专家答疑:“金三角”能否改善舒张性心衰或右心衰预后?

2018-12-09 朱燕林、方理刚 北京协和医院心内科 中国心血管杂志

“金三角”治疗即肾素-血管紧张素系统抑制剂(血管紧张素转换酶抑制剂、血管紧张素Ⅱ受体拮抗剂,ACEI/ARB)、β受体阻滞剂和醛固酮受体拮抗剂。诸多循证医学证据确立了“金三角”治疗适用于左室射血分数(LVEF)下降的心衰患者,是治疗LVEF减低心衰患者的基石,可以降低此类患者的全因死亡、心血管死亡、猝死和心衰住院风险,但其在舒张性心衰或右心衰治疗中的作用尚需探索。

“金三角”治疗即肾素-血管紧张素系统抑制剂(血管紧张素转换酶抑制剂、血管紧张素Ⅱ受体拮抗剂,ACEI/ARB)、β受体阻滞剂和醛固酮受体拮抗剂。诸多循证医学证据确立了“金三角”治疗适用于左室射血分数(LVEF)下降的心衰患者,是治疗LVEF减低心衰患者的基石,可以降低此类患者的全因死亡、心血管死亡、猝死和心衰住院风险,但其在舒张性心衰或右心衰治疗中的作用尚需探索。

舒张性心衰即射血分数保留的心力衰竭(HFpEF),其诊断标准为左室射血分数(LVEF)50%或以上、利钠肽(BNP)升高,并合并左室肥厚和(或)左房扩大或心脏舒张功能异常。同时需要排除患者症状是由非心脏疾病引起的。在诊断不明确时,可进行超声心动图或有创检查明确左室充盈压是否升高。心房颤动、高血压、冠状动脉粥样硬化性心脏病、糖尿病、慢性肾脏疾病可以作为HFpEF的基础疾病。因基础疾病的不同,病理生理机制差异很大,对于HFpEF的患者需要注意个体化和综合性治疗。

有液体潴留的HFpEF患者应使用利尿剂治疗。TOPCAT研究亚组分析显示,螺内酯可以降低HFpEF患者的因心衰住院风险。因此,对于BNP升高或1年内因心衰住院的HFpEF患者,可考虑使用醛固酮受体拮抗剂。

针对引起HFpEF的基础疾病治疗非常重要:

--高血压是最重要及最常见的HFpEF病因,有效控制血压可以降低心衰住院、心血管事件及死亡率。

--合并冠心病的HFpEF患者应积极药物治疗或联合血运重建术。

--房颤患者控制心室率或尝试恢复并维持窦性心律。

--糖尿病患者积极治疗并有效控制血糖。

临床研究如PEP-CHF、CHARM-Preserved、I-Preserve、J-DHF等未能证实ACEI/ARB、β受体阻滞剂能改善HFpEF患者的预后和降低病死率。

新的药物沙库巴曲缬沙坦可能为HFpEF的治疗带来转机。PARAMOUNT试验表明,沙库巴曲缬沙坦可改善HFpEF患者的左心室心肌形变能力,降低N末端B型利钠肽原(NT-proBNP),缩小左房体积。在PARAMOUNT试验基础上的PARAGON-HF研究以心血管疾病死亡或心衰住院为硬终点,有望明确沙库巴曲缬沙坦在HEpEF人群中是否优于血管紧张素Ⅱ受体拮抗剂。

引起右心衰竭的病因包括伴有右室受累的原发心肌病、右心室心肌缺血和梗死、各种引起右心室容量负荷增加的疾病(先天性心脏病、瓣膜性心脏病)以及压力负荷增加的疾病(各种原因所致的肺动脉高压、肺动脉瓣狭窄)。目前尚无针对右心衰竭治疗的大规模随机临床试验,而且缺乏促进右心室功能稳定和恢复的特异性治疗。治疗原则为积极治疗导致右心衰竭的上述原发疾病,减轻右心前后负荷和增强心肌收缩力,维持心脏收缩同步性。同时纠正感染、妊娠或分娩、高原反应等诱发因素。可以选择利尿剂降低前负荷,血管活性药物改善脏器灌注。而“金三角”治疗尚缺乏改善右心衰预后的证据。

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    2019-01-02 topnew

    厉害厉害继续学习

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    2018-12-09 医者仁心5538

    学习了

    0

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    2018-12-09 ylzr123

    好文,值得点赞,更值得收藏!慢慢领会学习的。给点个赞!

    0

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关于舒张性心衰:你应该知道的

心室的收缩与舒张是心动周期中互相依赖的两个过程,收缩功能或舒张功能异常均可能使心脏排血量降低并导致心力衰竭。虽然多年以前我们便认识到左心室舒张功能异常可能是导致心脏排血量降低的一种病理生理机制,但长期以来我们更多关注的是因心室收缩功能障碍所致的收缩性心衰,而对于舒张性心衰的病理生理机制以及诊疗策略却所知很少。然而研究资料显示,在临床实践中因心室舒张功能障碍所导致的心衰占患者总数的50%左右,其