Acute Coronary Syndrome wadi final

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By: drmay (42 month(s) ago)

thank you

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Slide 1: 

ACUTE CORONARY SYNDROME DR. ANISH JOSHI MD, IDCC JASLOK HOSPITAL & RESEARCH CENTRE, MUMBAI dranishjoshi@yahoo.com

Slide 2: 

Heart is capable of pumping blood to every cell in the body in under one minute During the course of the day, your heart will beat approx 100,000 times driving 2,000 gallons of oxygen-rich blood through 60,000 miles of blood vessels.

DEFINITION: : 

DEFINITION: STEMI : OR New Onset LBBB NSTEMI : ECG MAY SHOW ST-DEPRESSION,T-WAVE INVERSION, NON-SPECIFIC CHANGES OR NORMAL (NON-Q WAVE MI OR SUBENDOCARDIAL MI) UA: ANGINA OF INCREASING FREQUENCY OR SEVERITY, OCCURS ON MIN; EXERTION OR AT REST. ASSOCIATED WITH INCREASED RISK OF MI ACUTE MI

Clinical Spectrum : 

Clinical Spectrum None Positive Positive ECG early ST-segment depression and/or T-wave inversion ST-segment elevation ECG late No Q No Q Q develops Stable angina Unstable angina Non-STE MI STE MI ST-segment depression and/or T-wave inversion

Slide 5: 

Unstable Angina STEMI NSTEMI Non occlusive thrombus Non specific ECG Normal cardiac enzymes Occluding thrombus sufficient to cause tissue damage & mild myocardial necrosis ST depression +/- T wave inversion on ECG Elevated cardiac enzymes Complete thrombus occlusion ST elevations on ECG or new LBBB Elevated cardiac enzymes More severe symptoms

CLASSIFICATION OF MI : 

CLASSIFICATION OF MI Ischemic DiscomfortUnstable Symptoms No ST-segmentelevation ST-segmentelevation Unstable Non-Q Q-Waveangina AMI AMI ECG AcuteReperfusion HistoryPhysical Exam

PATHOPHYSIOLOGY : 

PATHOPHYSIOLOGY

Understanding myocardial ischemia : 

Understanding myocardial ischemia Imbalance

Understanding Myocardial Ischemia : 

Understanding Myocardial Ischemia  O2 supply  Demand INCREASED CARDIAC OUTPUT….. (THYROTOXICOSIS) MYOCARDIAL HYPERTROPHY (AS,HTN)

The integral role of platelets : 

The integral role of platelets Plaque Fissure or Rupture

RISK FACTORS : 

RISK FACTORS MODIFIABLE NON-MODIFIABLE

RISK FACTORS : 

RISK FACTORS NON-MODIFIABLE AGE. INCIDENCE INCREASES WITH AGE. RARE IN CHILDHOOD EXCEPT IN FAMILIAL HYPERLIPIDEMIA. MALE GENDER. MEN > PREMENUPAUSAL WOMEN. AFTER MENUPAUSE INCIDENCE IS ALMOST SAME. REASON LOSS OF PROTECTIVE EFFECT OF OESTROGEN FAMILY HX OF IHD.

MODIFIABLE RISK FACTORS SMOKING HYPERLIPIDEMIA HTN DM LACK OF EXERCISE BLOOD COAGULATION FACTORS CRP HOMOCYSTEINAEMIA PERSONALITY OBESITY GOUT SOFT WATER DRUGS……OCP,COX-2 INHIBITORS HEAVY ALCOHOL CONSUMPTION

Slide 16: 

2O% OF DEATHS FROM CAD IN MEN & 17% OF DEATHS FROM CAD IN WOMEN ARE D/T SMOKING SMOKING

DIET AND OBESITY : 

DIET AND OBESITY UPTO 30% OF DEATHS FROM CAD ARE D/T UNHEALTHY DIETS 5% OF DEATHS IN MEN 6% OF DEATHS IN WOMEN

LACK OF PHYSICAL ACTIVITY : 

LACK OF PHYSICAL ACTIVITY 36% OF DEATHS IN MEN AND 38% IN WOMEN SEDENTARY LIFE STYLE

HYPERTENSION : 

HYPERTENSION 14% OF DEATHS IN MEN AND 12% OF DEATHS IN WOMEN

HYPERLIPIDEMIA : 

