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Management of Coronary Artery Disease PowerPoint Presentation

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Description : Check out this medical PowerPoint presentation titled "Management of Coronary Artery Disease" by Saravanan Kuppuswamy MD.
This medical PowerPoint presentation talks about Management of Coronary Artery Disease (CAD).
Coronary artery disease (CAD) is a condition in which the arteries that supply blood to the heart become narrowed or blocked, leading to decreased blood flow and oxygen supply to the heart muscle. It is a leading cause of heart attacks and other cardiovascular events.
The management of CAD involves several approaches, including lifestyle modifications, medications, and procedures.

Tags : Coronary Artery Disease, heart attacks, Cardiothoracic Surgery, cardiology, cardiology PowerPoint presentation

Published on : Mar 19, 2023 | Views : 1111 | Downloads : 4

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Management of Coronary Artery Disease: Saravanan Kuppuswamy MD Division of Cardiology Department of Internal Medicine University of Missouri Hospital
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Coronary blood supply
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Micro circulation
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Temporal Trends in CAD CHD is the leading cause of death in adults in US (1/3 of all deaths in subjects over age 35) Mortality rates for cardiovascular death has fallen in most developed countries 24-28% since 1975 Estimated that 45 percent of mortality reduction in CHD is due to improvement of medical therapy and 55% is due to risk factor modification
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Etiology Congenital Acquired Infection Inflammation Neoplastic
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Management of CAD Acute Chronic
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ACS=acute coronary syndrome. UA=unstable angina. Bhatt DL. J Invasive Cardiol. 2003;15:3B-9B. Acute Plaque Rupture (UA/NSTEMI/STEMI) Presence of Multiple Coronary Plaques Persistent Hyperreactive Platelets Vascular Inflammation Clinical Subclinical ACS: The Tip of the Atherothrombotic “Iceberg” NSTEMI=non-ST-segment elevation myocardial infarction. STEMI=ST-segment elevation myocardial infarction.
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Chronic stable angina Levine’s sign Exercise capacity may vary Relieved by nitrates
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CCS classification
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Applying Classification of Recommendations and Level of Evidence
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Components of Secondary Prevention
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ABCDE Of Management
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A
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Antiplatelet Agents / Anticoagulation Recommendations
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Aspirin Recommendations Start and continue indefinitely aspirin 75 to 162 mg/d in all patients unless contraindicated For patients undergoing CABG, aspirin (100 to 325 mg/d) should be started within 48 hours after surgery to reduce saphenous vein graft closure Post-PCI-stented patients should receive 325 mg per day of aspirin for 1 month for bare metal stent, 3 months for sirolimus-eluting stent and 6 months for paclitaxel-eluting stent
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Aspirin Evidence: Secondary Prevention Antithrombotic Trialist Collaboration. BMJ 2002;324:71–86. Effect of antiplatelet therapy* on vascular events** *Aspirin was the predominant antiplatelet agent studied **Vascular events include MI, stroke, or death
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Aspirin Evidence: Dose and Efficacy Indirect Comparisons of Aspirin Doses on Vascular Events in High-Risk Patients Antithrombotic Trialists Collaboration. BMJ. 2002;324:71-86
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Mechanism of action of nitrates
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B
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b-blocker Recommendations
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Start and continue indefinitely in all post MI, ACS, LV dysfunction with or without HF symptoms, unless contraindicated. Consider chronic therapy for all other patients with coronary or other vascular disease or diabetes unless contraindicated. *Precautions but still indicated include mild to moderate asthma or chronic obstructive pulmonary disease, insulin dependent diabetes mellitus, severe peripheral arterial disease, and a PR interval >0.24 seconds. MI=Myocardial infarction, HF=Heart Failure b-blocker Recommendations
