Presentation on theme: "Acute Coronary Syndrome Garland Anderson MD September 29 th 2014."— Presentation transcript:
Acute Coronary Syndrome Garland Anderson MD September 29 th 2014
Goals and Objectives Review the etiologies of Acute Coronary Syndrome (ACS) Gain understanding of how to diagnose ACS Understand the different types of ACS Review the treatment of ACS Understand risk stratification in patients with unstable angina and non-ST segment elevation myocardial infarction Brief review of optimizing risk in secondary prevention after myocardial infarction
Etiologies Atherosclerosis is a diffuse arterial disease Endothelial dysFx Formation of plaques Treatment of most risk factors reduces the dysfunction Progression of plaques Foam cells →fibrous cap Prone to Rupture Result ACS
Acute Coronary Syndrome Diagnosis History and Physical Exam EKG Cardiac Biomarkers
History Chest pain Present in less than half of patients over 85 years of age Typically poorly localized to anterior chest +/- Radiation ( Arms, neck, epigastrium, or back) Dyspnea Most common “atypical” symptom Weakness Fatigue Nausea/Vomiting Diaphoresis
History Further define likelihood of ACS with chest pain Atherosclerotic risk factors Associated medical conditions (HTN/HLD) Age Smoking Similar pain with prior MI Chest pain characteristics not likely to represent ACS Worsens with Localized palpitation Deep breathing Movement of the affected area
Electrocardiogram Should be obtained within 10 minutes of presentation to the emergency department ST-segment elevation of 0.1 mV or more in at least 2 contiguous ECG leads Diagnostic of STEMI Degree of ST-segment elevation correlates with the amount of myocardium experiencing injury ST-segment depression and/or T-wave inversion can indicate ischemia Suggestive of, but not specific for, the diagnosis of unstable angina or NSTEMI
Electrocardiogram ECG results can be initially normal in up to 20% of patients experiencing ACS. Might not be helpful If patient’s baseline ECG is abnormal Preexisting ST-segment or T-wave changes Left bundle-branch block Left ventricular hypertrophy Left ventricular aneurysm Myocarditis Electrolyte abnormality Preexcitation syndrome Ventricular pacemaker rhythm
Cardiac Biomarkers Troponins Highly sensitive and specific markers of myocardial damage Elevated in patients with NSTEMI and STEMI but are normal in patients with unstable angina Typically do not increase until approximately 6 hours after onset of chest pain. ECG results consistent with ischemia, normal cardiac troponin levels should not be used in the decision to discharge a patient Serial levels should be measured at 8-hour intervals on the first day When levels are elevated, they can remain elevated for up to 10 days
Cardiac Biomarkers In ACS, the amount of troponin elevation is directly related to infarct size Normal serial troponin levels rule out an acute MI with a high negative predictive value Multiple nonischemic etiologies of elevated troponin
Treatment Critical to initiate therapy promptly to limit ongoing myocardial damage Must be tailored to the type of ACS and specific patient characteristics
Treatment Oxygen Supplemental oxygen is usually administered to all patients Recommended in patients with: Arterial oxygen saturation level less than 90% Respiratory distress Incipient heart failure
Treatment Relief of Anginal Pain Nitroglycerin (NTG) 0.4 mg should be administered sublingually every 5 minutes for up to 3 doses or until the pain resolves Patient should be in the seated or recumbent position when administered to optimize benefit and prevent systemic hypotension Ischemic chest pain continues or recurs, intravenous NTG is indicated Contraindicated in patients who have taken phosphodiesterase inhibitors (eg, sildenafil, tadalafil) within the previous 24 hours Use with caution in patients with right ventricular infarction or diastolic dysfunction to prevent systemic hypotension
Treatment Relief of Anginal Pain Morphine sulfate (2 to 5 mg) Major role in analgesia. Safety concerns have been raised about the use of morphine Some studies have found a higher likelihood of mortality in patients receiving morphine
Treatment Initial Antiplatelet Therapy Aspirin 162 to 325 mg should be started over the telephone or at the initial medical encounter, even if a dose was taken earlier that day. Administered to patients with STEMI whether or not they will receive fibrinolytic therapy. Chewed, rather than swallowed whole. 75 to 162 mg should then be continued indefinitely because it results in a significant reduction in mortality and MI.
Treatment Initial Antiplatelet Therapy Clopidogrel (Plavix) Patients who are intolerant of ASA because of allergy or major gastrointestinal disease. Loading dose of 300 mg 75 mg/day maintenance dosage
Cardioprotective Drugs Beta blockers Should be administered within the first 24 hours unless contraindicated. Marked first-degree atrioventricular (AV) block PR interval more than 240 ms Second- or third-degree AV block Acute heart failure Low cardiac-output states Active bronchospasm.
