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Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
Risk stratification and medical management of stemi
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Risk stratification and medical management of stemi

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  • 1. Dr . Ranjith MP 14-11-2011
  • 2.  Definition of MI  Risk stratification  Medical management
  • 3. (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;959-969)  Criteria for Acute, Evolving, or Recent MI  Either of the following criteria satisfies 1. Typical rise &/or fall of biochemical markers of myocardial necrosiswith at least one of the following: a) Ischemic symptoms b) ECG changes indicative of new ischemia (new ST elevation or new/presumed to be new LBBB) c) Development of pathological Q waves in the ECG d) Imaging e/o new loss of viable myocardium or new RWMA 2. Pathologic findings of an acute MI
  • 4. (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;959-969)  PCI periprocedural MI: increases of biomarkers >3 x 99th percentile URL  CABG-related MI Increases 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. (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;959-969)  Criteria for established MI.  Either of the following criteria satisfies 1. Development 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. 2. Pathologic findings of a healed or healing MI.
  • 6.  There is risk stratification within STEMI, but in general, STEMI is high-risk  Important to select greater-risk patients who warrant more aggressive strategies for prevention of future serious events such as reinfarction or sudden death
  • 7.  Occurs in several stages Initial presentation In-hospital course (CCU, intermediate CU) At the time of hospital discharge
  • 8.  Prior angina pectoris  Prior MI  Female gender  Hypertension  History of CHF  Hyperlipidemia  Diabetes  ECG Criteria  Markedly elevated cardiac enzymes  Elevated BUN  Complications  VSR/PMD-rupture  Myocardial rupture
  • 9.  Anterior MI/ Persisting ST elevation  Q waves in multiple leads  RVMI + IWMI  High sum of ST elevation  Reciprocal ( anterior ) ST depression  Persisting ST depression  Prolonged QT  Conduction defects/ heart block  Sinus tachycardia/atrial fibrillation
  • 10. Killip Classification % patients Mortality (%) I No CHF 30-50 5 II Rales, S3, Pulmonary venous hypertension 33 15-20 III Pulmonary edema 15 40 IV Cardiogenic shock 10 80-100 (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: 457-464 ) Left ventricular dysfunction is the single most important predictor of mortality
  • 11.  TIMI  GRACE  PURSUIT  ACI-TIPI  Goldman  best used to supplement—not replace— clinical judgment  less useful in atypical presentations, but indeed validated in an ED population . . .
  • 12. (David A et al. TIMI Risk Score for ………..: An Intravenous nPA for Treatment of Infarcting Myocardium Early II Trial Substudy. Circulation 2000, 102:2031-2037)
  • 13. (David A et al. TIMI Risk Score for ………..: An Intravenous nPA for Treatment of Infarcting Myocardium Early II Trial Substudy. Circulation 2000, 102:2031-2037)
  • 14. ( 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 trials  Based on age and vital signs, in predicting mortality among a large, community based, unselected, heterogeneous population  Heart rate [age/10 ]2 /systolic blood pressure  A strong and independent predictor of mortality at 24 h and at 30 days (p 0.0001)
  • 15.  Can 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 discharge  The tool is simple and applicable to patients across the complete spectrum of acute coronary syndrome
  • 16.  Exercise Testing  performed 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)
  • 17.  Sub maximal protocol Target workload =5 METS, 70 % MPHR or symptom limited  Predictors of poor outcome Ischemic ST depression > 1 mm is inconsistent predictor of mortality poor exercise tolerance < 3 minutes doubles one year mortality ( 7% to14%) Inability to exercise or contra-indication to TMT identifies High Risk patient.
  • 18. Late Risk Stratification - 4 to 8 weeks (Assessment of residual ischaemia)  TMT  Stress echocardiography  Adenosine/Dipyridamole Perfusion imaging  Un-interpretable ECG  Equivocal TMT  Inability to exercise
  • 19.  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
  • 20. EMS Transport Onset of symptoms of STEMI EMS Dispatch EMS on-scene • Encourage 12-lead ECGs. • Consider prehospital fibrinolytic if capable and EMS-to-needle within 30 min. GOALS PCI capable Not PCI capable Hospital fibrinolysis: Door-to-Needle within 30 min. Inter- Hospital Transfer Golden Hour = first 60 min. Total ischemic time: within 120 min. Patient EMS Prehospital fibrinolysis EMS-to-needle within 30 min. EMS transport EMS-to-balloon within 90 min. Patient self-transport Hospital door-to-balloon within 90 min. Dispatch 1 min. 5 min. 8 min.
