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Acute coronary syndrome


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Acute coronary syndrome

  1. 1. 1 MAGDI AWAD SASI 2013 ACS ( CARDIOLOGY)Acute coronary syndromeAcute coronary syndrome is a myocardial ischemia due to :1- myocardial infarction (NSTEMI or STEMI)2- unstable anginaNSTEMI = non-ST elevation myocardial infarctionSTEMI = ST elevation myocardial infarction• Unstable angina : is defined as angina at rest, new onset exertional angina(<2 months), recent acceleration of angina (<2 months), or postrevascularization angina.Acute myocardial infarction (MI) remains a leading cause of morbidity andmortality worldwide. Myocardial infarction occurs when myocardial ischemia, adiminished blood supply to the heart, exceeds a critical threshold andoverwhelms myocardial cellular repair mechanisms designed to maintain normaloperating function and homeostasis. Ischemia at this critical threshold level foran extended period results in irreversible myocardial cell damage or death.(Critical imbalance between oxygen supply and demand to the myocardium)ACUTE CORONARY SYNDROMENo ST Elevation ST ElevationUnstable Angina NQMI QwMIMyocardial InfarctionNSTEMI
  2. 2. 2 MAGDI AWAD SASI 2013 ACS ( CARDIOLOGY)ClassificationAnatomic or morphologicTransmural= Full thicknessNon-transmural= Partial thicknessECGQ wave MINon Q wave MIDoes not distinguish transmural from a non-transmural MI .DEFINITION:Myocardial infarction ((acute, evolving, recent))Typical rise and gradual fall (troponin) or more rapid rise and fall (CK-MB) ofbiochemical markers of myocardial necrosis with at least one of the following:– a) Ischemic symptoms;– b) Development of pathologic Q waves on the ECG;– c) ECG changes indicative of ischemia (ST segment elevation ordepression);( dynamic T wave changes) or– d) Coronary artery intervention (e.g., coronary angio-plasty).NSTEMI is an acute process of myocardial ischemia with sufficient severity andduration to result in myocardial necrosis.– The initial ECG in patients with NSTEMI does not show ST-segmentelevation.– NSTEMI is distinguished from UA by the detection of cardiac markersindicative of myocardial necrosis in NSTEMI .
  3. 3. 3 MAGDI AWAD SASI 2013 ACS ( CARDIOLOGY)Unstable angina—an acute process of myocardial ischemia that is not ofsufficient severity and duration to result in myocardial necrosis.PrevalenceIncidence of 600 per 100,000 peopleThe survival rate for U.S. pts hospitalized with MI is approximately 90%This represents a significant improvement in survival and is related toimprovements in emergency medical response and treatment strategies.Increase in the proportion of NSTEMI compared to STEMIApproximately 500,000 to 700,000 deaths are caused by heart diseaseannually in the United States.PATHOPHYSIOLOGY:The severity of an MI depends on three factors: 1.the level of the occlusion inthe coronary artery 2. the length of time of the occlusion, and 3. the presenceor absence of collateral circulation.Generally, the more proximal the coronary occlusion, the more extensive theamount of myocardium that will be at risk of necrosis. The larger the myocardialinfarction, the greater the chance of death because of a mechanicalcomplication or pump failure. The longer the period of vessel occlusion, thegreater the chances of irreversible myocardial damage distal to the occlusion.STEMI is usually the result of complete coronary occlusion after plaque rupture.This arises most often from a plaque that previously caused less than 50%occlusion of the lumen. NSTEMI isusually associated with greater plaqueburden without complete occlusion.This difference contributes to theincreased early mortality seen inSTEMI and the eventual equalization
  4. 4. 4 MAGDI AWAD SASI 2013 ACS ( CARDIOLOGY)of mortality between STEMI and NSTEMI after 1 year.Most myocardial infarctions are caused by a disruption in the vascularendothelium associated with an unstable atherosclerotic plaque that stimulatesthe formation of an intracoronary thrombus, which results in coronary arteryblood flow occlusion. If such an occlusion persists for more than 20 minutes,irreversible myocardial cell damage and cell death will occur.The atherosclerotic plaque occurs over a period of years to decades. The plaquehas a fibromuscular cap and an underlying lipid-rich core. Plaque erosion canoccur because of the actions of matrix metalloproteases and the release ofother collagenases and proteases in the plaque, which result in thinning of theoverlying fibromuscular cap. The action of proteases, in addition tohemodynamic forces applied to the arterial segment, can lead to a disruption ofthe endothelium and fissuring or rupture of the fibromuscular cap. The loss ofstructural stability of a plaque often occurs at the juncture of the fibromuscularcap and the vessel wall, a site otherwise known as the shoulder region.Disruption of the endothelial surface can cause the formation of thrombus viaplatelet-mediated activation of the coagulation cascade. If a thrombus is largeenough to occlude coronary blood flow, an MI can result.
