Left ventricular hypertrophy: pathogenesis, detection, and prognosis.
Left ventricular hypertrophy: pathogenesis, detection, and prognosis.
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DOI：
10.1161/01.cir.102.4.470
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发表时间：
2000-07
期刊：
影响因子：
37.8
通讯作者：
B. Lorell;B. Carabello
中科院分区：
文献类型：
--
作者：
B. Lorell;B. Carabello
当心脏面临血流动力学负担时，它可以做以下补偿：(1)使用Frank-Starling机制来增加交叉桥的形成；(2)增加肌肉质量来承受额外的负荷；(3)利用神经激素机制来增加收缩能力。第一种机制的范围有限，第三种机制作为一种慢性调整是有害的。因此，增加质量在血流动力学过载的补偿中起着关键作用。这种质量的增加是由于现有的心肌细胞肥大而不是增殖，因为心肌细胞在出生后不久就会发生终末分化。为了应对主动脉狭窄或高血压等情况下的压力超负荷，肌节的平行增加会导致心肌细胞宽度增加，进而增加壁厚。这种重塑导致向心性肥厚(壁厚/腔大小的比率增加)。根据拉普拉斯定律，心肌任一区域的负荷如下：(压力×半径)/(2×壁厚)；因此，压力的增加可以通过壁厚的增加来抵消。由于收缩应力(后负荷)是射血性能的主要决定因素，因此，收缩应力的正常化有助于维持正常的射血分数，即使在需要产生高水平收缩压的情况下也是如此。1慢性主动脉瓣反流、二尖瓣反流或贫血等情况下的容量超负荷会通过肌节的串联复制和心室容量的增加而导致心肌细胞延长。这种偏心性肥厚的模式(腔扩张，壁厚/腔尺寸的比率降低)最初也是代偿性的，因此心脏可以满足维持高每搏量的需求。然而，慢性肥厚可能是有害的，因为它增加了发生心力衰竭和过早死亡的风险。本文就压力与容量超负荷型左心室肥厚的发病机制、检测、…作一综述。
When the heart faces a hemodynamic burden, it can do the following to compensate: (1) use the Frank-Starling mechanism to increase crossbridge formation; (2) augment muscle mass to bear the extra load; and (3) recruit neurohormonal mechanisms to increase contractility. The first mechanism is limited in its scope, and the third is deleterious as a chronic adjustment. Thus, increasing mass assumes a key role in the compensation for hemodynamic overload. This increase in mass is due to the hypertrophy of existing myocytes rather than hyperplasia, because cardiomyocytes become terminally differentiated soon after birth. In response to pressure overload in conditions such as aortic stenosis or hypertension, the parallel addition of sarcomeres causes an increase in myocyte width, which in turn increases wall thickness. This remodeling results in concentric hypertrophy (increase in ratio of wall thickness/chamber dimension). According to LaPlace’s Law, the load on any region of the myocardium is given as follows: (pressure×radius)/(2×wall thickness); thus, an increase in pressure can be offset by an increase in wall thickness. Because systolic stress (afterload) is a major determinant of ejection performance, the normalization of systolic stress helps maintain a normal ejection fraction even when needing to generate high levels of systolic pressure.1 Volume overload in conditions such as chronic aortic regurgitation, mitral regurgitation, or anemia engenders myocyte lengthening by sarcomere replication in series and an increase in ventricular volume. This pattern of eccentric hypertrophy (cavity dilatation with a decrease in ratio of wall thickness/chamber dimension) is also initially compensatory, such that the heart can meet the demand to sustain a high stroke volume. However, chronic hypertrophy may be deleterious because it increases the risk for the development of heart failure and premature death. This review will focus on the pathogenesis of pressure- versus volume-overload types of left ventricular hypertrophy (LVH), detection, …