Kodama-Takahashi Koji, Kurata Akira, Ohshima Kiyotaka, Yamamoto Kozo, Uemura Shigeki, Watanabe Seiichiro, Iwata Takeru
Department of Internal Medicine, Yawatahama General Hospital, Japan.
Chest. 2003 Apr;123(4):1161-9. doi: 10.1378/chest.123.4.1161.
This study assessed whether the antiplatelet agent cilostazol, which has potent cyclic nucleotide phosphodiesterase type-3 inhibitory activity, affects the ventricular escape rate and neurohumoral factors in patients with third-degree atrioventricular block.
Prospective, but nonrandomized, study.
Cardiology division of an acute care hospital.
We studied 12 patients with third-degree intra-His or infra-His atrioventricular block who were in functional class II or III of the New York Heart Association classification. None of the patients had experienced Adams-Stokes attacks.
These patients were given cilostazol orally at a dose of 200 mg daily for at least 1 week.
Before and after treatment with cilostazol, continuous 24-h ECG monitoring and measurement of plasma natriuretic peptide concentrations were performed. Cilostazol significantly increased the mean (+/- SEM) total 24-h QRS count from 57,300 +/- 2,800 to 74,400 +/- 3,200 beats (p = 0.001) and significantly decreased the maximum geometric mean R-R interval over a 24-h period from 1,900 ms (95% confidence interval [CI], 1,700 to 2,100 ms) to 1,600 ms (95% CI, 1,400 to 1,900 ms; p = 0.02), although none of the patients showed the abolishment of the atrioventricular conduction abnormalities. The total 24-h count of premature ventricular beats was not different before treatment (15 beats; 95% CI, 5 to 44 beats) and after treatment (12 beats; 95% CI, 5 to 30 beats; p = 0.57). Treatment with cilostazol significantly decreased the concentration of plasma atrial natriuretic peptide from 88 pg/mL (95% CI, 49 to 160 pg/mL) to 51 pg/mL (95% CI, 32 to 80 pg/mL; p = 0.007) and of brain natriuretic peptide from 166 pg/mL (95% CI, 71 to 389 pg/mL) to 77 pg/mL (95% CI, 30 to 178 pg/mL; p = 0.02).
Cilostazol significantly increased the ventricular escape rate and significantly decreased the level of circulating natriuretic peptides. Thus, cilostazol could be safely given to selected patients over the short term with third-degree atrioventricular block.
本研究评估具有强效3型环核苷酸磷酸二酯酶抑制活性的抗血小板药物西洛他唑是否会影响三度房室传导阻滞患者的心室逸搏率和神经体液因子。
前瞻性但非随机研究。
一家急症医院的心脏病科。
我们研究了12例希氏束内或希氏束下三度房室传导阻滞患者,他们属于纽约心脏协会心功能分级的II级或III级。所有患者均未发生阿-斯综合征发作。
这些患者口服西洛他唑,剂量为每日200mg,至少服用1周。
在西洛他唑治疗前后,进行了24小时连续心电图监测和血浆利钠肽浓度测定。西洛他唑显著增加了24小时平均(±标准误)QRS波总数,从57300±2800次增加到74400±3200次(p = 0.001),并显著缩短了24小时内最大几何平均R-R间期,从1900毫秒(95%置信区间[CI],1700至2100毫秒)降至1600毫秒(95%CI,1400至1900毫秒;p = 0.02),尽管没有患者的房室传导异常消失。治疗前室性早搏的24小时总数(15次;95%CI,5至44次)与治疗后(12次;95%CI,5至30次;p = 0.57)无差异。西洛他唑治疗显著降低了血浆心房利钠肽浓度,从88pg/mL(95%CI,49至160pg/mL)降至51pg/mL(95%CI,32至80pg/mL;p = 0.007),以及脑利钠肽浓度,从166pg/mL(95%CI,71至389pg/mL)降至77pg/mL(95%CI,30至178pg/mL;p = 0.02)。
西洛他唑显著提高了心室逸搏率,并显著降低了循环利钠肽水平。因此,对于选定的三度房室传导阻滞患者,短期内可安全给予西洛他唑。