ST elevation myocardial infarction pathophysiology: Difference between revisions

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{{Infobox_Disease |
  Name          = Myocardial Infarction Pathophysiology|
  Image          = Plaque rupture2 copy.jpg|
  Caption        = Shown in yellow is atherosclerotic plaque, in red is clot that has formed inside the ruptured plaque and in the lumen of the coronary artery.|
  DiseasesDB    = 8664 |
  ICD10          = {{ICD10|I|21||i|20}}-{{ICD10|I|22||i|20}} |
  ICD9          = {{ICD9|410}} |
  ICDO          = |
  OMIM          = |
  MedlinePlus    = 000195 |
  eMedicineSubj  = med |
  eMedicineTopic = 1567 |
  eMedicine_mult = {{eMedicine2|emerg|327}} {{eMedicine2|ped|2520}} |
  MeshID        = |
}}
{{SI}}
{{CMG}}


'''Associate Editor-In-Chief:''' {{CZ}}
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==The role of plaque rupture in ST elevation myocardial infarction==
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__NOTOC__
[[Atherosclerosis]], or "hardening of the arteries," is the gradual buildup of [[cholesterol]] and fibrous tissue ([[collagen]] and [[smooth muscle cells]]) throughout the vascular tree.  When there is localized accumulation of lipids and scar tissue, this is called a "plaque".  Somewhat paradoxically, it is not the most severe plaque narrowings that lead to ST elevation MI.  Pathology studies indicate that it is often mild-to-moderate, lipid-laden, inflammed plaques that are the ones most likely to rupture and cause an ST elevation MI (STEMI) or a non ST elevation MI (NSTEMI). <ref name="pmid7634481">{{cite journal |author=Falk E, Shah PK, Fuster V |title=Coronary plaque disruption |journal=Circulation |volume=92 |issue=3 |pages=657–71 |year=1995 |month=August |pmid=7634481 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=7634481}}</ref>  The role of plaque rupture in STEMI and NSTEMI is supported by studies demonstrating that plaque rupture is present in about 70% and superficial erosion is present in 30% of patients who die suddenly in whom there is documented coronary artery disease. <ref name="pmid9113930">{{cite journal |author=Burke AP, Farb A, Malcom GT, Liang YH, Smialek J, Virmani R |title=Coronary risk factors and plaque morphology in men with coronary disease who died suddenly |journal=N. Engl. J. Med. |volume=336 |issue=18 |pages=1276–82 |year=1997 |month=May |pmid=9113930 |doi= |url=http://content.nejm.org/cgi/pmidlookup?view=short&pmid=9113930&promo=ONFLNS19}}</ref> Exposure of the blood stream to the thrombogenic components of the plaque leads to activation of the [[coagulation cascade]] and thrombus formation.  In STEMI, the clot completely occludes the epicardial artery, and there is a complete lack of blood flow to the involved territory. This causes transmural injury and ST elevation. In NSTEMI, there is partial obstruction with embolization.  This causes ischemia and subendocardial injury that are manifested by ST depression.
{{ST elevation myocardial infarction}}
 
{{CMG}}; {{AE}} {{CZ}}
''Shown below are multiple slices of the LAD. The proximal LAD is located to the left. Plaque rupture with thrombus formation begins in the second slice of the LAD.''
[[Image:Plaque rupture.jpg|500px]]
 
''Shown below is a magnified view of the second slice from the left. In yellow is atherosclerotic plaque, in red is clot that has formed inside the ruptured plaque and in the lumen of the coronary artery.''
[[Image:Plaque rupture2 copy.jpg|500px]]
 
Te following are excellent videos demonstrating the underlying pathophysiology:
 
<youtube v=L6EiPLli5x8/>


==Overview==
ST elevation myocardial infarction is largely influenced by the role of plaque rupture.


<youtube v=cOMzh2hf_Vw/>
==The Role of Plaque Rupture in ST Elevation Myocardial Infarction==
[[Atherosclerosis]], or hardening of the [[arteries]], is the gradual buildup of [[cholesterol]] and [[fibrous tissue]] ([[collagen]] and [[smooth muscle cells]]) throughout the [[vascular]] tree.  When there is localized accumulation of [[lipids]] and [[scar tissue]], this is called a "plaque".  Somewhat paradoxically, it is not the most severe plaque narrowing that leads to ST elevation MI.  [[Pathological]] studies indicate that it is often mild-to-moderate, [[lipid]]-laden, inflamed plaques that are the ones most likely to rupture and cause an ST elevation MI ([[STEMI]]) or a non ST elevation MI ([[NSTEMI]]). <ref name="pmid7634481">{{cite journal |author=Falk E, Shah PK, Fuster V |title=Coronary plaque disruption |journal=Circulation |volume=92 |issue=3 |pages=657–71 |year=1995 |month=August |pmid=7634481 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=7634481}}</ref>  The role of plaque rupture in STEMI and NSTEMI is supported by studies demonstrating that plaque rupture is present in about 70% and superficial erosion is present in 30% of patients who die suddenly in whom there is documented [[coronary artery disease]]. <ref name="pmid9113930">{{cite journal |author=Burke AP, Farb A, Malcom GT, Liang YH, Smialek J, Virmani R |title=Coronary risk factors and plaque morphology in men with coronary disease who died suddenly |journal=N. Engl. J. Med. |volume=336 |issue=18 |pages=1276–82 |year=1997 |month=May |pmid=9113930 |doi= |url=http://content.nejm.org/cgi/pmidlookup?view=short&pmid=9113930&promo=ONFLNS19}}</ref> Exposure of the [[blood stream]] to the [[Thrombogenicity|thrombogenic]] components of the plaque leads to activation of the [[coagulation cascade]] and [[thrombus]] formation.  In STEMI, the [[clot]] completely occludes the epicardial artery, and there is a complete lack of blood flow to the involved territory. This causes transmural injury and ST elevation. In NSTEMI, there is partial obstruction with [[embolus|embolization]].  This causes [[ischemia]] and [[subendocardial]] injury that are manifested by [[ST depression]].


[[Image:Plaque rupture.jpg|frame|none|500px|Shown here are multiple slices of the LAD. The proximal LAD is located to the left. Plaque rupture with thrombus formation begins in the second slice of the LAD.]]


<youtube v=a8Idk4EUYTs/>
[[Image:Plaque rupture2 copy.jpg|frame|none|500px|Shown here is a magnified view of the second slice from the left. In yellow is atherosclerotic plaque, in red is clot that has formed inside the ruptured plaque and in the lumen of the coronary artery.]]