HYPERLIPIDEMIA HIGH S.CHOLESTEROL LOW HDL HIGH TRGL 45% DEATHS IN MEN & 47% DEATHS IN WOMEN

DIABETES MELLITUS : 

DIABETES MELLITUS TYPE 2 DM MAGNIFIES THE EFFECT OF OTHER RISK FACTORS FOR CAD SUCH AS RAISED CHOLESTEROL LEVELS RAISED BP SMOKING OBESITY MEN 2-4 FOLD GREATER ANNUAL RISK WOMEN 3-5 FOLD

PSYCHOSOCIAL WELL-BEING : 

PSYCHOSOCIAL WELL-BEING WORK STRESS LACK OF SOCIAL SUPPORT DEPRESSION (ANXIETY) PERSONALITY (HOSTILITY)

ALCOHOL : 

ALCOHOL HIGH INTAKE IN BINGES MODERATE INTAKE 1 OR 2 DRINKS / DAY  REDUCED RISK

GENETIC FACTORS : 

GENETIC FACTORS ACE GENE CONTAINS AN INSERTION/DELETION (I/D) POLYMORPHISM THE DD TYPE

LIPOPROTEINS : 

LIPOPROTEINS HIGH PLASMA Lp(a) HOMOCYSTEINE

COAGULATION FACTORS : 

COAGULATION FACTORS S.FIBRINOGEN COAGULATION FACTOR VII

DRUGS : 

DRUGS OCP NSAIDS COX-2 INHIBITORS NUCLEOSIDE ANALOGUE COCAINE USE ROSIGLITAZONE SOFT WATER GOUT

DIAGNOSIS OF ACS : 

DIAGNOSIS OF ACS 2 OUT OF 3 TYPICAL HISTORY ECG CHANGES  CARDIAC ENZYMES

CLINICAL PRESENTATION : 

CLINICAL PRESENTATION

Focused History : 

Focused History Aid in diagnosis and rule out other causes Palliative/Provocative factors Quality of discomfort Radiation Symptoms associated with discomfort Risk factors Past medical history -especially cardiac Reperfusion questions Timing of presentation ECG c/w STEMI Contraindication to fibrinolysis Degree of STEMI risk

SYMPTOMS : 

SYMPTOMS ACUTE CENTRAL CHEST PAIN. BEWARE OF SILENT NAUSEA. SWEATING. DYSPNOEA. PALPITATION. SYNCOPE. EPIGASTRIC PAIN. VOMITING. POST-OP HYPOTENSION. OLIGURIA. ACUTE CONFUSIONAL STATE. STROKE. DIABETIC HYPERGLYCEMIC STATES.

Chest pain : 

Chest pain Substernal heaviness or pressure (>15 min) Localization or radiation to arms, back, throat, jaw Accompanying features Dyspnea Nausea/vomiting Diaphoresis Weakness Atypical: syncope,

Targeted Physical Examination : 

Targeted Physical Examination Vitals CVS RS GIT CNS Recognize factors that increase risk Hypotension Tachycardia Pulmonary rales, JVD, pulmonary edema, New murmurs/heart sounds Diminished peripheral pulses Signs of stroke

SIGNS : 

SIGNS DISTRESS. ANXIETY. PALLOR. SWEATINESS. TACHYCARDIA/BRAYCARDIA HYPO/HYPERTENSION S4/SIGNS OF HEART FAILURE PANSYSTOLIC MURMUR LOW GRADE PYREXIA PERICARDIAL FRICTION RUB EDEMA

DIFFERENTIAL DIAGNOSIS : 

DIFFERENTIAL DIAGNOSIS ANGINA PERICARDITIS MYOCARDITIS AORTIC DISSECTION PULMONARY EMBOLISM ESOPHAGEAL REFLUX/SPASM

Differential Diagnosis : 

Differential Diagnosis ANGINA PERICARDITIS MYOCARDITIS AORTIC DISSECTION PULMONARY EMBOLISM ESOPHAGEAL REFLUX/SPASM CHEST PAIN HEAVY,GRIPPING,TIGHTNESS RETROSTENAL MAY RADIATE TO JAW/ARM MAY PROVOKE SWEATING AND FEAR PROVOKED BY PHYSICAL EXERTION,AFTER MEALS, IN COLD AND WINDY WEATHER AGGRAVATED BY ANGER AND EXCITEMENT FADES QUICKLY WITH REST OR NITROGLYCERINE. LASTS < 15 MINUTES

