钙通道阻滞剂治疗左心室肥厚

左心室肥厚是心肌组织的肥厚,是心脏对长期动脉高压适应的结果。本文叙述了左心室肥厚的病理生理异常情况。阐明口服钙通道阻滞剂可降低血压和减轻左心室肥厚,并能改善左心室充盈功能,室性心律失常,心肌缺血和左心室收缩的功能。表明钙通道阻滞剂为治疗本病的有效药物。     

中药防治高血压左心室肥厚的研究进展

<正>高血压左心室肥厚是在高血压左心室后负荷升高状态下,为减少室壁张力,维持心脏功能,代偿出现的心肌肥厚。左心室肥厚是导致心肌梗死、心力衰竭、心律失常、猝死等心血管事件的独立危险因素,一旦临床确诊为左心室肥厚,则预后较差[1-2]。因此,高血压的治疗不仅要降压,而且必须预防和逆转左心室肥厚的发生和发展,从而减少心血管事件[3-4]。目前在临床上广泛使用的血管紧张素转换酶抑制剂类和血管紧张素Ⅱ受体拮抗剂类药物,能够改善左心室重     

左心室肥厚

本文综述了左心室肥厚,尤其是老年人左心室肥厚的病理生理、流行病学、类型、诊断和治疗的最新研究成果。     

关注左心室心肌肥厚的病因诊断

肥厚型心肌病(HCM)是一种临床常见的原发性心肌病,以心肌显著肥厚、家族遗传背景为特征,临床诊断依据超声心动图左心室室壁或(和)室间隔厚度超过15 mm[1].但是,引起左心室心肌肥厚(LVH)不仅仅限于HCM,如果忽视LVH的病因分析,有可能贻误诊断.     

左心室肥厚的影响因素及机制的研究进展

生理和病理条件下,血流动力学超负荷会引起左心室肥厚。目前尚未完全阐明引起心肌肥厚的主要的刺激因素是心脏自身机械拉伸,还是神经体液因子,抑或是两者的共同作用所致。刺激因素进入细胞后,通过引起细胞内生化改变导致第二信使和第三信使的激活,进一步调节转录,激活多种心肌肥厚相关基因的表达。左心室肥厚时会出现一系列的结构改变,包括心肌细胞肥大、间质结缔组织增生以及冠状循环微血管稀少。本文参考近年来相关文献,总结左心室肥厚的影响因素及机制研究方面的发展动态,旨在为读者阐明左心室肥厚的影响因素及机制的总体情况,提供可参考的研究靶点。     

左心室肥厚的发生与消退

左室肥厚是伴有左室压力或容量负荷过度的疾病中所发生的一种重要适应机制。左室肥厚对基础心脏病变的预后亦有重要的意义,当病因经内科或外科治疗纠正后左室肥厚可能会消退。本文复习左室肥厚的病理生理机制、发现方法和临床意义,并介绍记录到左室肥厚消退的资料。定义:左心室肥厚的病因学心肌肥厚。是指现存心肌纤维大小的增加,并非心肌细胞的增生,后者是指通过有丝分裂使心肌细胞数量增加。当所有左室壁几乎同等程度地增厚,左室肥厚可以是整体性的(弥漫性);当左室的一侧(室间隔或游离     

左心室肥厚的逆转

已经发现,主动脉狭窄或主动脉返流时行主动脉瓣置换术后,左心室重量可逐渐减轻,这是由于心肌细胞肥厚的逆转及心肌纤维含量减少所致。一些研究证实,高血压的药物治疗及非药物治疗,例如减轻体重、低钠饮食等可使左心室重量下降。在大多数试验中,左心室肥厚的逆转程度与收缩压的降低有关。几乎所有的降压药物如β阻滞剂、钙拮抗剂、血管紧张素转换酶抑制剂及肾上腺素能阻滞剂能使高血压患者的左心室重量减轻,然血管扩张剂如肼苯达嗪及长压定不能如此。这可能是上述血     

超声评价高血压左心室肥厚心肌密度特征的价值

<正> 高血压左心室肥厚独立于高血压的危险因素,现有研究表明,高血压患者左心室心肌纤维化的发生是其最重要的病理基础.本文旨在通过采用计算机辅助的灰阶分析声学组织密度定量新技术,对高血压患者的心肌组织进行研究,以评价超声诊断高血压左心室肥厚心肌纤维化的可行性.     