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Phase of Treatment Acute treatment Secondary prevention Overall Total # Patients 28,970 24,298 53,268 0.5 1.0 2.0 RR of death b-blocker better RR (95% CI) Placebo better 0.87 (0.77-0.98) 0.77 (0.70-0.84) 0.81 (0.75-0.87) b-blocker Evidence Antman E, Braunwald E. Acute Myocardial Infarction. In: Braunwald E, Zipes DP, Libby P, eds. Heart Disease: A textbook of Cardiovascular Medicine, 6th ed., Philadelphia, PA: W.B. Sanders, 2001, 1168. Summary of Secondary Prevention Trials of b-blocker Therapy CI=Confidence interval, RR=Relative risk
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6,644 patients with LVEF <0.40 after a MI with or without HF randomized to carvedilol or placebo for 24 months The CAPRICORN Investigators. Lancet. 2001;357:1385–1390. b-blocker Evidence: Post MI with Left Ventricular Dysfunction Carvedilol Post-Infarct Survival Control in LV Dysfunction (CAPRICORN)
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b-blocker Evidence: Benefit in HF and LVSD *Not an approved indication †Not a planned end point. #Not approved for severe HF or mortality reduction alone
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Goal: <140/90 mm Hg or <130/80 if diabetes or chronic kidney disease Blood Pressure Control Recommendations Blood pressure 120/80 mm Hg or greater: · Initiate or maintain lifestyle modification: weight control, increased physical activity, alcohol moderation, sodium reduction, and increased consumption of fresh fruits vegetables and low fat dairy products Blood pressure 140/90 mm Hg or greater (or 130/80 or greater for chronic kidney disease or diabetes) · As tolerated, add blood pressure medication, treating initially with beta blockers and/or ACE inhibitors with addition of other drugs such as thiazides as needed to achieve goal blood pressure
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Prospective Studies Collaboration. Lancet. 2002;360:1903-1913 Usual Diastolic BP (mm Hg) Usual Systolic BP (mm Hg) Ischemic Heart Disease Mortality 50-59 60-69 70-79 80-89 Age at Risk (Y) 40-49 256 128 64 32 16 8 4 2 1 0 120 140 160 180 50-59 60-69 70-79 80-89 Age at Risk (Y) 40-49 256 128 64 32 16 8 4 2 1 0 80 90 100 110 70 Blood Pressure: Lower is Better Ischemic Heart Disease Mortality Ischemic Heart Disease Mortality BP=Blood pressure
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0 0.5 1.0 1.5 2.0 0.79 (0.69 to 0.90) He J et al. Am Heart J 1999; 138:211-219 Better than placebo Worse than placebo Blood Pressure: Risk of CHD with Active Treatment CHD=Coronary heart disease
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Yes >100 >160 Stage 2 Hypertension Yes 90–99 140–159 Stage 1 Hypertension Yes 80–89 120–139 Pre- hypertension Encourage <80 <120 Normal With compelling indications Initial drug therapy Lifestyle modification DBP* mmHg SBP* mmHg BP classification JNC VII Guidelines for Management and Treatment ACEI=Angiotensin converting enzyme inhibitor, ARB=Angiotensin receptor blocker, BB=b-blocker, BP=Blood pressure, CCB=Calcium channel blocker, DBP=Diastolic blood pressure, SBP=Systolic blood pressure Chobanian AV et al. JAMA. 2003;289:2560-2572 *Treatment determined by highest blood pressure category. †Initial combined therapy should be used cautiously in those at risk for orthostatic hypotension. ‡Treat patients with chronic kidney disease or diabetes mellitus to blood pressure goal of <130/80 mmHg. Drug(s) for the compelling indications.‡ Other antihypertensive drugs (diuretics, ACEI, ARB, BB, CCB) as needed. Drug(s) for compelling indications. ‡
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JNC VII Lifestyle Modifications for BP Control Chobanian AV et al. JAMA. 2003;289:2560-2572 BMI=Body mass index, SBP=Systolic blood pressure
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Clinical-Trial Basis Compelling Indication ALLHAT, HOPE, ANBP2,LIFE, CONVINCE High CAD Risk ACC/AHA Post-MI Guideline, BHAT, SAVE, Capricorn, EPHESUS Post-MI MERIT-HF, COPERNICUS, CIBIS, SOLVD, AIRE, TRACE, Val-HeFT, RALES Initial Therapy Options Diuretic, BB, ACEI, CCB BB, ACEI, Aldo Ant Diuretic, BB, ACEI,ARB, Aldo Ant Heart Failure JNC VII Compelling Indications for Drug Classes ACEI=Angiotensin converting enzyme inhibitor, Aldo Ant=Aldosterone antagonist, ARB=Angiotensin receptor blocker, BB=b-blocker, CAD=Coronary artery disease, CCB=Calcium channel blocker, MI=Myocardial Infarction Chobanian AV et al. JAMA. 2003;289:2560-2572 Recurrent Stroke Prevention PROGRESS Diuretic, ACEI NKF-ADA Guideline,UKPDS, ALLHAT NKF Guideline, Captopril Trial, RENAAL, IDNT, REIN, AASK Diuretic, BB, ACEI,ARB, CCB ACEI, ARB Diabetes Mellitus Chronic Kidney Disease
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C
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Goal: Complete Cessation and No Exposure to Environmental Tobacco Smoke Cigarette Smoking Recommendations Ask about tobacco use status at every visit. Advise every tobacco user to quit. Assess the tobacco user’s willingness to quit. Assist by counseling and developing a plan for quitting. Arrange follow-up, referral to special programs, or pharmacotherapy (including nicotine replacement and bupropion. Urge avoidance of exposure to environmental tobacco smoke at work and home.
