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==Pathophysiology==
==Pathophysiology==
The pathophysiology of lesion irregularity is represented by pre-existing intimal disruption and/or increased [[turbulence]] and [[shear stress]]es, which lead to [[platelet activation]] evidenced by a large transcardiac gradient of serotonin (5-hydroxy-tryptamine).<ref name="van den Berg-1989">{{Cite journal  | last1 = van den Berg | first1 = EK. | last2 = Schmitz | first2 = JM. | last3 = Benedict | first3 = CR. | last4 = Malloy | first4 = CR. | last5 = Willerson | first5 = JT. | last6 = Dehmer | first6 = GJ. | title = Transcardiac serotonin concentration is increased in selected patients with limiting angina and complex coronary lesion morphology. | journal = Circulation | volume = 79 | issue = 1 | pages = 116-24 | month = Jan | year = 1989 | doi =  | PMID = 2910538 }}</ref> The irregular endothelial surfaces may serve as foci of platelet aggregation with [[subsequent thrombus]] formation and vasospasm induced by release of [[thrombaxane A2|thrombaxane A2 (TXA2)]].<ref name="Erhardt-1973">{{Cite journal  | last1 = Erhardt | first1 = LR. | last2 = Lundman | first2 = T. | last3 = Mellstedt | first3 = H. | title = Incorporation of 125 I-labelled fibrinogen into coronary arterial thrombi in acute myocardial infarction in man. | journal = Lancet | volume = 1 | issue = 7800 | pages = 387-90 | month = Feb | year = 1973 | doi =  | PMID = 4119704 }}</ref><ref name="Fuster-1981">{{Cite journal  | last1 = Fuster | first1 = V. | last2 = Chesebro | first2 = JH. | title = Antithrombotic therapy: role of platelet-inhibitor drugs. I. Current concepts of thrombogenesis: role of platelets. (first of three parts). | journal = Mayo Clin Proc | volume = 56 | issue = 2 | pages = 102-12 | month = Feb | year = 1981 | doi =  | PMID = 7007748 }}</ref><ref name="Hamberg-1975">{{Cite journal  | last1 = Hamberg | first1 = M. | last2 = Svensson | first2 = J. | last3 = Samuelsson | first3 = B. | title = Thromboxanes: a new group of biologically active compounds derived from prostaglandin endoperoxides. | journal = Proc Natl Acad Sci U S A | volume = 72 | issue = 8 | pages = 2994-8 | month = Aug | year = 1975 | doi =  | PMID = 1059088 }}</ref><ref name="Hirsh-1981">{{Cite journal  | last1 = Hirsh | first1 = PD. | last2 = Hillis | first2 = LD. | last3 = Campbell | first3 = WB. | last4 = Firth | first4 = BG. | last5 = Willerson | first5 = JT. | title = Release of prostaglandins and thromboxane into the coronary circulation in patients with ischemic heart disease. | journal = N Engl J Med | volume = 304 | issue = 12 | pages = 685-91 | month = Mar | year = 1981 | doi = 10.1056/NEJM198103193041201 | PMID = 6894016 }}</ref> The resulting [[endothelium|endothelial]] damage and lesion instability are associated with an increased risk of thrombotic occlusion and [[distal embolization]].<ref name="Falk-1985">{{Cite journal  | last1 = Falk | first1 = E. | title = 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. | journal = Circulation | volume = 71 | issue = 4 | pages = 699-708 | month = Apr | year = 1985 | doi =  | PMID = 3971539 }}</ref><ref name="Davies-1986">{{Cite journal  | last1 = Davies | first1 = MJ. | last2 = Thomas | first2 = AC. | last3 = Knapman | first3 = PA. | last4 = Hangartner | first4 = JR. | title = Intramyocardial platelet aggregation in patients with unstable angina suffering sudden ischemic cardiac death. | journal = Circulation | volume = 73 | issue = 3 | pages = 418-27 | month = Mar | year = 1986 | doi =  | PMID = 3948352 }}</ref>
The pathophysiology of lesion irregularity is represented by pre-existing intimal disruption and/or increased [[turbulence]] and [[shear stress]]es, which lead to [[platelet activation]] evidenced by a large transcardiac gradient of serotonin (5-hydroxy-tryptamine).<ref name="van den Berg-1989">{{Cite journal  | last1 = van den Berg | first1 = EK. | last2 = Schmitz | first2 = JM. | last3 = Benedict | first3 = CR. | last4 = Malloy | first4 = CR. | last5 = Willerson | first5 = JT. | last6 = Dehmer | first6 = GJ. | title = Transcardiac serotonin concentration is increased in selected patients with limiting angina and complex coronary lesion morphology. | journal = Circulation | volume = 79 | issue = 1 | pages = 116-24 | month = Jan | year = 1989 | doi =  | PMID = 2910538 }}</ref> The irregular endothelial surfaces may serve as foci of platelet aggregation with [[subsequent thrombus]] formation and vasospasm induced by release of [[thromboxane A2|thromboxane A2 (TXA2)]].