Department of Internal Medicine, Division of Cardiovascular and Respiratory Medicine, Akita University School of Medicine, 1-1-1 Hondo, Akita 010-8543, Japan.
J Cardiol. 2009 Oct;54(2):262-72. doi: 10.1016/j.jjcc.2009.05.012. Epub 2009 Jul 5.
Left ventricular (LV) diastolic dysfunction is related to increased cardiac sympathetic activity. We investigated the effect of cilnidipine, an L/N-type calcium channel blocker, on LV diastolic function and cardiac sympathetic activity in patients with hypertensive heart disease (HHD) using radionuclide myocardial imaging.
Thirty-two frame electrocardiography (ECG) -gated (99m)Tc-sestamibi (MIBI) myocardial single photon emission computed tomography (SPECT), and (123)I-metaiodobenzylguanidine (MIBG) imaging were performed before and 6 months after drug administration in 32 outpatients with HHD. Sixteen of the patients were treated with cilnidipine and the other 16 were treated with nifedipine retard. The parameters for assessing LV diastolic function evaluated using ECG-gated (99m)Tc-MIBI SPECT were peak filling rate (PFR), first-third filling rate (1/3FR), and time to peak filling (TPF). Cardiac sympathetic activity was assessed as early and delayed heart to mediastinum (H/M) ratios and a washout rate (WR), using (123)I-MIBG imaging. The PFR and 1/3FR significantly increased after 6 months of treatment with cilnidipine (p<0.05 for both), but did not with nifedipine retard. The H/M ratios significantly increased (p<0.05 for both) in conjunction with a decreased WR (p<0.05) in the cilnidipine group. Moreover, a significant positive correlation was seen between the rate of change in PFR and the rate of change in early and delayed H/M ratios in the cilnidipine group (p<0.05 for both). The same results were obtained for the relationship between the rate of change in 1/3FR and the rate of change in H/M ratios (p<0.05 for both). However, no such relationship was seen in the nifedipine group.
These data indicate that cilnidipine seems to suppress cardiac sympathetic overactivity via blockade of N-type calcium channels and improves LV diastolic function in patients with HHD.
左心室（LV）舒张功能障碍与心脏交感神经活动增加有关。我们通过放射性核素心肌成像研究了 L/N 型钙通道阻滞剂西尼地平对高血压心脏病（HHD）患者 LV 舒张功能和心脏交感神经活性的影响。
32 例 HHD 门诊患者在药物治疗前和治疗 6 个月后进行了 32 帧心电图（ECG）门控（99m）Tc-甲氧基异丁基异腈（MIBI）心肌单光子发射计算机断层扫描（SPECT）和（123）I-间碘苄胍（MIBG）成像。16 例患者接受西尼地平治疗，16 例患者接受硝苯地平控释片治疗。用 ECG 门控（99m）Tc-MIBI SPECT 评估 LV 舒张功能的参数为峰值充盈率（PFR）、1/3 充盈率（1/3FR）和达峰充盈时间（TPF）。用（123）I-MIBG 成像评估心脏交感神经活性为早期和延迟心脏与纵隔（H/M）比值和洗脱率（WR）。西尼地平治疗 6 个月后，PFR 和 1/3FR 显著增加（p<0.05），而硝苯地平控释片无变化。西尼地平组 H/M 比值显著增加（p<0.05），WR 降低（p<0.05）。此外，西尼地平组 PFR 变化率与早期和延迟 H/M 比值变化率呈显著正相关（p<0.05）。1/3FR 变化率与 H/M 比值变化率也呈显著正相关（p<0.05）。然而，硝苯地平组未见这种关系。
这些数据表明，西尼地平通过阻断 N 型钙通道似乎抑制了 HHD 患者的心脏交感神经过度活跃，并改善了 LV 舒张功能。