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0.1 1.0 10 Ceased smoking Continued smoking RR (95% Cl) Study Aberg, et al. 1983 0.67 (0.53-0.84) Herlitz, et al. 1995 0.99 (0.42-2.33) Johansson, et al. 1985 0.79 (0.46-1.37) Perkins, et al. 1985 3.87 (0.81-18.37) Sato, et al. 1992 0.10 (0.00-1.95) Sparrow, et al. 1978 0.76 (0.37-1.58) Vlietstra, et al. 1986 0.63 (0.51-0.78) Voors, et al. 1996 0.54 (0.29-1.01) Cigarette Smoking Cessation: Risk of Non-fatal MI* Critchley JA et al. JAMA. 2003;290:86-97. *Includes those with known coronary heart disease CI=Confidence interval, RR=Relative risk
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Grundy, S. et al. Circulation 2004;110:227-39. Lipid Management Goals: NCEP ATP=Adult Treatment Panel, CHD=Coronary heart disease, LDL-C=Low-density lipoprotein cholesterol, TLC=Therapeutic lifestyle changes
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Lipid Management Recommendations Start dietary therapy (<7% of total calories as saturated fat and <200 mg/d cholesterol) Adding plant stanol/sterols (2 gm/day) and viscous fiber (>10 mg/day) will further lower LDL Promote daily physical activity and weight management. Encourage increased consumption of omega-3 fatty acids in fish or 1 g/day omega-3 fatty acids in capsule form for risk reduction. I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III IIa IIa IIa IIb IIb IIb III III III For all patients
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Lipid Management Recommendations If baseline LDL-C > 100 mg/dL, initiate LDL-lowering drug therapy If on-treatment LDL-C > 100 mg/dL, intensify LDL-lowering drug therapy (may require LDL lowering drug combination) If baseline is LDL-C 70 to 100 mg/dL, it is reasonable to treat to LDL < 70 mg/dL Assess fasting lipid profile in all patients, and within 24 hours of hospitalization for those with an acute event. For patients hospitalized, initiate lipid-lowering medication as recommended below prior to discharge according to the following schedule: When LDL lowering medications are used, obtain at least a 30-40% reduction in LDL-C levels. I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III IIa IIa IIa IIb IIb IIb III III III
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Lipid Management Recommendations If TG are 200-499 mg/dL, non-HDL-C should be < 130 mg/dL Further reduction of non-HDL to < 100 mg/dL is reasonable Therapeutic options to reduce non-HDL-C: More intense LDL-C lowering therapy I (B) or Niacin (after LDL-C lowering therapy) IIa (B) or Fibrate (after LDL-C lowering therapy) IIa (B) If TG are > 500 mg/dL, therapeutic options to prevent pancreatitis are fibrate or niacin before LDL lowering therapy; and treat LDL-C to goal after TG-lowering therapy. Achieve non-HDL-C < 130 mg/dL, if possible I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III IIa IIa IIa IIb IIb IIb III III III
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Event Rate Ratio (95% CI) Statin Better Statin Worse 0.4 0.6 0.8 1.0 1.2 1.4 0.76 (0.72–0.81) P<0.0001 Heart Protection Study (HPS) HMG-CoA Reductase Inhibitor: Secondary Prevention 20,536 patients with CAD, other occlusive arterial disease, or DM randomized to simvastatin (40 mg) or placebo for 5.5 years CAD=Coronary artery disease, CI=Confidence interval, DM=Diabetes mellitus, HPS Collaborative Group. Lancet 2002;360:7-22
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Pravastatin or Atorvastatin Evaluation and Infection Therapy (PROVE-IT)—TIMI 22 Study 3 6 9 12 15 18 21 24 27 30 Follow-up (months) 30 25 20 15 10 5 0 P =0.005 Recurrent MI or Cardiac Death 16% RRR Atorvastatin Pravastatin ACS=Acute coronary syndrome, CV=Cardiovascular, MI=Myocardial infarction, RRR=Relative risk reduction Cannon CP et al. NEJM 2004;350:1495-1504 HMG-CoA Reductase Inhibitor: Secondary Prevention 4,162 patients with an ACS randomized to atorvastatin (80 mg) or pravastatin (40 mg) for 24 months
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LaRosa JC et al. NEJM. 2005;352:1425-1435 LDL-C=Low density lipoprotein cholesterol; TNT=Treating to New Targets; HPS=Heart Protection Study; CARE=Cholesterol and Recurrent Events Trial; LIPID=Long-term Intervention with Pravastatin in Ischaemic Disease; 4S=Scandinavian Simvastatin Survival Study. 30 25 20 15 10 5 0 0 70 90 110 130 150 170 190 210 LDL-C (mg/dL) TNT (atorvastatin 80 mg/d) TNT (atorvastatin 10 mg/d) HPS CARE LIPID LIPID CARE HPS Event (%) 4S 4S Statin Placebo Relationship between LDL Levels and Event Rates in Secondary Prevention Trials of Patients with Stable CHD HMG-CoA Reductase Inhibitor: Secondary Prevention
