Presentation on theme: "Acute Coronary Syndrome"— Presentation transcript:
1 Acute Coronary Syndrome Garland Anderson MDSeptember 29th 2014
2 Goals and ObjectivesReview the etiologies of Acute Coronary Syndrome (ACS)Gain understanding of how to diagnose ACSUnderstand the different types of ACSReview the treatment of ACSUnderstand risk stratification in patients with unstable angina and non-ST segment elevation myocardial infarctionBrief review of optimizing risk in secondary prevention after myocardial infarction
3 Etiologies Atherosclerosis is a diffuse arterial disease Endothelial dysFxFormation of plaquesTreatment of most risk factors reduces the dysfunctionProgression of plaquesFoam cells →fibrous capProne to RuptureResult ACS
8 Acute Coronary Syndrome DiagnosisHistory and Physical ExamEKGCardiac Biomarkers
9 History Chest pain Dyspnea Weakness Fatigue Nausea/Vomiting Present in less than half of patients over 85 years of ageTypically poorly localized to anterior chest+/- Radiation ( Arms, neck, epigastrium, or back)DyspneaMost common “atypical” symptomWeaknessFatigueNausea/VomitingDiaphoresis
10 History Further define likelihood of ACS with chest pain Atherosclerotic risk factorsAssociated medical conditions (HTN/HLD)AgeSmokingSimilar pain with prior MIChest pain characteristics not likely to represent ACSWorsens withLocalized palpitationDeep breathingMovement of the affected area
11 ElectrocardiogramShould be obtained within 10 minutes of presentation to the emergency departmentST-segment elevation of 0.1 mV or more in at least 2 contiguous ECG leadsDiagnostic of STEMIDegree of ST-segment elevation correlates with the amount of myocardium experiencing injuryST-segment depression and/or T-wave inversion can indicate ischemiaSuggestive of, but not specific for, the diagnosis of unstable angina or NSTEMI
12 ElectrocardiogramECG results can be initially normal in up to 20% of patients experiencing ACS.Might not be helpful If patient’s baseline ECG is abnormalPreexisting ST-segment or T-wave changesLeft bundle-branch blockLeft ventricular hypertrophyLeft ventricular aneurysmMyocarditisElectrolyte abnormalityPreexcitation syndromeVentricular pacemaker rhythm
19 Cardiac Biomarkers Troponins Highly sensitive and specific markers of myocardial damageElevated in patients with NSTEMI and STEMI but are normal in patients with unstable anginaTypically 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 patientSerial levels should be measured at 8-hour intervals on the first dayWhen levels are elevated, they can remain elevated for up to 10 days
20 Cardiac BiomarkersIn ACS, the amount of troponin elevation is directly related to infarct sizeNormal serial troponin levels rule out an acute MI with a high negative predictive valueMultiple nonischemic etiologies of elevated troponin
23 TreatmentCritical to initiate therapy promptly to limit ongoing myocardial damageMust be tailored to the type of ACS and specific patient characteristics
24 TreatmentOxygenSupplemental oxygen is usually administered to all patientsRecommended in patients with:Arterial oxygen saturation level less than 90%Respiratory distressIncipient heart failure
25 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 resolvesPatient should be in the seated or recumbent position when administered to optimize benefit and prevent systemic hypotensionIschemic chest pain continues or recurs, intravenous NTG is indicatedContraindicated in patients who have taken phosphodiesterase inhibitors (eg, sildenafil, tadalafil) within the previous 24 hoursUse with caution in patients with right ventricular infarction or diastolic dysfunction to prevent systemic hypotension
26 Treatment Relief of Anginal Pain Morphine sulfate (2 to 5 mg) Major role in analgesia.Safety concerns have been raised about the use of morphineSome studies have found a higher likelihood of mortality in patients receiving morphine
27 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.
28 Treatment Initial Antiplatelet Therapy Clopidogrel (Plavix) Patients who are intolerant of ASA because of allergy or major gastrointestinal disease.Loading dose of 300 mg75 mg/day maintenance dosage
30 Treatment Cardioprotective Drugs Beta blockers Should be administered within the first 24 hours unless contraindicated.Marked first-degree atrioventricular (AV) blockPR interval more than 240 msSecond- or third-degree AV blockAcute heart failureLow cardiac-output statesActive bronchospasm.
31 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
32 Treatment Cardioprotective Drugs Angiotensin-converting enzyme (ACE) inhibitorsShould 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
33 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
34 Treatment Management of STEMI Percutaneous Coronary Intervention (PCI) Coronary angiography and angioplasty with stent placement are the reperfusion therapies of choice in patients presenting withAcute STEMIACS with a new (or presumed new) left bundle-branch blockPosterior wall myocardial infarction (MI)Therapies of choice if they presentWithin 12 hours of symptom onsetHospital with PCI capabilityPCI can be performed within 90 minutes of first medical contactdoor-to-balloon time
35 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 unopposedBare-metal stent should be considered because of the possibility of poor long-term adherence to antiplatelet drug
36 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
37 Treatment Management of STEMI Coronary Artery Bypass Graft Surgery Associated with low rates of recurrent ischemia, complete revascularization, and few revascularizationPreferred therapy forLeft main coronary disease,Left main equivalent disease (ie, high-grade proximal stenosis of the left anterior descending and circumflex arteries)Diffuse 3-vessel diseaseSurgical 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.
38 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 aloneFibrinolysis = 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.
39 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.
40 Treatment Management of NSTEMI/UA Anti-Ischemic, Antiplatelet, and Anticoagulant therapyIdentical to management of STEMINon-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.
41 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 PresentationsCardiogenic ShockHemodynamic InstabilityClinical Heart FailureSevere Systolic Dysfunction (EF < 40%)Persistent or Recurrent IschemiaSustained Ventricular TachycardiaHigh-risk Thombolysis in Myocardial Infarction (TIMI) score
42 TIMI Risk Score for UA/NSTEMI TreatmentTIMI Risk Score for UA/NSTEMICalculation of Risk ScoreApplication of Risk ScoreCharacteristicPointScoreDeath/MI/Urgent Revascularization (14 d)Historical0-15%Age ≥ 65 y128%≥3 Risk factors for CAD313%Known CAD (stenosis ≥50%)420%Aspirin use in past 7 days526%Presentation6-741%Severe angina (≥ 2 episodes w/in 24h)ST deviation > 0.5 mm+ cardiac markers (Troponin, CK-MB)RISK SCORE = Total points(0-7)
45 Summary Acute coronary syndrome requires prompt diagnosis Early medical management is needed to reduce risk to myocardial tissueThe type of ACS guides the choice of treatment modalitiesRisk stratification/TIMI scores show what patients with NSTEMI/UA could benefit from early PCIRisk factor modification is important in secondary prevention of myocardial infarctions
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