Abdominal angina often has a one-year delay between symptoms and treatment, leading to complications like malnutrition or bowel infarction. Abdominal angina is more prevalent in females with a 3:1 ratio, and the average age of onset is 60 years. Abdominal angina was first described by Dr. Baccelli in 1918 as lower abdominal pain after eating.
Abdominal angina usually starts 30 minutes after eating and persists for one to three hours. Individuals typically express the pain as a dull ache by clenching their fists over the epigastrium (Levine sign).[3]
Sometimes people may reduce their caloric intake in an attempt to decrease pain which can lead to weight loss. There may also be changes in bowel habits, most commonly diarrhea from malabsorption or rarely constipation.[3]
Approximately 82% of those with abdominal angina have diabetes. Hyperlipidemia, which frequently causes peripheral vascular disease, raises the risk of abdominal angina by 70% and correlates with the atherosclerotic aspect of the disease process. Smoking plays a part in the development of abdominal angina. Smokers account for 75% to 80% of all abdominal angina cases. Age also plays a role. The average age of onset is more than 60. This data corresponds with the vascular damage that occurs with age. Gender appears to play a role in the development of abdominal angina. Women are threefold more likely to develop abdominal angina than men. Hypertension is another known risk factor. Six out of ten of those with abdominal angina will be hypertensive.[9]
The celiac, superior mesenteric, and inferior mesenteric arteries are the three primary blood vessels that support the digestive tract. Abdominal pain happens because the digestive processes require increased blood flow to the stomach. The stenotic or occluded artery cannot give adequate blood flow. The pain is caused by ischemia of the affected tissues, which do not receive the essential perfusion to preform digestion.[7]
The gastrointestinal system has significant collateral circulation, which may worsen in cases of vascular stenosis. Along with the protection provided by collateral blood flow, the colon possesses various other mechanisms to prevent ischemia, such as opening of all mesenteric capillaries, redistribution of intramural blood supply, and improved oxygen extraction. But if those are exceeded, these defensive mechanisms become overwhelmed and no longer provide protection.[8]
Some people with a single-vessel lesion experience symptoms, while others with up to three lesions are asymptomatic; hence, the number of arteries required to cause symptoms of ischemia is debatable. The occurrence of angina is determined by factors besides the number of arteries affected, such as the location of the lesion, the time of advancement of the lesions, and concurrent disorders that impact angiogenesis.[8]
Abdominal angina is treated differently based on the severity and cause. Antibiotics are often used in the case of colonic ischemia as there is often cooccuring infections. When possible the underlying cause of abdominal angina may be treated. This includes medications to treat heart failure, hypertension, dysrhythmia, or hyperlipidemia.[13]
The most effective treatment for chronic mesenteric ischemia is surgical revascularization and percutaneous treatment such as stents.[12] Surgical treatment may include transaortic endarterectomy of the effected arteries or creating a retrograde or anterograde bypass in the arteries.[14]
Similarly to other vascular disorders, abdominal angina can be slowly progressive. There is often a one-year delay between the onset of symptoms and treatment. Complications of abdominal angina such as malnutrition or bowel infarction can cause increased morbidity and mortality in this population.[4][15]
Epidemiology and history
The prevalence of abdominal angina is unknown. It is more prevalent in females than males with a ratio of 3:1. The mean age of those affected is 60 years old.[4]
The term "abdominal angina" was first used by Dr. Baccelli in 1918. He used the term to describe a group of patients who had developed lower abdominal pain after eating. In 1936 Dunphy made the connection between abdominal angina and gastrointestinal necrosis. 21 years later Mikkelson introduced a surgery which could help restore blood flow to the gastrointestinal system. Although there was early interest in research, there has been very little subsequent research in the years following.[16]
van Bockel, J.Hajo; Geelkerken, Robert H.; Wasser, Martin N. (February 2001). "Chronic splanchnic ischaemia". Best Practice & Research Clinical Gastroenterology. 15 (1). Elsevier: 99–119. doi:10.1053/bega.2001.0158. ISSN1521-6918. PMID11355903.
