(Circulation. 2005;111:125-126.)
© 2005 American Heart Association, Inc.
Editorial |
From the Division of Cardiology, Virginia Commonwealth University at Medical College of Virginia, Richmond.
Correspondence to Dr George W. Vetrovec, 1200 E Broad St, PO Box 980036, Richmond, VA 23298-0036. E-mail gvetrove@hsc.vcu.edu
Key Words: Editorials ischemia lesion stents plaque
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Death and myocardial infarction rates have been reduced significantly with the enhanced management of cardiovascular risk factors. Thats the good news. Conversely, a significant risk for subsequent adverse ischemic events remains, particularly after acute coronary syndromes (ACS). This risk of recurrent ischemic events appears to be highest early after the ACS event, decreasing over time to that of chronic stable angina by 6 to 12 months. The cause of increased events is a composite of disease progression, especially in the culprit vessel in the absence of intervention, but it also involves nonculprit lesions that appear to have a variable risk of progression.
See p 143
Much has been learned about the potential risk of late recurrent events. Vulnerable plaques,1 often in multiple lesions and vessels, have been described in patients with ACS via different imaging modalities, including plaque rupture as seen on intravascular ultrasound, increased plaque temperature, angioscopic descriptions of plaque disruption with intracoronary thrombus,2,3 and morphological markers identified by coronary angiography. Associated with these morphological definitions of plaque instability have been the systemic patient markers of inflammation,4 best described by C-reactive protein,5 which is a significant predictor of late adverse ischemic events.
Although all of the described markers have been associated with lesion instability, leading to an increased risk of late ischemic outcomes, the impact of therapeutic interventions has been harder to define. Late event rates appear to be related to lesion and clinical markers, suggesting the existence of a definable patient group with increased risk. The benefits of
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