Presentation on theme: "Risk stratification and Medical management of STEMI"— Presentation transcript:
1 Risk stratification and Medical management of STEMI Dr . Ranjith MP
2 OUTLINEDefinition of MIRisk stratificationMedical management
3 REVISED DEFINITION MI Criteria for Acute, Evolving, or Recent MI (Myocardial infarction redefined—a consensus document of The Joint European Society of Cardiology/American College of Cardiology committee for the redefinition of myocardial infarction:. J. Am. Coll. Cardiol. 2000;36; )Criteria for Acute, Evolving, or Recent MIEither of the following criteria satisfiesTypical rise &/or fall of biochemical markers of myocardial necrosis with at least one of the following:Ischemic symptomsECG changes indicative of new ischemia (new ST elevation or new/presumed to be new LBBB)Development of pathological Q waves in the ECGImaging e/o new loss of viable myocardium or new RWMAPathologic findings of an acute MI
4 REVISED DEFINITION MI PCI periprocedural MI: (Myocardial infarction redefined—a consensus document of The Joint European Society of Cardiology/American College of Cardiology committee for the redefinition of myocardial infarction:. J. Am. Coll. Cardiol. 2000;36; )PCI periprocedural MI:increases of biomarkers >3 x 99th percentile URLCABG-related MIIncreases of biomarkers >5 x 99th percentile URL plus either new pathological Q waves or new LBBB, or angiographically documented new graft or native coronary artery occlusion, or imaging evidence of new loss of viable myocardium.
5 REVISED DEFINITION MI Criteria for established MI. (Myocardial infarction redefined—a consensus document of The Joint European Society of Cardiology/American College of Cardiology committee for the redefinition of myocardial infarction:. J. Am. Coll. Cardiol. 2000;36; )Criteria for established MI.Either of the following criteria satisfiesDevelopment of new pathologic Q waves on serial ECGs. The patient may or may not remember previous symptoms. Biochemical markers of myocardial necrosis may have normalized, depending on the length of time that has passed since the infarct developed.Pathologic findings of a healed or healing MI.
7 Risk stratification of STEMI There is risk stratification within STEMI, but in general, STEMI is high-riskImportant to select greater-risk patients who warrant more aggressive strategies for prevention of future serious events such as reinfarction or sudden death
8 Risk Stratification Occurs in several stages Initial presentation In-hospital course (CCU, intermediate CU)At the time of hospital discharge
10 Acute Phase Risk Stratification: Electrocardiographic features Anterior MI/ Persisting ST elevationQ waves in multiple leadsRVMI + IWMIHigh sum of ST elevationReciprocal ( anterior ) ST depressionPersisting ST depressionProlonged QTConduction defects/ heart blockSinus tachycardia/atrial fibrillation
11 Acute Phase Risk Stratification: Importance of LV dysfunction (Killip T, and Kimball JT: Treatment of myocardial infarction in a coronary care unit: a two year experience of 250 patients. American Journal of Cardiology 1967; 20: )Left ventricular dysfunction is the single most important predictor of mortality
12 Risk Scores TIMI GRACE PURSUIT ACI-TIPI Goldman best used to supplement—not replace—clinical judgmentless useful in atypical presentations, but indeed validated in an ED population . . .
