Irregular lesion
Coronary Angiography | |
General Principles | |
---|---|
Anatomy & Projection Angles | |
Normal Anatomy | |
Anatomic Variants | |
Projection Angles | |
Epicardial Flow & Myocardial Perfusion | |
Epicardial Flow | |
Myocardial Perfusion | |
Lesion Complexity | |
ACC/AHA Lesion-Specific Classification of the Primary Target Stenosis | |
Lesion Morphology | |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
The appearence of irregular lesions with intraluminal filling defects and contrast staining is detected by coronary angiography and may indicate a fissured atherosclerotic plaque with adherent thrombus.[1]
Definition
A stenosis is classified as having irregular contour if the vascular margin is rough or has a jigged appearance and is characterized by ulceration, intimal flap, aneurysmal dilation, or “sawtooth” pattern.[2]
Feature | Definition |
Ulceration | Lesion with a small crater consisting of a discrete luminal widening in the area of the stenosis is noted, provided that it does not extend beyond the normal arterial lumen |
Intimal flap | A mobile, radiolucent extension of the vessel wall into the arterial lumen |
Aneurysmal dilation | Segment of arterial dilation larger than the dimensions of the normal arterial segment |
“Sawtooth pattern” | Multiple, sequential stenosis irregularities |
Pathophysiology
The pathophysiology of lesion irregularity is represented by pre-existing intimal disruption and/or increased turbulence and shear stresses, which lead to platelet activation causing a large transcardiac gradient of serotonin (5-hydroxy-tryptamine).[3] The resulting endothelial damage and lesion instability are associated with an increased risk of thrombotic occlusion and distal embolization.[4][5]
Grading of Lesion Irregularity
- Grade 0: Smooth – no irregularity.
- Grade 1: Mildly Irregular – lesion has an indistinct lumen edge.
- Grade 2: Sawtoothed/Grossly Irregular – lesion has defined jagged or “sawtoothed” lumen edges.
Clinical Significance
- The degree of irregularity is correlated with the risk of clinical instability in the next 10 days once the unstable features partially resolve over 5 to 10 days.[6]
- Greater irregularity of lesions are more likely to appear in the infarct-related artery than in lesions in the other coronary arteries of patients with acute infarction. and they are also related to the appearence of unstable angina.[7]
- The lesion irregularity is the second most important risk factor of diameter stenosis as a predictor of future infarction.[8]
Example
Treatment
A continued anticoagulation is already known as responsible for restabilize the coronary plaque after thrombolysis and so substantially reduce the risk of reinfarction. Due to these findings the anticoagulants may be used in patients in whom particularly irregular lesions are demonstrated by coronary angiography.[9]
References
- ↑ Davies, SW.; Marchant, B.; Lyons, JP.; Timmis, AD.; Rothman, MT.; Layton, CA.; Balcon, R. (1991). "Irregular coronary lesion morphology after thrombolysis predicts early clinical instability". J Am Coll Cardiol. 18 (3): 669–74. PMID 1869729. Unknown parameter
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ignored (help) - ↑ Ellis, SG.; Vandormael, MG.; Cowley, MJ.; DiSciascio, G.; Deligonul, U.; Topol, EJ.; Bulle, TM. (1990). "Coronary morphologic and clinical determinants of procedural outcome with angioplasty for multivessel coronary disease. Implications for patient selection. Multivessel Angioplasty Prognosis Study Group". Circulation. 82 (4): 1193–202. PMID 2401060. Unknown parameter
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ignored (help) - ↑ van den Berg, EK.; Schmitz, JM.; Benedict, CR.; Malloy, CR.; Willerson, JT.; Dehmer, GJ. (1989). "Transcardiac serotonin concentration is increased in selected patients with limiting angina and complex coronary lesion morphology". Circulation. 79 (1): 116–24. PMID 2910538. Unknown parameter
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ignored (help) - ↑ Falk, E. (1985). "Unstable angina with fatal outcome: dynamic coronary thrombosis leading to infarction and/or sudden death. Autopsy evidence of recurrent mural thrombosis with peripheral embolization culminating in total vascular occlusion". Circulation. 71 (4): 699–708. PMID 3971539. Unknown parameter
|month=
ignored (help) - ↑ Davies, MJ.; Thomas, AC.; Knapman, PA.; Hangartner, JR. (1986). "Intramyocardial platelet aggregation in patients with unstable angina suffering sudden ischemic cardiac death". Circulation. 73 (3): 418–27. PMID 3948352. Unknown parameter
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ignored (help) - ↑ Davies, SW.; Marchant, B.; Lyons, JP.; Timmis, AD.; Rothman, MT.; Layton, CA.; Balcon, R. (1990). "Coronary lesion morphology in acute myocardial infarction: demonstration of early remodeling after streptokinase treatment". J Am Coll Cardiol. 16 (5): 1079–86. PMID 2229751. Unknown parameter
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ignored (help) - ↑ Wilson, RF.; Holida, MD.; White, CW. (1986). "Quantitative angiographic morphology of coronary stenoses leading to myocardial infarction or unstable angina". Circulation. 73 (2): 286–93. PMID 3943163. Unknown parameter
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ignored (help) - ↑ Ellis, S.; Alderman, EL.; Cain, K.; Wright, A.; Bourassa, M.; Fisher, L. (1989). "Morphology of left anterior descending coronary territory lesions as a predictor of anterior myocardial infarction: a CASS Registry Study". J Am Coll Cardiol. 13 (7): 1481–91. PMID 2656822. Unknown parameter
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ignored (help) - ↑ "Randomised trial of intravenous streptokinase, oral aspirin, both, or neither among 17,187 cases of suspected acute myocardial infarction: ISIS-2. ISIS-2 (Second International Study of Infarct Survival) Collaborative Group". Lancet. 2 (8607): 349–60. 1988. PMID 2899772. Unknown parameter
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ignored (help)