Slide 37: 

ANGINA PERICARDITIS MYOCARDITIS AORTIC DISSECTION PULMONARY EMBOLISM ESOPHAGEAL REFLUX/SPASM SHARP CENTRAL CHEST PAIN EXACERBATED BY MOVEMENT,RESPIRATION,AND LYING DOWN. RELIEVED BY SITTING FORWARD MAY BE REFERRED TO NECK OR SHOULDER PERICARDIAL FRICTION RUB IN THREE PHASES OF CARDIAC CYCLE ATRIAL SYSTOLE VENTRICULAR SYSTOLE VENTRICULAR DIASTOLE BIPHASIC ‘TO AND FRO’ RUB FEVER LEUCOCYTOSIS LYMPHOCYTOSIS FEATURES OF PERICARDIAL EFFUSION Differential Diagnosis

Slide 39: 

ANGINA PERICARDITIS MYOCARDITIS AORTIC DISSECTION PULMONARY EMBOLISM ESOPHAGEAL REFLUX/SPASM ASYMPTOMATIC FATIGUE PALPITATIONS CHEST PAIN DYSPNOEA CCF/S3 SOFT HEART SOUNDS PERICARDIAL FRICTION RUB  ESR/CRP TROPONIN/CK +ve Differential Diagnosis

Slide 40: 

ANGINA PERICARDITIS MYOCARDITIS AORTIC DISSECTION PULMONARY EMBOLISM ESOPHAGEAL REFLUX/SPASM SEVERE CENTRAL CHEST PAIN. RADIATES TO BACK. SIGNS OF SHOCK NEUROLOGICAL SYMPTOMS RENAL FAILURE LOWER LIMB ISCHEMIA VISCERAL ISCHEMIA Differential Diagnosis

Slide 41: 

ANGINA PERICARDITIS MYOCARDITIS AORTIC DISSECTION PULMONARY EMBOLISM ESOPHAGEAL REFLUX/SPASM RVF Differential Diagnosis

Slide 42: 

ANGINA PERICARDITIS MYOCARDITIS AORTIC DISSECTION PULMONARY EMBOLISM ESOPHAGEAL REFLUX/SPASM 20% OF THE PTS; ADMITTED INTO CCU HAVE GORD

Disease Findings : 

Disease Findings Ischemia Injury Infarction Subendocardial Transmural

12-Lead ECG Variations : 

12-Lead ECG Variations

Concave Contour: Benign ? : 

Concave Contour: Benign ?

Convex Contour : Concerning : 

Convex Contour : Concerning

ECG : 

ECG NORMAL ST-DEPRESSION T-WAVE INVERSION PERSISTENT ST-ELEVATION OR LBBB PATTERN PREEXISTING LBBB will not allow classical MI pattern REPEAT ECG WHEN PATIENT IS IN PAIN CONTINUOUS ST – SEGMENT MONITORING

Causes of ST Elevation : 

Causes of ST Elevation "ELEVATION" E - Electrolytes L - LBBB E - Early Repolarization V - Ventricular hypertrophy A - Aneurysm T - Treatment - Pericardiocentesis I - Injury (AMI, contusion) O - Osborne waves (hypothermia) N - Non-occlusive vasospasm ST segment elevation =/>1mm above the TP baseline in limb leads or =/> 2 mm in two contiguous chest leads is significant. ST segment elevation in virtually all the leads can be pericarditis

Slide 52: 

‘R’ Wave Progression.

Slide 53: 

‘R’ Waves Voltage

Slide 54: 

Poor ‘R’ Wave Progression V3-V5

Slide 55: 

CORONARIES

ST-Elevation and Infarct Location : 

ST-Elevation and Infarct Location

AMI Localization : 

AMI Localization aVF inferior III inferior V3 anterior V6 lateral aVL lateral II inferior V2 septal V5 lateral aVR I lateral V1 septal V4 anterior

ST-Segment Elevation MI : 

ST-Segment Elevation MI

New LBBB : 

New LBBB QRS > 0.12 sec L Axis deviation Prominent R wave V1-V3Prominent S wave 1, aVL, V5-V6 with t-wave inversion

