Tct recognition of vulnerable plaque guidelines
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Tct recognition of vulnerable plaque guidelines
- 1. Total victims of new heart attacks in 2003 Will die before reaching hospital. >50% Damaged Myocardium Pre-Hospital Delay 10year mortality ticket issued on the way reaching hospital! Future heart failure… Cardiology of Today CANNOT Reach >50% of Its Target Population ~ 500,000 in the USA
- 2. Everybody has atherosclerosis, the question is who has vulnerable plaque Sudden Cardiac Death Acute MI Vulnerable Plaque
- 3. Carl von Rokitansky (1804-1878) Rokitansky gaveearly detailed descriptionsof arterial disease. Heis alleged to haveperformed 30,000 autopsies. Rokitansky in 1841 championed theThrombogenic Theory. Heproposed that the depositsobserved in theinner layer of thearterial wall derived primarily from fibrin and other blood elementsrather than being theresult of apurulent process. Subsequently, theatheroma resulted from thedegeneration of thefibrin and other blood proteinsasaresult of apreexisting crasisof theblood, and finally thesedepositsweremodified toward apulpy masscontaining cholesterol crystalsand fatty globules. Thistheory cameunder attack by Virchow
- 4. First studies on inflammation of vessels, particularly phlebitis, Started at a time when Cruveilhier2had just stated: La phlebite domine toute la pathologie.3 First a great number of preparatory studies on fibrin, leukocytes, meta-morphosis of blood, published separately. … Rudolf Virchow 1821-1902 The Father of Cellular Pathology Virchow appreciates prior works. Virchow presented hisinflammatory theory. Heutilized thenameof "endarteritisdeformans." By thishe meant that theatheromawasaproduct of an inflammatory processwithin theintimawith thefibrous thickening evolved asaconsequenceof areactivefibrosisinduced by proliferating connectivetissuecells within theintima.
- 5. Olcott 1931 “plaque rupture” Leary 1934 “rupture of atheromatous abscess” Wartman 1938 “rupture-induced occlusion” Horn 1940 “plaque fissure” Helpern 1957 “plaque erosion” Crawford 1961 “plaque thrombosis” Gore 1963 “plaque ulceration” Friedman 1964 “macrophage accumulation” Byers 1964 “thrombogenic gruel” Chapman 1966 “plaque rupture” Plaque Fissure in Human Coronary Thrombosis (Abstract) Fed. Proc. 1964, 23, 443 Paris Constantinidis “Thedestruction of thehyalinized wall separating lumen from theatheromawas almost alwaysobserved to bepreceded by or associated with itsinvasion by lipid containing macrophages.” Friedman and van den Bovenkamp 1965 Unheralded Pioneers
- 6. N Engl J Med 1999 “Atherosclerosis; an inflammatory disease” Ross R. Russell Ross Atherosclerosis; arterial “Response to Injury” N Engl J Med 1976 Aug 12;295(7):369-77 The pathogenesis of atherosclerosis (first of two parts). Ross R, Glomset JA.
- 7. James T. Willerson 1981 N Engl J Med 1981 Mar 19;304(12):685-91 Plaque Thrombosis
- 8. Erling Falk Michael Davies Autopsy Series Thin Fibrous Cap + Large Lipid Core + Dense Macrophage A culprit ruptured plaque 1981-1990
- 9. Seymour Glagov Compensatory Enlargement of Human Atherosclerotic Coronary Arteries N Engl J Med 1987 May 28;316(22):1371-5 <50% stenosis Luminal area is not endangered until more than 40% of internal elastic lamina is destructed and occupied by plaque Coronary artery disease is a disease of arterial wall disease not lumen. Positive(expansive) Remodeling <80% stenosis
- 10. Angiographic progression of coronary artery disease and the development of myocardial infarction. Ambrose JA, Tannenbaum MA, Alexopoulos D, Hjemdahl-Monsen CE, Leavy J, Weiss M, Borrico S, Gorlin R, Fuster V. Department of Medicine, New York Cardiac Center, Mount Sinai Medical Center, New York 10029. Simultaneously, Little et al, Haft et al reported that majority of culprit lesions are found on previously non-critical stenosis plaques. Conclusion: “Myocardial infarction frequently develops from non-severe lesions.” J Am Coll Cardiol 1988 Jul;12(1):56-62 Ambrose, Fuster, and colleagues Angiographically Invisible Plaques
- 11. Falk E., Shak P.K., Fuster V. Circulation 1995 Non-stenotic (<75%) plaques cause about 80% of deadly MI
- 12. Macrophage- driven MMPs soften plaquecap and prompt it to rupture P.K. Shah Peter Libby Thefateof atherosclerosisand itsthrombotic complication are governed by immunesystem. Goran Hansson and others Allard van der Wal and others
- 13. •Eroded Plaque Rupture-prone plaques are not the only type of vulnerable plaque •Calcium Nodule van der Wal - Netherlands Renu Virmani -USA Thiene - Italy Kolodgie F., Burk A.P., Farb A., and Virmani R.