13 TIMI 30-day MORTALITY(David A et al. TIMI Risk Score for ………..: An Intravenous nPA for Treatment of Infarcting Myocardium Early II Trial Substudy. Circulation 2000, 102: )
14 TIMI 1yr MORTALITY (30-day survivors) (David A et al. TIMI Risk Score for ………..: An Intravenous nPA for Treatment of Infarcting Myocardium Early II Trial Substudy. Circulation 2000, 102: )
15 The Thrombolysis In Myocardial Infarction (TIMI) risk index (TRI) ( Wiviott SD et al Performance of the TRI in the National Registry of Myocardial Infarction-3 and -4:. J Am Coll Cardiol 2004;44:783–9 )Derived from In TIME II trial & validated in TIMI-9 trialsBased on age and vital signs, in predicting mortality among a large, community based, unselected, heterogeneous populationHeart rate [age/10 ]2 /systolic blood pressureA strong and independent predictor of mortality at 24 h and at 30 days (p )
16 TIMI risk index and mortality ( Stephen D et al TIMI risk index and mortality ( Stephen D et al. Application of the Thrombolysis In Myocardial Infarction Risk Index in Non–ST-Segment Elevation Myocardial Infarction Evaluation of Patients in the National Registry of Myocardial Infarction, JAAC: Vol. 47, No. 8, 2006)
17 GRACE RISK SCORECan be used to predict the cumulative risk of death and death or myocardial infarction in the period from admission to hospital to six months after dischargeThe tool is simple and applicable to patients across the complete spectrum of acute coronary syndrome
19 Risk Stratification at Hospital Discharge Exercise Testingperformed either in the hospital or early after discharge in patients not selected for cardiac catheterization and without high-risk features to assess the presence and extent of inducible ischemia Class I (B)Exercise testing might be considered before discharge of patients recovering from STEMI to guide the post discharge exercise prescription or to evaluate the functional significance of a coronary lesion previously identified at angiography Class IIb (C)
20 Post MI Management: Pre-discharge TMT Sub maximal protocolTarget workload =5 METS, 70 % MPHR or symptom limitedPredictors of poor outcomeIschemic ST depression > 1 mm is inconsistent predictor of mortalitypoor exercise tolerance < 3 minutes doubles one year mortality ( 7% to14%)Inability to exercise or contra-indication to TMT identifies High Risk patient.
21 Post MI Management-Phases: Convalescence Late Risk Stratification - 4 to 8 weeks(Assessment of residual ischaemia)TMTStress echocardiographyAdenosine/Dipyridamole Perfusion imagingUn-interpretable ECGEquivocal TMTInability to exercise
23 Prehospital Chest Pain Evaluation and Treatment Prehospital EMS providers …162 to 325 mg of aspirin (chewed) …non–enteric-coated formulations.(goal is to quickly block thromboxane A2 formation in platelets)Previously on NTG take I tab S/L Not improving after 5 mts Seek medical help
24 Options for Transport of Patients With STEMI and Initial Reperfusion Treatment Hospital fibrinolysis:Door-to-Needlewithin 30 min.Not PCIcapableEMS on-sceneEncourage 12-lead ECGs.Consider prehospital fibrinolytic if capable and EMS-to-needle within 30 min.Onset of symptoms of STEMIEMSDispatchEMS Triage PlanInter-HospitalTransferPCIcapableGOALS5min.8min.EMS TransportPatientEMSPrehospital fibrinolysisEMS-to-needlewithin 30 min.EMS transportEMS-to-balloon within 90 min.Patient self-transportHospital door-to-balloonwithin 90 min.Dispatch1 min.Golden Hour = first 60 min.Total ischemic time: within 120 min.
25 Fibrinolysis preferred Early presentation (≤3 hr from symptom onset and delay to invasive strategy)Invasive strategy is not an option Catheterization laboratory occupied or not availableVascular access difficulties Lack of access to a skilled PCI laboratory Delay to invasive strategyProlonged transport (Door-to-balloon)–(door-to-needle) more than 1 hrMedical contact-to-balloon or door-to-balloon more than90 min
26 Invasive strategy preferred Skilled PCI laboratory is available with surgical backup Medical contact-to-balloon or door-to-balloon less than 90 minHigh risk from STEMICardiogenic shockKillip class ≥ 3Contraindications to fibrinolysisLate presentation (> 3 hr)Diagnosis of STEMI is in doubt
