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&M) area. Positive remodeling was defined as lesion/mean reference EEM > 1.0. Culprit lesions were identified by a combination of ECG, wall motion abnormalities (ventriculogram or echocardiogram), scintigraphic perfusion defects, and coronary angiogram. Culprit lesions contained more thrombus (23.7% versus 3.4% in nonculprit IRA plaques and 3.1% in non-IRA plaques; 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&M area (13.0±6.0, 7.5±3.7, 9.3±4.3 mm2, respectively; 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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 2889-2893 |
| Number of pages | 5 |
| Journal | Circulation |
| Volume | 107 |
| Issue number | 23 |
| DOIs | |
| State | Published - Jun 17 2003 |
| Externally published | Yes |
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Keywords
- Myocardial infarction
- Plaque
- Ultrasonics
ASJC Scopus subject areas
- Physiology
- Cardiology and Cardiovascular Medicine
Cite this
Intravascular ultrasound analysis of infarct-related and non-infarct-related arteries in patients who presented with an acute myocardial infarction. / Kotani, Jun ichi; Mintz, Gary S.; Castagna, Marco T.; Pinnow, Ellen; Berzingi, Chalak O.; Bui, Anh B.; Pichard, Augusto D.; Satler, Lowell F.; Suddath, William O.; Waksman, Ron; Laird, John R.; Kent, Kenneth M.; Weissman, Neil J.
In: Circulation, Vol. 107, No. 23, 17.06.2003, p. 2889-2893.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Intravascular ultrasound analysis of infarct-related and non-infarct-related arteries in patients who presented with an acute myocardial infarction
AU - Kotani, Jun ichi
AU - Mintz, Gary S.
AU - Castagna, Marco T.
AU - Pinnow, Ellen
AU - Berzingi, Chalak O.
AU - Bui, Anh B.
AU - Pichard, Augusto D.
AU - Satler, Lowell F.
AU - Suddath, William O.
AU - Waksman, Ron
AU - Laird, John R.
AU - Kent, Kenneth M.
AU - Weissman, Neil J.
PY - 2003/6/17
Y1 - 2003/6/17
N2 - 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&M) area. Positive remodeling was defined as lesion/mean reference EEM > 1.0. Culprit lesions were identified by a combination of ECG, wall motion abnormalities (ventriculogram or echocardiogram), scintigraphic perfusion defects, and coronary angiogram. Culprit lesions contained more thrombus (23.7% versus 3.4% in nonculprit IRA plaques and 3.1% in non-IRA plaques; 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&M area (13.0±6.0, 7.5±3.7, 9.3±4.3 mm2, respectively; 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.
AB - 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&M) area. Positive remodeling was defined as lesion/mean reference EEM > 1.0. Culprit lesions were identified by a combination of ECG, wall motion abnormalities (ventriculogram or echocardiogram), scintigraphic perfusion defects, and coronary angiogram. Culprit lesions contained more thrombus (23.7% versus 3.4% in nonculprit IRA plaques and 3.1% in non-IRA plaques; 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&M area (13.0±6.0, 7.5±3.7, 9.3±4.3 mm2, respectively; 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.
KW - Myocardial infarction
KW - Plaque
KW - Ultrasonics
UR - http://www.scopus.com/inward/record.url?scp=0037974163&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0037974163&partnerID=8YFLogxK
U2 - 10.1161/01.CIR.0000072768.80031.74
DO - 10.1161/01.CIR.0000072768.80031.74
M3 - Article
VL - 107
SP - 2889
EP - 2893
JO - Circulation
JF - Circulation
SN - 0009-7322
IS - 23
ER -