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Acute Coronary Syndrome Garland Anderson MD September 29 th 2014.

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Presentation on theme: "Acute Coronary Syndrome Garland Anderson MD September 29 th 2014."— Presentation transcript:

1 Acute Coronary Syndrome Garland Anderson MD September 29 th 2014

2 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

3 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

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6 Etiologies Rupture of Plaque Total Occlusion ST-segment elevation myocardial infarction (STEMI) Partial Occlusion-Spectrum of Disease Unstable Angina→ non- ST-segment elevation myocardial infarction (NSTEMI) Acute Coronary Syndrome Imbalance between coronary blood flow and myocardial oxygen demand

7 DDX Acute Chest Pain Anxiety/panic disorder Aortic dissection Costochondritis Esophageal Conditions (spasm) Gall bladder disease Myocarditis/pericarditis Peptic Ulcer Disease Pneumonia Pulmonary Embolus

8 Acute Coronary Syndrome Diagnosis History and Physical Exam EKG Cardiac Biomarkers

9 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

10 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

11 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

12 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

13 Electrocardiogram

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19 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

20 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

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22 Acute Coronary Syndrome

23 Treatment Critical to initiate therapy promptly to limit ongoing myocardial damage Must be tailored to the type of ACS and specific patient characteristics

24 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

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 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

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 morphine Some 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 mg 75 mg/day maintenance dosage

29 Treatment

30 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.

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) 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

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 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

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 unopposed Bare-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 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.

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 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.

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 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.

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 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

42 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)

43 Treatment

44 Secondary Risk Factor Prevention Blood Pressure Lipid Management Physical Activity Smoking Cessation Weight Management Other Considerations Diabetes Management Metabolic Syndrome Influenza Immunization

45 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

46 References AAFP-FP Comprehensive 2014 Lloyd-Jones D, Adams R, Carnethon M. Heart disease and stroke statistics—2009 update: a report from the Amercan Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation. 2009;119(3): Fuster V, Moreno PR, Fayad ZA. Atherothrombosis and high-risk plaque. J Am Coll Cardiol. 2005;46(6): [Review]. Thygesen K, Alpert JS, White HD. Universal definition of myocardial infarction. J Am Coll Cardiol. 2007;50(22): Brieger D, Eagle KA, Goodman SG. Acute coronary syndrome without chest pain, an underdiagnosed and undertreated high-risk group: insights from the Global Registry of Acute Coronary Events. Chest. 2004;126(2): Jones ID, Slovis CM. Emergency department evaluation of the chest pain patient. Emerg Med Clin North Am. 2001;19(2): [Review]. Swap CJ, Nagurney JT. Value and limitations of chest pain history in the evaluation of patients with suspected acute coronary syndrome. JAMA. 2005;294(20): [Review]. Erratum in JAMA. 2006;295(19):2250. Han JH, Lindsell CJ, Storrow AB. The role of cardiac risk factors burden in the diagnosing acute coronary syndromes in the emergency department setting. Ann Emerg Med. 2007;49(2): , 152.e1.

47 References Anderson JL, Adams CD, Antman EM. ACC/AHA 2007 guidelines for the management of patients with unstable angina/non-ST-Elevation myocardial infarction. J Am Coll Cardiol. 2007;50(7):e1-e157. Erratum in J Am Coll Cardiol. 2008;51(9):974. Piccini JP, Ohman EM. ECG interpretation in ST-elevation myocardial infarction: pattern recognition or caliper measurement? Heart. 2009;95(4): Turnipseed SD, Trythall WS, Diercks DB. Frequency of acute coronary syndrome in patients with normal electrocardiogram performed during presence or absence of chest pain. Acad Emerg Med. 2009;16(6): Meine TJ, Roe MT, Chen AY. Association of intravenous morphine use and outcomes in acute coronary syndromes: results from the CRUSADE Quality Improvement Initiative. Am Heart J. 2005;149(6): Gibler WB, Cannon CP, Blomkalns AL. Practical implementation of the guidelines for unstable angina/non-ST-segment elevation myocardial infarction in the emergency department: a scientific statement from the American Heart Association on Clinical Cardiology (Subcommittee on Acute Cardiac Care), Council on Cardiovascular Nursing, and Quality of Care and Outcomes Research Interdisciplinary Working Group, in Collaboration With the Society of Chest Pain Centers. Circulation. 2005;111(20): López-Sendón J, Swedberg K, McMurray J. Expert consensus document on beta-adrenergic receptor blockers. Eur Heart J. 2004;25(15): ACE Inhibitor Myocardial Infarction Collaborative Group. Indications for ACE inhibitors in the early treatment of acute myocardial infarction: systemic overview of individual data from 100,000 patients in randomized trials. Circulation. 1998;97(22):

48 References Spencer FA, Allegrone J, Goldberg RJ. Association of statin therapy with outcomes of acute coronary syndromes: the GRACE study. Ann Intern Med. 2004;140(11): Bavry AA, Mood G, Borek PP. Benefit of early statin therapy during acute coronary syndromes: a meta-analysis. J Am Coll Cardiol. 2006;47(4 Suppl A):205A. Cannon CP, Braunwald E, McCabe CH. Intensive versus moderate lipid lowering with statins after acute coronary syndromes. N Engl J Med. 2004;350(15): Erratum in N Engl J Med. 2006;354(7):778. Rodes-Cabau J, Tardif JC, Cossette M. Acute effects of statin therapy on coronary atherosclerosis following an acute coronary syndrome. Am J Cardiol. 2009;104(6): Marrow DA, Antman EM, Charlesworth A. TIMI risk score for ST- elevation myocardial infarction: a convenient bedside clinical score for the risk assessment at presentation. Circulation. 2000;102(17): King SB, Smith SC, Hirshfeld JW focused update of the ACC/AHA/SCAI 2005 guideline update for percutaneous coronary intervention. J Am Coll Cardiol. 2008;51(2):

49 References McNamara RL, Wang Y, Herrin J, Effects of door-to-balloon time on mortality in patients with ST-segment elevation myocardial infarction. J Am Coll Cardiol. 2006;47(11): Antman EM, Hand M, Armstrong PW focused update of the ACC/AHA 2004 guidelines for the management of patients with ST-elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2008;51(2): [Review]. Erratum in J Am Coll Cardiol. 2008;51(9):977. Huynh T, Perron S, O’Loughlin J. Comparison of primary percutaneous coronary intervention and fibrinolytic therapy in ST-segment-elevation myocardial infarction. Circulation. 2009;119(24): Mehta RH, Harjai KJ, Cox D. Clinical and angiographic correlates and outcomes of suboptimal coronary flow in patients with acute myocardial infarction undergoing primary percutaneous coronary intervention. J Am Coll Cardiol. 2003;42(10): Kushner FG, Hand M, Smith SC focused updates: ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction (updating the 2004 guideline and 2007 focused update). J Am Coll Cardiol. 2009;54(23):


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