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HDL-C=High-density lipoprotein cholesterol, LDL-C=Low-density lipoprotein cholesterol, TC=Total cholesterol, TG=Triglycerides *Daily dose of 40mg of each drug, excluding rosuvastatin. Lipid Management Pharmacotherapy
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Lipid Management Goal LDL-C should be less than 100 mg/dL Further reduction to LDL-C to < 70 mg/dL is reasonable *Non-HDL-C = total cholesterol minus HDL-C I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III IIa IIa IIa IIb IIb IIb III III III If TG >200 mg/dL, non-HDL-C should be < 130 mg/dL*
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D
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Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. JAMA 2001;285:2486-2497. ATP III Dietary Recommendations ATP=Adult Treatment Panel
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Weight Management Recommendations Goal: BMI 18.5 to 24.9 kg/m2 Waist Circumference: Men: < 40 inches Women: < 35 inches Assess BMI and/or waist circumference on each visit and consistently encourage weight maintenance/ reduction through an appropriate balance of physical activity, caloric intake, and formal behavioral programs when indicated. If waist circumference (measured at the iliac crest) >35 inches in women and >40 inches in men initiate lifestyle changes and consider treatment strategies for metabolic syndrome as indicated. The initial goal of weight loss therapy should be to reduce body weight by approximately 10 percent from baseline. With success, further weight loss can be attempted if indicated. *BMI is calculated as the weight in kilograms divided by the body surface area in meters2. Overweight state is defined by BMI=25-30 kg/m2. Obesity is defined by a BMI >30 kg/m2.
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Mhurchu N et al. Int J Epidemiol 2004;33:751-758 CV Risk Increases with Body Mass Index CV=Cardiovascular Body mass index is calculated as the weight in kilograms divided by the body surface area in meters2.
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Grundy, et al. Diagnosis and management of the metabolic syndrome: an AHA/NHLBI Scientific Statement. Circulation 2005;112:2735-2752. Definition of the Metabolic Syndrome Defined by presence of >3 risk factors HDL-C=High-density lipoprotein cholesterol
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3,234 patients with elevated fasting and post-load glucose levels randomized to placebo, metformin (850 mg twice daily), or lifestyle modification* for 2.8 years Lifestyle modification reduces the risk of developing DM Metabolic Syndrome: Risk of Developing DM Diabetes Prevention Program (DPP) Knowler WC et al. NEJM 2002;346:393-403 *Includes 7% weight loss and at least 150 minutes of physical activity per week
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Diabetes Mellitus Recommendations Goal: Hb A1c < 7% Lifestyle and pharmacotherapy to achieve near normal HbA1C (<7%). Vigorous modification of other risk factors (e.g., physical activity, weight management, blood pressure control, and cholesterol management as recommended). Coordinate diabetic care with patient’s primary care physician or endocrinologist. ) HbA1c = Glycosylated hemoglobin
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E
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Physical Activity Recommendations Assess risk with a physical activity history and/or an exercise test, to guide prescription Encourage 30 to 60 minutes of moderate intensity aerobic activity such as brisk walking, on most, preferably all, days of the week, supplemented by an increase in daily lifestyle activities Advise medically supervised programs for high-risk patients (e.g. recent acute coronary syndrome or revascularization, HF) Goal: 30 minutes 7 days/week, minimum 5 days/week
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Observational study of self-reported physical activity in 772 men with established coronary heart disease Light or moderate exercise is associated with lower risk Wannamethee SG et al. Circulation 2000;102:1358-1363 Exercise Evidence: Mortality Risk
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Renin-Angiotensin-Aldosterone System Blockers Recommendations
