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Pathogenesis of Acute Coronary Syndromes

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Viduranga Edirisinghe
Viduranga Edirisinghe

This presentation was prepared by Dr. Viduranga Edirisinghe; upon request made by the board certified Consultant Cardiologist, Dr.(Mrs). Nimali Fernando, MD

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Pathogenesis of ACSs
ACSs May result from new superimposed thrombosis on a pre-existing ("fixed") atherosclerotic occlusion and/or vasospasm of one or more coronary arteries.
Role of Acute Plaque Changes In most patients, unstable angina, infarction, and many cases of SCD all occur because of abrupt plaque change followed by thrombosis. Hence the term acute coronary syndrome.
Acute Plaque Changes Highly thrombogenic plaque constituents Rupture, fissuring, or Exposing ulceration Underlying subendothelial basement membrane Acute Coronary Syndromes Worsening of the luminal occlusion Hemorrhage into the Expansion of plaque core of plaques volume Plaque rupture
Pathogenesis of Acute Coronary Syndromes
Events that trigger the abrupt plaque changes Rupture reflects the inability of a plaque to withstand mechanical stresses. Triggers may be intrinsic or extrinsic Intrinsic factors Extrinsic factors Large atheromatous Adrenergic stimulation core Intense emotional stress Thickness of the fibrous cap
Integrity of the Plaque Fibrous caps are continuously remodeling collagen collagen synthesis degradation Collagen produced by smooth muscle cells Collagen degraded by the action of metalloproteinases (macrophages)
Role of Inflammation Inflammation plays an essential role at all stages of atherosclerosis Whats the contribution of Inflammation to acute coronary syndromes? Breakdown of Plaque Neutrophil Release of Inflammation collagen in the destabilization & infiltration metalloproteinases fibrous cap rupture
Role of Thrombus Formation of a thrombus on a disrupted atherosclerotic plaque Significant rapid stenosis Complete occlusion of the coronary arteries Mural thrombus in a coronary artery can also embolize Small fragments of thrombotic material Small infarcts
Acute Myocardial Infarction Ischemic necrosis of a part of the myocardium In a typical MI, A sudden disruption of an atheromatous plaque Platelets adhere, aggregate, become activated Release potent secondary aggregators(thromboxane A2, adenosine diphosphate, and serotonin) Other mediators activate the extrinsic pathway of coagulation Vasospasm (platelet aggregation and mediator release) Within minutes the thrombus can evolve to completely occlude the coronary lumen of the coronary vessel
Acute Myocardial Infarction Electrical instability of the Arrhythmias (ventricular myocardium fibrillation) Ischemia Death of myocardium Or a fatal mechanical failure Reduction in the contractility of the myocardium Reduction in the ejection fraction & increase in end systolic volume & pressure (Heart failure)
Irreversible injury of ischemic myocytes first occurs in the subendocardial zone (STEMI) With more prolonged ischemia Involve progressively more of the transmural thickness (NSTEMI)
Myocardial Infarction

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Pathogenesis of Acute Coronary Syndromes

  • 2. ACSs May result from new superimposed thrombosis on a pre-existing ("fixed") atherosclerotic occlusion and/or vasospasm of one or more coronary arteries.
  • 3. Role of Acute Plaque Changes In most patients, unstable angina, infarction, and many cases of SCD all occur because of abrupt plaque change followed by thrombosis. Hence the term acute coronary syndrome.
  • 4. Acute Plaque Changes Highly thrombogenic plaque constituents Rupture, fissuring, or Exposing ulceration Underlying subendothelial basement membrane Acute Coronary Syndromes Worsening of the luminal occlusion Hemorrhage into the Expansion of plaque core of plaques volume Plaque rupture
  • 6. Events that trigger the abrupt plaque changes Rupture reflects the inability of a plaque to withstand mechanical stresses. Triggers may be intrinsic or extrinsic Intrinsic factors Extrinsic factors Large atheromatous Adrenergic stimulation core Intense emotional stress Thickness of the fibrous cap
  • 7. Integrity of the Plaque Fibrous caps are continuously remodeling collagen collagen synthesis degradation Collagen produced by smooth muscle cells Collagen degraded by the action of metalloproteinases (macrophages)
  • 8. Role of Inflammation Inflammation plays an essential role at all stages of atherosclerosis Whats the contribution of Inflammation to acute coronary syndromes? Breakdown of Plaque Neutrophil Release of Inflammation collagen in the destabilization & infiltration metalloproteinases fibrous cap rupture
  • 9. Role of Thrombus Formation of a thrombus on a disrupted atherosclerotic plaque Significant rapid stenosis Complete occlusion of the coronary arteries Mural thrombus in a coronary artery can also embolize Small fragments of thrombotic material Small infarcts
  • 10. Acute Myocardial Infarction Ischemic necrosis of a part of the myocardium In a typical MI, A sudden disruption of an atheromatous plaque Platelets adhere, aggregate, become activated Release potent secondary aggregators(thromboxane A2, adenosine diphosphate, and serotonin) Other mediators activate the extrinsic pathway of coagulation Vasospasm (platelet aggregation and mediator release) Within minutes the thrombus can evolve to completely occlude the coronary lumen of the coronary vessel
  • 11. Acute Myocardial Infarction Electrical instability of the Arrhythmias (ventricular myocardium fibrillation) Ischemia Death of myocardium Or a fatal mechanical failure Reduction in the contractility of the myocardium Reduction in the ejection fraction & increase in end systolic volume & pressure (Heart failure)
  • 12. Irreversible injury of ischemic myocytes first occurs in the subendocardial zone (STEMI) With more prolonged ischemia Involve progressively more of the transmural thickness (NSTEMI)