依那普利或氯沙坦对SHR左室肥厚和心肌纤维化的影响

目的:观察自发性高血压大鼠(SHR)左室肥厚和心肌纤维化各指标的改变,以及依那普利和氯沙坦的保护作用.方法:雄性SHR(n=30)自第10周始服用依那普利(20mg@kg-1@d-1),或氯沙坦(25mg@kg-1@d-1),或二者合用(依那普利10mg@kg-1@d-1,氯沙坦12.5mg@kg-1@d-1)至第16周,并以年龄、性别、数量配对的未治疗SHR和Wistar-kyoto(WKY)大鼠作对照.测定收缩压(SBP)、左室重量(LVM)以及左室重量指数(LVMI)和左室心肌胶原含量;计算机图象分析心肌细胞大小、心肌胶原容积分数(CVF)和血管周围胶原面积(PVCA).结果:SHR的SBP、LVM、LVMI、心肌胶原含量、心肌细胞的横截面积、CVF和PVCA均显著高于WKY对照组(P＜0.001).SHR治疗组上述指标显著低于SHR未治疗组(P＜0.01),依那普利与氯沙坦之间无显著差别(P＜0.05).二者合用比单用依那普利或氯沙坦更有效(P＜0.05).结论:依那普利和氯沙坦可显著的降低血压、逆转SHR早期左室肥厚和心肌纤维化,而且二者合用在逆转左室肥厚和心肌纤维化方面效果更明显.     

依贝沙坦对自发性高血压大鼠左心室肥厚和心肌纤维化的影响

目的探讨依贝沙坦对自发性高血压大鼠(SHR)左心室肥厚(LVH)和心肌纤维化的影响。方法18只16周龄SHR,随机分为依贝沙坦治疗组(SHR-I)和SHR空白对照组(SHR-C);另设同源的WKY大鼠8只为正常对照组。治疗组口服依贝沙坦50mg.kg-1.d-1给药8周后处死动物,取左心室心肌称重,计算左心室/体重比(LVW/BW),Masson三色法染色观察左心室心肌胶原变化,计算机图象分析测量心肌切片的胶原容积分数(CVF)和血管周围胶原面积(PVCA)。结果SHR空白对照组的收缩压(SBP),LVW/BW,CVF,PVCA均显著高于WKY对照组(P<0.01),与SHR空白对照组相比,依贝沙坦治疗组能有效降低SHR的SBP,改善左心室肥厚(P<0.01)并使左心室内膜及心肌小动脉周围的胶原减少(P<0.01)。结论依贝沙坦可有效降低SHR血压,部分逆转心肌纤维化和左心室肥厚。     

厄贝沙坦治疗EH的降压效果及其对左心室肥厚和舒张功能的影响

目的 观察厄贝沙坦治疗原发性高血压（EH）的临床效果.方法 选择同期收治的40例EH并左心室肥厚患者,均予单药厄贝沙坦150～300 mg/d口服治疗36周;治疗前后记录血压变化,并用超声心动图测量左室结构和舒张功能指标.结果 40例患者厄贝沙坦治疗后收缩压和舒张压均显著下降（P均＜0.05）,室间隔厚度、舒张末期左室后壁厚度、舒张末期左室腔内径、左室重量指数均显著减小,舒张早期运动峰速度（Ea）、Ea/舒张晚期运动峰速度（Aa）显著增大（P均＜0.05）,且均无明显不良反应.结论 厄贝沙坦治疗EH降压效果确切、患者耐受性好,且对靶器官亦有较好的保护作用,是一种理想的一线抗高血压药物.     

依那普利或氯沙坦对SHR左室肥厚和心肌纤维化的影响

目的 :观察自发性高血压大鼠 (SHR)左室肥厚和心肌纤维化各指标的改变 ,以及依那普利和氯沙坦的保护作用。方法 :雄性 SHR(n=30 )自第 1 0周始服用依那普利 (2 0 mg.kg- 1 .d - 1 ) ,或氯沙坦 (2 5 mg.kg - 1 .d - 1 ) ,或二者合用 (依那普利1 0 mg.kg - 1 .d - 1 ,氯沙坦 1 2 .5 mg.kg - 1 .d - 1 )至第 1 6周 ,并以年龄、性别、数量配对的未治疗 SHR和 Wistar- kyoto(WKY)大鼠作对照。测定收缩压 (SBP)、左室重量 (L VM)以及左室重量指数 (L VMI)和左室心肌胶原含量 ;计算机图象分析心肌细胞大小、心肌胶原容积分数 (CVF)和血管周围胶原面积(PVCA)。结果 :SHR的 SBP、L VM、L VMI、心肌胶原含量、心肌细胞的横截面积、CVF和 PVCA均显著高于 WKY对照组 (P<0 .0 0 1 )。 SHR治疗组上述指标显著低于 SHR未治疗组 (P<0 .0 1 ) ,依那普利与氯沙坦之间无显著差别 (P<0 .0 5 )。二者合用比单用依那普利或氯沙坦更有效 (P<0 .0 5 )。结论 :依那普利和氯沙坦可显著的降低血压、逆转 SHR早期左室肥厚和心肌纤维化 ,而且二者合用在逆转左室肥厚和心肌纤维化方面效果更明显     

