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Am Heart J. 2010 Apr;159(4):584-92. doi: 10.1016/j.ahj.2009.12.036.

The relationship between coronary stenosis severity and compression type coronary artery movement in acute myocardial infarction.

Author information

1
Department of Cardiology, Royal Prince Alfred Hospital, Sydney, Australia.

Abstract

BACKGROUND:

Acute myocardial infarction is thought to occur at sites of minor coronary stenosis. Recent data challenge this and also propose a role for coronary artery movement (CAM) in plaque instability. We examined the relationship between coronary stenosis severity, CAM pattern, and infarct-related lesions (IRLs) in acute myocardial infarction.

METHODS:

We investigated 203 consecutive patients with ST-segment elevation myocardial infarction after successful fibrinolysis. Quantitative coronary angiography, CAM pattern, and extent score (atheroma burden) analysis was performed for each coronary artery segment.

RESULTS:

The IRL stenosis was at least moderate (>50%) and severe (>70%) in 78% and 31% of patients, respectively. Culprit arteries were associated with higher atheroma extent scores (25.2 vs 21.6, P < .001). Analysis of 2,228 coronary segments showed that stenosis severity and IRLs were highly correlated, such that the likelihood of being a culprit segment progressively increased with worsening stenosis (odds ratio [OR] 30.0, 95% confidence interval [CI] 19.0-47.6, P < .001, for >70% vs <30% stenosis). Compression CAM was also strongly associated with culprit segments (OR 3.4, 95% CI 2.6-4.5, P < .001). In addition, compression CAM and stenosis severity were strongly correlated, with the likelihood of a coronary segment having compression CAM progressively increasing with worsening stenosis (OR 56.4, 95% CI 37.9-83.8, P < .001, for >70% vs <30% stenosis).

CONCLUSIONS:

In patients with ST-segment elevation myocardial infarction, there is a strong relationship between stenosis severity and IRLs. Our study also raises the hypothesis that compression CAM may accelerate atherosclerosis and predispose to plaque vulnerability.

PMID:
20362716
DOI:
10.1016/j.ahj.2009.12.036
[Indexed for MEDLINE]

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