  5. 5. 5 MAGDI AWAD SASI 2013 ACS ( CARDIOLOGY)Risk factors for atherosclerosis:AgeMale genderSmokingHypercholesterolemia and triglyceridemiaDiabetes MellitusPoorly controlled hypertensionFamily HistorySedentary lifestyleType A personalitySigns and symptoms:The history is critical in making the diagnosis of MI and sometimes provide onlythe only clues that lead to the diagnosis in the initial phase of presentation.Acute MI can have unique manifestations in individual patients. The degree ofsymptoms ranges from none at all to sudden cardiac death. An asymptomaticMI is not necessarily less severe than a symptomatic event, but patients whoexperience asymptomatic MIs ((SILENT)) are more likely to be diabetic. Despitethe diversity of manifesting symptoms of MI, there are some characteristicsymptoms.TYPICAL SYMPTOM-chest pain or discomfort. You have to ask the patient aboutonset as the vascular insult is acute and ask about duration , aggravating orrelieving symptoms ,site , character, radiation, severity ,course and association.ONSET-all of a sudden , for first time in most of cases , awake ptSITE-anterior precordium , central , right or left sided ,interscapularDURATION- minutes to hours to days according to severity.
  6. 6. 6 MAGDI AWAD SASI 2013 ACS ( CARDIOLOGY)CHARACTER- pressure sensation, fullness, or squeezing in the midportionof the thorax, burning , heaviness, stabbing , piercing, heart burn, pinsand needles, colicky, tightness ,ANY TYPE .RADIATION-may radiate to jaw OR teeth, tip of shoulder, arm to the innersit of the upper limb more left or both limbs, and/or back ,anterior neckand epigastrium up and down to the jaw.AGGREVATING FACTORS- 60% no factors, others can be related tostressful event or exercise or heavy work or walking in windy weather orsudden heavy work or bad news.ASSOCITED SYMPTOMS Nausea with and without vomiting Diaphoresis or sweating Syncope or near syncope Dyspnea- angina equivalent, poor LV function NauseaSEVERITY-awake the patient from sleeping , fear of death, abstinencefrom work , can’t sleep or eat , interfere with daily activities , chestdiscomfort that is not relieved in any posture.ATYPICAL SYMPTOMSAs many as half of MI are clinically silent((DIABETICS AND ELDERY))Epigastric discomfort with or without nausea and vomiting.All of sudden epigastric pain in a patient above 40years wither heart burnor colicy abdominal pain or radiating up to the neck.Sudden dyspnea with out lung diseases.Syncope or near syncope without other causePalpitation all of sudden with fear of death in elder pt.Impairment of cognitive function without other cause.Profuse sweating all of sudden in diabetic with out hypoglycemia.Jaw pain all of sudden in elder patient.Fatigability al of suddenMI can occur at any time of the day, but most appear to be clusteredaround the early hours of the morning or are associated with demandingphysical activity, or both.
