of diastolic function. The decrease in LVH was more significant in the ID genotype group than in the II and DD groups. Thus, prolonged treatment with telmisartan is accompanied by an improvement in myocardial structure, expressed as a reduction in left ventricular mass and function that is more marked in patients with ID genotype of the ACE gene.     

The effects of left ventricular hypertrophy on the respiratory changes in transmitral Doppler flow patterns of hypertension patients

BACKGROUND: Left ventricular early diastolic fillings can be reduced by inspiration. However, the effects of left ventricular hypertrophy on such changes have not been studied before. This study was undertaken to investigate whether respiratory changes in transmitral Doppler flow were affected by left ventricular hypertrophy in hypertension patients. METHODS: Eighty-three patients (mean age 46 +/- 8 years, 49 males) with untreated essential hypertension were included in this study. Transmitral Doppler flow velocity was measured both at end-expiration and end-inspiration. Left ventricular mass was measured by M-mode echocardiography. We divided patients into two groups based on the presence of left ventricular hypertrophy or not. RESULTS: Twenty-one patients were diagnosed to have left ventricular hypertrophy. In patients without left ventricular hypertrophy, the peak early filling velocity decreased significantly (from 74 +/- 15 to 71 +/- 18 cm s(-1), P = 0.003), the peak atrial velocity increased significantly (from 65 +/- 17 to 74 +/- 15 cm s(-1), P < 0.001) and the early filling to atrial velocity ratio decreased significantly (from 1.2 +/- 0.3 to 1.1 +/- 0.3, P < 0.001) from end-expiration to end-inspiration. In patients with left ventricular hypertrophy, the parameters of transmitral Doppler flow pattern did not change during respiration. CONCLUSION: Respiratory changes in the transmitral Doppler flow velocity are blunted by left ventricular hypertrophy in hypertension patients. This phenomenon is probably contributed by the increased left ventricular wall stiffness in the left ventricular hypertrophy.     

Increased rat cardiac angiotensin converting enzyme activity and mRNA expression in pressure overload left ventricular hypertrophy. Effects on coronary resistance, contractility, and relaxation.

We compared the activity and physiologic effects of cardiac angiotensin converting enzyme (ACE) using isovolumic hearts from male Wistar rats with left ventricular hypertrophy due to chronic experimental aortic stenosis and from control rats. In response to the infusion of 3.5 X 10(-8) M angiotensin I in the isolated buffer perfused beating hearts, the intracardiac fractional conversion to angiotensin II was higher in the hypertrophied hearts compared with the controls (17.3 +/- 4.1% vs 6.8 +/- 1.3%, P less than 0.01). ACE activity was also significantly increased in the free wall, septum, and apex of the hypertrophied left ventricle, whereas ACE activity from the nonhypertrophied right ventricle of the aortic stenosis rats was not different from that of the control rats. Northern blot analyses of poly(A)+ purified RNA demonstrated the expression of ACE mRNA, which was increased fourfold in left ventricular tissue obtained from the hearts with left ventricular hypertrophy compared with the controls. In both groups, the intracardiac conversion of angiotensin I to angiotensin II caused a comparable dose-dependent increase in coronary resistance. In the control hearts, angiotensin II activation had no significant effect on systolic or diastolic function; however, it was associated with a dose-dependent depression of left ventricular diastolic relaxation in the hypertrophied hearts. These novel observations suggest that cardiac ACE is induced in hearts with left ventricular hypertrophy, and that the resultant intracardiac activation of angiotensin II may have differential effects on myocardial relaxation in hypertrophied hearts relative to controls.     

Prognostic value of matrix metalloproteinases (MMP-2 and MMP-9) in Hodgkin's and non-Hodgkin's lymphoma

Matrix metalloproteinases (MMPs) are responsible for the degradation of extracellular matrix and have an important role in tumour metastases. We investigated the role of MMP-2 and MMP-9 in Hodgkin's disease (HD) and non-Hodgkin's lymphoma (NHL). The serum samples of patients with HD (n = 12), NHL (n = 30) and healthy control (n = 22) were analysed for MMP-2 and MMP-9. An immunoassay method was used for the determination of MMP-2 and MMP-9 levels. No statistical significance was found between HD and NHL groups for levels of MMP-2. There were no relation between MMP-2, MMP-9 levels and clinical characteristics of patients. The mean MMP-9 levels were found to be 555.6 +/- 140 ng/ml, 446.6 +/- 53.6 ng/ml and 111.2 +/- 10.3 ng/ml in HD, NHL and control groups, respectively. Our results suggest that MMP-9 levels are substantially increased in HD and NHL when compared with controls and may probably be used for distinguishing the benign diseases from malign lymphomas.     

