■先前的研究报道,与不使用他法米米治疗的患者相比,他法米米治疗在甲状腺素运载蛋白淀粉样心肌病(ATTR-CM)患者中具有更好的预后。因此,我们旨在系统评估tafamidis治疗与ATTR-CM患者结局的相关性.
■本系统评价和荟萃分析的方案已在PROSPERO(CRD42022381985)中注册。Pubmed,OvidEmbase,Scopus,科克伦图书馆,和WebofScience被询问以确定评估tafamidis对ATTR-CM预后影响的研究,从2000年1月1日至2023年6月1日。使用随机效应模型来确定不良终点的合并风险比(RR)。此外,主要结局包括全因死亡或心脏移植,复合终点包括全因死亡,心脏移植,心脏辅助装置植入,心力衰竭恶化,和住院。
■15项研究包括2765名患者(平均年龄75.9±9.3岁;男性占83.7%),平均随访时间为18.7±17.1个月。左心室射血分数(LVEF)降低(标准平均差(SMD:-0.17;95%置信区间(CI),-0.31至-0.03;P=0.02),但在tafamidis治疗后,心室内间隔(IVS)厚度或整体纵向应变(GLS)没有显着差异。然而,亚组分析显示,野生型ATTR患者在tafamidis治疗后LVEF无明显恶化(SMD:-0.11;95%CI,-0.34~0.12,P=0.34).此外,与未接受治疗的患者相比,接受tafamidis治疗的患者发生全因死亡或心脏移植的风险降低(合并RR,0.44;95%CI,0.31-0.65;P<0.01)。亚组分析显示,tafamidis对野生型或遗传性ATTR患者的预后没有显着差异(RR,0.44;95%CI,0.27-0.73对0.21,95%CI,0.11-0.40,P=0.08)。此外,Tafamidis治疗与复合终点风险较低相关(RR,0.57;95%CI,0.42-0.77;P<0.01)。
■我们的研究结果表明,野生型ATTR患者在tafamidis治疗后LVEF没有明显恶化。此外,tafamidis治疗与全因死亡和不良心血管事件的低风险相关.
■这项工作得到了四川省自然科学基金[资助号:23NSFSC4589]和国家自然科学基金[资助号:82202248]的资助。
UNASSIGNED: Previous studies have reported that tafamidis treatment was associated with better outcomes in patients with transthyretin amyloid cardiomyopathy (
ATTR-CM) compared with those without tafamidis treatment. Therefore, we aimed to systematically assess the association of tafamidis treatment with outcomes in patients with
ATTR-CM.
UNASSIGNED: The protocol for this systematic review and meta-analysis was registered in the PROSPERO (CRD42022381985). Pubmed, Ovid Embase, Scopus, Cochrane Library, and Web of Science were interrogated to identify studies that evaluated the impact of tafamidis on prognosis in
ATTR-CM, from January 1, 2000 to June 1, 2023. A random-effects model was used to determine the pooled risk ratio (RR) for the adverse endpoints. In addition, the main outcomes included all-cause death or heart transplantation, the composite endpoints included all-cause death, heart transplantation, cardiac-assist device implantation, heart failure exacerbations, and hospitalization.
UNASSIGNED: Fifteen studies comprising 2765 patients (mean age 75.9 ± 9.3 years; 83.7% male) with a mean follow-up duration of 18.7 ± 17.1 months were included in the meta-analysis. There was a decrease in left ventricular ejection fraction (LVEF) (standard mean differences (SMD: -0.17; 95% confidence interval (CI), -0.31 to -0.03; P = 0.02) but were no significant differences in intraventricular septum (IVS) thickness or global longitudinal strain (GLS) after tafamidis treatment. However, subgroup analysis showed no significant deterioration in LVEF in the patients with wild-type ATTR after tafamidis treatment (SMD: -0.11; 95% CI, -0.34 to 0.12, P = 0.34). In addition, the group with tafamidis treatment had a decreased risk for all-cause death or heart transplantation compared to patients without treatment (the pooled RR, 0.44; 95% CI, 0.31-0.65; P < 0.01). Subgroup analysis showed that there was no significant difference of tafamidis on the outcomes in patients with wild-type or hereditary
ATTR (RR, 0.44; 95% CI, 0.27-0.73 versus 0.21, 95% CI, 0.11-0.40, P = 0.08). Furthermore, tafamidis treatment was associated with a lower risk of the composite endpoint (RR, 0.57; 95% CI, 0.42-0.77; P < 0.01).
UNASSIGNED: Our findings suggested that there was no significant deterioration in LVEF in the patients with wild-type ATTR after tafamidis treatment. In addition, tafamidis treatment was associated with a low risk of all-cause death and adverse cardiovascular events.
UNASSIGNED: This work was supported by grants from the Natural Science Foundation of Sichuan Province [Grant Number: 23NSFSC4589] and the National Natural Science Foundation of
China [Grant Number: 82202248].