27 Initial Recognition and Management in the Emergency Department 1. Airway, Breathing, Circulation (ABC) 2. Vital signs, general observation 3. Presence or absence of jugular venous distension 4. Pulmonary auscultation for rales 5. Cardiac auscultation for murmurs and gallops 6. Presence or absence of stroke
28 Laboratory examinations should be performed, but should not delay the implementation of reperfusion therapy.Serum biomarkers for cardiac damageComplete blood count (CBC) with plateletsInternational normalized ratio (INR)Activated partial thromboplastin time (aPTT)Electrolytes and magnesiumBlood urea nitrogen (BUN),creatinineGlucoseComplete Lipid Profile
29 Cardiac Biomarkers in STEMI 10050Cardiac troponin-no reperfusion20Cardiac troponin-reperfusionMultiples of the URLCKMB- no reperfusion10CKMB- reperfusion52Cardiac biomarkers in ST-elevation myocardial infarction (STEMI).Typical cardiac biomarkers that are used to evaluate patients withSTEMI include the MB isoenzyme of CK (CK-MB) and cardiac specific troponins. The horizontal line depicts the upper reference limit (URL)for the cardiac biomarker in the clinical chemistry laboratory. The URL is that value representing the 99th percentile of a reference control group without STEMI. The kinetics of release of CK-MB and cardiac troponin in patients who do not undergo reperfusion are shown in the solid green and red curves as multiples of the URL. Note that when patients with STEMI undergo reperfusion, as depicted in the dashed green and red curves, the cardiac biomarkers are detected sooner, rise to a higher peak value, but decline more rapidly, resulting in a smaller area under the curve and limitation of infarct size. Modified with permission from Alpert et al. J Am Coll Cardiol 2000;36:959 and Wu et al. Clin Chem 1999;45:1104.Upper reference limit1Days After Onset of STEMIURL = 99th %tile ofReference Control Group
30 Control of cardiac pain Pain contribute to the heightened sympathetic activityTypically accomplished with combination of nitrates, analgesics, oxygen and β-blockersOxygenArterial oxygen desaturation (SaO2 < 90%) Class I(B)Uncomplicated STEMI during the first 6 hours Class II(A)
31 Control of cardiac pain Nitroglycerin Class I (C)Patients with ongoing ischemic discomfort0.4 mg every 5 minutes for a total of 3 dosesIntravenous NTGOngoing ischemic discomfort that responds to nitrate therapycontrol of hypertensionmanagement of pulmonary congestion.Nitrates should not be administered to patients with:systolic pressure < 90 mm Hg or ≥ to 30 mm Hg below baselinesevere bradycardia (< 50 bpm)tachycardia (> 100 bpm)suspected RV infarction.who have received a phosphodiesterase
32 Control of cardiac pain AnalgesiaMorphine sulfate (2 to 4 mg intravenously) Class I (C)NSAIDS Increase risk of cardiovascular events so should be discontinued[A sub study analysis from the ExTRACT TIMI-25 trial showed increased risk of death, reinfarction, heart failure, or shock among patients on NSAIDs within 7 days of enrollment].AspirinShould be chewed by patients who have not taken aspirin before presentation with STEMI. The initial dose should be 162 mg Class I (A) to 325 mg. Class I (C)
33 REPERFUTION THERAPYThe principal goal of fibrinolysis is prompt restoration of full IRA patencyStreptokinase , tPA,, TNK, rPATNK and rPA - bolus fibrinolyticsPromote conversion of plasminogen to plasmin, which subsequently lyses fibrin thrombi
34 Importance of time to reperfusion in patients undergoing fibrinolysis (National Cardiovascular Data Registry )
35 Data from 22 trials of fibrinolytic therapy (Boersma E, et al: Early thrombolytic treatment in acute myocardial infarction: Reappraisal of the golden hour. Lancet 348:771, 1996)
36 Contraindications and Cautions for Fibrinolysis in STEMI Absolute Contraindications:Any prior intracranial hemorrhageKnown structural cerebral vascular lesionKnown malignant intracranial neoplasmIschemic stroke within 3 months EXCEPT acute ischemic stroke within 3 hoursSuspected aortic dissectionActive bleeding or bleeding diathesis (excluding menses)Significant closed-head or facial trauma within 3 monthsNote: Age restriction for fibrinolysis has been removed compared with prior guidelines.