厄贝沙坦对兔肥厚心肌钙调蛋白激酶活性及室性心律失常发生的影响

目的:研究厄贝沙坦对兔肥厚心肌局部钙调蛋白激酶活性的影响和对恶性心律失常发生的预防作用。方法:家兔30只,随机分为左心室肥厚组(手术组,腹主动脉缩窄术制备心肌肥厚模型),对照组(只暴露主动脉而不行缩窄)和厄贝沙坦干预组(干预组,行腹主动脉缩窄后予厄贝沙坦口服)。8周后,在体同步测量肥厚心肌3层的APD100以及透壁弥散复极化(TDR),用程序电刺激方法诱导心律失常发生。术后测量全心重量、室壁厚度和心肌局部钙调蛋白激酶活性。结果:手术组,3层心肌细胞的APD100,TDR较对照组明显延长,局部钙调蛋白激酶活性明显升高,更容易诱发室性心律失常;干预组APD100、TDR较手术组缩短,局部钙调蛋白激酶活性降低,而且不易诱发心律失常。结论:肥厚心肌发生电生理重构,局部钙调蛋白激酶活性增加,更容易发生恶性心律失常,厄贝沙坦能够部分恢复肥厚心肌的电重构,降低心肌局部的钙调蛋白激酶活性,从而减少心律失常的发生。     

厄贝沙坦对慢性心力衰竭和心肌纤维化的影响研究

目的 探讨厄贝沙坦对心力衰竭患者心功能和心肌纤维化的影响.方法 选择心力衰竭患者（NYHA分级为Ⅱ～Ⅳ级）100例,随机分为常规治疗组和厄贝沙坦组.每组50例;在治疗前和治疗后12周应用心脏彩色超声测定心功能变化（测量LVEF）,采用放射免疫法检测血浆脑钠肽（BNP）、血清Ⅲ型前胶原氨基末端肽（PⅢNP）和透明质酸（HA）的浓度.结果 ①厄贝沙坦组BNP、PⅢNP和HA治疗后比常规治疗组治疗后降低效果更明显（P＜0.05）;两组患者LVEF值治疗后比治疗前明显升高（P＜0.01）,而且厄贝沙坦组治疗后与常规治疗组治疗后相比升高明显（P＜0.05）.②血清PⅢNP、HA与BNP值呈正相关,血清PⅢNP、HA与LVEF值呈负相关.结论 在常规治疗慢性心衰的基础上加用厄贝沙坦更能有效地抑制心脏HA和Ⅲ型胶原的产生,可以起到抗心肌纤维化、改善心功能的作用.     

厄贝沙坦对老年原发性高血压患者降压和逆转左心室肥厚的作用

目的观察厄贝沙坦对老年原发性高血压患者降压和逆转左心室肥厚（LVH）的作用。方法对85例老年原发性高血压合并LVH患者采用厄贝沙坦治疗,观察治疗前后血压、心率及超声心动图的变化情况。结果与治疗前比较,治疗后收缩压、舒张压下降（P均〈0．05）;室间隔厚度、左心室后壁厚度、左心室舒张末期内径、左心室质量指数降低（P均〈0．05）,心率无明显变化（P〉0．05）。结论厄贝沙坦能逆转原发性高血压引起的LVH并改善左心室舒张功能,明显改善老年原发性高血压患者预后。     

自发性高血压大鼠左室肥厚及心肌纤维化的动态变化

目的 生高血压大鼠（ＳＨＲ）血压增高的初期。增高期和稳定期左室肥厚和心肌纤维化参数的改变,探讨高血压左室肥厚和心肌纤维化的动态演化规律。方法 应用生化测定、病一检查结合计算机分析等方法,检测ＳＨＲ及其照ＷＫＹ在６周、１４周和２４周的收缩压、左室重量及左室重量指数、心肌细胞面积及横径、民胶原只分数（ＣＶＦ）、血管周围胶原面积（ＰＶＣＡ）及心肌组织内羟脯氨酸浓度。结果ＳＨＲ左室重量及左室重量指数、心肌     

