Abdominal angina pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]


Abdominal angina is an unusual cause of intermittent abdominal pain.The term angina is used because the pain develops only after eating, due to diminshed arterial supply that's needed to meet the increased demands to support digestion [1]. It's due to reduced mesenteric blood flow, the reduced oxygen content of red blood cells distributed via the mesenteric arterial circulation, or mesenteric venous stasis, any of which can lead to tissue hypoxia and ischemic injury[1]


  • The pathophysiology is similar to that seen in angina pectoris and intermittent claudication.
  • Abdominal angina occurs due to narrowing of the mesenteric vessels that causes decreased blood flow.[2]
  • Atherosclerotic vascular disease at ostia of the mesenteric vessels is the most common cause of abdominal angina . Superior mesenteric artery occlusion is often found in patients presenting symptomatic occlusive mesenteric ischemia. Patients with abdominal angina are unable to increase flow in the mesenteric vessels in response to eating and that's why they develop postprandial pain.[2]
  • Low perfusion can cause intestinal injury when mesenteric perfusion pressure is reduced to about 30 mmHg or reduction of 45 mmHg in mean mesenteric arterial pressure. Physiologically, the intestine can compensate for about a 75% decrease in mesentery blood flow for 12 hours without significant injury due to vasodilation of collateral circulation and increased oxygen extraction. But after an extended period of low perfusion or hypoxemia, progressive vasoconstriction leads to diminished collateral flow and subsequently full-thickness necrosis of the intestinal wall and perforation. Reperfusion injury after ischemia can be observed due to the release of toxic byproducts of ischemic injury, free oxygen radicals, and neutrophil activation.[3]

Acute Mesenteric ischemia Pathophysiology

  • Acute mesenteric arterial embolism has usually cardiogenic origin and commonly affects the superior mesenteric artery, it can occur following atrial tachyarrhythmia, congestive heart failure, myocardial ischemia or infarction, cardiomyopathy, and ventricular aneurysm, which results in thrombus formation that can embolizes to cause ischemia. Patients with acute mesenteric arterial thrombosis commonly have an underlying atherosclerotic disease. Vasospasm in the superior mesenteric artery usually accompanies non-occlusive mesenteric ischemia secondary to cardiac failure, peripheral hypoxemia, or reperfusion injury. Rarely, vasopressors (e.g., cocaine and norepinephrine) and ergotamines may cause non-occlusive mesenteric ischemia. These agents cause vasoconstriction and decreased blood flow in the mesentery, which may result in ischemia of the bowel[4].

Chronic mesenteric ischemia Pathophysiology

  • The mesenteric circulation consists mainly of three vessels that supply blood to the small and large bowel: the celiac artery, superior mesenteric artery (SMA), and inferior mesenteric artery (IMA). Blood flow through these arteries raises within an hour post-prandially due to an increase in metabolic demand of the intestinal mucosa. Diffuse atherosclerosis, often occurring at the origin of these vessels, is the primary mechanism and accounts for 95% of Chronic mesenteric ischemia. Chronic occlusion of a single vessel allows collateral blood flow to compensate, but symptoms do not typically manifest until at least two primary vessels are occluded. Less common causes include vasculitis, fibromuscular dysplasia, and radiation.[5]


  1. 1.0 1.1 "www.sciencedirect.com".
  2. 2.0 2.1 "Abdominal Angina - StatPearls - NCBI Bookshelf".
  3. "Bowel Ischemia - StatPearls - NCBI Bookshelf".
  4. "Acute Mesenteric Ischemia - StatPearls - NCBI Bookshelf".
  5. "Chronic Mesenteric Ischemia - StatPearls - NCBI Bookshelf".