LAUSR

The risk of acute coronary syndrome (ACS) in patients with inflammatory bowel disease (IBD) has to this point not been studied prospectively. A meta-analysis of 9 retrospective studies including approximately 150 000 patients with IBD demonstrated an increase of 18% in the risk of myocardial infarction (MI) and stroke compared to the general population. This observation has been challenged by a more recent study that included more than 550 000 inpatients with IBD from a US Nationwide Database and demonstrated a significantly lower risk of MI in these patients. The etiology of ACS in the IBD population comprises 2 distinctive but potentially overlapping pathophysiological entities—ACS secondary to rupture of the atheromatous plaque in the context of coronary atherosclerosis or ACS secondary to acute intracoronary thrombosis. There is an increasing number of mainly small studies that utilized noninvasive markers of atherosclerosis, such as carotid intima-media thickness and aortic stiffness as estimated by carotid-femoral pulse wave velocity, to predict the risk of cardiovascular disease (CVD) in these patients. Several of these studies have demonstrated early changes in the arterial wall reflecting increased risk of atherosclerosis and CVD events. It has been hypothesized that chronic systemic inflammation can precipitate proatherogenic changes via the circulation of proinflammatory cytokines, such as tumor necrosis factor a and interleukin 6. These changes include endothelial dysfunction, atherogenic dyslipidemia, homocysteinemia, insulin resistance, and oxidative stress and may lead to the development of atheroma. In this issue of Angiology, Tsigkas et al report a case of MI secondary to thrombosis of the left main coronary artery in a young patient with recent acute exacerbation of ulcerative colitis. Inflammatory bowel disease is associated with a 3-fold increase in the risk of deep venous thrombosis and pulmonary embolism in adults and 2-fold risk in children and adolescents. Thrombosis has been less commonly described in the venous splanchnic circulation, such as portal vein thrombosis and acute Budd-Chiari syndrome secondary to hepatic vein thrombosis, or in the cerebral venous sinuses. Arterial thrombotic events are less common and have been described in several sites including the cerebral and coronary arteries. Reports of ACS secondary to thrombosis of the coronary arteries in the absence of atherosclerosis in patients with IBD are scarce. The risk of thromboembolism (TE) is higher in the context of acute exacerbations of IBD or in the postoperative setting and correlates with disease activity/severity. Hypercoagulability in IBD is mainly driven by the systemic inflammatory state that precipitates changes in coagulation parameters, such as increased levels of procoagulant factors, reduced levels of anticoagulant factors, defects in fibrinolysis, and alterations in platelet number and function. Inherited prothrombotic disorders, such as factor V Leiden mutation, have been also described in IBD, but there is not enough evidence to support an increased prevalence in this population. Acute phase inflammation is associated with instability of the atheromatous plaque and increased risk of ACS. The hypercoagulable state that characterizes the acute flares of IBD can result in both venous and arterial TE events, including the coronary arteries. Acute coronary syndrome, however, secondary to acute thrombosis of the coronary arteries in the absence of atheromatous plaques is very rare. Prophylactic anticoagulation is recommended in the setting of acute IBD exacerbations and in the postoperative period. Therapeutic anticoagulation therapy is required in patients with TE events, and lifelong treatment is advocated in case of recurrent episodes or concomitant prothrombotic disorders. The question as to whether patients with IBD are at increased risk of CVD remains open, but the hypothesis that patients with higher inflammatory burden, that is, severe disease activity, recurrent flares, longer disease duration, and more extensive intestinal involvement, might be at higher risk compared to patients with milder disease is plausible. The goal of reducing the risk of CVD and TE in the IBD population comprises 2 components. First, effective suppression of the underlying systemic inflammation with the use of potent anti-inflammatory strategies should aim at mucosal healing and