阿托伐他汀联合厄贝沙坦治疗高血压左心室肥厚的临床研究

目的探讨阿托伐他汀联合厄贝沙坦对原发性高血压患者左心室肥厚（LVH）的临床疗效。方法将160例原发性高血压LVH患者随机分为厄贝沙坦组和阿托伐他汀联合厄贝沙坦组。治疗前后检测左心室质量指数（LVM I）及24 h动态血压。结果两组治疗后血压及LVM I较治疗前显著降低（P均〈0.05）,治疗后两组间血压的差异无统计学意义。治疗后阿托伐他汀联合厄贝沙坦组的LVM I明显低于厄贝沙坦组（P〈0.05）。结论阿托伐他汀与厄贝沙坦联合治疗在逆转LVH方面较厄贝沙坦单药治疗具有更加显著的作用,且这些作用独立于降压疗效之外。     

福辛普利对SHR左室肥厚和心肌纤维化的影响

目的探讨福辛普利对自发性高血压大鼠(SHR)左心室肥厚(LVH)和心肌纤维化的影响。方法18只16周龄SHR大鼠,随机分为福辛普利治疗组(SHR-F)和SHR空白对照组(SHR-C);另设同源的WKY大鼠8只为正常对照组。治疗组口服福辛普利20mg·kg-1·d-1,给药8周后处死动物,取左心室心肌称重,计算左心室/体重比(LVW/BW),Masson三色法染色观察左心室心肌胶原变化,计算机图像分析测量心肌切片的胶原容积分数(CVF)和血管周围胶原面积(PVCA)。结果SHR空白对照组的SBP、LVW/BW、CVF、PVCA均显著高于WKY对照组(P<0.01),与SHR空白对照组相比,福新普利治疗组能有效降低SHR的SBP,改善SHR左心室肥厚(P<0.01〉并使左心室内膜及心肌小动脉周围的胶原减少(P<0.01〉。结论福辛普利可有效降低SHR血压,部分逆转心肌纤维化和左室肥厚。     

心肌组织多普勒成像技术评估左室肥厚对左室收缩运动协调性的影响

目的评价左室肥厚对左室收缩运动协调性和功能的影响。方法正常对照组18例(组1)、高血压性心脏病患者18例(组2)和肥厚型心肌病患者16例(组3)。应用组织多普勒成像技术测量左室收缩期电机械运动的时间离散度(DTQ-S)、室间隔和左室侧壁6个位点的心肌收缩期峰值速率(Vs)。结果与组1相比,组3DTQ-S延长(P<0.001),各位点Vs值降低(P<0.05);组2上述数值无明显变化。结论肥厚型心肌病存在左室运动收缩协调障碍和收缩功能下降。     

Remodeling of myocardial interstitium in left ventricular hypertrophy and myocardial infarction

Structural and biochemical modifications of the myocardium (remodeling) occur during the development of left ventricular hypertrophy and acute myocardial infarction. An important part of this process of myocardial remodeling occurs in the interstitial compartment. The myocardial interstitium is composed mainly of fibrillar collagen. These changes are associated to modifications in ventricular function that could be deleterious and have clinical manifestations. Some salutory effects of the treatment of both conditions are related to modifications of the process of myocardial interstitial remodeling.     

替米沙坦对自发性高血压大鼠左心室重塑的影响

目的探讨替米沙坦对自发性高血压大鼠(SHR)左心室重塑的影响。方法l6只16周龄雄性SHR,随机分为替米沙坦治疗组和SHR空白对照组;另设同源的WKY大鼠8只为正常对照组。治疗组给予替米沙坦10mg·kg-1·d-1灌胃给药,8周后处死动物,测量左心室心肌厚度并称重,计算左心室与体重比(LVW/BW);通过Van Gieson染色法观察左心室心肌胶原变化,对左心室心肌胶原容积分数(CVF)和血管周围胶原面积(PVCA)进行定性和半定量分析;电镜和HE染色观察左室心肌病理及超微结构。结果与WKY组相比,SHR空白对照组的尾动脉收缩压(SBP)、LVW/BW、左室壁厚度、CVF、PVCA、均显著增高(P<0.01);与SHR空白对照组相比,替米沙坦治疗组能有效降低SHR的SBP,改善左心室肥厚(P<0.01),减少心肌间质及心肌小动脉周围的胶原(P<0.01),组织病理及电镜显示,替米沙坦治疗能显著改善SHR左心室重塑。结论替米沙坦能有效降低SHR血压,改善左心室重塑。     

Irbesartan and atenolol improve diastolic function in patients with hypertensive left ventricular hypertrophy

