Risk factors[edit]
Unlike classical angina pectoris, traditional cardiovascular risk factors are not thought to be significantly associated with coronary vasospasm.[9] The exception to this is with smoking, which is known to be a modifiable risk factor for vasospastic angina.[9][10]
There are several risk factors that are thought to precipitate, or trigger, episodes of coronary vasospasm. Many of these factors work by exerting effects on the autonomic nervous system. One of the mechanisms through which this occurs is via increasing sympathetic nervous system activity. The resulting increased sympathetic outflow leads to vasoconstrictive effects on blood vessels.[9] For example, cocaine use can trigger vasospasm in coronary arteries through its actions on adrenergic receptors causing vasoconstriction.[11] Exercise, cold weather, physical activity or exertion, mental stress, hyperventilation are additional precipitating factors.[9][7]
The exact pathophysiology behind coronary vasospasm has not been elucidated. Instead, a combination of different factors has been proposed to contribute to coronary vasospasm.[12] In general, it is thought that an abnormality within a coronary artery causes it to become hyperreactive to vasoconstrictor stimuli. This abnormality can be located in one segment of the coronary artery, or it may be diffuse and present throughout the entire artery. If and when vasoconstrictor stimuli act upon the hyperreactive segment of the artery, then vasospasm can result.[9] Ultimately, when large coronary arteries undergo vasospasm, this can lead to either complete or transient occlusion of blood flow within the artery. As a result, ischemia to the tissues served by the artery can occur. Symptoms due to ischemia can follow.[13]
Some of the factors that have been proposed to contribute to coronary vasospasm include the following:[1][12]
History[edit]
Chest pain due to coronary vasospasm was described in the medical literature by Prinzmetal et al. in 1959.[2] This discovery led to this type of angina being referred to in the literature as Prinzmetal angina.[3][20] A following study further distinguished this angina from classical angina pectoris due to the fact that the results showed that the patients with chest pain due to coronary vasospasm lacked evidence of atherosclerosis on cardiac catheterization.[3][20] Angina due to coronary vasospasm is also known as variant angina.[20]
During the 70’s and 80’s, intense research[21] headed by Dr. Robert A. Chahine resulted in the delineation of Spasm's role in Prinzmetal's angina, allowing for easy identification and effective treatment.[22]