Inflammation: a possible pathogenic link to cardiac syndrome X.
Cardiac syndrome X is defined as a typical angina pectoris, positive treadmill exercise test, negative intravenous ergonovine test and normal coronary angiography. The pathogenesis of cardiac syndrome X has previously ascribed to myocardial ischemia that may be caused by microvascular dysfunction and increased sensitivity to intracardiac pain. Despite the extensive studies, the pathophysiological mechanisms in cardiac syndrome, however, remain unclear. More recently, the data has been suggested that chronic inflammation has been associated with cardiac syndrome X. The evidence for the hypotheses included that inflammatory marker are increased, and associated with the disease activity in patients with cardiac syndrome X. And also, statin, a lipid-lowering as well as anti-inflammatory drug, has significantly modified the disease process in this special syndrome. Despite the good prognosis of cardiac syndrome X, the chronic, frequent nature of the persistent angina and reduced exercise tolerance can significantly impair quality of life. Thus, lowering inflammatory response by, for example, use of statin and/or aspirin, might improve coronary microvascular dysfunction. Whether this is a valid approach, however, is still unknown and deserves further investigation. Indeed, as mediators of inflammation are multiple, the strategy of identifying triggers and mechanisms of inflammation in each special clinical setting and directing treatment at the special triggers or to rate limiting steps in effector pathways appears more reasonable or a promising strategy.
Li
Jian-Jun
JJ
Center of Diagnosis and Treatment of Coronary Artery Disease, Fu Wai Hospital, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing 100037, People's Republic of China. lijnjn@yahoo.com.cn
Li
Yi-Shi
YS
Zhang
Yuen
Y
Gao
Zhan
Z
Li
Zheng
Z
Qian
Hai-Yan
HY
D003331:Coronary Vessels / Q000473:pathology; D006801:Humans; D007249:Inflammation / Q000150:complications*; D018836:Inflammation Mediators / Q000627:therapeutic use; D008833:Microcirculation; D017566:Microvascular Angina / Q000188:drug therapy / Q000209:etiology* / Q000503:physiopathology*
D018836:Inflammation Mediators