==Pathophysiology of and risk factors for plaque rupture==
==Pathophysiology of and Risk Factors for Plaque Rupture==
#[[Macrophage]] accumulation has been shown to be present to a greater degree in patients with [[acute coronary syndromes]] than in those patients with [[chronic stable angina]] <ref name="pmid8044947">{{cite journal |author=Moreno PR, Falk E, Palacios IF, Newell JB, Fuster V, Fallon JT |title=Macrophage infiltration in acute coronary syndromes. Implications for plaque rupture |journal=Circulation |volume=90 |issue=2 |pages=775–8 |year=1994 |month=August |pmid=8044947 |doi= |url=}}</ref>  <ref name="pmid8281670">{{cite journal |author=van der Wal AC, Becker AE, van der Loos CM, Das PK |title=Site of intimal rupture or erosion of thrombosed coronary atherosclerotic plaques is characterized by an inflammatory process irrespective of the dominant plaque morphology |journal=Circulation |volume=89 |issue=1 |pages=36–44 |year=1994 |month=January |pmid=8281670 |doi= |url=}}</ref>  These activated macrophages can release enzymes  such as metalloproteinases, interstitial collagenase, gelatinase, and stromelysin that degrade collagen, elastin, and proteoglycans. <ref name="pmid7664441">{{cite journal |author=Shah PK, Falk E, Badimon JJ, ''et al'' |title=Human monocyte-derived macrophages induce collagen breakdown in fibrous caps of atherosclerotic plaques. Potential role of matrix-degrading metalloproteinases and implications for plaque rupture |journal=Circulation |volume=92 |issue=6 |pages=1565–9 |year=1995 |month=September |pmid=7664441 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=7664441}}</ref> This enzymatic degradation in turn leads to breakdown of the fibrous cap. The thin shoulders or edges of the fibrous cap appear to be particularly vulnerable to erosion and breakdown.
#[[Macrophage]] accumulation has been shown to be present to a greater degree in patients with [[acute coronary syndromes]] than in those patients with [[chronic stable angina]] <ref name="pmid8044947">{{cite journal |author=Moreno PR, Falk E, Palacios IF, Newell JB, Fuster V, Fallon JT |title=Macrophage infiltration in acute coronary syndromes. Implications for plaque rupture |journal=Circulation |volume=90 |issue=2 |pages=775–8 |year=1994 |month=August |pmid=8044947 |doi= |url=}}</ref>  <ref name="pmid8281670">{{cite journal |author=van der Wal AC, Becker AE, van der Loos CM, Das PK |title=Site of intimal rupture or erosion of thrombosed coronary atherosclerotic plaques is characterized by an inflammatory process irrespective of the dominant plaque morphology |journal=Circulation |volume=89 |issue=1 |pages=36–44 |year=1994 |month=January |pmid=8281670 |doi= |url=}}</ref>  These activated [[macrophages]] can release enzymes  such as [[metalloproteinases]], [[collagenase|interstitial collagenase]], [[gelatinase]], and stromelysin that degrade [[collagen]], [[elastin]], and [[proteoglycan|proteoglycans]]. <ref name="pmid7664441">{{cite journal |author=Shah PK, Falk E, Badimon JJ, ''et al'' |title=Human monocyte-derived macrophages induce collagen breakdown in fibrous caps of atherosclerotic plaques. Potential role of matrix-degrading metalloproteinases and implications for plaque rupture |journal=Circulation |volume=92 |issue=6 |pages=1565–9 |year=1995 |month=September |pmid=7664441 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=7664441}}</ref> This [[enzymatic]] degradation in turn leads to breakdown of the [[fibrous]] cap. The thin shoulders or edges of the [[fibrous]] cap appear to be particularly vulnerable to erosion and breakdown.
#Neovascularization of the plaque Moreno et have shown that microvessel density was increased in ruptured plaques when compared with nonruptured plaques (P=0.0001). Furthermore, among lesions with severe macrophage infiltration at the fibrous cap, microvessel density was increased (P=0.0001) was well as at the edges or shoulders of the plaque (P=0.0001). Intraplaque hemorrhage was also associated with an increase in microvessel density (P=0.04) as was the presence of thin-cap fibroatheromas (P=0.038).  Microvessel density at the base of the plaque was identified as an independent (P=0.003)  correlate of plaque rupture. <ref name="pmid15451780">{{cite journal |author=Moreno PR, Purushothaman KR, Fuster V, ''et al'' |title=Plaque neovascularization is increased in ruptured atherosclerotic lesions of human aorta: implications for plaque vulnerability |journal=Circulation |volume=110 |issue=14 |pages=2032–8 |year=2004 |month=October |pmid=15451780 |doi=10.1161/01.CIR.0000143233.87854.23 |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=15451780}}</ref>  
#[[Neovascularization]] of the plaque Moreno et have shown that microvessel density was increased in ruptured plaques when compared with nonruptured plaques (P=0.0001). Furthermore, among lesions with severe [[macrophage]] infiltration at the fibrous cap, [[microvessel]] density was increased (P=0.0001) was well as at the edges or shoulders of the plaque (P=0.0001). [[hemorrhage|Intraplaque hemorrhage]] was also associated with an increase in [[microvessel]] density (P=0.04) as was the presence of thin-cap fibroatheromas (P=0.038).  [[Microvessel]] density at the base of the plaque was identified as an independent (P=0.003)  correlate of plaque rupture. <ref name="pmid15451780">{{cite journal |author=Moreno PR, Purushothaman KR, Fuster V, ''et al'' |title=Plaque neovascularization is increased in ruptured atherosclerotic lesions of human aorta: implications for plaque vulnerability |journal=Circulation |volume=110 |issue=14 |pages=2032–8 |year=2004 |month=October |pmid=15451780 |doi=10.1161/01.CIR.0000143233.87854.23 |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=15451780}}</ref>  
# High oscillatory shear stress
# High oscillatory shear stress
# Vasoconstriction
# [[Vasoconstriction]]
# [[Spontaneous coronary dissection]]
# [[Spontaneous coronary dissection]]


==Pathophysiology of and risk factors for thrombosis following plaque rupture==
==Pathophysiology of and Risk Factors for Thrombosis Following Plaque Rupture==
There are numerous systemic risk factors associated with thrombus formation following plaque rupture:
There are numerous systemic risk factors associated with thrombus formation following plaque rupture:


