Acute coronary syndrome

Question 1

What is acute coronary syndrome

Answer 1

•Any array of clinical symptoms resulting from underlying acute myocardial ischemia. Almost always associated with rupture of an atherosclerotic plaque and partial or complete thrombosis of the infarct-related coronary artery

Question 2

Causes of acute coronary syndrome

Answer 2

•Atherosclerotic plaque rupture with thrombus, Vasculitic syndromes, Coronary embolism, Congenital anomalies, Coronary trauma or aneurysm, Severe coronary artery spasm
Increased blood viscosity, Spontaneous coronary dissection, Markedly increased myocardial O2 demand

Question 3

How does atherosclerosis lead to coronary thrombosis?

Answer 3

Plaque rupture can cause platelet activation or coagulation cascade activation. Dysfunctional endothelium can cause decreased vasodilator effect and decreased antithrombotic effect

Question 4

Describe steps that lead to occlusion of vessel

Answer 4

Endothelial cells are activated then express adhesion molecules that recruit inflammatory cells > lipid formation in intima > macrophages engulf lipoprotein and become foam cells > lesion grows > Fibrous cap weakens b/c inflammatory mediators and proteinases > fibrous cap ruptures > thrombogenic tissue factor is exposed to blood and thrombosis begins > partial occlusion > total occlusion

Question 5

compare transmural to subendocardial ischemia

Answer 5

transmural is usually due to total occlusion. Subendocardialis usually due to partial occlusion, and is particularly susceptible to ischeima b/c it is subjected to highest pressure from ventricular chamber and has little collateral flow.

Question 6

What causes ST depression? ST elevation?

Answer 6

ST depression is caused by subendocardial ischemia b/c the ST vector is directed toward the inner layer of affected ventricle and awa from the overlying leads. ST elevation is caused by transmural ischemia b/c ST vector is directed towards overlying leads.

Question 7

Serum markers of MI

Answer 7

Troponin I and T- sensitive and specific for myocardium. Begin to rise 3-4 hours after onset of pain, Peak at 18-36 hours. Creatine kinase-MB: Not as specific for myocardium. Begins to rise 3-8 hours after onset of pain. Peaks at 24 hours

Question 8

Clinical symptoms of MI

Answer 8

Angina: chest pain / pressure / tightness or its equivalent (stable or unstable). Shortness of breath, sweating, nausea, vomiting, weakness

Question 9

Compare unstable Angina to MI: symptoms, vessel occlusion, serum biomarkers, ECG

Answer 9

unstable angina: escalating symptoms at rest with new onset angina, partial occlusion, no serum biomarkers, ST depression. MI: prolonged chest pain, more severe than unstable angina, Partial (NSTEMI) or total (STEMI) occlusion, serum biomarkers present, ST depression (NSTEMI) or ST elevation (STEMI)

Question 10

Treatment of ST elevated MI

Answer 10

Open artery! Catheter (if done within 90 minutes) or fibrinolytic agent. Reduce myocardial oxygen demand with BB or nitrates

Question 11

Treatment of unstable angina/ Non-ST elevated MI

Answer 11

Halt propagation of clot , reduce myocardial oxygen demand (BB, nitrates),

Question 12

How do you halt propagation of clot in unstable angina/ NSTEMI?

Answer 12

Antiplatelet agents: Aspirin plus P2Y12 inhibitor (Clopidogrel, Prasugrel or Ticagrelor) plus Glycoprotein Iia/IIIb inhibitorif catheterization (Eptifibatide, Tirofiban). Anticoagulants: Choose one of unfractionated heparin, enoxaparin, fondaparinux, possibly Bivalirudin