Impaired subendocardial function in tachycardia-induced cardiac failure.
Impaired subendocardial function in tachycardia-induced cardiac failure.
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心动过速引起的心力衰竭中心内膜下功能受损。
DOI：
10.1152/ajpheart.1995.268.5.h1788
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发表时间：
1995
期刊：
影响因子：
--
通讯作者：
Covell,JW
中科院分区：
文献类型：
--
作者：
LeGrice,IJ;Takayama,Y;Holmes,JW;Covell,JW
慢性心室快速起搏（CRVP）在许多实验模型中诱导心室扩张，射血分数降低和症状性充血性心力衰竭。我们研究了5只汉福德迷你猪在crvp诱发心力衰竭前后左心室壁的全壁机械功能。三柱直径1mm的不透射线标记物通过正中胸骨切开术植入左室前壁。将一对左室起搏导线缝入心肌，在下腔静脉（IVC）周围放置气压袖带，在左室心尖植入两根充液硅胶导管。手术后两周，猪被吊在吊带上保持清醒，并用双翼放射照相追踪标记物。心脏起搏3周（225-240次/分钟），并在关闭起搏器的情况下重复研究。使用生理盐水输注和IVC闭塞来改变左室舒张末压（EDP），以便在匹配的左室EDP下进行控制-失效比较。采用有限元法定量计算周向（E11）、纵向（E22）和跨壁（E33）方向的收缩末期应变。心内膜下的E11和E33显著降低：E11从-0.27降至-0.18；在E33，从0.83到0.46。心内膜下E22或任何外壁正常菌株均无明显变化。这些结果表明CRVP导致心内膜下功能的显著降低，而不是心外膜下功能的显著降低；结合先前显示心内膜下灌注不足的数据，这些结果支持了血流和氧气需求之间的不平衡在该模型中心力衰竭病因学中起作用的论点。
Chronic rapid ventricular pacing (CRVP) in many experimental models induces ventricular dilatation, reduced ejection fraction, and symptomatic congestive heart failure. We have investigated transmural mechanical function in the left ventricular (LV) wall of five Hanford miniature swine before and after CRVP-induced failure. Three columns of radiopaque markers 1 mm in diameter were implanted in the anterior LV wall through a median sternotomy. A pair of LV pacing wires were sutured into the myocardium, a pneumatic cuff was placed around the inferior vena cava (IVC), and two fluid-filled Silastic catheters were implanted into the LV apex. Two weeks after surgery, the pigs were suspended awake in a sling, and markers were tracked with biplane cineradiography. The hearts were paced for 3 wk (225-240 beats/min), and the study was repeated with the pacemaker off. Saline infusion and IVC occlusion were used to vary LV end-diastolic pressure (EDP) so control-to-failure comparisons could be made at matched LV EDPs. End-systolic strains in the circumferential (E11), longitudinal (E22), and transmural (E33) directions were quantified using finite element methods. There was a significant reduction in E11 and E33 for the subendocardium: in E11, from -0.27 to -0.18; in E33, from 0.83 to 0.46. There were no significant changes in subendocardial E22 or in any of the outer wall normal strains. These results indicate that CRVP causes substantial reduction of subendocardial, but not subepicardial, function; taken together with previous data indicating subendocardial hypoperfusion, these results support the contention that an imbalance between blood flow and oxygen demand plays a role in the etiology of heart failure in this model.