Acute coronary syndrome (ACS) results from diminished blood flow due to plaque rupture and clot formation. It includes unstable angina, STEMI, and NSTEMI. STEMI is identified by elevated cardiac enzymes and ECG changes, while unstable angina has normal enzymes. Treatment goals are restoration of blood flow and prevention of complications. Pharmacotherapy includes aspirin, anticoagulants, fibrinolytics if within 12 hours of STEMI onset, and P2Y12 inhibitors like clopidogrel. Long-term secondary prevention focuses on risk factor modification and use of aspirin, statins, beta-blockers, and ACE inhibitors.
Acute coronary syndrome (ACS) results from diminished blood flow due to plaque rupture and clot formation. It includes unstable angina, STEMI, and NSTEMI. STEMI is identified by elevated cardiac enzymes and ECG changes, while unstable angina has normal enzymes. Treatment goals are restoration of blood flow and prevention of complications. Pharmacotherapy includes aspirin, anticoagulants, fibrinolytics if within 12 hours of STEMI onset, and P2Y12 inhibitors like clopidogrel. Long-term secondary prevention focuses on risk factor modification and use of aspirin, statins, beta-blockers, and ACE inhibitors.
Acute coronary syndrome (ACS) results from diminished blood flow due to plaque rupture and clot formation. It includes unstable angina, STEMI, and NSTEMI. STEMI is identified by elevated cardiac enzymes and ECG changes, while unstable angina has normal enzymes. Treatment goals are restoration of blood flow and prevention of complications. Pharmacotherapy includes aspirin, anticoagulants, fibrinolytics if within 12 hours of STEMI onset, and P2Y12 inhibitors like clopidogrel. Long-term secondary prevention focuses on risk factor modification and use of aspirin, statins, beta-blockers, and ACE inhibitors.
Acute coronary syndrome (ACS) results from diminished blood flow due to plaque rupture and clot formation. It includes unstable angina, STEMI, and NSTEMI. STEMI is identified by elevated cardiac enzymes and ECG changes, while unstable angina has normal enzymes. Treatment goals are restoration of blood flow and prevention of complications. Pharmacotherapy includes aspirin, anticoagulants, fibrinolytics if within 12 hours of STEMI onset, and P2Y12 inhibitors like clopidogrel. Long-term secondary prevention focuses on risk factor modification and use of aspirin, statins, beta-blockers, and ACE inhibitors.
flow secondary to Plaque rupture and clot formation • Unstable angina with normal troponin while STE MI and NSTE MI with elevated troponin level • According to ECG, MI is classified into STE MI and NSTE ACS (MI and UA) • NSTE is usually smaller than STE MI • Ventricular remodeling following acute MI Unstable Angina • Cardiac enzymes (Troponine and CK MB) are NOT elevated • Treatment Goal (main): restoration of blood flow • Prevention of death • Prevention of coronary artery occlusion • Relief of ischemic chest discomfort • Restoration of ST segment and T wave changes on ECG STE MI • Elevated Troponin • Early pharmacologic therapy for STE MI: • Fibrinolytic therapy: • Within the 1st 12 hrs • If within 6 hrs, more specific agent is recommended (alteplase, reteplase) • Side effect: ICH and systemic bleeding Aspirin
• Drug of choice for all ACS patients
• Other NSAIDs should be discontinued at the time of STE MI • Side effects: dyspepsia, nausea, bleeding • Platelets P2Y12 inhibitors: • Clopidogril, prasugrel and ticagrelor • prasugrel and ticagrelor more potent than cloppidogril • Coadministration of aspirin with P2Y12 inhibitors is recommended for all pts with STE MI • For STE MI with undergoing PCI coadministration is recommended to prevent stent thrombosis • Prasugrel is contraindicated in the presence of previous history of stroke • Duration of treatment: at least 12 month after stent • Nonadherence is a major risk factor for stent thrombosis • Side effect of ticagrelor is dyspnea Glycoprotien IIb/ IIIa receptor inhibitors:
• In patients with STE MI undergoing PCI who
have treated with UFH, abxiximab, eptifibatide, or tirofiban may be administered • Bleeding is the most significant side effect Anticoagulants
• If undergoing PCI, either UFH or bivalirudin is
preferred • For fibrinolysis, enoxaparin is preferred • Bivalirudin has similar efficacy but better safety than UFH • Side effect: Bleeding (highest risk with UFH), HIT (Except Bivalirudine and Fondaparinux) • Fondaparinux is contraindicated when GFR is declined Nitrates
• SL NTG every 5 minutes
• IV NTG should be initiated for all pts with ACS and persistent ischemia, HF, uncontrolled BP BP Control
• B blockers and ACE/ARB are drug of choice for
patients with ACS • CCBs Usually should be avoided, but If contraindications to Β-blockers • Nefidipine should be avoided Pharmacotherapy of NSTE MI:
• Elevated troponine levels
• Similar pharmacotherapy to that of STE MI • In absence of contraindications, all pts should be treated with intranasal oxygen, SL NTG, aspirin, and anticoagulant • Fibrinolytic therapy is not indicated in any pt with NSTE ACS Prevention following MI
• The long term goals after MI are:
• Control modifiable CHD risk factors • Prevent development of HF • Prevent recurrence • Prevent death • Prevent stent thrombosis following PCI • Following MI, all patients should receive indefinite treatment with aspirin, B-blockers and ACEI for secondary prevention of death, stroke or recurrent infarction • ALL pts will receive statins • P2Y12 inhibitor should be continued for at least 12 months after PCI • Clopidogril should be continued for 14 days in pts with STE MI not undergoing PCI • Treatment of modifiable risk factors • The use of meneralocorticoid receptor antagonists: • Administration of eplerenone or spironolactone should be considered within the 1st 2 wks following MI in all pts who already receive ACEI and B-blocker and have LVEF less than 40% and either HF or DM Lipid lowering agents
• All pts with CAD should receive dietary
counceling and pharmacotherapy to reduce LDL cholesterol to less than 100 mg/dL • Statins shown anti-inflammatory and antithrombotic properties • Studies with fibrates have produced less definitive results