Slide 62: 

Case 13. A 53 year old man with 3 hours of "crushing" chest pain. Interpretation Acute inferior myocardial infarctionST elevation in the inferior leads II, III and aVF reciprocal ST depression in the anterior leads

Slide 63: 

Case 16. 51 yr old male with no prior cardiac history presents with mid-sternal chest discomfort Questions  1. Is there ECG evidence of injury or ischemia? 2. Is this patient having an MI? If so, in what anatomic distribution? Interpretation  1. YES 2. YES, ANTEROSEPTAL

Slide 64: 

post thrombolysis ECG

BIOCHEMICAL MARKERS : 

BIOCHEMICAL MARKERS

Cardiac enzymes : 

Cardiac enzymes TROP. I TROP T CK-MB MYOBLOBIN WBC LIPID PROFILE TRANSTHORACIC ECHOCARDIOGRAPHY (TTE) OTHER BLOOD INVESTIGATIONS CARDIAC TROPONONS

Cardiac markers : 

Cardiac markers Troponin ( T, I) Very specific and more sensitive than CK Rises 4-8 hours after injury May remain elevated for up to two weeks Can provide prognostic information Troponin T may be elevated with renal dis., poly/dermatomyositis CK-MB isoenzyme Rises 4-6 hours after injury and peaks at 24 hours Remains elevated 36-48 hours Positive if CK/MB > 5% of total CK and 2 times normal Elevation can be predictive of mortality False positives with exercise, trauma, muscle dz,

Slide 68: 

Anderson, J. L. et al. J Am Coll Cardiol 2007;50:e1-e157 Timing of Release of Various Biomarkers After Acute Myocardial Infarction

Slide 69: 

Timings Initial Peak Normal Myoglobin 1-4hr 6-7hr 24hr Nonspecific CK-MB 3-12hr 24hr 48-72hr Also elevated with skmuscle TroponinI 3-12hr 24hr 5-10d Highly sensitive/ specific

Slide 70: 

MANAGEMENT

Cardiac Care Goals : 

Cardiac Care Goals Decrease amount of myocardial necrosis Preserve LV function Prevent major adverse cardiac events Treat life threatening complications

MANAGEMENT : 

MANAGEMENT 2 KEY QUESTIONS IS THERE ST-SEGMENT ELEVATION? IS THERE A RISE IN TROPONINS? 1 2 RIGHT ANSWER LEADS TO SUCCESSFUL MANAGEMENT

TIMI RISK SCORE IN ACS NSTEMI/UA : 

TIMI RISK SCORE IN ACS NSTEMI/UA

TIMI RISK SCORE IN ACS NSTEMI/UA : 

TIMI RISK SCORE IN ACS NSTEMI/UA

Chest pain suggestive of ischemia : 

Chest pain suggestive of ischemia 12 lead ECG Initial cardiac enzymes electrolytes, cbc lipids, bun/cr, glucose, coags CXR Immediate assessment within 10 Minutes Establish diagnosis Read ECG Identify complications Assess for reperfusion Initial labs and tests Emergent care History & Physical IV access Cardiac monitoring Oxygen Aspirin Nitrates

Slide 77: 

ONSET OF SYMPYOMS EMS ARRIVAL PRE-HOSP ECG HOSP ARRIVAL REPERFUSION REPERFUSION GOALS DOOR TO NEEDLE DOOR-TO-BALLOON SYMPTOM ONSET –TO-REPERFUSION <30 MIN <90 MIN <120 MIN INCREASING LOSS OF MYOCYTES GOLDEN HOUR: 1ST 60 MINUTES DOOR TO ECG: 10 MINUTES

MONA + BAH : 

MONA + BAH Morphine (class I, level C) Analgesia Reduce pain/anxiety—decrease sympathetic tone, systemic vascular resistance and oxygen demand Careful with hypotension, hypovolemia, respiratory depression Oxygen (2-4 liters/minute) (class I, level C) Up to 70% of ACS patient demonstrate hypoxemia May limit ischemic myocardial damage by increasing oxygen delivery/reduce ST elevation

Slide 79: 