37 Contraindications and Cautions for Fibrinolysis in STEMI Relative Contraindications:Severe uncontrolled hypertension on presentation (SBP > 180 or DBP > 110)Prior ischemic stroke >3 monthsTraumatic or prolonged (> 10 mt.) CPR or major surgery (< 3 weeks)Recent (< 2 to 4 weeks) internal bleedingNoncompressible vascular puncturesFor streptokinase/anistreplase: prior exposure (> 5 days ago) or prior allergic reaction to these agentsPregnancy, Active peptic ulcerCurrent use of anticoagulants
38 Comparison of Approved Fibrinolytic Agents (Antman EM et al: ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction. Circulation 110:e82, 2004.)PARAMETERSTREPTOKINASEALTEPLASERETEPLASETNK t-PADose1.5 MU in 30-60 minUp to 100 mg in 90 min (based on weight)10 U ? 2 (30 min apart) each over 2 min30-50 mg based on weightBolus administrationNoYesAntigenicAllergic reactions hypotension most commonSystemic fibrinogen depletionMarkedMildModerateMinimal90-min patency rates (%)≈50≈75TIMI grade 3 flow (%)32546063Cost per dose (Rs)250039375 (50mg)
39 CHOICE OF FIBRINOLYTICS WP-4 hr. t-PA is the preferred treatmentstreptokinase t-PA equivalent choices -risk of death is low , and increased risk of ICH .WP-4 to 12 hr . streptokinase and t-PA are equivalent options, but streptokinase is probably preferable to t-PA because of cost considerations
40 Late fibrinolysis LATE and EMERAS trials Fibrinolytics between 12 and 24 hoursNo mortality benefitIncreases risk of cardiac rupture
41 Assessment of Reperfusion after fibrinolysis Noninvasive findings s/o reperfusion include:Relief of symptomsMaintenance and restoration of hemodynamic and/or electrical instabilityReduction of ≥ 50% of the initial STE pattern on follow-up ECG 60 to 90 minutes after initiation of therapy.Class II(A)
42 TIMI grading system Flow in the IRA angiographically Gd. 0, compl. OcclussionGd. 1, some penetrationGd.2, entire vessel withImpaired flowGd.3, entire vessel withNormal flow
43 Anticoagulant therapy Prevention of DVT, pulmonary embolism, ventricular thrombus, cerebral embolization.Establishing & maintaining patency of IRA.Trials shown that more prolonged anticoagulant therapy is beneficial (duration of index hospita- lization) in patients receiving thrombolytic therapay
45 Anticoagulant therapy Consensus IV Unfractionated HeparinSelective Fibrinolytic – Bolus of 60 U/kg (maximum 4000 U) followed by an infusion of 12 U/kg/hr (maximum 1000 U) (Level of Evidence: C)Nonselective fibrinolytic agents- who are at high risk for systemic emboli (large or anterior MI, atrial fibrillation (AF), previous embolus, or known LV thrombus) (Level of Evidence: B)LMWH- 30mg iv followed by 1mg/kg every 12hr.
46 AntiplateletsAspirin should be given indefinitely to all STEMI pts. without a true aspirin allergy Class I (A)Patients undergoing PCI are also given aspirin loadingClass I (B)Patients not on aspirin therapy should be given nonenteric aspirin 325 mg before PCI.Class I(B)After PCI, use of aspirin should be continued indefinitelyClass I (A)
47 ThienopyridinesAddition of P2Y12 inhibitor to aspirin warranted for most patients with STEMI (COMMIT & CLARITY-TIMI22)In patients for whom PCI is planned, clopidogrel should be started and continued: Class I (B)Patients receiving a stent (BMS or DES) clopidogrel 75 mg daily or prasugrel 10 mg for at least 12 months;If the risk of bleeding outweighs the anticipated benefit afforded by thienopyridine therapy, earlier discontinuation .Continuation of thienopyridines beyond 15 months may be considered in patients undergoing DES placement
48 ThienopyridinesPrior history of stroke and TIA for whom primary PCI is planned, prasugrel is not recommendedCABG planned ?... the drug should be withheld for at least 5 days in patients receiving clopidogrel and at least 7 days in patients receiving prasugrel, Class I (B)Probably indicated in patients receiving fibrinolytic therapy who are unable to take aspirin because of hypersensitivity or GI intolerance Class I (C)
49 Glycoprotein IIb/IIIa Inhibitors It is reasonable to start abciximab as early as possible before primary PCI (with or without stenting) in patients with STEMI.Tirofiban or eptifibatide may be considered before primary PCI (with or without stenting) in patients with STEMI.
