Is slow coronary flow associated with inflammation?
Cardiologists are familiar with the phenomenon of slow progression of angiographic contrast in the coronary arteries in the absence of stenosis in the epicardial vessels in some patients presenting with chest pain. This phenomenon is called as coronary slow flow phenomenon, and firstly described in 1972, while it remains scantily studied. The pathophysiological mechanisms of coronary slow flow phenomenon remain uncertain. Several hypotheses however, have been suggested for slow coronary flow phenomenon, including a form of early phase of atherosclerosis, small vessel dysfunction, Hagen-Poiseuille's equation model, imbalance between vasoconstrictor and vasodilatory factors, and platelet function disorder. More recently, there has been mounting evidence that inflammation plays an important role in the initiation, development as well as evolution of atherosclerosis, suggesting that atherosclerosis is an inflammation disease. New evidence has also indicated that inflammation may be involved in the development of slow coronary flow phenomenon. Coronary slow flow phenomenon is an important clinical entity because it may be the cause of angina at rest or during exercise, acute myocardial infarction, and hypertension. Despite the good prognosis of this kind of patients, the chronic, frequent nature of the persistent uncomfortable chest can significantly impair the quality of life. Whether this is really a new kind of coronary disease involving in inflammation, however, is still unknown and deserves further investigation.
Li
Jian-Jun
JJ
Center for Diagnosis and Treatment of Coronary Artery Disease, Fu Wai Hospital, Department of Cardiology, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing 100037, PR China. lijnjn@yahoo.com.cn
Xu
Bo
B
Li
Zi-Cheng
ZC
Qian
Jie
J
Wei
Bing-Qi
BQ
D000792:Angiography / Q000379:methods; D000818:Animals; D001783:Blood Flow Velocity; D002318:Cardiovascular Diseases / Q000473:pathology; D003327:Coronary Disease / Q000473:pathology; D006801:Humans; D007249:Inflammation / Q000473:pathology*; D008954:Models, Biological; D008962:Models, Theoretical