心臟猝死的其他機(jī)制及其防治

　　花生四烯酸受環(huán)氧化酶作用產(chǎn)生的化合物在血管內(nèi)皮上形成前列腺素I₂（PGI₂)，同樣的化合物在血小板里卻形成血栓素（TXA₂)。兩種化合物的血管活性作用正相反，前者使血管舒張，而后者使之收縮。PGI₂還有抑制血小板凝聚的作用。若能增加PGI₂的活性，抑制TXA₂的生成，就能改善冠脈缺血狀態(tài)及預(yù)防隨著缺血伴發(fā)的心律失常。

　　阿司匹林、潘生丁、磺酰吡唑酮（Sulfinpyrazone,Auturane小板凝)、消炎痛有抑制環(huán)氧化酶的作用，所以用以抗血小板凝集治療。表5-9是幾種大系列的觀察報(bào)告。阿司匹林lg反而增加了病死率和猝死率。小劑量阿司匹林可以選擇性地抑制TXA₂而不影響PGI₂的合成，有減少病死率和猝死率的效果�；酋１冗蛲�試驗(yàn)組，共1558例心梗后25～35天患者，24個(gè)月隨訪時(shí)間，與對(duì)照組比較，猝死率在用藥組中減少43%（P<0.05)。這種差別在6個(gè)月以內(nèi)尤為明顯，而此時(shí)期正是心梗的高危階段。

表5-9 抑制血小板藥物在心肌梗死后的預(yù)防作用

　　^* 有統(tǒng)計(jì)學(xué)意義。

　�。ㄟx自Gelman & Mehta: Suddun Cardiac Death,ed by Mark E Josephson,F A Davis Co.,Philadelphia,1985,P.65)

　　心得安有改變血小板功能的作用，抑制ADP、腎上腺素、膠原、血栓素造成的血小板凝集。其機(jī)制不清楚，可能與血小板結(jié)合改變膜的性能，對(duì)促凝集物質(zhì)不敏感。臨床尚無(wú)心得安等β受體阻滯劑抑制血小板的研究報(bào)道。

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