Natural history of asymptomatic mesenteric artery occlusive disease and predictors of symptomatic progression.

OBJECTIVE

The objective of this study was to characterize the natural history of incidentally identified asymptomatic mesenteric artery stenosis and to identify clinical and radiographic predictors that differentiate patients with asymptomatic mesenteric artery occlusive disease (MAOD) and patients with symptomatic chronic mesenteric ischemia (CMI) diagnosed at the index study.

METHODS

This single-institution retrospective analysis included patients diagnosed with >70% stenosis of the celiac or superior mesenteric artery (SMA) on axial imaging or duplex ultrasound examination in an institutional radiology database. Patients were grouped into asymptomatic MAOD and symptomatic CMI cohorts according to their clinical presentation at index study. The primary end point was progression of disease from asymptomatic stenosis to CMI. Demographic, clinical, and imaging features at index study were also compared between asymptomatic and symptomatic cohorts.

RESULTS

Seventy-nine patients met the inclusion criteria, with 43 in the asymptomatic group and 36 in the symptomatic group. Patients in the asymptomatic group were followed for mean 32.7 ± 30.2 months; 60.5% (n = 26) were referred to and followed by a vascular surgeon for 21.5 ± 27.8 months. No asymptomatic patients developed symptoms during the follow-up period. All patients in the symptomatic group were evaluated by a vascular surgeon and underwent procedural intervention for CMI within 6 months of diagnosis. Patients with CMI were more likely to have a history of smoking (P = .02) and less likely to be anticoagulated (P < .01) than patients with asymptomatic MAOD. Symptomatic patients trended toward a greater prevalence of coronary artery disease (P = .06) and a lower prevalence of arrhythmia (P = .08). On imaging, the symptomatic cohort was more likely to have severe SMA stenosis (P < .001), multivessel mesenteric disease (P = .001), calcified aortic plaque (P = .01), and severe stenosis in one or both internal iliac arteries (P < .001). On multivariable analysis, a lack of anticoagulation use (P < .01) and severe SMA stenosis (P < .001) were associated independently with higher odds of symptomatic mesenteric stenosis. Although statistically insignificant, calcified aortic plaque (P = .08) and smoking history (P = .06) trended toward higher odds of symptomatic index presentation.

CONCLUSIONS

The rate of progression from asymptomatic MAOD to CMI seems to be exceedingly low in the first 2 to 3 years after diagnosis, suggesting that prophylactic revascularization is mostly unnecessary. Surveillance of asymptomatic MAOD may be personalized based on clinical and radiographic features of disease. SMA stenosis severity, anticoagulation use, and possibly smoking history and the presence of aortic plaque calcification may be promising markers to stratify the risk of ischemic progression.