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ACE Inhibitor Recommendations Use in all patients with LVEF < 40%, and those with diabetes or chronic kidney disease indefinitely, unless contraindicated Consider for all other patients Among lower risk patients with normal LVEF where cardiovascular risk factors are well controlled and where revascularization has been performed, their use may be considered optional ACE=Angiotensin converting enzyme, LVEF= left ventricular ejection fraction
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STEMI Clinical finding EKG Serum markers Risk assessment Non-cardiacchest pain Stableangina UA NSTEMI Negative Positive ST-T wave changes ST elevation Lowprobability Medium-high risk ThrombolysisPrimary PCI Aspirin + GP IIb/IIIa inhibitor clopidogrel + heparin/ LMWH + anti-ischemic RxEarly invasive Rx Discharge Negative Diagnostic rule out MI/ACS pathway STEMI Negative Atypical pain Low risk Aspirin, heparin/low-molecular-weight heparin (LMWH) + clopidogrelAnti-ischemic Rx Early conservative therapy Ongoing pain DM=diabetes mellitus. Cannon, Braunwald. Heart Disease. 2001. Rest pain, Post-MI, DM, Prior Aspirin Exertional pain The Spectrum of ACS
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Acute Coronary Syndromes: Management of STEMI
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Balloon angioplasty
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Stents
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Acute Coronary Syndromes: Management of UA/NSTEMI
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Acute Management of UA/NSTEMI Anti-Ischemic Therapy Oxygen, bed rest, ECG monitoring Nitroglycerin -Blockers ACE inhibitors UA, unstable angina; NSTEMI, non-ST-segment elevation myocardial infarction; ECG, electrocardiogram; ACE, angiotensin-converting enzyme. Braunwald E, et al. J Am Coll Cardiol. 2000;36:970-1062. Antithrombotic Therapy Antiplatelet therapy Anticoagulant therapy
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Rationale for Use: Pharmacologic Intervention in Thrombosis UFH=unfractionated heparin. LMWH=low-molecular-weight heparin ADP=adenosine diphosphate. TFPI=tissue factor pathway inhibitor Selwyn A. Am J Cardiol. 2003;91:3H-11H. Coagulation cascade Platelets LMWH Thienopyridines GP IIb/IIIa inhibitors Thrombolytics LMWH UFH LMWH UFH Direct thrombin inhibitors Tissue factor Factor Xa Prothrombin Thrombin Platelets A2 vWF ADP Activated platelets Fibrinogen cross-linking Platelet aggregation Aspirin Fibrinogen Fibrin Fibrin degradation Collagen Leukocytes TFPI Anti-thrombin Anti-thrombin Thromboxane Plasmin Thrombus
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Efficacy of Aspirin Doses on Vascular Events in High Risk Patients Adapted with permission from the BMJ Publishing Group. Anti-thrombotic Trialists’ Collaboration. BMJ. 2002;324:71-86. 0 0.5 1.0 1.5 2.0 500–1500 mg 34 19 160–325 mg 19 26 75–150 mg 12 32 <75 mg 3 13 Any aspirin 65 23 Anti - platelet Better Anti - platelet Worse Aspirin Dose # Trials OR* (%) *Odds reduction. Treatment effect P < 0.0001. Odds Ratio
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RR: Death/MI ASA Alone 68/655=10.4% Heparin + ASA 55/698=7.9% B B B B B B B 0.1 1 10 Summary Relative Risk 0.67 (0.44-0.1.02) Theroux RISC Cohen 1990 ATACS Holdright Gurfinkel Comparison of Heparin + ASA vs ASA Alone ASA, acetylsalicylic acid; RISC, Research on InStability in Coronary artery disease; ATACS, Antithrombotic Therapy in Acute Company Syndromes; RR, relative risk; MI, myocardial infarction. Oler A, et al. JAMA. 1996;276:811-815. (with permission)
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TIMI, Thrombosis in Myocardial Infarction; ESSENCE, Efficacy and Safety of Subcutaneous Enozapam in Non–Q-Wave Coronary Events; UHF, unfractionated heparin; ENOX, enoxaparin; MI, myocardial infarction; OR, odds ratio. Antman EM, et al. Circulation. 1999;100:1602-1608. (with permission) TIMI IIB/ESSENCE Metanalysis:Enoxaparin vs Unfractionated Heparin
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LMWH Limitations Indirect inhibition: dependent on antithrombin Inability to inhibit clot-bound thrombin Catheterization lab: slower onset, longer half-life, and with enoxaparin, no standard test to measure levels/effect CABG: concerns regarding the long half-life Monitoring for Factor Xa: possible, but what is the therapeutic target, increased time, expense? Not all LMWHs are the same CABG=coronary artery bypass graft.