组织多普勒显像技术评价西尼地平对高血压左室舒张功能的影响

目的借组织多普勒显像(TDI)技术评价西尼地平对高血压患者左室舒张功能的影响。方法37例高血压患者分为非左室肥厚(NLVH)组及左室肥厚(LVH)组,给予西尼地平治疗8周,治疗前、后用TDI技术测量收缩期运动速度(Sa)、舒张早期运动速度(Ea)、舒张晚期运动速度(Aa)及Ea/Aa,并与血流多普勒指标E波速度(E)、A波速度(A)、E/A进行比较,观察降压效果及对左室舒张功能的影响。结果(1)高血压LVH组较NLVH组Ea降低(P<0.01),Ea/Aa降低(P<0.05);而E、E/A等指标两组间差异无统计学意义;(2)西尼地平治疗8周后收缩压(SBP)、舒张压(DBP)均较治疗前下降(P<0.001),HR与治疗前比较无统计学意义;(3)治疗后E波减速时间(EDT)较治疗前降低(P<0.05),治疗后E、E/A、Ea均较治疗前升高(P<0.01),Ea/Aa较治疗前升高(P<0.001),等容舒张期(IVRT)较治疗前降低(P<0.001)。治疗后A、Sa、Aa与治疗前比较差异无统计学意义。结论TDI技术在评价左室舒张功能方面较二尖瓣血流频谱更准确;西尼地平对轻中度高血压患者具有良好的降压作用,不引起反射性心率加快,且能改善患者左室舒张功能。     

Structural-functional alterations in the heart affecting dynamics of transmitral blood flow during a hemodialysis session

AIM: To study dynamics of transmitral circulation (TMC) during a hemodialysis (HD) session in patients with chronic renal failure (CRF) regarding structural-functional alterations of the heart and baseline condition of the diastolic function of left ventricular (LV) myocardium. MATERIAL AND METHODS: Sixty one patients (34 females and 27 males, mean age 47 +/- 11 years) on programmed HD free of heart valvular disease, ischemic heart disease, acute myocardial infarction, atrial fibrillation. Before and after HD session the patients underwent echocardiography, including Doppler regime. RESULTS: Normal LV geometry was detected in 3 (4.9%) patients, concentric remodeling - in 9 (14.8%), concentric LV hypertrophy (LVH) - in 37 (60.7%), excentric LVH - in 12 (19.7%) patients. The ejection fraction was under 45% in 5 (8.2%) patients. Diastolic dysfunction of LV myocardium was found in 42 (68.9%) patients, TMC characteristic of slow relaxation was registered most frequently (47.6%). A pseudonormal type of TMC was recorded in 16 (38.1%) patients. HD did not change TMC significantly in patients with normal diastolic function (before HD E peak velocity was 88.7 +/- 19.8 cm/s, after - 80.0 +/- 24.6 cm/s, p > 0.05). In patients with initially disturbed relaxation the velocity of early diastolic flow (Vp) (color M-mode Doppler) increased (before HD, Vp was 67.6 +/- 17.1 cm/s, after - 72.9 +/- 15.7 cm/s, p < 0.05), E/Vp reduced (before HDm E/Vp was 1.2 +/- 0.4, after 1.0 +/- 0.4, p < 0.05). The subgroup with initially pseudonormal TMC showed decreased velocity in the E peak (before HD - 103.4 +/- 13.5 cm/s, after - 76.8 +/- 24.0 cm/s, p < 0.001). In restrictive TMC this velocity also decreased - 129.0 +/- 17.8 cm/s and 108.8 +/- 14.7 cm/s, p < 0.05, respectively). CONCLUSION: TMC alteration during a HD session depends more on initial type of diastolic dysfunction than on LV geometry. A HD session improves intracardiac hemodynamics in patients with pseudonormal TMC.     

定量组织速度成像及应变率成像对高血压病患者左室舒张功能的研究

目的:探讨二尖瓣环舒张早期峰值速度及应变率与舒张晚期峰值速度及应变率评价左室舒张功能的价值。方法:取心尖四腔心切面,获取44例高血压病患者及20例正常人的二尖瓣前后叶瓣环的组织速度曲线和应变率曲线,分别测量舒张期峰值速度(Ve、Va)及舒张期峰值应变率(e、a);计算前后瓣环的平均峰值速度(EVe、EVa)及比率(EVe?蛐EVa);平均峰值应变率(Ee、Ea)及比率(Ee/Ea)。用血流多普勒法测定二尖瓣口血流峰值速度(E、A)及比率(E/A),并进行比较。结果:与对照组相比,高血压病患者EVe,EVe/EVa和Ee,Ee/Ea明显降低,且高血压肥厚组(LVH组)比非肥厚组(non-LVH组)降低更甚,EVa则明显升高,Ee/Ea比率与EVe/EVa比率呈高度显著相关(rs’=0.890,P<0.001),二者对左室舒张功能异常的检出率明显高于E/A比率(P<0.001)。结论:QTVI及SRI能便捷准确地定量高血压病患者二尖瓣环舒张期运动速度及应变率,揭示左心室舒张功能的改变,有助于舒张功能受损程度的判断,优于传统的血流多普勒法,为又一无创检测左室舒张功能的新方法。