Triposkiadis F, Moyssakis I, Hadjinikolaou L, Makris T, Zioris H, Hatzizaharias A, Kyriakidis M
University of Thessaly, Faculty of Health Sciences, School of Medicine, Larissa, Greece.
Eur J Clin Invest. 1999 Nov;29(11):905-12. doi: 10.1046/j.1365-2362.1999.00563.x.
Left atrial systolic dysfunction, unexplained by altered loading conditions, has been reported in idiopathic dilated cardiomyopathy suggesting left atrial involvement in the myopathic process.
Seventeen patients with idiopathic dilated cardiomyopathy, 16 with ischemic dilated cardiomyopathy and 18 normal controls were studied with transthoracic echocardiography and cardiac catheterization. Transmitral diastolic flow was evaluated with pulsed Doppler. Left atrial volume (cm3/m2) at mitral valve opening (maximal, Vmax.), onset of atrial systole (P wave of the electrocardiogram, Vp), and mitral valve closure (minimal, Vmin. ) was determined with two-dimensional echocardiography using the biplane area-length method. The left atrial active emptying fraction (ACTEF = [Vp-Vmin.] x 100/Vp) served as an index of systolic function.
The peak early diastolic transmitral flow velocity (cm/sec) was similar in the three groups (idiopathic: 60 +/- 16, ischemic: 58 +/- 20, control: 56 +/- 22; P = NS), whereas the late diastolic transmitral flow velocity was lower but not significantly different in idiopathic compared to ischemic cardiomyopathy, and in both was lower than control (26 +/- 12 vs. 34 +/- 13 vs. 44 +/- 14, respectively; P < 0.05). Vmax. and Vp were similar in idiopathic and ischemic cardiomyopathy and greater than control (44.6 +/- 13.6 vs. 48.2 +/- 18.3 vs. 26.9 +/- 6.2; P < 0.05, and 34.6 +/- 13.4 vs. 30.8 +/- 10.9 vs. 16.7 +/- 3.7, respectively; P < 0.05). ACTEF was lower in idiopathic than in ischemic cardiomyopathy and in the latter it was similar to control (18 +/- 10% vs. 32 +/- 10% vs. 36 +/- 10%, respectively; P < 0.05). Moreover, ACTEF was inversely related to left atrial tension at end-of atrial systole both in idiopathic and in ischemic cardiomyopathy (r2 = 0.52, P = 0.001 and r2 = 0.57, P = 0.0007, respectively). However, at any given level of left atrial tension at end of atrial systole, ACTEF was lower in idiopathic than ischemic cardiomyopathy.
Left atrial systolic function is depressed in idiopathic and preserved in ischemic dilated cardiomyopathy despite similar left atrial loading conditions. This finding suggests left atrial myopathy in the former, and may be related to the differences in the response to medical treatment and clinical outcome observed between the two conditions.
特发性扩张型心肌病患者中曾有报道称,在负荷条件未改变的情况下出现左心房收缩功能障碍,提示左心房参与了肌病过程。
对17例特发性扩张型心肌病患者、16例缺血性扩张型心肌病患者和18名正常对照者进行经胸超声心动图检查和心导管检查。采用脉冲多普勒评估二尖瓣舒张期血流。使用双平面面积-长度法通过二维超声心动图测定二尖瓣开放时(最大,Vmax.)、心房收缩开始时(心电图P波,Vp)和二尖瓣关闭时(最小,Vmin.)的左心房容积(cm³/m²)。左心房主动排空分数(ACTEF = [Vp - Vmin.]×100/Vp)作为收缩功能指标。
三组患者二尖瓣舒张早期血流峰值速度(cm/秒)相似(特发性:62±16,缺血性:58±20,对照:56±22;P = 无显著性差异),然而,特发性扩张型心肌病患者二尖瓣舒张晚期血流速度低于缺血性扩张型心肌病患者,但差异无统计学意义;两者均低于对照组(分别为26±12、34±22和44±14;P < 0.05)。特发性和缺血性心肌病患者的Vmax.和Vp相似且高于对照组(分别为44.6±13.6、48.2±18.3和26.9±6.;P < 0.05,以及分别为34.6±13.4、30.8±10.9和均低于对照组(分别为26±12、34±22和44±14;P < 0.05)。特发性扩张型心肌病患者的Vmax.和Vp相似且高于对照组(分别为44.6±13.6、48.2±18.3和26.9±6.2;P < 0.05,以及分别为34.6±13.4、30.8±10.9和16.7±3.7,P < 0.05)。特发性扩张型心肌病患者的ACTEF低于缺血性扩张型心肌病患者,后者与对照组相似(分别为18±10%、32±%和36±10%;P < 0.05)。此外,特发性和缺血性心肌病患者的ACTEF均与心房收缩末期的左心房张力呈负相关(r² = 0.52,P = 0.001和r² = 0.57,P = 0.0007)。然而,在心房收缩末期左心房张力的任何给定水平下,特发性扩张型心肌病患者的ACTEF均低于缺血性扩张型心肌病患者。
尽管左心房负荷条件相似,但特发性扩张型心肌病患者的左心房收缩功能降低,而缺血性扩张型心肌病患者的左心房收缩功能得以保留。这一发现提示前者存在左心房肌病,可能与两种疾病在药物治疗反应和临床结局方面观察到的差异有关。