  7. 7. 7 MAGDI AWAD SASI 2013 ACS ( CARDIOLOGY)Physical signs:Most of the patients has no signs on presentation(completely normal).Others , they may present with left ventricular failure (dyspnea) or sweatingand cold extremities in others.The physical exam can often be unremarkableHypertension , HypotensionTachycardia , bradycardia.Sweating , dyspnea , apprehensiveAcute valvular dysfunction may be presentRales on chest examinationNeck vein distentionThird heart sound may be presentA fourth heart sound--- poor LV complianceDysrhythmiasLow grade fever( fever in MI develop after a day of MI).CAUSES OF MI OTHER THAN PLAQUE:Coronary artery vasospasmVentricular hypertrophyHypoxiaCoronary artery emboliCocaine
  8. 8. 8 MAGDI AWAD SASI 2013 ACS ( CARDIOLOGY)ArteriesCoronary anomaliesAortic dissectionPediatrics Kawasaki disease, Takayasu arteritisIncreased afterload which increases myocardial demandAcute coronary syndromes can also be due to secondarycauses:– Thyrotoxicosis– Anemia– Tachycardia– Hypotension– Hypoxemia– Arterial inflammation (infection, arteritis)Differentials4 IMPORTANT LIFE SAVING DIAGNOSIS NOT TO BE MISSED:1. Acute coronary syndrome2. Pulmonary embolism3. Aortic Dissection4. PneumothoraxOther D/DEndocarditis Myocarditis PericarditisAnxiety Aortic stenosis AsthmaCholecystitis and biliary colic CholethiasisEsophagitis Pneumonia COPD
  9. 9. 9 MAGDI AWAD SASI 2013 ACS ( CARDIOLOGY)DiagnosisDx of acute coronary syndrome is based on 1- History, 2- Physical exam, 3- ECG, 4- Cardiac enzymes
  10. 10. 10 MAGDI AWAD SASI 2013 ACS ( CARDIOLOGY)INVESTIGATION:2 OF 3 ARE DIAGNOSTIC FOR MI:1. CHEST PAIN2. ECG3. CARDIAC ENZYMES1.Complete blood count:CBC is indicated if anemia is suspected as precipitantLeukocytosis may be observed within several hours aftermyocardial injury and returns to levels within the referencerange within one week.2.Renal function test and electrolytes:Potassium and magnesium levels should be monitored andcorrected ( rhythmogenic).Decrease cardiac output may lead to renal impairment .Creatinine levels must be considered before using contrast dyefor coronary angiography and percutanous revascularization3. ElectrocardiogramA normal ECG does not exclude ACSThe first diagnostic test is electrocardiography (ECG), which maydemonstrate that a MI is in progress or has already occurredHigh probability include ST segment elevation in two contiguousleads or presence of q wavesIntermediate probability ST depression
  11. 11. 11 MAGDI AWAD SASI 2013 ACS ( CARDIOLOGY)In addition to ST-segment elevation, 81% of electrocardiogramsduring STEMI demonstrate reciprocal ST-segment depression aswell.T wave inversions are less specific in NSTEMILocalization of MIST elevation only Inferior wall- II, III, aVF Lateral wall_ I, aVL, V4-V6 Anteroseptal- V1-V3 Anterolateral- V1-V6 Right ventricular- RV4, RV5 Posterior- R/S ratio >1 in V1 and T wave inversion4. Cardiac BiomarkersCardiac biomarkers are protein molecules released into the bloodstream from damaged heart muscle .Living myocardial cells contain enzymes and proteins (e.g.,creatine kinase, troponin I and T, myoglobin) associated withspecialized cellular functions. When a myocardial cell dies,cellular membranes lose integrity, and intracellular enzymes andproteins slowly leak into the blood stream. These enzymes andproteins can be detected by a blood sample analysis. Thesevalues vary depending on the assay used in each laboratory.Given the acuity of a STEMI and the need for urgent intervention,the laboratory tests are usually not available at the time ofdiagnosis. Thus, good history taking and an ECG are used toinitiate therapy in the appropriate situations.