Nitroglycerin (class I, level B) Analgesia—titrate infusion to keep patient pain free Dilates coronary vessels—increase blood flow Reduces systemic vascular resistance and preload Careful with recent ED meds, hypotension, bradycardia, tachycardia, RV infarction Aspirin (160-325mg chewed & swallowed) (class I, level A) Irreversible inhibition of platelet aggregation Stabilize plaque and arrest thrombus Reduce mortality in patients with STEMI Careful with active PUD, hypersensitivity, bleeding disorders

Slide 80: 

Beta-Blockers (class I, level A) Mortality benfit Contraindications (CHF, Heart block, Hypotension) Reassess for therapy as contraindications resolve ACE-Inhibitors / ARB (class I, level A) Start in patients with anterior MI, pulmonary congestion, LVEF < 40% in absence of contraindication/hypotension Start in first 24 hours ARB as substitute for patients unable to use ACE-I

Slide 81: 

Heparin LMWH or UFH (max 4000u bolus, 1000u/hr) Indirect inhibitor of thrombin Less supporting evidence of benefit in era of reperfusion Adjunct to surgical revascularization and thrombolytic / PCI reperfusion 24-48 hours of treatment Coordinate with PCI team (UFH preferred) Used in combo with aspirin and/or other platelet inhibitors Changing from one to the other not recommended Aldosterone blockers (class I, level A) Post-STEMI patients no significant renal failure (cr < 2.5 men or 2.0 for women) No hyperkalemis > 5.0 LVEF < 40% Symptomatic CHF or DM

WHICH? : 

WHICH? Fibrinolysis preferred if: <3 hours from onset PCI not available/delayed door to balloon > 90min Door to needle goal <30min No contraindications PCI preferred if: PCI available Door to balloon < 90min Fibrinolysis contraindications Late Presentation > 3 hr STEMI dx in doubt

THROMBOLYSIS : 

THROMBOLYSIS MORTALITY BENEFIT GREATEST BENEFIT IF GIVEN <12 H OF ONSET OF PAIN.

Mechanism of action : 

Mechanism of action Conversion of fibrin bound plasminogen to active plasmin, which subsequently lyses fibrin thrombi and dissolution of clots.

Absolute contraindications : 

Absolute contraindications Any prior ICH Known structural cerebral vascular lesion (e.g., AVM) Known malignant intracranial neoplasm (primary or metastatic) Ischemic stroke within 3 months EXCEPT acute ischemic stroke within 3 hours Suspected aortic dissection Active bleeding or bleeding diathesis (excluding menses) Significant closed-head or facial trauma within 3 months

Relative contraindications : 

Relative contraindications History of chronic, severe, poorly controlled hypertension SBP > 180 mm Hg or DBP > 110 mmHg History of prior ischemic stroke greater than 3 months, dementia, or known intracranial pathology not covered in contraindications Traumatic or prolonged (greater than 10 minutes) CPR or major surgery (less than 3 weeks) Recent (within 2-4 weeks) internal bleeding Noncompressible vascular punctures For streptokinase/anistreplase: prior exposure (more than 5 days ago) or prior allergic reaction to these agents Pregnancy Active peptic ulcer Current use of anticoagulants: the higher the INR, the higher the risk of bleeding

STREPTOKINASE : 

STREPTOKINASE Obtained from β- hemolytic Streptococci group C Decreases fibrinogen & plasminogen levels Increases PT,aPTT,TT Allergic reactions Build up of neutralizing antibodies with repeated use Elevates Bil.,SGOT, SGPT, GGT (unknown mechanism) Reported cases of GBS Dose – 1.5 mu iv over 60 mins

UROKINASE : 

UROKINASE Enzyme isolated from human urine, now prepared from cultured human kidney cells Non – antigenic Allergic phenomenon rare Dose – 2,50,000 U iv over 10 mins f/b 5,00,000 U over 60 mins

ALTEPLASE (tPA) : 

ALTEPLASE (tPA) Dose – 15 mg iv bolus + 50mg iv over 30 mins + 35 mg/kg over 60 mins Lesser incidence of allergic reactons Metabolised in liver

RETEPLASE (rPA) : 

RETEPLASE (rPA) Dose – 10 Units as iv bolus and repeat in 30 mins Bolus doses are easier to give and produce more rapid clot lysis than tPA Should not be infused in the same iv access as heparin

TENECTEPLASE (TNK) : 

