Riccardi M, Pagnesi M, Sciatti E, Lombardi C M, Inciardi R M, Metra M, Vizzardi E
Department of Medical and Surgical Specialties, Radiological Sciences, and Public Health, Cardiology Unit, University of Brescia, Spedali Civili Di Brescia, 23123, Brescia, Italy.
Heart Fail Rev. 2023 Jan;28(1):137-148. doi: 10.1007/s10741-022-10251-9. Epub 2022 Jun 1.
Patients with heart failure (HF) often have pulmonary hypertension (PH), which is mainly post-capillary; however, some of them also develop a pre-capillary component. The exact mechanisms leading to combined pre- and post-capillary PH are not yet clear, but the phenomenon seems to start from a passive transmission of increased pressure from the left heart to the lungs, and then continues with the remodeling of both the alveolar and vascular components through different pathways. More importantly, it is not yet clear which patients are predisposed to develop the disease. These patients have some characteristics similar to those with idiopathic pulmonary arterial hypertension (e.g., young age and frequent incidence in female gender), but they share cardiovascular risk factors with patients with HF (e.g., obesity and diabetes), with both reduced and preserved ejection fraction. Thanks to echocardiography parameters and newly introduced scores, more tools are available to distinguish between idiopathic pulmonary arterial hypertension and combined PH and to guide patients' management. It may be hypothesized to treat patients in whom the pre-capillary component is predominant with specific therapies such as those for idiopathic pulmonary arterial hypertension; however, no adequately powered trials of PH-specific treatment are available in combined PH. Early evidence of clinical benefit has been proven in some trials on phosphodiesterase type 5 inhibitors, while data on prostacyclin analogues, endothelin-1 receptor antagonists, and soluble guanylate cyclase stimulators are still controversial.
心力衰竭(HF)患者常伴有肺动脉高压(PH),主要为毛细血管后性肺动脉高压;然而,其中一些患者也会出现毛细血管前性肺动脉高压成分。导致毛细血管前和毛细血管后性肺动脉高压合并存在的确切机制尚不清楚,但这种现象似乎始于左心压力升高向肺部的被动传导,然后通过不同途径继续发展为肺泡和血管成分的重塑。更重要的是,尚不清楚哪些患者易患该病。这些患者具有一些与特发性肺动脉高压患者相似的特征(如年轻、女性发病率高),但他们与心力衰竭患者有共同的心血管危险因素(如肥胖和糖尿病),包括射血分数降低和保留的患者。得益于超声心动图参数和新引入的评分,现在有更多工具可用于区分特发性肺动脉高压和合并性肺动脉高压,并指导患者的管理。可以假设,对于毛细血管前性肺动脉高压成分占主导的患者,采用针对特发性肺动脉高压的特定疗法进行治疗;然而,在合并性肺动脉高压中,尚无足够大样本量的肺动脉高压特异性治疗试验。在一些关于5型磷酸二酯酶抑制剂的试验中已证实有早期临床获益证据,而关于前列环素类似物、内皮素-1受体拮抗剂和可溶性鸟苷酸环化酶刺激剂的数据仍存在争议。