Can J Cardiol:加拿大声明,心脏淀粉样变合并心衰有5特征!

2020-08-17 岱西 中国循环杂志

心脏淀粉样变性,进展快,预后差,但临床漏诊和误诊率高。为了更好诊治这种疾病, 加拿大心血管学会联合加拿大心力衰竭学会发布了一份立场声明。

心脏淀粉样变性,进展快,预后差,但临床漏诊和误诊率高。为了更好诊治这种疾病, 加拿大血管学会联合加拿大心力衰竭学会发布了一份立场声明。

心脏淀粉样变性主要有免疫球蛋白轻链型和转甲状腺素蛋白型两个亚型,后者较前者通常相对年龄大,心室壁厚,但症状轻,左心室射血分数低。

这项声明总结了患者合并心力衰竭症状和体征的 5个临床特征:

(1)无法解释的左心室壁厚度增加;

(2)60 岁以上的低流量、低压力阶差的主动脉瓣狭窄且LVEF>40%;

(3)无法解释的周围感觉运动神经病和(或)自主神经功能障碍;

(4)双侧腕管综合征病史;

(5)已确诊心外系统淀粉样变性。

当有任何这些临床特征时,需要高度怀疑心脏淀粉样变性,建议进行相关诊断检查,对于病因未明的进行性心力衰竭患者,必须高度怀疑心脏淀粉样变性可能,以免延误诊断。

建议对疑似患者行心衰常规检查,及超声心动图左心室纵向应变检查或心脏磁共振钆延迟强化显像和T1成像检查,评估有无心脏淀粉样变性特征,以及有无心衰其它病因。

心衰标准检查时提示心脏淀粉样变性的患者均应接受确诊检查(图 1)。声明建议首先需行血清/尿液蛋白电泳检查。

注:CMR:心脏磁共振成像;BNP:脑钠肽;NT-proBNP:N 末端脑钠肽前体;AL-CA:轻链淀粉样变性;ATTR-CA:转甲状腺素蛋白淀粉样变性;PYP:焦磷酸盐;hATTR:遗传型转甲状腺素蛋白型淀粉样变性;wtATTR:野生型转甲状腺素蛋白型淀粉样变性

图1 疑似 CA 诊断流程图

心内膜心肌活检仍是诊断金标准

声明建议现有无创检查结果不明确或与临床表现不符时,需要进行心内膜心肌活检,并行质谱或免疫组织化学/免疫荧光法分析,以进行诊断和分型。

心肌活检样本需行刚果红染色,偏振光显微镜观察淀粉样沉积物呈苹果绿双折射即可确诊。

鉴定亚型需要进行免疫组织化学染色、免疫荧光或激光显微切割行质谱分析。转甲状腺素蛋白淀粉样变性的诊断需要组织活检确认。

筛查时发现有单克隆免疫球蛋白的患者需行骨髓活检,以排除是否并发多发性骨髓瘤。

若心外部位活检结果阳性并且伴有心脏受累的影像学证据,无需心肌活检确诊。

确诊转甲状腺素蛋白淀粉样变性后,应进行基因测序以区分遗传型与野生型。这与预后评估、心外组织累及可能性、家系筛查以及治疗相关。一旦发现有ATTR基因突变,建议行遗传咨询。

治疗主要针对已受累靶器官和预防淀粉样蛋白进一步沉积的缓解治疗。

避免使用地高辛和钙拮抗剂

心脏淀粉样变性心衰患者对常规心衰用药耐受性差;地高辛和钙拮抗剂会增加局

部毒性风险,应避免使用;限钠和利尿仍是主要手段。

声明建议对于因淀粉样变性而致重度心力衰竭患者,如无明显心外器官累及,且预测疾病进展风险低和(或)疾病缓解治疗反应良好,可考虑进行心脏移植。

对于伴发房颤者,声明建议无论脑卒中或系统性血栓栓塞风险评分如何,无禁忌证者应常规抗凝。

高危患者使用ICD

心脏淀粉样变性患者猝死风险高,建议依据常规适应证植入 ICD 用于二级预防,用于一级预防要个体化。

抑制异常产生的游离轻链可减缓轻链淀粉样变性疾病进展。通常建议在符合条件患者中进行化疗,并可考虑行自体干细胞移植(ASCT)。

声明建议应用氯苯唑酸治疗NYHA心功能Ⅰ~Ⅲ级转甲状腺素蛋白心脏淀粉样变性患者,应用 TTR RNA 沉默剂治疗家族性淀粉样变多发性神经病患者。

声明建议定期复查BNP/NT-proBNP水平、超声心动图和心脏核磁共振,以监测患者心脏病进展和(或)对治疗的反应。

多建议每 6~48 个月和(或)临床恶化时复查超声心动图或心脏核磁共振。目前尚不建议用骨放射性示踪剂核素显像来监测疾病的进展和(或)对治疗的反应。

原始出处:Fine NM, Davis MK, Anderson K, et al. Canadian Cardiovascular Society/Canadian Heart Failure Society Joint Position Statement on the Evaluation and Management of Patients With Cardiac Amyloidosis. Can J Cardiol, 2020, 36(3)∶322-334.

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