TENECTEPLASE (TNK) DOSE - < 60 kg – 30mg iv bolus 60 – 69 kg – 35 mg iv bolus 70 – 79 kg – 40 mg iv bolus 80 – 89 kg – 45 mg iv bolus >90 kg - 50 mg iv bolus Most clot specific and rapidly acting lytic agent. Single bolus dose

ACUTE MANAGENT OF ACS WITHOUT ST-SEGMENT ELEVATION (NSTEMI)contd: : 

ACUTE MANAGENT OF ACS WITHOUT ST-SEGMENT ELEVATION (NSTEMI)contd: Infusion of a GP11b/111a antagonist. Abciximab (250microgram/kg IV OVER 1 Min. THEN 125 nanogram/kg/min IV) Eptifibatide Tirofiban Urgent angiography. Add clopidogrel High Risk Pts. Persistent ischemia Recurrent ischemia ST-Depression DM Increased Troponins Beta-blocker Ca2+; ch antagonist ACE-I Nitrates Intensive statin regimens OPTIMIZE DRUGS PREVENT PLT AGGRGN BY BLOCKING BINDING OF FIBRINOGEN TO RECEPTOR ON PLT. 300mg po stat then 75mg/d With ASA

Slide 93: 

URGENT CAG URGENT ANGIOPLASTY OR CABG IF SYMPTOMS FAIL TO IMPROVE High Risk Pts.

ACUTE MANAGENT OF ACS (NSTEMI) CONTD: : 

ACUTE MANAGENT OF ACS (NSTEMI) CONTD: Wean off NTG infusion when stabilized on oral drugs. Stop heparin when pain-free for 24h.(give atleast 3-5 days therapy). Check serial ECGs. For 2-3 days. Check serial cardiac enzymes for 2-3 days. Address modifiable risk factors Smoking HTN Hyperlipidemia DM Gentle mobilization. Further measures:

POST-MI DRUG THERAPY : 

POST-MI DRUG THERAPY ASA 75-150 mg/day A BETA-BLOCKER TO MAINTAIN HR <60/MIN. (METOPROLOL 50 mg BD) ACEi (RAMIPRIL 2.5MG BD TITRATED TO MAX TOLERATED OR TARGET DOSE) IF INTOLERANT OF ACE-INH USE ARB (VALSARTAN 20MG BID) STATINS (ATORVASTATIN 20-80 mg/day) CLOPIDOGREL 75 mg/day FOR 9-12 MONTHS NTG SPRAY FOR SYMPTOMATIC RELIEF OF ANGINA ALDOSTERONE ANTAGONIST (EPLERENONE 25 mg/day FOR REDUCED EF AND HF PTS

Slide 96: 

MANAGEMENT OF AMI ECG O2 IV ACCESS TAKE LABS BRIEF ASSESSMENT ASPIRIN 300 MG NTG S/L 2 PUFFS OR 1 TAB. MORPHINE 2.5-5mg IV +METOCLOPRAMIDE 10mG THROMBOLYSIS BETA-BLOCKER CXR CONSIDER GLUCOSE,INSULIN,& POTASSIUM INFUSION FOR DM PTs. CONT;MEDICATION EXCEPT Ca;CHANNEL ANTAGONIST (UNLESS SPECIFIC INDICATIONS) CONSIDER DVT PROPHYLAXIS

It is what we think we know already ,that often prevents us fromlearning. : 

It is what we think we know already ,that often prevents us fromlearning. Claude Bernard Thank You !!

Slide 98: 

Risk Stratification to Determine the Likelihood of Acute Coronary Syndrome

ACS risk criteria : 

ACS risk criteria Low Risk ACS No intermediate or high risk factors <10 minutes rest pain Non-diagnositic ECG Non-elevated cardiac markers Age < 70 years Intermediate Risk ACS Moderate to high likelihood of CAD >10 minutes rest pain, now resolved T-wave inversion > 2mm Slightly elevated cardiac markers

Slide 100: 

High Risk ACS Elevated cardiac markers New or presumed new ST depression Recurrent ischemia despite therapy Recurrent ischemia with heart failure High risk findings on non-invasive stress test Depressed systolic left ventricular function Hemodynamic instability Sustained Ventricular tachycardia PCI with 6 months Prior Bypass surgery

Slide 101: 

Low risk High risk Conservative therapy Invasive therapy Chest Pain center Intermediate risk