急性心肌梗死后溶血磷脂酸水平与心肌重塑的关系

目的　研究急性心肌梗死 (AMI)后溶血磷脂酸 (LPA)水平的变化及其与左室重塑的相关关系 ,及LPA在AMI后心肌重塑中的作用。方法　选择AMI患者 86例 ,分别于入院即刻及第 4天测定患者血浆溶血磷脂酸和Ⅲ型前胶原蛋白的水平 ,并于入院即刻和发病第 8～ 10天对患者进行心脏彩色超声的检查 ,测定左室舒张末期直径 (LVDEd)和左室射血分数 (EF) ,并计算心肌梗死占左室面积的百分比。正常对照 4 0例 ,测定其血浆溶血磷脂酸和Ⅲ型前胶原蛋白的水平。根据入院第 4天所测得的LPA水平把患者分为两组 :LPA水平较低组 (LPA <6 0 μmol/L)为A组 ,4 5例 ;LPA水平较高组(LPA≥ 6 0 μmol/L)为B组 ,4 1例 ,比较各组参数的差异性 ,分析它们的相关关系。 结果 (1)AMI后患者血溶血磷脂酸水平较正常对照明显升高 (5 1μmol/L± 1 1μmol/L和 6 4 μmol/L± 1 3μmol/Lvs 2 5μmol/L± 1 1μmol/L ,P =0 0 0 0 1) ;(2 )溶血磷脂酸水平较高组患者与溶血磷脂酸水平较低组患者相比其左室舒张末期直径较大 (5 4 0mm± 3 3mmvs 5 1 1mm± 2 7mm ,P <0 0 5 ) ,心肌梗死面积占左室总面积的百分比较高 (114 %± 6 %vs2 6 %± 12 % ,P <0 0 5 ) ,PCⅢ水平高 (136 μg/L± 10 μg/Lvs113μg/L± 12 μg/L ,P <0

The relationship between the levels of lysophosphatidic acid and left ventricular remodeling after acute myocardial infarction

OBJECTIVE: To investigate the relationship between the levels of lysophsophatidic acid (LPA) and function of left ventricular after acute myocardial infarction (AMI) and the role of LPA in ventricular remodeling and the potential mechanism. METHODS: In this study, we selected 86 patients with AMI and measured the levels of LPA and type III procollagen (PCIII) on admission and 4 day after admission, and performed echocardiographic examinations on admission and 8 approximately 10 day after admission. And according to their serum LPA value at day 4 patients were stratified into two group (group A, LPA < 6.0 micro mol/L, n = 45; group B, LPA >/= 6.0 micro mol/L, n = 41). In 40 normal individuals, level of LPA and PCIII were measured. RESULTS: (1) The patient's levels of LPA after AMI were increased (5.1 micro mol/L +/- 1.1 micro mol/L and 6.4 micro mol/L +/- 1.3 micro mol/L vs 2.5 micro mol/L +/- 1.1 micro mol/L, P = 0.0001). (2) PCIII was significantly higher in group B than that in group A (136 micro g/L +/- 10 micro g/L vs 113 micro g/L +/- 12 micro g/L, P < 0.05). Left ventricular end-diastolic diameter was significantly higher in group B than in group A (54.0 mm +/- 3.3 mm vs 51.1 mm +/- 2.7 mm, P < 0.05). (3) The elevation of LPA after AMI was closed related to the function of left ventricular (P < 0.05). CONCLUSION: The levels of LPA after AMI were increased, which may play a role in ventricular remodeling. The potential mechanism may be that LPA can stimulate cardiac myocyte hypertrophy and cardiac fibroblast proliferation and cause collagen production increasing.