Treatment Cardioprotective Drugs Beta blockers Initial dose should be based on the heart rate and blood pressure. Reduce oxygen demand, ventricular fibrillation risk, cardiac remodeling, and progression of coronary disease. Help control heart rate and hypertension
Treatment Cardioprotective Drugs Angiotensin-converting enzyme (ACE) inhibitors Should be administered at a low dose within the first 24 hours of hospitalization. Reduce mortality and morbidity rates, prevent cardiac remodeling, and are of extra benefit in the presence of anterior wall infarctions, hypertension, and systolic dysfunction. Prevents approximately 1 mortality per 200 treated patients. Angiotensin receptor blockers can be substituted if the patient is intolerant of ACE inhibitors
Treatment Cardioprotective Drugs Statins Shown to be of long-term benefit in patients with ACS. Patients already taking a statin when presenting with ACS are less likely to have STEMI or acute in-hospital arrhythmias. Should be started in all patients with ACS during hospital admission, regardless of the LDL level. Plaque stabilization, reversal of endothelial dysfunction, decreased thrombogenicity, reduced inflammation independent of the long- term cholesterol level-lowering benefit. Early regression of coronary atherosclerosis, decrease in mortality rates, and significant reduction in the rate of major cardiovascular end points
Treatment Management of STEMI Percutaneous Coronary Intervention (PCI) Coronary angiography and angioplasty with stent placement are the reperfusion therapies of choice in patients presenting with Acute STEMI ACS with a new (or presumed new) left bundle-branch block Posterior wall myocardial infarction (MI) Therapies of choice if they present Within 12 hours of symptom onset Hospital with PCI capability PCI can be performed within 90 minutes of first medical contact door-to-balloon time
Treatment Management of STEMI Special situations Hospitals Without PCI Capability. These patients with STEMI should be transferred to a PCI center if the PCI can be performed within 90 minutes of first medical contact. Lack of Onsite Surgical Backup. Clinical studies indicate that patients at hospitals with PCI and stent capabilities but without onsite surgical backup can experience outcomes that are better than those associated with coronary fibrinolysis, if PCI is performed in a high- volume center by expert operators. Cocaine Users. Beta blocker use should always be avoided in cocaine users to prevent the vasoconstriction that can occur when beta blockers leave alpha stimulation unopposed Bare-metal stent should be considered because of the possibility of poor long-term adherence to antiplatelet drug
Treatment Management of STEMI Fibrinolysis Patients who cannot be transferred to a PCI center within 90 minutes should undergo urgent intravenous fibrinolysis. Most effective when administered within the first 4 hours, and especially within the first 30 to 60 minutes. Still beneficial up to 12 hours after symptom onset. Results in normal coronary perfusion in 55% of patients
Treatment Management of STEMI Coronary Artery Bypass Graft Surgery Associated with low rates of recurrent ischemia, complete revascularization, and few revascularization Preferred therapy for Left main coronary disease, Left main equivalent disease (ie, high-grade proximal stenosis of the left anterior descending and circumflex arteries) Diffuse 3-vessel disease Surgical mortality rates after CABG for patients with STEMI are higher in the first week after MI. when possible, surgery should be postponed for at least 1 week in patients in stable condition.
Treatment Management of STEMI Anticoagulants Recommended for all patients with STEMI. Unfractionated heparin (UFH) Low-molecular-weight heparin (LMWH) Synthetic heparin (fondaparinux [Arixtra]) Direct thrombin inhibitors (bivalirudin) Should be administered before invasive procedures are started. Choice of anticoagulant be guided by the reperfusion therapy planned and the individual’s risk of bleeding. PCI = UFH plus a glycoprotein inhibitor IIb/IIIa, or bivalirudin alone Fibrinolysis = UFH, LMWH, or fondaparinux If bleeding is a concern, LMWH is associated with a lower rate of reinfarction at 30 days than UFH, but it is also associated with more major bleeding.
Treatment Management of STEMI Antiplatelets ASA is indicated for all patients with STEMI whether they receive reperfusion therapy with PCI, fibrinolysis, or bypass surgery. Thienopyridines. If PCI is to be performed, clopidogrel should be administered in addition to ASA before the procedure (loading dose of 300 to 600 mg, followed by 75 mg/day). These drugs are indicated even when patients receive anticoagulants. Glycoprotein IIb/IIIa inhibitors (eg, abciximab [Reopro], eptifibatide [Integrilin], tirofiban [Aggrastat]) Not recommended for STEMI patients already receiving dual antiplatelet therapy plus an anticoagulant. Might have a role in the catheterization laboratory in select patients with large thrombi or those who have not received adequate pre-procedure thienopyridine therapy. More potent than clopidogrel, faster in onset, and more consistent in platelet inhibition.
Treatment Management of NSTEMI/UA Anti-Ischemic, Antiplatelet, and Anticoagulant therapy Identical to management of STEMI Non-ST-segment elevation MIs occur more frequently than STEMIs, but are associated with similar long-term outcomes. In contrast to STEMIs, for which urgent revascularization is required because of complete or near-complete vessel occlusion, urgent intervention is less often required for NSTEMIs because the involved vessel is partially patent in 60% to 85% of patients.
Treatment Predicting Mortality Risk The Thrombolysis in Myocardial Infarction (TIMI) risk score helps determine the risk of mortality within the first 30 days of presentation. High-Risk Clinical Presentations Cardiogenic Shock Hemodynamic Instability Clinical Heart Failure Severe Systolic Dysfunction (EF < 40%) Persistent or Recurrent Ischemia Sustained Ventricular Tachycardia High-risk Thombolysis in Myocardial Infarction (TIMI) score
Treatment TIMI Risk Score for UA/NSTEMI Calculation of Risk ScoreApplication of Risk Score CharacteristicPointScoreDeath/MI/Urgent Revascularization (14 d) Historical0-15% Age ≥ 65 y128% ≥3 Risk factors for CAD1313% Known CAD (stenosis ≥50%)1420% Aspirin use in past 7 days1526% Presentation6-741% Severe angina (≥ 2 episodes w/in 24h)1 ST deviation > 0.5 mm1 + cardiac markers (Troponin, CK-MB)1 RISK SCORE = Total points(0-7)
Summary Acute coronary syndrome requires prompt diagnosis Early medical management is needed to reduce risk to myocardial tissue The type of ACS guides the choice of treatment modalities Risk stratification/TIMI scores show what patients with NSTEMI/UA could benefit from early PCI Risk factor modification is important in secondary prevention of myocardial infarctions
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