  12. 12. 12 MAGDI AWAD SASI 2013 ACS ( CARDIOLOGY)Since ECG can be inconclusive , biomarkers are frequently used toevaluate for myocardial injuryThese biomarkers have a characteristic rise and fall pattern.a. Troponin T and I• These isoforms are very specific for cardiac injury.• Preferred markers for detecting myocardial cell injury.• Rise 2-6 hours after injury• Peak in 12-16 hours• Stay elevated for 5-14 daysb. Creatinine Kinase ( CK-MB) Creatinine Kinase is found in heart muscle (MB), skeletal muscle(MM), and brain (BB) Increased in over 90% of myocardial infraction However, it can be increased in muscle trauma, physical exertion,post-op, convulsions, and other conditions Time sequence after myocardial infarction Begins to rise 4-6 hours Peaks 24 hours returns to normal in 2 days MB2 released from heart muscle and converted to MB1. A level of MB2 > or = 1 and a ratio of MB2/MB1 > 1.5 indicatesmyocardial injury
  13. 13. 13 MAGDI AWAD SASI 2013 ACS ( CARDIOLOGY)c. MyoglobinDamage to skeletal or cardiac muscle release myoglobin intocirculation.Time sequence after infarctionRises fast 2hours Peaks at 6-8 hoursReturns to normal in 20-36 hoursHave false positives with skeletal muscle injury and renal failure5. Chest X-Ray Chest radiography may provide clues to an alternativediagnosis ( aortic dissection or pneumothorax) Chest radiography also reveals complications of myocardialinfarction such as heart failure(CONGESTED LUNG-WHITE).
  14. 14. 14 MAGDI AWAD SASI 2013 ACS ( CARDIOLOGY)5. Echocardiography Use 2-dimentional and M mode echocardiography whenevaluating overall ventricular function and wall motionabnormalities, intracardiac thrombus. Echocardiography can also identify complications of MI ( eg.Valvular or pericardial effusion, VSD) The presence of wall motion abnormalities on the ECHO may bethe result of an acute MI or previous (old) MI or other myopathicprocesses, limiting its overall diagnostic utility.Complications of MI:Arrhythmic Complications of MIAbout 90% of patients who have an acute myocardial infarction (AMI)develop some form of cardiac arrhythmia during or immediately after theevent. In 25% of patients, such rhythm abnormalities manifest within the first24 hours. In this group of patients, the risk of serious arrhythmias, such asventricular fibrillation, is greatest in the first hour and declines thereafter.The incidence of arrhythmia is higher with an ST-elevation myocardialinfarction (STEMI) and lower with a non–ST-elevation myocardial infarction.The clinician must be aware of these arrhythmias, in addition to reperfusionstrategies, and must treat those that require intervention to avoidexacerbation of ischemia and subsequent hemodynamic compromise. Mostperi-infarct arrhythmias are benign and self-limited. However, those thatresult in hypotension, increase myocardial oxygen requirements, and/orpredispose the patient to develop additional malignant ventriculararrhythmias should be aggressively monitored and treated.Pathophysiology of arrhythmic complicationsAMI is characterized by generalized autonomic dysfunction that results inenhanced automaticity of the myocardium and conduction system. Electrolyteimbalances (eg, hypokalemia and hypomagnesemia) and hypoxia furthercontribute to the development of cardiac arrhythmia.
  15. 15. 15 MAGDI AWAD SASI 2013 ACS ( CARDIOLOGY)The damaged myocardium acts as substrate for re-entrant circuits, due tochanges in tissue refractoriness.Enhanced efferent sympathetic activity, increased concentrations of circulatingcatecholamines, and local release of catecholamines from nerve endings in theheart muscle itself have been proposed to play roles in the development of peri-infarction arrhythmias. Furthermore, transmural infarction can interruptafferent and efferent limbs of the sympathetic nervous system that innervatesmyocardium distal to the area of infarction. The net result of this autonomicimbalance is the promotion of arrhythmias.Classification of peri-infarction arrhythmiasSupraventricular tachyarrhythmias, including sinus tachycardia,premature atrial contractions, paroxysmal supraventricular tachycardia,atrial flutter, and atrial fibrillationAccelerated junctional rhythmsBradyarrhythmias, including sinus bradycardia and junctional bradycardiaAtrioventricular (AV) blocks, including first-degree AV block, second-degree AV block, and third-degree AV blockIntraventricular blocks, including left anterior fascicular block, rightbundle branch block (RBBB), and left bundle branch block (LBBB)Ventricular arrhythmias, including premature ventricular contractions(PVCs), accelerated idioventricular rhythm, ventricular tachycardia, andventricular fibrillationReperfusion arrhythmiasMechanical Complications of MI:Left ventricular failure due to1. Ventricular free wall rupture (VFWR)2.ventricular septal rupture (VSR)3. papillary muscle rupture with severe mitral regurgitation (MR).