#[[Smoking]]: Smoking increases platelet aggregation and plasma epinephrine levels <ref name="pmid7586342">{{cite journal |author=Hung J, Lam JY, Lacoste L, Letchacovski G |title=Cigarette smoking acutely increases platelet thrombus formation in patients with coronary artery disease taking aspirin |journal=Circulation |volume=92 |issue=9 |pages=2432–6 |year=1995 |month=November |pmid=7586342 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=7586342}}</ref>
#[[Smoking]]: Smoking increases [[platelet aggregation]] and [[plasma]] [[epinephrine]] levels <ref name="pmid7586342">{{cite journal |author=Hung J, Lam JY, Lacoste L, Letchacovski G |title=Cigarette smoking acutely increases platelet thrombus formation in patients with coronary artery disease taking aspirin |journal=Circulation |volume=92 |issue=9 |pages=2432–6 |year=1995 |month=November |pmid=7586342 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=7586342}}</ref>
#[[Fibrinogen]]: Elevated levels of fibrinogen have been associated with thrombosis including abnormal levels of fibrinogen <ref name="pmid7845427">{{cite journal |author=Thompson SG, Kienast J, Pyke SD, Haverkate F, van de Loo JC |title=Hemostatic factors and the risk of myocardial infarction or sudden death in patients with angina pectoris. European Concerted Action on Thrombosis and Disabilities Angina Pectoris Study Group |journal=N. Engl. J. Med. |volume=332 |issue=10 |pages=635–41 |year=1995 |month=March |pmid=7845427 |doi= |url=http://content.nejm.org/cgi/pmidlookup?view=short&pmid=7845427&promo=ONFLNS19}}</ref>
#[[Fibrinogen]]: Elevated levels of [[fibrinogen]] have been associated with [[thrombosis]] including abnormal levels of [[fibrinogen]] <ref name="pmid7845427">{{cite journal |author=Thompson SG, Kienast J, Pyke SD, Haverkate F, van de Loo JC |title=Hemostatic factors and the risk of myocardial infarction or sudden death in patients with angina pectoris. European Concerted Action on Thrombosis and Disabilities Angina Pectoris Study Group |journal=N. Engl. J. Med. |volume=332 |issue=10 |pages=635–41 |year=1995 |month=March |pmid=7845427 |doi= |url=http://content.nejm.org/cgi/pmidlookup?view=short&pmid=7845427&promo=ONFLNS19}}</ref>
#[[von Willebrand factor]] antigen <ref name="pmid7845427">{{cite journal |author=Thompson SG, Kienast J, Pyke SD, Haverkate F, van de Loo JC |title=Hemostatic factors and the risk of myocardial infarction or sudden death in patients with angina pectoris. European Concerted Action on Thrombosis and Disabilities Angina Pectoris Study Group |journal=N. Engl. J. Med. |volume=332 |issue=10 |pages=635–41 |year=1995 |month=March |pmid=7845427 |doi= |url=http://content.nejm.org/cgi/pmidlookup?view=short&pmid=7845427&promo=ONFLNS19}}</ref>
#[[Von Willebrand factor]] antigen <ref name="pmid7845427">{{cite journal |author=Thompson SG, Kienast J, Pyke SD, Haverkate F, van de Loo JC |title=Hemostatic factors and the risk of myocardial infarction or sudden death in patients with angina pectoris. European Concerted Action on Thrombosis and Disabilities Angina Pectoris Study Group |journal=N. Engl. J. Med. |volume=332 |issue=10 |pages=635–41 |year=1995 |month=March |pmid=7845427 |doi= |url=http://content.nejm.org/cgi/pmidlookup?view=short&pmid=7845427&promo=ONFLNS19}}</ref>
#[[tissue plasminogen activator]] <ref name="pmid7845427">{{cite journal |author=Thompson SG, Kienast J, Pyke SD, Haverkate F, van de Loo JC |title=Hemostatic factors and the risk of myocardial infarction or sudden death in patients with angina pectoris. European Concerted Action on Thrombosis and Disabilities Angina Pectoris Study Group |journal=N. Engl. J. Med. |volume=332 |issue=10 |pages=635–41 |year=1995 |month=March |pmid=7845427 |doi= |url=http://content.nejm.org/cgi/pmidlookup?view=short&pmid=7845427&promo=ONFLNS19}}</ref>
#[[Tissue plasminogen activator]] <ref name="pmid7845427">{{cite journal |author=Thompson SG, Kienast J, Pyke SD, Haverkate F, van de Loo JC |title=Hemostatic factors and the risk of myocardial infarction or sudden death in patients with angina pectoris. European Concerted Action on Thrombosis and Disabilities Angina Pectoris Study Group |journal=N. Engl. J. Med. |volume=332 |issue=10 |pages=635–41 |year=1995 |month=March |pmid=7845427 |doi= |url=http://content.nejm.org/cgi/pmidlookup?view=short&pmid=7845427&promo=ONFLNS19}}</ref>
#[[Anticardiolipin antibodies]] <ref name="pmid7805207">{{cite journal |author=Vaarala O, Mänttäri M, Manninen V, ''et al'' |title=Anti-cardiolipin antibodies and risk of myocardial infarction in a prospective cohort of middle-aged men |journal=Circulation |volume=91 |issue=1 |pages=23–7 |year=1995 |month=January |pmid=7805207 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=7805207}}</ref>
#[[Anticardiolipin antibodies]] <ref name="pmid7805207">{{cite journal |author=Vaarala O, Mänttäri M, Manninen V, ''et al'' |title=Anti-cardiolipin antibodies and risk of myocardial infarction in a prospective cohort of middle-aged men |journal=Circulation |volume=91 |issue=1 |pages=23–7 |year=1995 |month=January |pmid=7805207 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=7805207}}</ref>
# Cross-linked [[fibrin-degradation products]] <ref name="pmid7955179">{{cite journal |author=Ridker PM, Hennekens CH, Cerskus A, Stampfer MJ |title=Plasma concentration of cross-linked fibrin degradation product (D-dimer) and the risk of future myocardial infarction among apparently healthy men |journal=Circulation |volume=90 |issue=5 |pages=2236–40 |year=1994 |month=November |pmid=7955179 |doi= |url=}}</ref>
# Cross-linked [[fibrin-degradation products]] <ref name="pmid7955179">{{cite journal |author=Ridker PM, Hennekens CH, Cerskus A, Stampfer MJ |title=Plasma concentration of cross-linked fibrin degradation product (D-dimer) and the risk of future myocardial infarction among apparently healthy men |journal=Circulation |volume=90 |issue=5 |pages=2236–40 |year=1994 |month=November |pmid=7955179 |doi= |url=}}</ref>
# Polymorphisms of a platelet glycoprotein receptor <ref name="pmid8598867">{{cite journal |author=Weiss EJ, Bray PF, Tayback M, ''et al'' |title=A polymorphism of a platelet glycoprotein receptor as an inherited risk factor for coronary thrombosis |journal=N. Engl. J. Med. |volume=334 |issue=17 |pages=1090–4 |year=1996 |month=April |pmid=8598867 |doi= |url=http://content.nejm.org/cgi/pmidlookup?view=short&pmid=8598867&promo=ONFLNS19}}</ref>
# [[Polymorphisms]] of a [[platelet]] [[glycoprotein]] receptor <ref name="pmid8598867">{{cite journal |author=Weiss EJ, Bray PF, Tayback M, ''et al'' |title=A polymorphism of a platelet glycoprotein receptor as an inherited risk factor for coronary thrombosis |journal=N. Engl. J. Med. |volume=334 |issue=17 |pages=1090–4 |year=1996 |month=April |pmid=8598867 |doi= |url=http://content.nejm.org/cgi/pmidlookup?view=short&pmid=8598867&promo=ONFLNS19}}</ref>


==Gross Pathology Findings in Plaque Rupture==
==Gross Pathology Findings in Plaque Rupture==
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[[Image:Slow-wavefront.gif|left|Time dependent wavefront of necrosis working its way from the subendocardium to the subepicardium]]
[[Image:Slow-wavefront.gif|left|Time dependent wavefront of necrosis working its way from the subendocardium to the subepicardium]]
In 1940, Blumgart ligated or tied off the coronary artery in dogs and cats and for the first time demonstrated a wavefront of cell death folllowing vessel occlusion <ref>Blumgart HL, Schlesinge MJ, Davis D: Studies on the relation of the clinical manifestations of angina pectoris, coronary thrombosis, and myocardial infarction to the pathologic findings, with particular reference to the significance of collateral circulation. Amer Heart J 19: 1, 1940 </ref> <ref> Blumgart HL, Zoll PM, Freedberg AS, Gilligan DR: The experimental production of intercoronary arterial anastomoses and their functional significance. Circulation 1: 10, 1950 PMID 15401193 </ref> <ref> Blumgart HL, Zoll PM, Kurland CS: Discussion of direct relief of coronary occlusion. Arch Intern Med (Chicago) 104: 862, 1959 PMID 13801751 </ref> <ref> Blumgart HL, Zoll PM. Pathologic physiology of angina pectoris and acute myocardial infarction. Circulation. 1960 Aug;22:301-7. PMID 13801752 </ref>
In 1940, Blumgart ligated or tied off the coronary artery in dogs and cats and for the first time demonstrated a wavefront of cell death folllowing [[Blood vessel|vessel]] occlusion <ref>Blumgart HL, Schlesinge MJ, Davis D: Studies on the relation of the clinical manifestations of angina pectoris, coronary thrombosis, and myocardial infarction to the pathologic findings, with particular reference to the significance of collateral circulation. Amer Heart J 19: 1, 1940 </ref> <ref>Blumgart HL, Zoll PM, Freedberg AS, Gilligan DR: The experimental production of intercoronary arterial anastomoses and their functional significance. Circulation 1: 10, 1950 PMID 15401193 </ref> <ref>Blumgart HL, Zoll PM, Kurland CS: Discussion of direct relief of coronary occlusion. Arch Intern Med (Chicago) 104: 862, 1959 PMID 13801751 </ref> <ref>Blumgart HL, Zoll PM. Pathologic physiology of angina pectoris and acute myocardial infarction. Circulation. 1960 Aug;22:301-7. PMID 13801752 </ref>
<ref> Blumgart HL, Zoll PM, Clinical Pathologic Correlations in Coronary Artery Disease, Circulation, Volume XLVII, No 6, June 1973, 1139-43 PMID 4575525 </ref>
<ref>Blumgart HL, Zoll PM, Clinical Pathologic Correlations in Coronary Artery Disease, Circulation, Volume XLVII, No 6, June 1973, 1139-43 PMID 4575525 </ref>