50 Beta-BlockersRelieve ischemic pain, reduce need for analgesics, reduce infarct size and life-threatening arrhythmiasContra indications:signs of heart failureevidence of a low output stateincreased risk for cardiogenic shockother relative contraindications (PR interval > 0.24 S. 2nd or 3rd degree AV block, or reactive airway disease)
52 Beta-BlockersFavorable effects with metoprolol, atenolol, carvedilol and timolol,Beta blockers with intrinsic sympathomimetic activity probably should not be chosen.Trial of esmolol in the presence of relative contraindications.
53 Inhibitors of the RAASFavorable impact on ventricular remodeling, improvement in hemodynamics, and reductions in congestive heart failureAngiotensin-converting enzyme inhibitorsAngiotensin II receptor blockersAldosterone blockade
54 ACE inhibitors on mortality after MI- from long-term trials.
55 ACE inhibitors on mortality after MI- from short-term trials.
56 Angiotensin II receptor blockers VALIANT TRIAL-Mortality
57 Angiotensin II receptor blockers VALIANT TRIAL-MACE
58 Aldosterone blockadeEPHESUS trial: Eplerenone, 25 mg/day titrated to 50 mg/day for high-risk patients following STEMI (EF ≤40%, clinical HF, DM)Mean follow-up 16 months, there was a 15% reduction in the RR of mortality
59 Calcium Channel Antagonists Immediate-release preparation of nifedipine increased risk of in-hospital mortalityVerapamil & diltiazem can be given for relief of ongoing ischemia or slowing of a rapid ventricular response in AF in patients with contraindication to beta blockers.INTERCEPT trial compared 300 mg of diltiazem with placebo and Diltiazem did not reduce cardiac death, nonfatal reinfarction, during a 6-month follow-up
60 Intensive Glucose Control in STEMI It is reasonable to use an insulin based regimen to achieve and maintain glucose levels less than 180 mg/dl while avoiding hypoglycemia for patients with STEMI with either a complicated or uncomplicated course Class IIa(B)
61 Physical activityIn the absence of complications patients need not be confined to bed for more than 12 hoursProgression of activity should be individualized
62 Pericarditis first day and as late as 6 weeks after STEMI Radiation of the pain to either trapezius ridge.Treatment consists of aspirin doses of 650 mg orally every 4 to 6 hours may be necessary.NSAIDs and steroids should be avoided
63 Left Ventricular Thrombus Anticoagulation- heparin to elevate the aPTT to 1.5 to 2 times that of control, followed by a minimum of 3 to 6 months of warfarin in the following clinical situations:An embolic event has already occurred orThe patient has a large anterior infarction whether or not a thrombus is visualized echocardiographically
64 Post MI myocardial rupture More in older patients, women , hypertensiveMore frequently in the left than right ventricle1 day and 3 weeks, most commonly 1 to 4 daysNear the junction of infarct and normal muscleMost often in patients without previous infarctsFibrinolytic therapy more than PCI
65 Cardiac arrhythmias in MI CATEGORYARRHYTHMIAOBJECTIVE OF TREATMENTTHERAPEUTIC OPTIONSElectrical instabilityVentricular premature beatsCorrection of electrolyte deficits and increased sympathetic tonePotassium and magnesium solutions, beta blockerVentricular tachycardiaProphylaxis against ventricular fibrillation, restoration of hemodynamic stabilityAntiarrhythmic agents; cardioversion/defibrillationVentricular fibrillationUrgent reversion to sinus rhythmDefibrillation; bretylium tosylateAccelerated idioventricular rhythmObservation unless hemodynamic function is compromisedIncrease sinus rate (atropine, atrial pacing); antiarrhythmic agentsNonparoxysmal atrioventricular junctional tachycardiaSearch for precipitating causes (e.g., digitalis intoxication); suppress arrhythmia only if hemodynamic function is compromisedAtrial overdrive pacing; antiarrhythmic agents; cardioversion relatively contraindicated if digitalis intoxication present