  16. 16. 16 MAGDI AWAD SASI 2013 ACS ( CARDIOLOGY)4.RV infarction5.Infarct expansion, aneurysm, LV remodeling6. Intracardiac ThrombusTreatment of ACS:The goals of therapy in acute MI are 1. the expedient restoration of normal coronary bloodflow and 2. the maximum salvage of functional myocardium. These goals can be met by anumber of medical interventions and adjunctive therapies. The primary obstacles toachieving these goals are the patients failure to recognize MI symptoms quickly and thedelay in seeking medical attention. When patients present to a hospital, there are a variety ofinterventions to achieve treatment goals. “Time is muscle” guides the managementdecisions in acute STEMI, and an early invasive approach is the standard of care for acuteNSTEMITreatment of STEMI ((6A))ADMISSION & CANNULAASSURANCEANALGESIAANGESIEDASPIRIN 600MG CRUSHEDAIR- OXYGENTHROMBOLYSIS FOR STEMI & LBBB/NG &HEPARIN FOR NSTEMI• ASA• NTG (consider MSO4 if pain not relieved)• Beta Blocker• Heparin/LMWH• ACE-I after 24 hrs• +/-Clopidogrel• +/- Statin• Activate the Cath Lab!!!Pain ControlPain from MI is often intense and requires prompt and adequate analgesia.The agent of choice is morphine sulfate, IV at 5 to 15 minute intervals atdoses of 2 to 4 mg OR pethidine 50mg-150mg. Reduction in myocardialischemia also serves to reduce pain, so oxygen therapy, nitrates, and betablockers remain the mainstay of therapy.
  17. 17. 17 MAGDI AWAD SASI 2013 ACS ( CARDIOLOGY)FibrinolyticsRestoration of coronary blood flow in MI patients can be accomplishedpharmacologically with the use of a fibrinolytic agent. Fibrinolytic therapy isindicated for patients who present with a STEMI within 12 hours of symptomonset without a contraindication. These are streptokinase. Metalase , tissueplasminogen activator.Absolute contraindications to fibrinolytic therapy1. Allergy to thrombolysis2. History of intracranial hemorrhage3. Ischemic stroke or closed head injury within the past 3 months4. Presence of an intracranial malignancy5. Signs of an aortic dissection6. Active bleeding(duodenal ulcer,varices, haemophylia).Fibrinolytic therapy is primarily used at facilities without access to anexperienced interventionalist within 90 minutes of presentation.Cautions/Relative Contraindications■ Severe uncontrolled hypertension on presentation (BP >180/110 mm Hg)■ History of prior cerebrovascular accident or known intracerebral diseasenot covered in contraindications■ Current use of anticoagulants in therapeutic doses (internationalnormalized ratio [INR] ≥2:3); known bleeding diathesis■ Recent trauma (within 2–4 weeks), including head traumaor traumatic or prolonged (>10 minutes) cardiopulmonary resuscitation(CPR) or major surgery (<3 weeks)As a class, the plasminogen activators have been shown to restore normalcoronary blood flow in 50% to 60% of STEMI patients. The successful use offibrinolytic agents provides a definite survival benefit that is maintained for
  18. 18. 18 MAGDI AWAD SASI 2013 ACS ( CARDIOLOGY)years. The most critical variable in achieving successful fibrinolysis is time fromsymptom onset to drug administration. A fibrinolytic is most effective withinthe first hour of symptom onset and when the door-to-needle time is 30minutes or lessSupplemental OxygenOxygen should be administered to patients with symptoms or signs ofpulmonary edema or with pulse oximetry less than 90% saturation.AIM- the erythrocytes will be saturated to maximum carrying capacity.Because MI impairs the circulatory function of the heart, oxygen extraction bythe heart and by other tissues may be diminished. In some cases, elevatedpulmonary capillary pressure and pulmonary edema can decrease