Irreversible injury of ischemic myocytes occurs first in the subendocardial zone. With more extended ischemia, a wavefront of cell death moves through the myocardium to involve progressively more of the transmural thickness of the ischemic zone. The precise location, size, and specific morphologic features of an [[acute myocardial infarction]] depend on:
Irreversible injury of ischemic myocytes occurs first in the subendocardial zone. With more extended [[ischemia]], a wavefront of cell death moves through the myocardium to involve progressively more of the transmural thickness of the ischemic zone. The precise location, size, and specific morphologic features of an [[acute myocardial infarction]] depend on:


#The location, severity, and rate of development of coronary atherosclerotic obstructions,
#The location, severity, and rate of development of coronary atherosclerotic obstructions,
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#The extent of collateral blood vessels
#The extent of collateral blood vessels


Decrease of ATP levels in myocytes in reaction to ischemia starts within seconds and causes loss of contractility in first two minutes. If ischemia persists, ATP levels reduced to its half level within 10 minutes and to 1/10 within 40 minutes. Irreversible cell injury occurs between 20-40 minutes and microvascular level injury starts if ischemia lasts more than an hour.<ref>Robbins Pathologic Basis of Disease, Kumar V, 7th ed</ref>
Decrease of ATP levels in myocytes in reaction to ischemia starts within seconds and causes loss of [[contractility]] in first two minutes. If [[ischemia]] persists, [[Adenosine triphosphate|ATP]] levels reduced to its half level within 10 minutes and to 1/10 within 40 minutes. Irreversible cell injury occurs between 20-40 minutes and [[Microvascular bed|microvascular]] level injury starts if [[ischemia]] lasts more than an hour.<ref>Robbins Pathologic Basis of Disease, Kumar V, 7th ed</ref>


If impaired blood flow to the heart lasts long enough, it triggers a process called the [[ischemic cascade]]; the heart cells die (chiefly through  [[necrosis]]) and do not grow back. A [[collagen]] [[scar]] forms in its place. Recent studies indicate that another form of cell death called [[apoptosis]] also plays a role in the process of tissue damage subsequent to myocardial infarction.<ref name="Krijnen-2002">{{cite journal | author=Krijnen PA, Nijmeijer R, Meijer CJ, Visser CA, Hack CE, Niessen HW. | title=Apoptosis in myocardial ischaemia and infarction. | journal=J Clin Pathol | year=2002 | volume=55 | issue=11 | pages=801-11 | id=PMID 12401816}}</ref>  As a result, the patient's heart can be permanently damaged. This scar tissue also puts the patient at risk for potentially life threatening arrhythmias.
If impaired [[blood]] flow to the heart lasts long enough, it triggers a process called the [[ischemic cascade]]; the [[Myocardium|heart cells]] die (chiefly through  [[necrosis]]) and do not grow back. A [[collagen]] [[scar]] forms in its place. Recent studies indicate that another form of cell death called [[apoptosis]] also plays a role in the process of [[Tissue (biology)|tissue]] damage subsequent to myocardial infarction.<ref name="Krijnen-2002">{{cite journal | author=Krijnen PA, Nijmeijer R, Meijer CJ, Visser CA, Hack CE, Niessen HW. | title=Apoptosis in myocardial ischaemia and infarction. | journal=J Clin Pathol | year=2002 | volume=55 | issue=11 | pages=801-11 | id=PMID 12401816}}</ref>  As a result, the patient's heart can be permanently damaged. This [[scar tissue]] also puts the patient at risk for potentially life threatening [[arrhythmias]].


==Pathophysiology of ST segment elevation on the electrocardiogram==
==Pathophysiology of ST segment elevation on the electrocardiogram==
In ST segment myocaridal infarction (STEMI), the ST segments on the ECG are by definition elevated and there is myonecrosis (death of myocytes) as reflected by elevation of biomarkers such as [[creatine kinase]] MB fraction (CK-MB) or [[troponin]] T or I (tn)).  The ST segments are elevated due to full thickness injury of the myocardium.  Other causes of ST segment elevation that are not due to vessel occlusion are discussed below.
In ST segment myocaridal infarction (STEMI), the [[ST segments]] on the [[The electrocardiogram|ECG]] are by definition elevated and there is [[myonecrosis]] (death of [[myocytes]]) as reflected by elevation of [[Cardiac biomarkers|biomarkers]] such as [[creatine kinase]] MB fraction ([[CK-MB]]) or [[troponin]] T or I (tn).  The [[ST segments]] are elevated due to full thickness injury of the [[myocardium]].
 
==Differential Diagnosis of Causes of ST Segment Elevation in the Absence of Myonecrosis==
Acute epicardial artery occlusion by [[thrombus]] is certainly one cause of ST segment elevation, but other causes of ST segment elevation which are not associated with myonecrosis include the following: (listed in alphabetical order) <ref name="pmid14645641">{{cite journal |author=Wang K, Asinger RW, Marriott HJ |title=ST-segment elevation in conditions other than acute myocardial infarction |journal=N. Engl. J. Med. |volume=349 |issue=22 |pages=2128–35 |year=2003 |month=November |pmid=14645641 |doi=10.1056/NEJMra022580 |url=}}</ref><ref name="pmid15014192">{{cite journal |author=Ako J, Honda Y, Fitzgerald PJ |title=Conditions associated with ST-segment elevation |journal=N. Engl. J. Med. |volume=350 |issue=11 |pages=1152–5; author reply 1152–5 |year=2004 |month=March |pmid=15014192 |doi=10.1056/NEJM200403113501118 |url=}}</ref>
 
* [[Aneurysm]] of the ventricle can result in persistent ST segment elevation that can be exacerbated with tachycardia.
 
* [[Arrhythmogenic right ventricular cardiomyopathy]]
 
* Balloon inflation in a coronary artery during percutaneous coronary intervention
 
* [[Brugada syndrome]]
 
* [[Cardioversion|Transthoracic cardioversion]]
 
* [[Coronary artery]] rupture during percutaneous coronary intervention
 
* [[Early repolarization]] is a normal variant that can result in ST segment elevation. It is more common in males of younger age. The ST elevation is exacerbated by [[bradycardia]].
 
* [[Hyperkalemia]] known as the "dialyzable current of njury" hyperkalemia may cause hyperacute ECG changes due to changes in membrane polarity
 
* [[Left bundle branch block]] is associated with ST segment elevation in those leads that are discordant to the QRS. Stated differently, if the QRS is predominantly of a negative deflection, it is normal to observe ST segment elevation in the same leads. The presence of ST elevation in leads where the QRS deflection is upright (concordance) may be a marker of myocardial injury.
 
* [[Myopericarditis]] can cause injury to the subepicardial myocytes and ST segment elevation.
 
* [[Myocarditis]] can cause injury to the subepicardial myocytes and ST segment elevation.
 
* [[Pericardiocentesis]] when the needle comes into contact with the myocardium, there can be ST segment elevation reflecting local injury of the myocardium.
 
* [[Pericarditis]] can cause injury to the subepicardial myocytes and ST elevation.
 
* [[Pulmonary Embolism]]
 
* [[Prinzmetal's angina]] is associated with ST segment elevation due to transient epicardial coronary artery spasm either in the absence or presence of atherosclerosis. If the condition persists long enough, myonecrosis can be observed.
 
