TY - JOUR
T1 - Sildenafil reduces pulmonary vascular resistance in single ventricular physiology
AU - Mori, Hiroki
AU - Park, In Sam
AU - Yamagishi, Hiroyuki
AU - Nakamura, Makoto
AU - Ishikawa, Shiro
AU - Takigiku, Kiyohiro
AU - Yasukochi, Satoshi
AU - Nakayama, Tomotaka
AU - Saji, Tsutomu
AU - Nakanishi, Toshio
N1 - Funding Information:
This study was partially supported by a research grant H27-022 from Japanese Ministry of Health and Welfare , a research grant 16ek0109146h0002 from Japan Agency for Medical Research and Development , and grant-in-aid from Pfizer Inc .
PY - 2016/10/15
Y1 - 2016/10/15
N2 - Background High pulmonary vascular resistance (PVR) may be a risk factor for early and late mortality in both Glen shunt and Fontan operation patients. Furthermore, PVR may increase long after the Fontan operation. Whether pulmonary vasodilators such as phosphodiesterase 5 inhibitors can decrease PVR in patients with single ventricular physiology remains undetermined. Methods and results This was a prospective, multicenter study. Patients with single ventricular physiology who have a PVR index higher than 2.5 Wood units·㎡ (WU) were enrolled. Cardiac catheterization was performed before and after administration of sildenafil in all patients. After the Fontan operation, a six minute walk test (6 MWT) was also performed. A total of 42 patients were enrolled. PVR was significantly decreased in each stage of single ventricular physiology after sildenafil administration: from 4.3 ± 1.5 WU to 2.1 ± 0.6 WU (p < 0.01) in patients before a Glenn shunt, from 3.2 ± 0.5 WU to 1.6 ± 0.6 WU (p < 0.001) in patients after a Glenn shunt, and from 3.9 ± 1.7 WU to 2.3 ± 0.8 WU (p < 0.001) in patients after Fontan. In patients after Fontan, the 6 MWT increased from 416 ± 74 m to 485 ± 72 m (p < 0.01), and NYHA functional class improved significantly (p < 0.05) after sildenafil administration. No major side effects were observed in any patients. Conclusions Sildenafil reduced PVR in patients with single ventricle physiology. Sildenafil increased exercise capacity and improved NYHA functional class in patients after a Fontan operation. This implies that pulmonary vasodilation is a potential therapeutic target in selected patients with elevated PVR with single ventricle physiology. Long-term clinical significance warrants further study.
AB - Background High pulmonary vascular resistance (PVR) may be a risk factor for early and late mortality in both Glen shunt and Fontan operation patients. Furthermore, PVR may increase long after the Fontan operation. Whether pulmonary vasodilators such as phosphodiesterase 5 inhibitors can decrease PVR in patients with single ventricular physiology remains undetermined. Methods and results This was a prospective, multicenter study. Patients with single ventricular physiology who have a PVR index higher than 2.5 Wood units·㎡ (WU) were enrolled. Cardiac catheterization was performed before and after administration of sildenafil in all patients. After the Fontan operation, a six minute walk test (6 MWT) was also performed. A total of 42 patients were enrolled. PVR was significantly decreased in each stage of single ventricular physiology after sildenafil administration: from 4.3 ± 1.5 WU to 2.1 ± 0.6 WU (p < 0.01) in patients before a Glenn shunt, from 3.2 ± 0.5 WU to 1.6 ± 0.6 WU (p < 0.001) in patients after a Glenn shunt, and from 3.9 ± 1.7 WU to 2.3 ± 0.8 WU (p < 0.001) in patients after Fontan. In patients after Fontan, the 6 MWT increased from 416 ± 74 m to 485 ± 72 m (p < 0.01), and NYHA functional class improved significantly (p < 0.05) after sildenafil administration. No major side effects were observed in any patients. Conclusions Sildenafil reduced PVR in patients with single ventricle physiology. Sildenafil increased exercise capacity and improved NYHA functional class in patients after a Fontan operation. This implies that pulmonary vasodilation is a potential therapeutic target in selected patients with elevated PVR with single ventricle physiology. Long-term clinical significance warrants further study.
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U2 - 10.1016/j.ijcard.2016.06.322
DO - 10.1016/j.ijcard.2016.06.322
M3 - Article
C2 - 27400308
AN - SCOPUS:84978131614
SN - 0167-5273
VL - 221
SP - 122
EP - 127
JO - International Journal of Cardiology
JF - International Journal of Cardiology
ER -