June 4, 2003Circulation206 citations
Intravascular Ultrasound Analysis of Infarct-Related and Non–Infarct-Related Arteries in Patients Who Presented With an Acute Myocardial Infarction
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Key Result
Culprit lesions in AMI patients had significantly more thrombus (23.7% vs 3.4% in nonculprit IRA plaques; P=0.0011) and positive remodeling (79.4% vs 59.0%; P=0.0155), indicating local instability.
Study Design
Type
Observational (n=38)
Structured PICO
Does IVUS analysis reveal different plaque morphologies and markers of instability in culprit lesions compared to nonculprit and non-infarct-related lesions in patients with AMI?
P
Population
38 consecutive patients presenting with acute myocardial infarction (AMI)
I
Intervention
Intravascular ultrasound (IVUS) analysis of culprit lesions in infarct-related arteries
C
Comparator
IVUS analysis of nonculprit lesions in infarct-related arteries, non-infarct-related arteries, and a control group of chronic stable angina patients
O
Outcome
Plaque morphology and markers of instability (thrombus, echogenicity, lesion length, external elastic membrane area, plaque plus media area, lumen area, positive remodeling, plaque rupture/dissection)surrogate
In patients with AMI, markers of plaque instability such as thrombus, positive remodeling, and large plaque mass are predominantly localized to culprit lesions rather than being diffusely present throughout the coronary tree.
Main Result
Absolute Event Rate: 23.7% vs 3.4%
p-value: p=0.0011
Abstract
BACKGROUND: Previous studies have reported diffuse destabilization of atherosclerotic plaques in acute myocardial infarction (AMI). METHODS AND RESULTS: We used intravascular ultrasound (IVUS) to assess 78 coronary arteries (38 infarct-related arteries IRAs with culprit and nonculprit lesions and 40 non-IRAs) from 38 consecutive AMI patients. IVUS analysis included qualitative and quantitative measurements of reference and lesion external elastic membrane (EEM), lumen, and plaque plus media (P P=0.0011). Culprit lesions were predominantly hypoechoic (63.2% versus 37.9% of nonculprit IRA plaques and 28.1% of non-IRA plaques; P=0.0022). Culprit lesions were longer (17.5+/-10.1, 9.8+/-4.0, and 10.3+/-5.7 mm, respectively; P<0.0001), had larger EEM area (15.0+/-6.0, 11.5+/-5.7, and 12.6+/-5.6 mm2, respectively; P=0.0353) and P P<0.0001), smaller lumens (2.0+/-0.9, 4.1+/-3.1, and 3.4+/-2.5 mm2, respectively; P=0.0009), and more positive remodeling (79.4%, 59.0%, and 50.8%, respectively; P=0.0155). The frequency of plaque rupture/dissection was greater in culprit, nonculprit IRA, and non-IRA plaques in AMI patients than in a control group of chronic stable angina patients with multivessel IVUS imaging. CONCLUSIONS: Culprit plaques have more markers of instability (thrombus, positive remodeling, and large plaque mass); however, these markers of instability are not typically found elsewhere. This suggests that the vascular event in AMI patients is determined by local pre-event lesion morphologies.
Cite This Study
Kotani et al. (2003) conducted an observational in Acute Myocardial Infarction (n=38). Intravascular ultrasound (IVUS) of culprit lesions vs. IVUS of nonculprit infarct-related artery (IRA) and non-IRA plaques was evaluated on Presence of thrombus (p=0.0011). Culprit lesions in AMI patients had significantly more thrombus (23.7% vs 3.4% in nonculprit IRA plaques; P=0.0011) and positive remodeling (79.4% vs 59.0%; P=0.0155), indicating local instability.