* [[Stroke]] [[Intracranial hemorrhage]] can in some cases cause ST segment elevation due to direct [[myocyte]] injury from a hyperadrenergic stimulation emanating from the central nervous system.
 
==Differential Diagnosis of Causes of ST Segment Elevation in the Presence of Myonecrosis (STEMI)==
 
While plaque rupture is the most common cause of ST segment elevation MI, other conditions can cause ST elevation and myocardial necrosis. In order to expeditiously treat an alternate underlying cause of myonecrosis, it is important to rapidly identify conditions other than plaque rupture that may also cause ST elevation and myonecrosis. Indeed, the management of some of these conditions might be differ substantially from that of plaque rupture: [[cocaine]] induced STEMI would not be treated with [[beta-blocker]]s, and [[myocardial contusion]] would not be treated with an [[antithrombin]]. These conditions include the following:
 
{|style="width:100%; height:100px" border="1"
|style="height:100px"; style="width:25%" border="1" bgcolor="LightSteelBlue" | '''Cardiovascular'''
|style="height:100px"; style="width:75%" border="1" bgcolor="Beige" | [[Aortic dissection]] more often extends to occlude the ostium of the [[right coronary artery]]
 
[[Aortic stenosis]] can cause subendocardial ischemia and infarction if demand grossly exceeds supply
 
 
|-
|-bgcolor="LightSteelBlue"
| '''Chemical / poisoning'''
|bgcolor="Beige"| [[Carbon monoxide poisoning]]
|-
|-bgcolor="LightSteelBlue"
| '''Dermatologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Drug Side Effect'''
|bgcolor="Beige"| [[Oral contraceptive pills]], particularly among women who smoke
 
[[Anabolic steroids]]
|-
|-bgcolor="LightSteelBlue"
| '''Ear Nose Throat'''
|bgcolor="Beige"| A recent [[upper respiratory tract infection]]s has been associated with a 4.9 fold rise in the risk of [[trigger of MI|MI]]
|-
|-bgcolor="LightSteelBlue"
| '''Endocrine'''
|bgcolor="Beige"| [[Thyrotoxicosis]]
|-
|-bgcolor="LightSteelBlue"
| '''Environmental'''
|bgcolor="Beige"| Blizzards and snow shoveling, and inhalation of fine particulate matter in areas with air pollution and high traffic have been identified as [[triggers of MI]].
|-
|-bgcolor="LightSteelBlue"
| '''Gastroenterologic'''
|bgcolor="Beige"| A heavy meal has been associated with a 4 fold rise in the risk of [[trigger of MI|MI]], and it is not clear if this is mediated by hyperadrenergic tone<ref name="pmid15609883">{{cite journal |author=Lipovetzky N, Hod H, Roth A, Kishon Y, Sclarovsky S, Green MS |title=Heavy meals as a trigger for a first event of the acute coronary syndrome: a case-crossover study |journal=Isr. Med. Assoc. J. |volume=6 |issue=12 |pages=728–31 |year=2004 |month=December |pmid=15609883 |doi= |url=}}</ref>;
|-
|-bgcolor="LightSteelBlue"
| '''Genetic'''
|bgcolor="Beige"| [[Familial hypercholesterolemia]]
|-
|-bgcolor="LightSteelBlue"
| '''Hematologic'''
|bgcolor="Beige"| [[Disseminated intravascular coagulation]] ([[DIC]])
 
[[Hypercoagulable states]]
 
[[Polycythemia vera]]
 
[[Thrombocytosis]]
|-
|-bgcolor="LightSteelBlue"
| '''Iatrogenic'''
|bgcolor="Beige"| [[Epinephrine]] overdose
 
Sudden withdrawal of [[Beta blockers]] or [[nitrates]]
|-
|-bgcolor="LightSteelBlue"
| '''Infectious Disease'''
|bgcolor="Beige"| A recent [[upper respiratory tract infection]]s has been associated with a 4.9 fold rise in the risk of [[trigger of MI|MI]]
 
[[Infectious endocarditis]] may STEMI as a result of embolization
|-
|-bgcolor="LightSteelBlue"
| '''Musculoskeletal / Ortho'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Neurologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Nutritional / Metabolic'''
|bgcolor="Beige"| A heavy meal has been associated with a 4 fold rise in the risk of [[trigger of MI|MI]] and it is not clear if this is mediated by hyperadrenergic tone<ref name="pmid15609883">{{cite journal |author=Lipovetzky N, Hod H, Roth A, Kishon Y, Sclarovsky S, Green MS |title=Heavy meals as a trigger for a first event of the acute coronary syndrome: a case-crossover study |journal=Isr. Med. Assoc. J. |volume=6 |issue=12 |pages=728–31 |year=2004 |month=December |pmid=15609883 |doi= |url=}}</ref>;


[[Amyloidosis]]
==Videos of STEMI pathophysiology==
The following are excellent videos demonstrating the underlying pathophysiology.
{{#ev:youtube|L6EiPLli5x8}}
{{#ev:youtube|cOMzh2hf_Vw}}
{{#ev:youtube|a8Idk4EUYTs}}