OBJECTIVES AND DESIGN: An abnormal diastolic filling is common in hypertensive left ventricular (LV) hypertrophy, a condition that may lead to heart failure and death. The renin-angiotensin-aldosterone system has been implicated in the development of LV hypertrophy. This study examines the effects of 48 weeks of double-blind treatment with the AT1 receptor blocker irbesartan and the beta-blocker atenolol on diastolic function. METHODS: Diastolic function was evaluated in 115 hypertensive patients with LV hypertrophy by Doppler echocardiography mitral inflow velocities calculated from the peak of early (E) and peak of late (A) diastolic velocities (E/A ratio), the E-wave deceleration time, the isovolumic relaxation time, the pulmonary venous flow velocity, and by the atrioventricular valve plane displacement method. RESULTS: By similar reductions in blood pressure both groups progressively reduced the LV mass index, with a greater reduction in the irbesartan group (P = 0.024). Diastolic function was improved similarly by irbesartan and atenolol; for example, the E/A ratio by 12 and 14% (P = 0.022 and P < 0.001), and the pulmonary venous flow velocity by 10 and 7% (P = 0.036 and P = 0.001), respectively. The isovolumic relaxation time was improved by irbesartan (P = 0.040) only, and was related to changes in LV geometry (P < 0.001). For atenolol, improvement in diastolic function was associated only with the reduction in blood pressure (P = 0.048). An improvement in diastolic function appeared greater in concentric LV hypertrophy than in eccentric LV hypertrophy. CONCLUSIONS: Treatment based on atenolol or irbesartan improves diastolic function in patients with hypertensive LV hypertrophy to the same degree, but through different mechanisms.     

Ventricular arrhythmias in hypertensive left ventricular hypertrophy. Relationship to coronary artery disease, left ventricular dysfunction, and myocardial fibrosis

Ventricular arrhythmias occur with increased frequency in hypertensive patients with left ventricular hypertrophy (LVH). The relationships, however, between ventricular arrhythmias and coexistent coronary artery disease, left ventricular dysfunction and left ventricular fibrosis have not been examined in hypertensive LVH. We carried out coronary arteriography on fifteen hypertensive patients with LVH and nonsustained ventricular tachycardia (greater than or equal to 3 consecutive ventricular complexes) of whom nine (60%) were free of significant (greater than 50% stenosis) coronary disease. To identify other possible correlates of left ventricular arrhythmias, 28 patients with LVH, comprising 17 with ventricular tachycardia and 11 without ventricular arrhythmias, underwent quantitative assessment of left ventricular function (angiographic ejection fraction), left ventricular mass (echocardiography), and left ventricular fibrosis (endomyocardial biopsy). Ejection fraction was not significantly different between the two groups (53 +/- 8% v 62 +/- 2%, P = NS). However, left ventricular mass was significantly greater (442 +/- 28 g v 339 +/- 34 g, P less than .05) and percentage fibrosis significantly higher (19 +/- 4% v 3 +/- 1%, P less than .001) in those patients with ventricular tachycardia. Thus ventricular arrhythmias in hypertensive patients with LVH cannot be entirely attributed to coexistent coronary disease, nor to left ventricular dysfunction, but are related to the degree of cardiac hypertrophy and subendocardial fibrosis.     

Midwall myocardial shortening in athletic left ventricular hypertrophy

BACKGROUND: Patients with pathological left ventricular hypertrophy have depressed midwall systolic shortening in spite of normal indices of left ventricular chamber function and a reduced midwall function has been observed to be an independent predictor of cardiovascular risk. Whether midwall shortening is depressed in physiological hypertrophy is unknown. METHODS: Forty-two subjects, 27 athletes and 15 age- and sex-matched normal control subjects (group 1) were studied. The athletes were divided into those with eccentric hypertrophy (group 2) and those with concentric hypertrophy (group 3). Systolic left ventricular function was assessed at the midwall and endocardium using two-dimensional echocardiography in all subjects. RESULTS: Left ventricular mass index was significantly greater in both athletic groups than in controls (group 1, 101+/-5.8 g/m(2), group 2, 141+/-11.1*, group 3, 155+/-5.8*; *P<0.01 compared with group 1). Left ventricular systolic function assessed at the endocardium was similar among all three groups (ejection fraction: group 1, 66.2+/-2.38, group 2, 66.8+/-1.44, group 3, 63.7+/-1.66%; endocardial fractional shortening: group 1, 37.1+/-1.71, group 2, 37.6+/-1.13, group 3, 35.1+/-1.25%). However, fractional shortening at the midwall was reduced in the concentric hypertrophy athletes compared with the other two groups (midwall fractional shortening: group 1, 21.9+/-1.1, group 2, 21.9+/-0.86, group 3, 18.4+/-0.96*%; P<0.05 compared with groups 1 and 2). CONCLUSION: Subjects with physiological concentric hypertrophy have depressed midwall fractional shortening. This suggests that the observed discrepancy between midwall and endocardial shortening in patients with left ventricular hypertrophy is likely to be a function of the geometry and not necessarily a reflection of pathology within the myocardium.