原发性高血压患者左心室后壁心肌肥厚与碱性成纤维细胞生长因子之间的关系

目的探讨原发性高血压患者左心室心肌肥厚与碱性成纤细胞生长因子(bFGF)之间的临床关系及意义。方法住院高血压患者共243例,行彩色超声心动图检查,其中高血压左心室后壁心肌肥厚>11.1mm108例;高血压左心室后壁厚度≤11mm 135例。采用ELISA方法测定bFGF。结果高血压左心室后壁心肌肥厚组、高血压非左心室后壁肥厚组bFGF水平分别为(342.42±11.611)μg/ml、(269.43±8.01)μg/ml,与对照组比较有显著差异(P<0.001)。结论bFGF水平高血压左心室后壁心肌肥厚组>高血压非左心室后壁肥厚组>正常对照组。bFGF在心肌重构、心肌肥厚及高血压的发生发展过程中起重要作用。对了解病情,判断预后有一定临床意义。     

高血压与左心室肥厚

心脏是高血压的一个主要靶器官。一方面,高血压导致以左心室肥厚(LVH)为主要特征的心脏病变;另一方面,高血压引起冠状动脉粥样硬化,这两种情况使心脏疾病成为高血压的主要并发症和死亡原因,包括充血性心力衰竭、心肌梗塞、严重心律失常、猝死等。本文着重从临床角度对高血压性左心室肥厚予以论述。     

Multiple left ventricular thrombi in a patient with left ventricular noncompaction

The major clinical features of myocardial noncompaction are heart failure, arrhythmias, and thromboembolic events. Prominent myocardial trabeculae and deep recesses characteristic of myocardial noncompaction can cause stagnant blood flow and the formation of left ventricular clots. We describe the case of a 62-year-old woman who presented with symptoms of heart failure secondary to left ventricular noncompaction. Transthoracic and transesophageal echocardiography revealed multiple left ventricular thrombi, which had formed despite the patient's long-term therapy with aspirin.Anticoagulative therapy should be considered for patients with myocardial noncompaction who also have risk factors for thromboembolism, such as atrial fibrillation, a history of systemic embolism, or severe left ventricular systolic dysfunction. However, chronic antiplatelet therapy may not sufficiently prevent clot formation in patients who have myocardial noncompaction and severe left ventricular systolic dysfunction.     

Isolated left ventricular noncompaction mimicking ventricular mass

Isolated left ventricular noncompaction is an inherited cardiomyopathy characterized by multiple prominent trabeculations with deep intertrabecular recesses. The diagnosis is often missed because echocardiography poses inherent problems of poor echo window in assessment of the LV apex, which is most commonly involved in noncompaction. We report a case in which conventional 2D echocardiography failed to demonstrate multiple prominent trabeculations. Contrast echocardiography confirmed the presence of multiple trabeculations with deep intertrabecular recesses. This report emphasizes the importance of contrast echocardiography in the diagnosis of ventricular noncompaction.     

Impaired left ventricular functional reserve in hypertensive patients with left ventricular hypertrophy

To determine whether patients with hypertension and especially those with left ventricular hypertrophy have subtle changes in cardiac function, we measured the increase in left ventricular ejection fraction and in systolic blood pressure to end-systolic volume index ratio with exercise in 40 hypertensive patients and 16 age-matched normotensive volunteers. Twenty-two hypertensive patients without hypertrophy had normal end-systolic wall stress at rest and exercise responses. In contrast, the 18 patients with echocardiographic criteria for left ventricular hypertrophy demonstrated a significant increase in end-systolic wall stress at rest compared with normal subjects (69 +/- 16 vs. 55 +/- 15 10(3) x dyne/cm2, p less than 0.05) despite having normal resting left ventricular size and ejection fraction. In patients with left ventricular hypertrophy, the increase in ejection fraction with exercise was less than in the normotensive control subjects (7 +/- 7 vs. 12 +/- 8 units, p less than 0.05), and delta systolic blood pressure to end-systolic volume with exercise was reduced (3.3 +/- 3.8 vs. 8.3 +/- 7.7 mm Hg/ml/m2, p less than 0.05). The hypertensive patients with hypertrophy displayed a shift downward and to the right in the relation between systolic blood pressure to end-systolic volume ratio and end-systolic wall stress compared with control subjects and hypertensive patients without left ventricular hypertrophy. Thus, hypertensive patients with left ventricular hypertrophy by echocardiography and normal resting ejection fraction exhibit abnormal ventricular functional responses to exercise. This finding may have implications in identifying patients at higher risk for developing heart failure.     

Subacute left ventricular rupture supported with a percutaneous left ventricular assist device

Cardiac rupture is a fatal complication of transmural myocardial infarction that is associated with high mortality. We describe the successful management of a case of subacute cardiac rupture and cardiogenic shock supported by a percutaneous left ventricular assist device (LVAD) as a bridge to surgery.     

Salmonella-infected left ventricular thrombus

A 64-year-old man had an anterior AMI in 1996 leaving him withan ejection fraction of 40% but symptom free on treatment withACE-inhibitor. In