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0.00 0.02 0.04 0.06 0.08 0.10 0.12 0.14 Cumulative Hazard Rate Clopidogrel + Aspirin* 3 6 9 Placebo + Aspirin* Months of Follow-Up P<0.001 N=12,562 0 12 *Other standard therapies were used as appropriate. CV=cardiovascular. CURE Trial Investigators. N Engl J Med. 2001;345:494-502. 20% Relative-riskReduction CURE: Primary Endpoint: MI/Stroke/CV Death
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Before PCI Post-PCI PCI n=2754 p=0.001 +24 h +48 h 8.0% 4.9% 0% 2% 4% 6% 8% 10% Death/MI 0 2.9% 0% 2% 4% 6% 8% 10% n=12,296 p=0.001 +24 h +48 h +72 h 4.3% Death/MI Boersma E, et al. Circulation. 1999;100:2045-2048. Early Use of GP IIb/IIIa Inhibition Improves PCI: CAPTURE, PURSUIT, PRISM-PLUS
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In-hospital Mortality is Lower With Early GP IIb/IIIa Inhibitor Use (within 24 hrs) † ∆ 42% p<0.0001 Includes patients who received late GP IIb/IIIa inhibitor (> 24 hrs) therapy. † Unadjusted for risk.
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TIMI, thrombosis in myocardial infarction; UA, unstable angina; NSTEMI, non–ST-segment elevation myocardial infarction; CAD, coronary artery disease.Antman EM, et al. JAMA. 2000;284:835-842. TIMI Risk Score for UA/NSTEMI: 7 Independent Predictors Aged ≥65 years ≥3 CAD risk factors Prior CAD (stenosis >50%) Aspirin in last 7 days >2 anginal events in ≤24 hours ST deviation Elevated cardiac markers (CK-MB or troponin)
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TIMI risk score predicts 30 day mortality after a myocardial infarction The TIMI risk score has a continuous association with 30-day mortality in patients with an ST elevation (STE) myocardial infarction who are eligible for fibrinolytic therapy. Morrow, DA, Antman, EM, Charlesworth, A, et al Circulation 2000; 102:2031.
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TIMI risk score predicts 14 day outcome for NSTEMI and UA The TIMI risk score has a continuous association with 14-day mortality, recurrent MI and target vessel revascularization in patients with an NSTEMI and unstable angina (UA) Antman, EM, Cohen, et al, JAMA 2000; 284:835.
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Chest Pain Classification/Triage Class I Class II Class III Class IV Class V Class “x”
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Class I STEMI Chest pain with STE or new LBBB Acute revascularization followed by CICU admission
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Class II Unstable Angina/NSTEMI (high risk) Positive initial cardiac markers ST depression > 1mm in two contiguous leads TIMI risk score > 5 Continued angina requiring IV NTG drip CHF SBP < 90mmHg or > 180mmHg New mitral regurgitaiton Recent ACS (< 30 days) Admit to CICU by cardiology
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Class III Unstable Angina No initial increase in cardiac markers Normal ECG or ST depression < 1mm No CHF No recent ACS TIMI risk score 3-4 Admit to telemetry by cardiology
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Class IV Unstable Angina with normal ECG No initial increase in cardiac markers No history of CAD TIMI risk score < 3 No ongoing or recurring pain Admit to Chest Pain Service or Chest Pain Center in ER
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Class V Non-cardiac Chest Pain Workup in ER with appropriate referral
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Class “x” Critical causes of acute chest pain other than ACS or ACS combined with other acute critical/life-threatening illnesses Admit to intensive care (MICU, SICU or CICU) as appropriate
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Chest pain algorithm