- 14. Muller JE, Abela GS, Nesto RW, Tofler GH. Triggers, acute risk factors and vulnerable plaques: the lexicon of a new frontier. J Am Coll Cardiol. 1994 Mar 1;23(3):809-13 James E. Muller 1994 Muller coined the term of “Vulnerable” Plaque Muller likened Vulnerable Plaques to American nuclear missiles stored underground in Nevada desert where they could be vulnerable to Russians’ long-range missile attack! “Vulnerableto disruption and thrombosis”
- 16. Total victims of new heart attacks in 2003 Will die before reaching hospital. >50% Damaged Myocardium Pre-Hospital Delay 10year mortality ticket issued on the way reaching hospital! Future heart failure… The major underlying cause of this long standing failure in cardiology. ~ 500,000 in the USA
- 18. Potential Underlying Cause of All (fatal and non-fatal) Heart Attacks (Sudden Cardiac Death + Acute Coronary Syndrome) With Occlusive Thrombi With Rupture >70% Stenosis With Significant Atherosclerosis or Ischemic Heart <70% Stenosis Without Significant Atherosclerosis or Atherosclerosis-Derived Myocardial Damage Without Occlusive Thrombi Without Rupture With Old Myocardial Damage Without Old Myocardial Damage Only Myocardial-Derived Factors (conductive disorders, …) Erosion Calcified Nodule Others With Critical Stenosis Without Critical Stenosis With Expansive Remodeling Without Expansive Remodeling
- 19. Ruptured Plaques (~70%) 1. Stenotic (~20%) 2. Non-stenotic (~50%) Non-ruptured Plaques (~ 30%) 1. Erosion (~20%) 2. Calcified Nodule (~5%) Plaque Pathology Responsible for Coronary Thrombotic Death In summary:
- 20. Terminology: Culprit Plaque: a Retrospective Terminology Vulnerable Plaque: a Prospective Terminology
- 21. Different Types of Vulnerable Plaques Major Underlying Cause of Acute Coronary Events Normal Rupture-prone Fissured Eroded Critical Stenosis Hemorrhage Naghavi et al, Cur Ath Rep 2001
- 22. Rupture-Prone Plaque Vulnerable Plaque Naghavi et al, Cur Ath Rep 2001 Macrophage Necrotic lipid core Thin fibrouscap
- 23. Eroded Plaque Vulnerable Plaque Naghavi et al, Cur Ath Rep 2001 Endothelial denudation Proteoglycans
- 24. Fissured / Healed Plaque Vulnerable Plaque Naghavi et al, Cur Ath Rep 2001 Mural thrombi Wounded plaque
- 25. Plaque with a Intimal Calcified Nodule Vulnerable Plaque Naghavi et al, Cur Ath Rep 2001 Calcified nodule
- 26. Intra-Plaque Hemorrhage with Intact Cap Vulnerable Plaque Naghavi et al, Cur Ath Rep 2001 Leaking angiogenesisor ruptureof vasa vaserum
- 27. Critically Stenotic but Asymptomatic Plaque Naghavi et al, Cur Ath Rep 2001Vulnerable Plaque >75% lumina narrowing
- 28. Different Types of Vulnerable Plaques Major Underlying Cause of Acute Coronary Events Normal Rupture-prone Fissured Eroded Critical Stenosis Hemorrhage Naghavi et al, Cur Ath Rep 2001
- 29. Proposed Histopathological and Clinical Criteria for Definition of Vulnerable Plaque • Major Criteria: 1. Active Inflammation (monocyte/ macrophage infiltration) 2. Thin Cap with Large Lipid Core 3. Endothelial Denudation with Superficial Platelet Aggregation 4. Fissured / Wounded Plaque
- 30. Proposed Histopathological and Clinical Criteria for Definition of Vulnerable Plaque • Minor Criteria: 1. Superficial Calcified nodule 2. Glistening Yellow 3. Intraplaque Hemorrhage 4. Critical Stenosis 5. Positive Remodeling?
- 31. From “Vulnerable Plaque” To “Vulnerable Patient” A Call For New DefinitionsAnd Risk Assessment Strategies
- 35. A plaquewith high likelihood of causing thrombusOR rapid progression.
- 37. A thrombogenic blood that exhibitsincreased coagulability or decreased endogenous thrombolytic activity.
- 39. A myocardium with electrical instability that hastendency to develop fatal arrhythmiaupon ischemia.
- 41. A patient with high likelihood of having an acuteevent: -Sudden Cardiac Death -Myocardial Infarction -AcuteCoronary Syndrome
- 42. In search of “vulnerable patient”
- 43. 1,400,000 Annual Heart Attacks 140,000,000 Americans>35y Home-Based Screening Non-invasive Imaging Office-Based Screening Invasive2-3 millions 40-50 millions 50-60 millions Chol, CRP, Genetic Screening, Age– Sex – Family History Calcium MRI / MRA Thermography, OCT, Spectroscopy, … CT-Angio
- 46. Association for Eradication of Heart Attack www.VP.org