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目的:观察醛固酮拈抗剂——螺内酯(spironolactone)对急性心肌梗塞(AMI)患者早期血清Ⅰ型前胶原 (procollagcn I．PCI)端肽,Ⅲ型前胶原(PCⅢ)端肽含量的影响,探讨螺内酯能否抑制AMI后胶原合成以及阻抑 AMI后早期左室重塑。方法:44例AMI未经静脉溶栓或溶栓未成功的患者随机分为常规治疗组11例,螺内酯组17 例,卡托普利组16例,采用放射免疫法测44例患者发病后1周、4周血清Ⅰ型前胶原氨基末端肽(PINP)和Ⅲ型前 胶原氨基末端肽(PⅢNP)含量,超声心电图测左室舒张末期内径,室间隔厚度,左室后壁厚度,计算左室重量。结 果:①AMI后4周,螺内酯组血清PⅠNP,PⅢNP含量显著低于常规治疗组(P<0．05)．而Ⅰ／Ⅲ高于常规治疗且 与卡托普利组无明显差异;②螺内酯组治疗21天后其血清PⅠNP,PⅢNP及左室重量,左室舒张末期内径均较治疗 前下降,而Ⅰ／Ⅲ比值升高(P<0．05);③AMI后28天血清PⅢNP含量与左室重量,左室舒张末期内径呈正相关 (r=0．711、P<0．01,r=0．480、P<0．01)。结论:螺内酯可以抑制AMI后PC Ⅰ、PCⅢ合成,从而减轻左室重量, 抑制心室腔扩张,阻抑AMI后早期左室重塑,其效果与血管紧张素转换酶抑制剂卡托普利相近。
OBJECTIVE: To investigate the effect of aldosterone antagonist spironolactone on serum procollagen Ⅰ end-peptide and procollagen Ⅲ end-peptide levels in patients with acute myocardial infarction (AMI) Spironolactone can inhibit collagen synthesis after AMI and inhibit AMI after early left ventricular remodeling. Methods: Forty-four AMI patients without intravenous thrombolysis or unsuccessful thrombolysis were randomly divided into routine treatment group (n = 11), spironolactone group (n = 17) and captopril group (n = 16) Week, the content of serum type Ⅰ procollagen aminopeptidase (PINP) and type Ⅲ procollagen aminoterminal peptide (PⅢNP), the left ventricular end-diastolic diameter, the thickness of interventricular septum and the thickness of left ventricular posterior wall by echocardiography, weight. Results: ① At 4 weeks after AMI, the contents of PⅠNP and PⅢNP in spironolactone group were significantly lower than those in the conventional treatment group (P <0.05). The serum levels of PⅠNP, PⅢNP, left ventricular mass and left ventricular end-diastolic diameter in spironolactone group decreased compared with that before treatment, while Ⅰ / Ⅲ was higher than conventional treatment and no significant difference with captopril group. (P <0.05). (3) Serum PⅢNP levels at 28 days after AMI were positively correlated with left ventricular mass and left ventricular end diastolic diameter (r = 0.711, P <0.01, r = 0.480, P <0.01). CONCLUSIONS: Spironolactone can inhibit the synthesis of PC Ⅰ and PC Ⅲ after AMI, so as to reduce the weight of left ventricle, inhibit the expansion of ventricular cavity and inhibit the early left ventricular remodeling after AMI. The effect is similar to that of captopril, an angiotensin converting enzyme inhibitor.