oxygenuptake as a result of impaired pulmonary alveolar-capillary diffusion.Supplemental oxygen increases the driving gradient for oxygen uptake.Arterial blood that is at its maximum oxygen-carrying capacity can potentiallydeliver oxygen to myocardium in jeopardy during an MI via collateral coronarycirculation. The recommended duration of supplemental oxygen administrationin a MI is 2 to 6 hours, longer if congestive heart failure occurs or arterial oxygensaturation is less than 90%Aspirin• Aspirin is an antiplatelet agent that initiates the irreversible inhibition ofcyclooxygenase, thereby preventing platelet production of thromboxane A2and decreasing platelet aggregation• Administration of ASA in ACS reduces cardiac endpoints The nidus of an occlusive coronary thrombus is the adhesion of activatedplatelets at the site of intimal disruption in an unstable atherosclerotic plaque. Its beneficial effect is observed early in therapy and persists for years withcontinued use. The long-term benefit is sustained, even at doses as low as75 mg/dayACC/AHA Guidelines for Aspirin TherapyAspirin should be given in a dose of 75-325 mg/day to allpatients with ACS unless there is a contraindication (in whichcase, clopidogrel should be given)
  19. 19. 19 MAGDI AWAD SASI 2013 ACS ( CARDIOLOGY)NitratesNitroglycerin is considered a cornerstone of anti-anginal therapy,despite little objective evidence for its benefit.Mechanism of Action-Relaxes vascular smooth muscle- Benefit is thought to occur via reduction in myocardial O2 demandsecondary to venodilation induced reduction in preload as well ascoronary vasodilation and afterload reduction.Titrate to relief of chest pain; chest pain = death of myocardial cellsNo documented mortality benefitContraindications :1.BP<100mm Hg2.Pt. Has already taken maximum dose of three doses (1.2mg)Dose– .4mg sublingual Tablet or Metered-dose Spray– .4mg Trans-dermal patch May repeat at 5 minute intervals up to 3 .If tablet form - Protect potencyStore in original brown bottle,Keep tightly sealedProtect from light, air, heat, Secure new supply every 4 - 6 monthsIntravenous nitroglycerin in patients with persistent chest pain afterthree sublingual nitroglycerin tablets, as well as in patients withhypertension or HF. However, nitrates must be used with caution oravoided in settings in which hypotension is likely or could result in serioushemodynamic decompensation, such as right ventricular infarction orsevere aortic stenosis. In addition, nitrates are contraindicated in patientswho have taken a phosphodiesterase inhibitor for erectile dysfunction (orpulmonary hypertension) within the previous 24 hours
  20. 20. 20 MAGDI AWAD SASI 2013 ACS ( CARDIOLOGY)Beta Blockers• Beta Blockers reduce myocardial oxygen demand by reducing heart rate,contractility, and ventricular wall tension• Administration of beta blockers in ACS reduces cardiac endpointsAHA/ACC Guidelines for Beta Blocker Therapy• Intravenous beta blockers should be usedinitially in all patients (without contraindication)followed by oral beta blockers with the goal beingdecrease in heart rate to 60 beats per minute• A combination of beta blockers and nitrates canbe viewed as first line therapy in all patients withACSHeparin• Heparin (unfractionated heparin or UFH) has traditionally beenthe mainstay of therapy in acute coronary syndromes as its efficacyhas been documented in several large, randomized trialsLMWH• More recent studies indicate that low molecular weight heparinis also effective in the reduction of end points such as myocardial infarctionor death, DVT ,INTRACARDIAC THROMBUS OR PE.• Some studies report that LMWH, when used in combination with ASA,may be superior to continuous infusion of Heparin.ACC/AHA Guidelines for Heparin Therapy• All patients with acute coronary syndromes shouldbe treated with a combination of ASA (325 mg/day)and low molecular weight heparin unless one of thedrugs is contraindicated
