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Clinical Investigations: CARDIOLOGY |

Effect of Cilostazol on the Ventricular Escape Rate and Neurohumoral Factors in Patients With Third-Degree Atrioventricular Block*

Koji Kodama-Takahashi; Akira Kurata; Kiyotaka Ohshima; Kozo Yamamoto; Shigeki Uemura; Seiichiro Watanabe; Takeru Iwata
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*From the Department of Internal Medicine, Yawatahama General Hospital, Yawatahama, Japan.

Correspondence to: Koji Kodama-Takahashi, MD, Department of Internal Medicine, Yawatahama General Hospital, 1-638 Ohira, Yawatahama-shi, Ehime 796-8502, Japan; e-mail: koji0911@sage.ocn.ne.jp



Chest. 2003;123(4):1161-1169. doi:10.1378/chest.123.4.1161
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Study objectives: 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.

Design: Prospective, but nonrandomized, study.

Setting: Cardiology division of an acute care hospital.

Patients: 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.

Interventions: These patients were given cilostazol orally at a dose of 200 mg daily for at least 1 week.

Measurements and results: 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).

Conclusions: 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.

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