Therapeutic development in cardiac syndrome X: a need to target the underlying pathophysiology.
Morbidity of patients with cardiac syndrome X (typical anginal-like chest pain and normal coronary arteriogram) is high with continuing episodes of chest pain and frequent hospital readmissions. Management of this syndrome represents a major challenge for the treating physician. Conventional therapies with antianginal agents such as nitrates, calcium channel antagonists, classic beta-adrenoceptor blockers and nicorandil have been tried, with variable success. However, this might be related to a failure to target the underlying pathophysiology and, clearly, more effective therapies are needed. Supporting evidence for the important role of endothelial dysfunction and oxidative stress in the pathogenesis of cardiac syndrome X has come from the recent observation that basal superoxide production predicts future cardiovascular events in this patient group. This review will discuss the pathophysiology, current medical management and potential new pharmacological treatment for patients with cardiac syndrome X which target endothelial dysfunction and oxidative stress. What's already known about this topic? Morbidity of patients with cardiac syndrome X is high. The important role of endothelial dysfunction and oxidative stress in the pathogenesis of cardiac syndrome X. What does this article add? This review will discuss the pathophysiology, current medical management and potential new pharmacological treatment for patients with cardiac syndrome X which target endothelial dysfunction and oxidative stress.
Lim
Tiong K
TK
Division of Medicine and Therapeutics, University of Dundee, Dundee, UK.
Choy
AnnaMaria J
AJ
Khan
Faisel
F
Belch
Jill J F
JJ
Struthers
Allan D
AD
Lang
Chim C
CC
D000818:Animals; D000975:Antioxidants / Q000627:therapeutic use*; D002317:Cardiovascular Agents / Q000627:therapeutic use*; D015928:Cognitive Behavioral Therapy; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000503:physiopathology; D015914:Estrogen Replacement Therapy; D004967:Estrogens / Q000172:deficiency; D015444:Exercise; D006801:Humans; D007249:Inflammation / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy; D007333:Insulin Resistance; D008833:Microcirculation / Q000187:drug effects; D017566:Microvascular Angina / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D017202:Myocardial Ischemia / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy; D018384:Oxidative Stress / Q000187:drug effects*; D016896:Treatment Outcome
D000975:Antioxidants; D002317:Cardiovascular Agents; D004967:Estrogens