Overview Acute Coronary Syndromes Rabeea Aboufakher, MD, FACC, FSCAI Section Chief of Cardiology Altru Health System Grand Forks, ND Epidemiology Pathophysiology Clinical features and diagnosis STEMI management NSTEMI/UA management Introduction/Epidemiology Introduction/Epidemiology CAD is a major cause of death and disability worldwide ACS will strike 935,000 people a year in the US, an estimated 250,000 of those will be STEMIs Responsible for one third of all deaths in individuals over age 35 In ND 43% of adults have 3 or more risk factors for Cardiovascular disease 17.6 million persons in the US have CAD CV disease is the #1 leading cause of death in ND Age adjusted death rates for coronary heart disease by race/ethnicity and sex, US, 1999 to 2008 Deaths from cardiovascular disease, US, 1900 to 2008 Prevalence of CAD and CAD mortality have declined over the past 4 decades in the US 1
CAD PATHOPHYSIOLOGY Spectrum of presentation silent ischemia exertion-induced angina unstable angina acute myocardial infarction STEMI NSTEMI Acute coronary syndromes Stable Vs. Unstable Pathophysiology of ACS Slowly accruing high-grade stenoses of epicardial coronary arteries may progress to complete occlusion but do not usually precipitate ACS Stable angina Silent ischemia Abrupt and catastrophic transition may occur characterized by plaque disruption by rupture of the fibrous cap or erosion of the surface ACS The shift in our understanding of ACSs Pathophysiology of ACS The Vulnerable Plaque Most lesions that cause ACSs are not severely stenotic 2
Chest Pain CLINICAL FEATURES Atypical presentations are common in women, diabetics and the elderly ECG Extensive Anterior STEMI Septal: V1 and V2 Anterior: V3 and V4 Lateral: V5 and V6 Anteroseptal: V1-V4 Anterolateral: V3-V6 Extensive anterior: V1-V6 Inferior: II, III, avf High Lateral: I, avl Always look for the reciprocal changes Posterior: R wave and ST depression in V1-V2 Inferior STEMI with Posterior and Lateral Involvement Isolated Posterior STEMI 3
LBBB ST Depression T Wave Inversion Cardiac Enzymes Coronary Angiography 4
STEMI: Time is muscle!! STEMI MANAGEMENT ACC/AHA GUIDELINES STEMI What is 1/5/2015 2010, American Heart Association Mission: Lifeline ND Hospitals Mission: Lifeline will: Promote ideal STEMI systems of care Help STEMI patients get the life-saving care they need in time Bring together healthcare resources into an efficient, synergistic system Improve overall quality of care The initiative is unique in that it: Addresses the continuum of care for STEMI patients Preserves a role for the local STEMI-referral hospital Understands the issues specific to rural communities Promotes different solutions/protocols for rural vs. urban/suburban areas Recognizes there is no one-size-fits-all solution Knows the issues of implementing national recommendations on a community level Improving the System of Care for STEMI Patients 5
Pre-hospital Care (EMS) Initial Recognition and Management in the ED Non-enteric-coated aspirin (162-325 mg chewed) Class I Pre-hospital ECG Class IIa Oxygen Class I IV access Morphine as needed for pain control Class I Sublingual nitroglycerine Class I Hospitals should develop guideline-based, institutionspecific written protocols for triaging and managing pts with symptoms suggestive of STEMI Class I Door to needle time should be < 30 minutes Class I Door to balloon time should be < 90 minutes Class I Focused history and physical to make sure other important diagnoses are not missed ECG 12 lead ECG should be performed and shown to the ED physician within 10 minutes of arrival Class I If the ECG is not diagnostic but symptoms continue repeat ECG in 5-10 minutes Class I If inferior ST elevation a right sided ECG should be done to assess for RV infarction Class I Beta Blockers Class I Oral beta-blocker therapy should be administered promptly to those patients without a contraindication Class IIa It is reasonable to administer IV beta-blockers promptly to patients without contraindications, especially if a tachyarrhythmia or hypertension is present Reperfusion Therapy: Primary PCI vs. Fibrinolysis Reperfusion Therapy 6