<ref name="Erhardt-1973">{{Cite journal  | last1 = Erhardt | first1 = LR. | last2 = Lundman | first2 = T. | last3 = Mellstedt | first3 = H. | title = Incorporation of 125 I-labelled fibrinogen into coronary arterial thrombi in acute myocardial infarction in man. | journal = Lancet | volume = 1 | issue = 7800 | pages = 387-90 | month = Feb | year = 1973 | doi =  | PMID = 4119704 }}</ref><ref name="Fuster-1981">{{Cite journal  | last1 = Fuster | first1 = V. | last2 = Chesebro | first2 = JH. | title = Antithrombotic therapy: role of platelet-inhibitor drugs. I. Current concepts of thrombogenesis: role of platelets. (first of three parts). | journal = Mayo Clin Proc | volume = 56 | issue = 2 | pages = 102-12 | month = Feb | year = 1981 | doi =  | PMID = 7007748 }}</ref><ref name="Hamberg-1975">{{Cite journal  | last1 = Hamberg | first1 = M. | last2 = Svensson | first2 = J. | last3 = Samuelsson | first3 = B. | title = Thromboxanes: a new group of biologically active compounds derived from prostaglandin endoperoxides. | journal = Proc Natl Acad Sci U S A | volume = 72 | issue = 8 | pages = 2994-8 | month = Aug | year = 1975 | doi =  | PMID = 1059088 }}</ref><ref name="Hirsh-1981">{{Cite journal  | last1 = Hirsh | first1 = PD. | last2 = Hillis | first2 = LD. | last3 = Campbell | first3 = WB. | last4 = Firth | first4 = BG. | last5 = Willerson | first5 = JT. | title = Release of prostaglandins and thromboxane into the coronary circulation in patients with ischemic heart disease. | journal = N Engl J Med | volume = 304 | issue = 12 | pages = 685-91 | month = Mar | year = 1981 | doi = 10.1056/NEJM198103193041201 | PMID = 6894016 }}</ref> The resulting [[endothelium|endothelial]] damage and lesion instability are associated with an increased risk of thrombotic occlusion and [[distal embolization]].<ref name="Falk-1985">{{Cite journal  | last1 = Falk | first1 = E. | title = 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. | journal = Circulation | volume = 71 | issue = 4 | pages = 699-708 | month = Apr | year = 1985 | doi =  | PMID = 3971539 }}</ref><ref name="Davies-1986">{{Cite journal  | last1 = Davies | first1 = MJ. | last2 = Thomas | first2 = AC. | last3 = Knapman | first3 = PA. | last4 = Hangartner | first4 = JR. | title = Intramyocardial platelet aggregation in patients with unstable angina suffering sudden ischemic cardiac death. | journal = Circulation | volume = 73 | issue = 3 | pages = 418-27 | month = Mar | year = 1986 | doi =  | PMID = 3948352 }}</ref>


==Grading of Lesion Irregularity==
==Grading of Lesion Irregularity==

Revision as of 21:08, 21 November 2013

Coronary Angiography

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Lesion Complexity

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Preprocedural Lesion Morphology

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Lesion Morphology

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Irregular Lesion
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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 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. Unknown parameter |month= ignored (help)
  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. Unknown parameter |month= ignored (help)
  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. Unknown parameter |month= ignored (help)
  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. Unknown parameter |month= ignored (help)
  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. Unknown parameter |month= ignored (help)
  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. Unknown parameter |month= ignored (help)
  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. doi:10.1056/NEJM198103193041201. PMID 6894016. Unknown parameter |month= ignored (help)
  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. Unknown parameter |month= ignored (help)
  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. Unknown parameter |month= ignored (help)
  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. Unknown parameter |month= ignored (help)
  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. Unknown parameter |month= ignored (help)
  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. Unknown parameter |month= ignored (help)
  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. doi:10.1016/j.amjcard.2004.03.038. PMID 15219518. Unknown parameter |month= ignored (help)
  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. Unknown parameter |month= ignored (help)


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