The role of inflammatory stress in acute coronary syndrome.
OBJECTIVE
To summarize current understanding of the roles of anti-inflammatory and proinflammatory mechanisms in the development of atherosclerosis and acute coronary syndrome and to postulate the novel concept of inflammation stress as the most important factor triggering acute coronary syndrome. Moreover, markers of inflammation stress and ways to block involved pathways are elucidated.


METHODS
A literature search (MEDLINE 1997 to 2002) was performed using the key words "inflammation and cardiovascular disease". Relevant book chapters were also reviewed.


METHODS
Well-controlled, prospective landmark studies and review articles on inflammation and acute coronary syndrome were selected.


METHODS
Data and conclusions from the selected articles providing solid evidence to elucidate the mechanisms of inflammation and acute coronary syndrome were extracted and interpreted in the light of our own clinical and basic research.


RESULTS
Inflammation is closely linked to atherosclerosis and acute coronary syndrome. Chronic and long-lasting inflammation stress, present both systemically or in the vascular walls, can trigger acute coronary syndrome.


CONCLUSIONS
Inflammation stress plays an important role in the process of acute coronary syndrome. Drugs which can modulate the balance of pro- and anti-inflammatory processes and attenuate inflammation stress, such as angiotensin-converting enzyme (ACE) inhibitors/angiotensin II receptor blockers, statins, and cytokine antagonists may play active roles in the prevention and treatment of acute coronary syndrome when used in addition to conventional therapies (glycoprotein IIb/IIIa receptor antagonists, mechanical intervention strategies, etc).
Shen
Cheng-xing
CX
Department of Cardiology, Zhongda Hospital, Southeast University, Nanjing 210009, China.
Chen
Hao-zhu
HZ
Ge
Jun-bo
JB
D000787:Angina Pectoris / Q000209:etiology; D001161:Arteriosclerosis / Q000209:etiology; D015415:Biomarkers / Q000097:blood; D001808:Blood Vessels / Q000503:physiopathology; D006801:Humans; D007249:Inflammation / Q000150:complications* / Q000188:drug therapy / Q000503:physiopathology; D009203:Myocardial Infarction / Q000209:etiology*; D013312:Stress, Physiological / Q000150:complications*; D013577:Syndrome
D015415:Biomarkers