Coronary artery irregularity

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Coronary Angiography

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General Principles

Overview
Historical Perspective
Contraindications
Appropriate Use Criteria for Revascularization
Complications
Technique
Film Quality

Anatomy & Projection Angles

Normal Anatomy

Coronary arteries
Dominance
Right System
Left System
Left Main
Left Anterior Descending
Circumflex
Median Ramus

Anatomic Variants

Separate Ostia
Anomalous Origins
Fistula

Projection Angles

Standard Views
Left Coronary Artery
Right Coronary Artery

Epicardial Flow & Myocardial Perfusion

Epicardial Flow

TIMI Frame Count
TIMI Flow Grade
TIMI Grade 0 Flow
TIMI Grade 1 Flow
TIMI Grade 2 Flow
TIMI Grade 3 Flow
TIMI Grade 4 Flow
Pulsatile Flow
Deceleration

Myocardial Perfusion

TIMI Myocardial Perfusion Grade
TMP Grade 0
TMP Grade 0.5
TMP Grade 1
TMP Grade 2
TMP Grade 3

Lesion Complexity

ACC/AHA Lesion-Specific Classification of the Primary Target Stenosis

Preprocedural Lesion Morphology

Eccentricity
Irregularity
Ulceration
Intimal Flap
Aneurysm
Sawtooth Pattern
Length
Ostial location
Angulation
Proximal tortuosity
Degenerated SVG
Calcification
Total occlusion
Coronary Artery Thrombus
TIMI Thrombus Grade
TIMI Thrombus Grade 0
TIMI Thrombus Grade 1
TIMI Thrombus Grade 2
TIMI Thrombus Grade 3
TIMI Thrombus Grade 4
TIMI Thrombus Grade 5
TIMI Thrombus Grade 6

Lesion Morphology

Quantitative Coronary Angiography
Definitions of Preprocedural Lesion Morphology
Irregular Lesion
Disease Extent
Arterial Foreshortening
Infarct Related Artery
Restenosis
Degenerated SVG
Collaterals
Aneurysm
Bifurcation
Trifurcation
Ulceration

Left ventriculography

Technique
Quantification of LV Function
Quantification of Mitral Regurgitation

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Vanessa Cherniauskas, M.D. [2]

Overview

The appearence of irregular lesions with intraluminal filling defects and contrast staining is detected by coronary angiography and may indicate a fissuredatherosclerotic 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 evidenced by a large transcardiac gradient of serotonin (5-hydroxy-tryptamine).[3] The irregular endothelial surfaces may serve as foci of platelet aggregation with subsequent thrombus formation and vasospasm induced by release of thromboxane A2 (TXA2).[4][5][6][7] The resulting endothelial damage and lesion instability are associated with an increased risk of thrombotic occlusion and distal embolization.[8][9]

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.[10]
  • Greater irregularity of lesions are more likely to appear in the infarct-related artery than in lesions in other coronary arteries of patients with acute infarction and they are also related to the appearence of unstable angina.[11]
  • The lesion irregularity is the second most important risk factor of diameter stenosis as a predictor of future infarction.[12]
  • Greater lesion complexity is associated with worse epicardial flow characteristics and decreased myocardial perfusion at 60 minutes and after percutaneous coronary intervention and with a higher risk of shock and mortality rate within 30 days.[13]

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.[14]

References

  1. 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. 
  2. 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. 
  3. 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. 
  4. Erhardt, LR.; Lundman, T.; Mellstedt, H. (1973). "Incorporation of 125 I-labelled fibrinogen into coronary arterial thrombi in acute myocardial infarction in man.". Lancet. 1 (7800): 387–90. PMID 4119704. 
  5. Fuster, V.; Chesebro, JH. (1981). "Antithrombotic therapy: role of platelet-inhibitor drugs. I. Current concepts of thrombogenesis: role of platelets. (first of three parts).". Mayo Clin Proc. 56 (2): 102–12. PMID 7007748. 
  6. Hamberg, M.; Svensson, J.; Samuelsson, B. (1975). "Thromboxanes: a new group of biologically active compounds derived from prostaglandin endoperoxides.". Proc Natl Acad Sci U S A. 72 (8): 2994–8. PMID 1059088. 
  7. Hirsh, PD.; Hillis, LD.; Campbell, WB.; Firth, BG.; Willerson, JT. (1981). "Release of prostaglandins and thromboxane into the coronary circulation in patients with ischemic heart disease.". N Engl J Med. 304 (12): 685–91. PMID 6894016. doi:10.1056/NEJM198103193041201. 
  8. 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. 
  9. 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. 
  10. 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. 
  11. 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. 
  12. 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. 
  13. Gibson, CM.; Bigelow, B.; James, D.; Tepper, MR.; Murphy, SA.; Kirtane, AJ.; Giugliano, RP.; Cannon, CP.; Antman, EM. (2004). "Association of lesion complexity following fibrinolytic administration with mortality in ST-elevation myocardial infarction.". Am J Cardiol. 94 (1): 108–11. PMID 15219518. doi:10.1016/j.amjcard.2004.03.038. 
  14. "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. 

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