Reperfusion Therapy Relative Risk of In-Hospital Death with Each Additional 15 Minute Interval in Door to Balloon Time As Compared to Less Than 90 Minutes Nallamothu B et al. N Engl J Med 2007;357:1631-1638 Heparin UFH bolus of 60 U/kg (maximum 4000 U) followed by an initial infusion of 12 U/kg per hour (maximum 1000 U/hr) adjusted to maintain aptt at 1.5 to 2.0 times Should be given with fibrinolysis Class I Should also be given to pts treated with primary PCI Class I LMWH especially enoxaparin is an acceptable alternative to UFH in pts who undergo PCI or fibrinolysis but is contraindicated in Patients older than 75 years Patients with renal dysfunction (Cr >2.5 in men and >2.0 in women) Class IIb Glycoprotein IIb/IIIa Inhibitors Direct Thrombin Inhibitors: Bivalirudin It is reasonable to start treatment with abciximab or other GP IIb/IIIa inhibitors before PCI Class IIa Have fallen out of favor due to increased bleeding and use of better antiplatelet and anticoagulant agents May have a role in the high risk patient with large burden of thrombus and low risk of bleeding The most significant advance in antithrombotic agents during PCI Has several advantages over heparin Specific thrombin inhibitor so activity is predictable (no need for ACT testing Short half-life (25-30 minutes) No risk of heparin-induced thrombocytopenia Lower risk of bleeding 7
Bivalirudin in Primary PCI Antiplatelet Therapy Aspirin should be continued indefinitely after STEMI Class I A loading dose of P2Y12 antagonist is recommended when PCI is planned Class I Clopidogrel 300 or 600 mg Prasugrel 60 mg Ticagrelor 180 mg The duration of treatment should be at least 12 months after stenting Class I Should be discontinued 5 days before CABG ACE-I and ARB An ACE-I or an ARB should be given orally within the first 24 hours of STEMI In pts with anterior infarct, pulmonary congestion or with EF<40% Class I In all patient with STEMI Class IIa IV ACE-I or ARB should not be given in the first 24 hours to avoid hypotension Class III Summary of Initial Treatment in ED MONA ECG with interpretation within 10 minutes Decision on reperfusion therapy (fibrinolysis or primary PCI) Activate cath lab if PCI center Decision on transfer if non-pci center Load with a P2Y12 antagonist (confirm with cardiologist) UFH or LMWH Consider glycoprotein IIb/IIIa inhibitor (only after discussion with cardiologist) BB if no contraindication UA/NSTEMI MANAGEMENT ACC/AHA GUIDELINES NSTEMI and Unstable Angina The only difference is cardiac enzyme elevation due to more severe ischemia Same symptoms, pathophysiology and management guidelines 8
Unstable Angina TIMI Risk Score Angina occurring at rest and prolonged, usually greater than 20 min New-onset angina of at least CCS class III severity Previously diagnosed angina that has become distinctly more frequent, longer in duration, or lower in threshold (i.e., increased by 1 or more CCS class to at least CCS class III severity) Age > 65 yrs > 3 risk factors for CAD Prior coronary stenosis > 50% ST segment deviation on admission ECG > 2 anginal episodes in prior 24 hrs Elevated serum cardiac biomarkers Use of ASA in prior 7 days TIMI Risk Score for Non-ST Elevation ACS High-Risk Patients Pt. Characteristics Older age (>75 yrs) Hemodynamic instability Signs and symptoms of CHF Ventricular arrhythmias Disease severity Crescendo, recurrent or refractory angina Positive serum cardiac biomarkers ST-segment deviation Initial Medical Treatment Similar to STEMI management with MONA, beta blockers and ACE-I inhibitors No beta blockers if Signs of HF Patient is at risk of cardiogenic shock (bradycardia or hypotension) Severe asthma or reactive airway disease 9
Nitroglycerine Antiplatelet Therapy Give if ongoing ischemic discomfort Do not give if: SBP < 90 HR < 50 Tachycardia Suspected RV infarct Treatment with PDE inhibitors Aspirin Clopidogrel (300-600 mg loading dose followed by 75 mg daily) Prasugrel (60 mg loading dose followed by 10 mg daily) (only for patients undergoing PCI in the cath lab) Ticagrelor (180 mg loading dose followed by 90 mg BID) Aspirin in UA/NSTEMI Clopidogrel in UA/NSTEMI Prasugrel in ACS Ticagrelor in ACS Prasugrel Less MI Less stent thrombosis More bleeding Not useful/ harmful History of CVA or TIA Age > 75 years Weight < 60 kg Ticagrelor Less vascular death and MI Less stent thrombosis No major difference in bleeding STEMI and NSTEMI/UA Aspirin < 100 mg 10
GP IIb/IIIa Inhibitors Anticoagulation Selective rather than routine use is advised due to high risk of bleeding in certain groups of patients with triple antiplatelet therapy Do not use if no plans for PCI Abciximab is preferred for STEMI Eptifibitide and tirofiban are associated with less thrombocytopenia and shorter half lives Initial invasive strategy UFH Enoxaparin Bivalirudin (direct thrombin inhibitor) Fondaparinux (Factor X inhibitor) Initial conservative strategy UFH Enoxaparin Fondaparinux Bivalirudin in Acuity Initial Invasive Vs. Initial Conservative Strategy Similar ischemic events Less bleeding events Superior net clinical outcome Initial Invasive Vs. Initial Conservative Strategy Most patients with UA/NSTEMI should undergo initial invasive strategy with angiography and intention to revascularize Thank you for your attention Initial conservative strategy Patients with multiple co-morbidities Patients with chest pain unlikely to be cardiac Low risk ACS especially in older underweight women if stress testing is low risk QUESTIONS? 11