[[Fabry disease]]
[[Homocystinuria]]
[[Mucopolysaccharidoses]] or [[Hurler disease]]
[[Pseudoxanthoma elasticum]]
[[Thiamine deficiency]] has been associated with ST elevation and myonecrosis <ref name="pmid16020883">{{cite journal |author=Kawano H, Koide Y, Toda G, Yano K |title=ST-segment elevation of electrocardiogram in a patient with Shoshin beriberi |journal=Intern. Med. |volume=44 |issue=6 |pages=578–85 |year=2005 |month=June |pmid=16020883 |doi= |url=http://joi.jlc.jst.go.jp/JST.JSTAGE/internalmedicine/44.578?from=PubMed}}</ref> <ref>Hundley JM, Ashburn LL, Sebrell WH. The electrocardiogram in chronic thiamine deficiency in rats. Am J Physiol 144: 404–414, 1954. </ref>  <ref name="pmid7197132">{{cite journal |author=Read DH, Harrington DD |title=Experimentally induced thiamine deficiency in beagle dogs: clinical observations |journal=Am. J. Vet. Res. |volume=42 |issue=6 |pages=984–91 |year=1981 |month=June |pmid=7197132 |doi= |url=}}</ref>
|-
|-bgcolor="LightSteelBlue"
| '''Obstetric/Gynecologic'''
|bgcolor="Beige"| Spontaneous coronary [[dissection]] in the setting of [[pregnancy]]
|-
|-bgcolor="LightSteelBlue"
| '''Oncologic'''
|bgcolor="Beige"| [[Radiation therapy]] can accelerate atherosclerosis particularly in the distribution of the left anterior descending artery;
|-
|-bgcolor="LightSteelBlue"
| '''Opthalmologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Overdose / Toxicity'''
|bgcolor="Beige"| [[Cocaine]] ingestion which may result in direct myocyte injury due to an adrendergic surge, vasoconstriction of the microvasculature or plaque rupture and thrombus formation;
[[Marijuana]] ingestion has been identified as a [[trigger of MI]].
|-
|-bgcolor="LightSteelBlue"
| '''Psychiatric'''
|bgcolor="Beige"| Anger, [[anxiety]], [[bereavement]], work-related stress, earthquakes, bombings and other psychosocial stressors have been identified as [[triggers of MI]], and it is not clear if the mechanism is plaque rupture or hyperadrenergic tone;
[[Stress cardiomyopathy]] or [[Broken heart syndrome]] causes ST segment elevation most often in the anterior precordium and is thought to be due to direct [[myocyte]] injury from a hyperadrenergic stimulation emanating from the central nervous system.
|-
|-bgcolor="LightSteelBlue"
| '''Pulmonary'''
|bgcolor="Beige"| A recent [[upper respiratory tract infection]]s has been associated with a 4.9 fold rise in the risk of [[trigger of MI|MI]]
|-
|-bgcolor="LightSteelBlue"
| '''Renal / Electrolyte'''
|bgcolor="Beige"| [[Homocystinuria]]
|-
|-bgcolor="LightSteelBlue"
| '''Rheum / Immune / Allergy'''
|bgcolor="Beige"| Takayasus
|-
|-bgcolor="LightSteelBlue"
| '''Sexual'''
|bgcolor="Beige"| Sexual activity has been identified as a [[trigger of MI]]
|-
|-bgcolor="LightSteelBlue"
| '''Trauma'''
|bgcolor="Beige"| Both penetrating and non-penetrating trauma to the heart or [[myocardial contusion]], [[commotio cordis]] can be associated with ST elevation and myonecrosis.
|-
|-bgcolor="LightSteelBlue"
| '''Urologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Miscellaneous'''
|bgcolor="Beige"| [[Hypotension]] particularly if it is prolonged
|-
|}
==Sources==
*The 2004 ACC/AHA Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction <ref name="pmid15339869">{{cite journal |author=Antman EM, Anbe DT, Armstrong PW, Bates ER, Green LA, Hand M, Hochman JS, Krumholz HM, Kushner FG, Lamas GA, Mullany CJ, Ornato JP, Pearle DL, Sloan MA, Smith SC, Alpert JS, Anderson JL, Faxon DP, Fuster V, Gibbons RJ, Gregoratos G, Halperin JL, Hiratzka LF, Hunt SA, Jacobs AK |title=ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Revise the 1999 Guidelines for the Management of Patients with Acute Myocardial Infarction) |journal=Circulation |volume=110 |issue=9 |pages=e82–292 |year=2004 |month=August |pmid=15339869 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=15339869}}</ref>
*The 2007 Focused Update of the ACC/AHA 2004 Guidelines for the Management of Patients with ST-Elevation Myocardial Infarction <ref name="pmid18071078">{{cite journal |author=Antman EM, Hand M, Armstrong PW, ''et al'' |title=2007 Focused Update of the ACC/AHA 2004 Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines: developed in collaboration With the Canadian Cardiovascular Society endorsed by the American Academy of Family Physicians: 2007 Writing Group to Review New Evidence and Update the ACC/AHA 2004 Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction, Writing on Behalf of the 2004 Writing Committee |journal=Circulation |volume=117 |issue=2 |pages=296–329 |year=2008 |month=January |pmid=18071078 |doi=10.1161/CIRCULATIONAHA.107.188209 |url=}}</ref>
==References==
==References==
{{Reflist|2}}
{{Reflist|2}}
Line 382: Line 176:
* Appelbaum E, Kirtane AJ, Clark A, Pride YB, Gelfand EV, Harrigan CJ, Kissinger KV, Manning WJ, Gibson CM. Association of TIMI Myocardial Perfusion Grade and ST-segment resolution with cardiovascular magnetic resonance measures of microvascular obstruction and infarct size following ST-segment elevation myocardial infarction. J Thromb Thrombolysis. 2008 Feb 2. [Epub ahead of print] PMID 18246410
* Appelbaum E, Kirtane AJ, Clark A, Pride YB, Gelfand EV, Harrigan CJ, Kissinger KV, Manning WJ, Gibson CM. Association of TIMI Myocardial Perfusion Grade and ST-segment resolution with cardiovascular magnetic resonance measures of microvascular obstruction and infarct size following ST-segment elevation myocardial infarction. J Thromb Thrombolysis. 2008 Feb 2. [Epub ahead of print] PMID 18246410
* Leshnower BG, Sakamoto H, Hamamoto H, Zeeshan A, Gorman JH 3rd, Gorman RC. Progression of myocardial injury during coronary occlusion in the collateral-deficient heart: a non-wavefront phenomenon. Am J Physiol Heart Circ Physiol. 2007 Sep;293(3):H1799-804. Epub 2007 Jul 20. PMID 17644569
* Leshnower BG, Sakamoto H, Hamamoto H, Zeeshan A, Gorman JH 3rd, Gorman RC. Progression of myocardial injury during coronary occlusion in the collateral-deficient heart: a non-wavefront phenomenon. Am J Physiol Heart Circ Physiol. 2007 Sep;293(3):H1799-804. Epub 2007 Jul 20. PMID 17644569
{{refend}}
{{refend}}
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==External Links==
[[Category:Disease]]
 
[[Category:Cardiology]]
* [http://hp2010.nhlbihin.net/atpiii/calculator.asp?usertype=pub Risk Assessment Tool for Estimating Your 10-year Risk of Having a Heart Attack - based on information of the Framingham Heart Study from the United States National Heart, Lung and Blood Institute]
[[Category:Ischemic heart diseases]]
* [http://www.nlm.nih.gov/medlineplus/heartattack.html Heart Attack overview from MedlinePlus]
[[Category:Intensive care medicine]]
* [http://ww2.heartandstroke.ca/Page.asp?PageID=1975&ArticleID=5288 Heart Attack Warning Signals from the Heart and Stroke Foundation of Canada]
* [http://www.regionalpci-stemi.org/index.html A Regional PCI and Resource Center for STEMI]
* [http://www.stemisystems.org/ STEMI Systems' Quarterly newsletter]
* [http://d2b.acc.org/ American College of Cardiology (ACC) Door to Balloon (D2B) Initiative.]
* [http://www.americanheart.org/heartattack American Heart Association's Heart Attack web site]
 
{{STEMI}}
 
[[Category:Pathology]]
[[Category:Emergency medicine]]
[[Category:Emergency medicine]]
[[Category:Cardiology]]
[[Category:Mature chapter]]
 
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Latest revision as of 21:17, 25 January 2023

https://https://www.youtube.com/watch?v=GeX7-sxxOn4%7C350}}

Acute Coronary Syndrome Main Page

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2]

Overview

ST elevation myocardial infarction is largely influenced by the role of plaque rupture.

The Role of Plaque Rupture in ST Elevation Myocardial Infarction

Atherosclerosis, or hardening of the arteries, is the gradual buildup of cholesterol and fibrous tissue (collagen and smooth muscle cells) throughout the vascular tree. When there is localized accumulation of lipids and scar tissue, this is called a "plaque". Somewhat paradoxically, it is not the most severe plaque narrowing that leads to ST elevation MI. Pathological studies indicate that it is often mild-to-moderate, lipid-laden, inflamed plaques that are the ones most likely to rupture and cause an ST elevation MI (STEMI) or a non ST elevation MI (NSTEMI). [1] The role of plaque rupture in STEMI and NSTEMI is supported by studies demonstrating that plaque rupture is present in about 70% and superficial erosion is present in 30% of patients who die suddenly in whom there is documented coronary artery disease. [2] Exposure of the blood stream to the thrombogenic components of the plaque leads to activation of the coagulation cascade and thrombus formation. In STEMI, the clot completely occludes the epicardial artery, and there is a complete lack of blood flow to the involved territory. This causes transmural injury and ST elevation. In NSTEMI, there is partial obstruction with embolization. This causes ischemia and subendocardial injury that are manifested by ST depression.

Shown here are multiple slices of the LAD. The proximal LAD is located to the left. Plaque rupture with thrombus formation begins in the second slice of the LAD.
Shown here is a magnified view of the second slice from the left. In yellow is atherosclerotic plaque, in red is clot that has formed inside the ruptured plaque and in the lumen of the coronary artery.

