Hepatic artery thrombosis (HAT) and other vascular comIn patients with a history of cigarette smoking, incidence of vascular complications was higher than in those without history of cigarette smoking (17.8% v 8%, P ؍ .02). Having quit cigarette smoking 2 years before liver transplantation reduced the incidence of vascular complications by 58.6% (24.4% v 11.8%, P ؍ .04). The incidence of arterial complications was also higher in patients with a history of cigarette smoking compared with those without such history (13.5% v 4.8%, P ؍ .015). Cigarette smoking cessation for 2 years also reduced the risk of arterial complications by 77.6% (21.8% v 5.9%, P .)500.؍ However, the incidence of venous complications was not associated with cigarette smoking. Furthermore, there was no significant association between development of vascular complications and all other characteristics studied. Cigarette smoking is associated with a higher risk for developing vascular complications, especially arterial complications after liver transplantation. Cigarette smoking cessation at least 2 years before liver transplantation can significantly reduce the risk for vascular complications. Cigarette smoking cessation should be an essential requirement for liver transplantation candidates to decrease the morbidity C hanges in coagulation after successful liver transplantation (LT) include a tendency toward a hypercoagulable state leading to an increased incidence of vascular complications. Such changes have been known and studied in animals and humans for more than 30 years. 1,2 In particular, hepatic artery thrombosis (HAT) and other vascular complications (hepatic artery stenosis [HAS], portal vein thrombosis [PVT] and deep vein thrombosis [DVT]) remain devastating complications after LT. 2,3 The reported incidence of HAT is estimated to be 25% in living related allografts, 4 10% to 25% in pediatric cadaver liver recipients, 5-8 2.6% to 20% in adult cadaver liver recipients, 9 and as high as 30% in children younger than 1 year old. 10 Early onset HAT usually develops within the first 2 months, 11,12 especially the first 5 days after LT. 13 Clinical presentations include acute, massive hepatic necrosis leading to fulminant hepatic failure, relapsing bacteremia with recurrent biliary sepsis from cholangitis, biliary tract ischemia leading to bile duct necrosis and leaks, and asymptomatic presentation with normal liver function tests. 7,14,15 HAT occurring early after LT is more likely to be associated with an aggressive course and higher rate of allograft loss in comparison to late onset HAT (beyond 2 months after LT). 11,14 Some evidence suggests that a prompt and accurate diagnosis by duplex ultrasonography [16][17][18][19] with confirmation by hepatic artery angiography 20 or exploratory laparotomy, followed by urgent allograft rescue modalities (e.g., interventional radiology, surgical and medical therapy) can provide temporary or permanent support, avoiding higher morbidity and mortality from retransplantation. 21,22 The repo...