Department of Cardiology, Congenital Heart Diseases and Electrotherapy, Silesian University of Medicine, Zabrze, Poland.
Kardiol Pol. 2011;69(10):1043-51.
The concept of cardiac resynchronisation therapy (CRT) is based on biventricular pacing in symptomatic, chronic heart failure (HF) patients with systolic left ventricular (LV) dysfunction and QRS ≥ 120 ms. The response to CRT is determined by clinical and echocardiographic parameters. The change of biochemical status (e.g. natriuretic peptides or metalloproteinase levels) caused by CRT is not well explored.
To analyse the clinical and haemodynamic changes caused by CRT in relation to patients' biochemical status and to assess factors determining a favourable response to CRT.
Fifty patients with chronic systolic HF (NYHA IV: two patients), wide QRS complex (160 ± 31 ms) and reduced LV ejection fraction (26 ± 5.8%) under optimal pharmacotherapy, who underwent CRT, were enrolled. Data on NT-proBNP and C-reactive protein serum levels, as well as standard echocardiography with tissue Doppler measurements, were collected before CRT and after six months of pacing. The levels of matrix metalloproteinase-9 (MMP-9) were assessed in a subgroup of 18 patients. Patients were regarded as responders if LV end-systolic volume decreased by 10% compared to baseline.
Thirty five (70%) patients responded favourably to CRT. Cardiac resynchronisation therapy resulted in an improvement of max. ventilatory oxygen uptake (12.9 ± 3.8 vs 16.6 ± 4.7 mL/kg/min; p < 0.05), a of NT-proBNP decrease (2,579 ± 2,598 vs 1,339 ± 1,088 pg/mL, p < 0.05), and decrease of atrio-, inter- and intra-LV dyssynchrony. A greater baseline dyssynchrony was observed in responders. A decrease of MMP-9 level following CRT was observed in 12 (67%) patients. Significant MMP-9 decrease was observed only in the subgroup of ischaemic HF patients (26,100 ± 7,624 pg/mL vs 23,360 ± 6,258 pg/mL; p = 0.03). In patients with MMP-9 decrease during CRT, a lower C-reactive protein concentration at baseline was observed (2.12 ± 1.6 vs 4.7 ± 4.1 mg/L). The reduction in LV end-diastolic diameter correlated with the changes in MMP-9 level (r = 51; p = 0.03). Baseline left atrial end-diastolic diameter measured in parasternal long-axis view £ 46 mm had a sensitivity of 83% and a specificity of 67% in predicting MMP-9 decrease (AUC 0.83; 95% CI 0.59-0.96).
The CRT induces favourable myocardial remodelling, resulting in NT-proBNP level decrease, improvement of regional and global biventricular function, and MMP-9 level reduction, in ischaemic HF patients. The changes of MMP-9 level may be predicted by baseline left atrial end-diastolic diameter and correlate with LV end-diastolic diameter change during CRT.
心脏再同步治疗（CRT）的概念基于双心室起搏，适用于有症状的慢性心力衰竭（HF）患者，这些患者存在左心室收缩功能障碍伴 QRS 波群≥120ms。对 CRT 的反应由临床和超声心动图参数决定。CRT 引起的生化状态变化（如利钠肽或金属蛋白酶水平）尚未得到充分探讨。
分析 CRT 引起的临床和血液动力学变化与患者生化状态的关系，并评估决定 CRT 反应的因素。
入选了 50 例接受优化药物治疗的慢性收缩性 HF（NYHA IV：2 例）、宽 QRS 波群（160±31ms）和左心室射血分数降低（26±5.8%）的患者，这些患者接受了 CRT。在 CRT 前和起搏 6 个月后，收集了 NT-proBNP 和 C-反应蛋白血清水平以及标准超声心动图和组织多普勒测量数据。在 18 例患者亚组中评估了基质金属蛋白酶-9（MMP-9）的水平。如果与基线相比 LV 收缩末期容积减少 10%，则认为患者对 CRT 有良好反应。
35 例（70%）患者对 CRT 反应良好。CRT 导致最大通气氧摄取增加（12.9±3.8 比 16.6±4.7 mL/kg/min；p<0.05）、NT-proBNP 降低（2579±2598 比 1339±1088 pg/mL，p<0.05）和房室、室间和室内不同步的改善。在有反应的患者中，基线不同步程度更大。在 12 例（67%）患者中观察到 CRT 后 MMP-9 水平降低。仅在缺血性 HF 患者亚组中观察到显著的 MMP-9 降低（26100±7624 pg/mL 比 23360±6258 pg/mL；p=0.03）。在 CRT 期间 MMP-9 降低的患者中，基线时 C-反应蛋白浓度较低（2.12±1.6 比 4.7±4.1 mg/L）。LV 舒张末期直径的减少与 MMP-9 水平的变化相关（r=51；p=0.03）。胸骨旁长轴切面测量的左心房舒张末期直径≤46mm 预测 MMP-9 降低的敏感性为 83%，特异性为 67%（AUC 0.83；95%CI 0.59-0.96）。
CRT 可诱导有利的心肌重塑，导致缺血性 HF 患者 NT-proBNP 水平降低、区域性和整体双心室功能改善以及 MMP-9 水平降低。MMP-9 水平的变化可以通过基线左心房舒张末期直径预测，并与 CRT 期间 LV 舒张末期直径的变化相关。