Pathophysiology of and Risk Factors for Plaque Rupture

  1. Macrophage accumulation has been shown to be present to a greater degree in patients with acute coronary syndromes than in those patients with chronic stable angina [3] [4] These activated macrophages can release enzymes such as metalloproteinases, interstitial collagenase, gelatinase, and stromelysin that degrade collagen, elastin, and proteoglycans. [5] This enzymatic degradation in turn leads to breakdown of the fibrous cap. The thin shoulders or edges of the fibrous cap appear to be particularly vulnerable to erosion and breakdown.
  2. Neovascularization of the plaque Moreno et have shown that microvessel density was increased in ruptured plaques when compared with nonruptured plaques (P=0.0001). Furthermore, among lesions with severe macrophage infiltration at the fibrous cap, microvessel density was increased (P=0.0001) was well as at the edges or shoulders of the plaque (P=0.0001). Intraplaque hemorrhage was also associated with an increase in microvessel density (P=0.04) as was the presence of thin-cap fibroatheromas (P=0.038). Microvessel density at the base of the plaque was identified as an independent (P=0.003) correlate of plaque rupture. [6]
  3. High oscillatory shear stress
  4. Vasoconstriction
  5. Spontaneous coronary dissection

Pathophysiology of and Risk Factors for Thrombosis Following Plaque Rupture

There are numerous systemic risk factors associated with thrombus formation following plaque rupture:

  1. Smoking: Smoking increases platelet aggregation and plasma epinephrine levels [7]
  2. Fibrinogen: Elevated levels of fibrinogen have been associated with thrombosis including abnormal levels of fibrinogen [8]
  3. Von Willebrand factor antigen [8]
  4. Tissue plasminogen activator [8]
  5. Anticardiolipin antibodies [9]
  6. Cross-linked fibrin-degradation products [10]
  7. Polymorphisms of a platelet glycoprotein receptor [11]

Gross Pathology Findings in Plaque Rupture

Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology

  • Left anterior descending coronary artery: Atherosclerosis Plaque Ruptured with Thrombosis: Gross; natural color; four cross sections, close-up view (acute anterior myocardial infarction with rupture)

    Left anterior descending coronary artery: Atherosclerosis Plaque Ruptured with Thrombosis: Gross; natural color; four cross sections, close-up view (acute anterior myocardial infarction with rupture)

  • Coronary artery: Atherosclerotic Plaque: Gross natural color close-up view of a typical plaque

    Coronary artery: Atherosclerotic Plaque: Gross natural color close-up view of a typical plaque

  • Coronary Atherosclerosis: Gross, natural color, close-up view of large atherosclerotic plaque with soft atheroma (a quite good example in 54yo male. Smoker with hypertension). This slide shows the left main artery

    Coronary Atherosclerosis: Gross, natural color, close-up view of large atherosclerotic plaque with soft atheroma (a quite good example in 54yo male. Smoker with hypertension). This slide shows the left main artery

  • Coronary artery: Atherosclerotic Plaque: Gross, natural color, close-up view of plaque with atheroma core causing more than 90% lumen occlusion (an excellent example)

    Coronary artery: Atherosclerotic Plaque: Gross, natural color, close-up view of plaque with atheroma core causing more than 90% lumen occlusion (an excellent example)

  • Coronary artery: Atherosclerotic Plaque with Hemorrhage and Thrombosis: Gross, natural color, cross section, close-up, an excellent example of right coronary artery in 71yo female.

    Coronary artery: Atherosclerotic Plaque with Hemorrhage and Thrombosis: Gross, natural color, cross section, close-up, an excellent example of right coronary artery in 71yo female.

  • Coronary artery: Atherosclerotic Plaque with Hemorrhage and Thrombosis: Gross, natural color, cross sections; there is excellent example of hemorrhagic plaque and thrombus at and just below the origin of first diagonal artery. Another one (a more acute one) was in the right coronary artery.

    Coronary artery: Atherosclerotic Plaque with Hemorrhage and Thrombosis: Gross, natural color, cross sections; there is excellent example of hemorrhagic plaque and thrombus at and just below the origin of first diagonal artery. Another one (a more acute one) was in the right coronary artery.

  • Coronary artery: Atherosclerotic Plaque with Thrombus: Gross natural color, close-up of cross section.

    Coronary artery: Atherosclerotic Plaque with Thrombus: Gross natural color, close-up of cross section.

  • Coronary artery: Atherosclerotic Plaque with Hemorrhage: Gross fixed tissue, cross sections. LAD and 1st diagonal with large plaques and several apparent areas of hemorrhage.

    Coronary artery: Atherosclerotic Plaque with Hemorrhage: Gross fixed tissue, cross sections. LAD and 1st diagonal with large plaques and several apparent areas of hemorrhage.

  • Coronary artery: Atherosclerosis: Gross, an excellent close-up atherosclerosis with hemorrhage into plaque.

    Coronary artery: Atherosclerosis: Gross, an excellent close-up atherosclerosis with hemorrhage into plaque.

  • Coronary artery: Atherosclerosis: Gross, cross sections coronary artery with hemorrhage into plaque (image shows full length of the artery).

    Coronary artery: Atherosclerosis: Gross, cross sections coronary artery with hemorrhage into plaque (image shows full length of the artery).

  • Coronary artery: Atherosclerosis: Gross, cross sections of artery showing plaques (an excellent example)

    Coronary artery: Atherosclerosis: Gross, cross sections of artery showing plaques (an excellent example)

  • Coronary artery: Atherosclerosis: Gross natural color in situ cross section with large fibrocalcific plaque with hemorrhage (an excellent example)

    Coronary artery: Atherosclerosis: Gross natural color in situ cross section with large fibrocalcific plaque with hemorrhage (an excellent example)

Plaque Rupture Histopathological Findings

Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology

  • Coronary artery: Atherosclerosis: Micro H&E med mag; A good example of plaque rupture with thrombosis.

    Coronary artery: Atherosclerosis: Micro H&E med mag; A good example of plaque rupture with thrombosis.

  • Right coronary artery: Ruptured Plaque: Micro low mag H&E; Ruptured plaque with foam cell lesion (near rupture site).

    Right coronary artery: Ruptured Plaque: Micro low mag H&E; Ruptured plaque with foam cell lesion (near rupture site).

  • Right coronary artery: Atherosclerosis Plaque Ruptured with Thrombus: Micro low mag H&E; an excellent view of ruptured plaque with thrombus and some old fibrin in it.

    Right coronary artery: Atherosclerosis Plaque Ruptured with Thrombus: Micro low mag H&E; an excellent view of ruptured plaque with thrombus and some old fibrin in it.

  • Right coronary artery: Atherosclerosis Plaque Ruptured with Thrombus: Micro low mag trichrome.

    Right coronary artery: Atherosclerosis Plaque Ruptured with Thrombus: Micro low mag trichrome.

  • Right coronary artery: Atherosclerosis Plaque Ruptured: Micro low mag H&E; large plaque with hemorrhage; (an excellent example of hemorrhage).

    Right coronary artery: Atherosclerosis Plaque Ruptured: Micro low mag H&E; large plaque with hemorrhage; (an excellent example of hemorrhage).

  • Coronary artery: Atherosclerosis: Micro H&E low mag injected artery fairly typical uncomplicated atheromatous plaque

    Coronary artery: Atherosclerosis: Micro H&E low mag injected artery fairly typical uncomplicated atheromatous plaque

  • Coronary artery: Atherosclerosis: Micro H&E low mag, injected artery has typical fibrous plaque with small hemorrhage in atheroma.

    Coronary artery: Atherosclerosis: Micro H&E low mag, injected artery has typical fibrous plaque with small hemorrhage in atheroma.

