Prinzmetal’s Angina, Am J Cardiology

Charles J. Glueck et al, 3/15/10

Anginal pain usually reflects reduced blood flow and oxygenation to the heart muscle due to cholesterol-laden plaques which block flow. Sometimes, however, anginal pain occurs when there is no significant plaque in the artery, and is attributed to temporary, usually intermittent spasm of the artery, thus reducing oxygenation to heart. This is a serious problem, called Prinzmetal’s angina, occasionally leading to heart attack, but more commonly causing recurrent severe anginal pain. Prinzmetal’s angina can be treated with calcium channel blocking drugs, which often provide pain relief, but not always. In the past, the cause of the coronary artery spasm has not been understood.

In their original data publication in the American Journal of Cardiology, published March 15, 2010, Dr Charles Glueck and colleagues at the Jewish Hospital Cholesterol Center have reported the following important new information:

1. Patients with Prinzmetal’s angina are much more likely than normals to have a mutation in the eNOS gene (eNOS T786C mutation), which reduces the body’s ability to process the amino acid, L-arginine, into nitric oxide (NO), the most powerful vasodilator of the coronary arteries. The result is coronary artery spasm.
2. By providing 9 g/day of over the counter L-arginine, the amino acid building block for NO, Glueck et al have reported significant symptomatic relief from Prinzmetal’s Angina, probably because more NO is being produced.
3. Understanding the cause for Prinzmetal’s Angina opens approaches to further therapies, and opens a simple, inexpensive avenue to over the counter treatment for this serious cardiac condition.