67 Cardiac arrhythmias in MI CATEGORYARRHYTHMIAOBJECTIVE OF TREATMENTTHERAPEUTIC OPTIONSBradyarrhythmias and conduction disturbancesSinus bradycardiaAcceleration of heart rate only if hemodynamic function is compromisedAtropine; atrial pacingJunctional escape rhythmAcceleration of sinus rate only if loss of atrial “kick” causes hemodynamic compromiseAtrioventricular block and intraventricular blockInsertion of pacemaker
71 Post MI Management-Phases: Convalescence At time of discharge patient should be on:ASA unless contra-indicationClopidogrel if PCI/NSTEMI (duration minimum1 year)Longer duration of clopidogrel if DES in critical location or complex lesion-blocker unless contra-indicationACE inhibitor for CHF or LV dysfunctionAll for vascular protection?Statin for LDL to < 70mg%(minimum 50% reduction)
72 Indications for Angiography High Riskextensive ECG changesanterior/ infero-posterior/ prior MIResidual ischaemiapost MI anginapositive TMT/ perfusion scannon-Q MIischaemia at a distanceComplicated MICHF/ flash pulmonary edemashockheart blockRBBBsustained ventricular arrhythmiasAnxiety/ physical labor/ young age
74 LIFE-STYLE MODIFICATION Smoking Goal: Complete CessationWith in 2yrs risk of nonfatal MI falls to normalBlood pressure control:Goal: < 140/90 mm Hg or <130/80 mm Hg if chronic kidney disease or diabetesPhysical activity:Minimum goal: 30 minutes 3 to 4 days per week; Optimal daily
75 Secondary Prevention and Long Term Management Weight management:Goal: BMI 18.5 to 24.9 kg/m2Waist circumference: Women < 35 in Men: < 40 in.Diabetes management:Goal: HbA1c < 7%Lipid management: Primary goal: LDL-C <70mg%Start dietary therapy in all patients (< 7% of total calories as saturated fat and < 200 mg/d cholesterol). Promote physical activity and weight management. Encourage increased consumption of omega-3 fatty acids.Assess fasting lipid profile in all patients, preferably within 24 hours of STEMI. Add drug therapy according to the following guide:
76 Secondary Prevention and Long Term Management LDL-C < 100 mg/dL (baseline or on treatment):Statins should be used to lower LDL-C.LDL-C ≥ 100 mg/dL (baseline or on treatment):Intensify LDL-C–lowering therapy with drug treatment, giving preference to statins.If TGs are ≥ 150 mg/dL or HDL-C is < 40 mg/dL:Emphasize weight management and physical activity. Advise smoking cessation.If TG is 200 to 499 mg/dL:After LDL-C–lowering therapy, consider adding fibrate or niacin.If TG is ≥ 500 mg/dL:Consider fibrate or niacin before LDL-C–lowering therapy.Consider omega-3 fatty acids as adjunct for high TG.
77 Secondary Prevention and Long Term Management Hormone therapy:with estrogen plus progestin should not be given de novo to postmenopausal women after STEMI for secondary prevention of coronary events. Class III (A)Postmenopausal women who are already taking estrogen plus progestin at the time of STEMI should not continue hormone therapy Class II (B)However, women who are beyond 1 to 2 years after initiation of hormone therapy who wish to continue such therapy for another compelling indication should weigh the risks and benefits Class III (A)Antioxidant vitamins:such as vitamin E and/or vitamin C supplements should not be prescribed to patients recovering from STEMI to prevent cardiovascular disease
78 Secondary Prevention and Long Term Management Psychosocial status of the patient should be evaluated, including inquiries regarding symptoms of depression, anxiety, or sleep disorders and the social support environment Class I (C)Treatment with cognitive-behavioral therapy and selective serotonin reuptake inhibitors can be useful for STEMI patients with depression that occurs in the year after hospital discharge. Class IIa (A)
79 Potential Cumulative Impact of 2° Prevention Treatments ( Yusuf, S. Two decades of progress in preventing vascular disease. Lancet 2002; 360: 2-3).RRR2yr Event RateNone8%ASA25%6% -Blockers4.5%Lipid lowering30%3.0%ACE-inhibitors2.3%Cumulative relative risk reduction if all four drugs are used is about 75%