  • Coronary artery: Atherosclerosis: Micro H&E low mag, injected artery is a very good example of marked lumen stenosis due to typical fibrous plaque with calcification

    Coronary artery: Atherosclerosis: Micro H&E low mag, injected artery is a very good example of marked lumen stenosis due to typical fibrous plaque with calcification

The Consequence of Plaque Rupture and Vessel Occlusion: The Time Dependent Wavefront of Necrosis

Time dependent wavefront of necrosis working its way from the subendocardium to the subepicardium
Time dependent wavefront of necrosis working its way from the subendocardium to the subepicardium

In 1940, Blumgart ligated or tied off the coronary artery in dogs and cats and for the first time demonstrated a wavefront of cell death folllowing vessel occlusion [12] [13] [14] [15] [16]

Irreversible injury of ischemic myocytes occurs first in the subendocardial zone. With more extended ischemia, a wavefront of cell death moves through the myocardium to involve progressively more of the transmural thickness of the ischemic zone. The precise location, size, and specific morphologic features of an acute myocardial infarction depend on:

  1. The location, severity, and rate of development of coronary atherosclerotic obstructions,
  2. The size of the vascular bed perfused by the obstructed vessels
  3. The duration of the coronary artery occlusion
  4. The metabolic / oxygen needs of the myocardium at risk,
  5. The extent of collateral blood vessels

Decrease of ATP levels in myocytes in reaction to ischemia starts within seconds and causes loss of contractility in first two minutes. If ischemia persists, ATP levels reduced to its half level within 10 minutes and to 1/10 within 40 minutes. Irreversible cell injury occurs between 20-40 minutes and microvascular level injury starts if ischemia lasts more than an hour.[17]

If impaired blood flow to the heart lasts long enough, it triggers a process called the ischemic cascade; the heart cells die (chiefly through necrosis) and do not grow back. A collagen scar forms in its place. Recent studies indicate that another form of cell death called apoptosis also plays a role in the process of tissue damage subsequent to myocardial infarction.[18] As a result, the patient's heart can be permanently damaged. This scar tissue also puts the patient at risk for potentially life threatening arrhythmias.

Pathophysiology of ST segment elevation on the electrocardiogram

In ST segment myocaridal infarction (STEMI), the ST segments on the ECG are by definition elevated and there is myonecrosis (death of myocytes) as reflected by elevation of biomarkers such as creatine kinase MB fraction (CK-MB) or troponin T or I (tn). The ST segments are elevated due to full thickness injury of the myocardium.

Videos of STEMI pathophysiology

The following are excellent videos demonstrating the underlying pathophysiology. {{#ev:youtube|L6EiPLli5x8}} {{#ev:youtube|cOMzh2hf_Vw}} {{#ev:youtube|a8Idk4EUYTs}}

References

  1. ↑ Falk E, Shah PK, Fuster V (1995). "Coronary plaque disruption". Circulation. 92 (3): 657–71. PMID 7634481. Unknown parameter |month= ignored (help)
  2. ↑ Burke AP, Farb A, Malcom GT, Liang YH, Smialek J, Virmani R (1997). "Coronary risk factors and plaque morphology in men with coronary disease who died suddenly". N. Engl. J. Med. 336 (18): 1276–82. PMID 9113930. Unknown parameter |month= ignored (help)
  3. ↑ Moreno PR, Falk E, Palacios IF, Newell JB, Fuster V, Fallon JT (1994). "Macrophage infiltration in acute coronary syndromes. Implications for plaque rupture". Circulation. 90 (2): 775–8. PMID 8044947. Unknown parameter |month= ignored (help)
  4. ↑ van der Wal AC, Becker AE, van der Loos CM, Das PK (1994). "Site of intimal rupture or erosion of thrombosed coronary atherosclerotic plaques is characterized by an inflammatory process irrespective of the dominant plaque morphology". Circulation. 89 (1): 36–44. PMID 8281670. Unknown parameter |month= ignored (help)
  5. ↑ Shah PK, Falk E, Badimon JJ; et al. (1995). "Human monocyte-derived macrophages induce collagen breakdown in fibrous caps of atherosclerotic plaques. Potential role of matrix-degrading metalloproteinases and implications for plaque rupture". Circulation. 92 (6): 1565–9. PMID 7664441. Unknown parameter |month= ignored (help)
  6. ↑ Moreno PR, Purushothaman KR, Fuster V; et al. (2004). "Plaque neovascularization is increased in ruptured atherosclerotic lesions of human aorta: implications for plaque vulnerability". Circulation. 110 (14): 2032–8. doi:10.1161/01.CIR.0000143233.87854.23. PMID 15451780. Unknown parameter |month= ignored (help)
  7. ↑ Hung J, Lam JY, Lacoste L, Letchacovski G (1995). "Cigarette smoking acutely increases platelet thrombus formation in patients with coronary artery disease taking aspirin". Circulation. 92 (9): 2432–6. PMID 7586342. Unknown parameter |month= ignored (help)
  8. ↑ 8.0 8.1 8.2 Thompson SG, Kienast J, Pyke SD, Haverkate F, van de Loo JC (1995). "Hemostatic factors and the risk of myocardial infarction or sudden death in patients with angina pectoris. European Concerted Action on Thrombosis and Disabilities Angina Pectoris Study Group". N. Engl. J. Med. 332 (10): 635–41. PMID 7845427. Unknown parameter |month= ignored (help)
  9. ↑ Vaarala O, Mänttäri M, Manninen V; et al. (1995). "Anti-cardiolipin antibodies and risk of myocardial infarction in a prospective cohort of middle-aged men". Circulation. 91 (1): 23–7. PMID 7805207. Unknown parameter |month= ignored (help)
  10. ↑ Ridker PM, Hennekens CH, Cerskus A, Stampfer MJ (1994). "Plasma concentration of cross-linked fibrin degradation product (D-dimer) and the risk of future myocardial infarction among apparently healthy men". Circulation. 90 (5): 2236–40. PMID 7955179. Unknown parameter |month= ignored (help)
  11. ↑ Weiss EJ, Bray PF, Tayback M; et al. (1996). "A polymorphism of a platelet glycoprotein receptor as an inherited risk factor for coronary thrombosis". N. Engl. J. Med. 334 (17): 1090–4. PMID 8598867. Unknown parameter |month= ignored (help)
  12. ↑ Blumgart HL, Schlesinge MJ, Davis D: Studies on the relation of the clinical manifestations of angina pectoris, coronary thrombosis, and myocardial infarction to the pathologic findings, with particular reference to the significance of collateral circulation. Amer Heart J 19: 1, 1940
  13. ↑ Blumgart HL, Zoll PM, Freedberg AS, Gilligan DR: The experimental production of intercoronary arterial anastomoses and their functional significance. Circulation 1: 10, 1950 PMID 15401193
  14. ↑ Blumgart HL, Zoll PM, Kurland CS: Discussion of direct relief of coronary occlusion. Arch Intern Med (Chicago) 104: 862, 1959 PMID 13801751
  15. ↑ Blumgart HL, Zoll PM. Pathologic physiology of angina pectoris and acute myocardial infarction. Circulation. 1960 Aug;22:301-7. PMID 13801752
  16. ↑ Blumgart HL, Zoll PM, Clinical Pathologic Correlations in Coronary Artery Disease, Circulation, Volume XLVII, No 6, June 1973, 1139-43 PMID 4575525
  17. ↑ Robbins Pathologic Basis of Disease, Kumar V, 7th ed
  18. ↑ Krijnen PA, Nijmeijer R, Meijer CJ, Visser CA, Hack CE, Niessen HW. (2002). "Apoptosis in myocardial ischaemia and infarction". J Clin Pathol. 55 (11): 801–11. PMID 12401816.

Additional Resources

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