  21. 21. 21 MAGDI AWAD SASI 2013 ACS ( CARDIOLOGY)Enoxaparin 1mg/Kg bd• UFH if primary PCI• After thrombolysis continue until hospital discharge?ACE-ITo reduce ventricular remodeling over days to weeks after myocardialdamage.However, there is data that a mortality benefit exists whenthese agents are used early in the course of ACS.• Administration of ACE-I in ACS reduces cardiac endpointsAHA/ACC Guidelines for ACE-I Therapy• ACE-I should be administered to all patientsin the first 24 hours of ACS provided hypotensionand other clear cut contraindications are absentStatins• Statins may be of benefit in ACS• Mechanisms ---plaque stabilization, reversal of endothelial dysfunction,decreased thrombogenicity, and reduction of inflammation.IIBIIIA Inhibitors• More potent inhibition of platelet aggregation may be of importancein patients with ACS that is associated with unstable coronary lesionand thrombus formation.This can be achieved by the use of GP IIBIIIA inhibitors• Administration of IIBIIIA inhibitors reduces cardiac endpoints
  22. 22. 22 MAGDI AWAD SASI 2013 ACS ( CARDIOLOGY)AHA/ACC Guidelines for use of IIBIIIA inhibitors• A IIBIIIA inhibitor should be administered to all patients in whom apercutaneous intervention is planned (in addition to heparin/ASA)• Eptifibatide or Tirofiban should be administered to patients withACS in whom PCI is not planned if other high risk features arepresent (TIMI risk score >3)Score of 3 or less = low riskScore of 4-5 = intermediate risk (use IIBIIIA)Score of 6-7 = high risk (use IIBIIIA)Clopidogrel• Clopidogrel is a potent antiplatelet agent• It should be administered to all patients who cannot take ASA• The CURE trial suggests a benefit to adding Clopidogrel to ASA/Heparin inpatients going for PCI,STEMI ,NSTEMI.• Give 300 mg loading dose followed by 75mg/dayTIMI Risk Score• Age >65 yrs• Daily ASA Therapy (>7 days prior to event)• Symptoms of Unstable Angina• Documented CAD (stenosis > 50%)• 3 or more traditional cardiac risk factors• Elevated cardiac enzymes• ECG changes
  23. 23. 23 MAGDI AWAD SASI 2013 ACS ( CARDIOLOGY)AHA/ACC Guidelines for Clopidogrel• Clopidogrel should be administered to patients who cannottake ASA because of hypersensitivity or gastrointestinal intolerance• In hospitalized patients in whom an early, noninterventional approach isplanned, clopidogrel should be added to ASA as soon as possible onadmission and administered for at least 1 month and up to 9 months.Do not use clopidogrel if there is any possibility patient may be candidatefor CABGEmergent Revascularization• In the setting of STEMI primary PCI is associated with better outcomes thanthrombolysis• Emergent PCI is also indicated in the setting of a new LBBBPCI = percutaneous coronary interventionAHA/ACC Guidelines for Primary PCI• Primary PCI is indicated as an alternative to thrombolysis whenthe following criteria are met:– STEMI or new LBBB– Can undergo PCI within 12 hours of the onset of symptoms– The MD doing the intervention does more than 75 PCI’s/yr– The procedure is done in a center that does more than 200 PCI’s/yrand has surgical backupTreatment of NSTEMI/USA• ASA• NTG (consider MSO4 if pain not relieved)• Beta Blocker• Heparin/LMWH• ACE-I• +/- Statin• +/- Clopidogrel (don’t give if CABG is a possibility)• +/- IIBIIIA inhibitors (based on TIMI risk score)ANTIAARYTHMIC FOR ARRTHMIA AND DIURETIC FOR FAILUREDILTIAZEM (CCB) FOR CORONARY SPASM