Abdominal angina is defined as the postprandial pain that occurs in individuals who have mesenteric vascular occlusive disease that has advanced to the point where blood flow cannot increase enough to meet visceral demands. This mechanism is similar to that of the angina pectoris that occurs in individuals with coronary artery disease or the intermittent claudication that accompanies peripheral vascular disease.
Schnitzler first described the clinical picture of postprandial pain in 1901. However, the true description of postprandial abdominal angina is attributed to Baccelli or Goodman (1918). In 1957, Mikkelsen proposed surgical treatment of occlusive mesenteric vascular disease. Shaw and Maynard reported the first transarterial thromboendarterectomy of the superior mesenteric artery (SMA) in 1958. With the advancements in imaging technology, the degree of stenosis in mesenteric arteries can be defined accurately and treated accordingly.
Pathophysiology and Etiology
Intestinal ischemia results from the imbalance of oxygen supply to and oxygen consumption by the gastrointestinal (GI) tract. Diminished blood flow results from narrowing of the mesenteric vessels. The most common cause of abdominal angina is atherosclerotic vascular disease. It commonly involves the ostia of the mesenteric vessels. 
The three arteries supplying the gut are the celiac artery, the SMA, and the inferior mesenteric artery (IMA; see the image below). There are collaterals between the celiac artery and the SMA (pancreaticoduodenal arcades) and between the SMA and the IMA (meandering mesenteric artery). In cases of severe ostial narrowing, internal iliac arteries also serve as important sources of collateral hindgut and midgut perfusion in the presence of inferior mesenteric arterial occlusion.
SMA occlusion almost invariably is observed in patients with symptomatic occlusive mesenteric ischemia.
Within a few minutes of eating, there is increased blood flow in the celiac and superior mesenteric vessels in normal individuals. Patients with abdominal angina are unable to sufficiently increase flow in the mesenteric vessels. This leads to fear associated with eating and significant weight loss.
The etiology includes the following:
The syndrome is extremely rare, and the true incidence is unknown.
The mean age of affected individuals is slightly older than 60 years. Median arcuate ligament syndrome (see Pathophysiology and Etiology) has been reported in young individuals. In contrast to the usual male predilection of atherosclerotic vascular disease, females outnumber males by approximately 3 to 1 in most series. No data are available regarding relative incidence figures among different races.
Reocclusion is more prevalent in males than in females.
Several series have demonstrated that 86-96% of patients remain asymptomatic at 5 and 10 years, with similar graft patency rates.
Research suggests that after successful endovascular treatment, symptom relief is immediately achieved in 85% of patients. An overall morbidity of 30.8% has been reported. The most common complication has been reported to be access site hematoma/pseudoaneurysm/thrombosis (15.4%), followed by bowel infarction (4.6%). 
A retrospective review by Sundermeyer et al (N=27) found endovascular SMA treatment to be suitable and safe for patients with chronic mesenteric ischemia, though the authors noted that long-term results were limited. 
Cai et al carried out a meta-analysis comparing the clinical outcomes of endovascular revascularization for chronic mesenteric ischemia with those of open revascularization.  The two approaches were similar with regard to 30-day mortality and 3-year cumulative survival rate. The endovascular approach was associated with a lower rate of in-hospital complications but a higher rate of recurrence within the 3 years following revascularization.