  • 21.  Early presentation (≤3 hr from symptom onset and delay to invasive strategy)  Invasive strategy is not an option  Catheterization laboratory occupied or not available  Vascular access difficulties  Lack of access to a skilled PCI laboratory  Delay to invasive strategy Prolonged transport (Door-to-balloon)–(door-to-needle) more than 1 hr Medical contact-to-balloon or door-to-balloon more than90 min
  • 22.  Skilled PCI laboratory is available with surgical backup Medical contact-to-balloon or door-to-balloon less than 90 min  High risk from STEMI Cardiogenic shock Killip class ≥ 3  Contraindications to fibrinolysis  Late presentation (> 3 hr)  Diagnosis of STEMI is in doubt
  • 23. 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
  • 24.  should be performed, but should not delay the implementation of reperfusion therapy. Serum biomarkers for cardiac damage Complete blood count (CBC) with platelets International normalized ratio (INR) Activated partial thromboplastin time (aPTT) Electrolytes and magnesium Blood urea nitrogen (BUN),creatinine Glucose Complete Lipid Profile
  • 25. 0 1 2 3 4 5 6 7 8 Cardiac troponin-no reperfusion Days After Onset of STEMI MultiplesoftheURL Upper reference limit 1 2 5 10 20 50 URL = 99th %tile of Reference Control Group 100 Cardiac troponin-reperfusion CKMB- reperfusion CKMB- no reperfusion
  • 26.  Pain contribute to the heightened sympathetic activity  Typically accomplished with combination of nitrates, analgesics, oxygen and β-blockers  Oxygen Arterial oxygen desaturation (SaO2 < 90%) Class I(B) Uncomplicated STEMI during the first 6 hours Class II(A)
  • 27.  Nitroglycerin Class I (C)  Patients with ongoing ischemic discomfort  0.4 mg every 5 minutes for a total of 3 doses  Intravenous NTG  Ongoing ischemic discomfort that responds to nitrate therapy control of hypertension management of pulmonary congestion.  Nitrates should not be administered to patients with:  systolic pressure < 90 mm Hg or ≥ to 30 mm Hg below baseline  severe bradycardia (< 50 bpm)  tachycardia (> 100 bpm)  suspected RV infarction.  who have received a phosphodiesterase
  • 28.  Analgesia Morphine 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].  Aspirin Should 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)
  • 29.  The principal goal of fibrinolysis is prompt restoration of full IRA patency  Streptokinase , tPA,, TNK, rPA  TNK and rPA - bolus fibrinolytics  Promote conversion of plasminogen to plasmin, which subsequently lyses fibrin thrombi
  • 30.  Absolute Contraindications: Any prior intracranial hemorrhage Known structural cerebral vascular lesion Known malignant intracranial neoplasm 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 Note: Age restriction for fibrinolysis has been removed compared with prior guidelines.
  • 31.  Relative Contraindications: Severe uncontrolled hypertension on presentation (SBP > 180 or DBP > 110) Prior ischemic stroke >3 months Traumatic or prolonged (> 10 mt.) CPR or major surgery (< 3 weeks) Recent (< 2 to 4 weeks) internal bleeding Noncompressible vascular punctures For streptokinase/anistreplase: prior exposure (> 5 days ago) or prior allergic reaction to these agents Pregnancy, Active peptic ulcer Current use of anticoagulants
  • 32. (Antman EM et al: ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction. Circulation 110:e82, 2004.) PARAMETER STREPTOKINASE ALTEPLASE RETEPLASE TNK t-PA Dose 1.5 MU in 30-60 min Up to 100 mg in 90 min (based on weight) 10 U ? 2 (30 min apart) each over 2 min 30-50 mg based on weight Bolus administration No No Yes Yes Antigenic Yes No No No Allergic reactions hypotension most common Yes No No No Systemic fibrinogen depletion Marked Mild Moderate Minimal 90-min patency rates (%) ≈50 ≈75 ≈75 ≈75 TIMI grade 3 flow (%) 32 54 60 63 Cost per dose (Rs) 2500 39375 (50mg)
  • 33.  WP-4 hr. t-PA is the preferred treatment  streptokinase 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
  • 34.  LATE and EMERAS trials  Fibrinolytics between 12 and 24 hours  No mortality benefit  Increases risk of cardiac rupture
  • 35.  Noninvasive findings s/o reperfusion include:  Relief of symptoms  Maintenance and restoration of hemodynamic and/or electrical instability  Reduction of ≥ 50% of the initial STE pattern on follow-up ECG 60 to 90 minutes after initiation of therapy. Class II(A)
  • 36.  Flow in the IRA angiographically  Gd. 0, compl. Occlussion  Gd. 1, some penetration  Gd.2, entire vessel with Impaired flow  Gd.3, entire vessel with Normal flow
  • 37.  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
  • 38.  IV Unfractionated Heparin  Selective 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.
  • 39.  Aspirin should be given indefinitely to all STEMI pts. without a true aspirin allergy. Class I (A)  Patients undergoing PCI are also given aspirin loading Class 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 indefinitely Class I (A)
  • 40.  Addition 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
  • 41.  Prior history of stroke and TIA for whom primary PCI is planned, prasugrel is not recommended  CABG 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)
  • 42.  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.
  • 43.  Relieve ischemic pain, reduce need for analgesics, reduce infarct size and life-threatening arrhythmias  Contra indications:  signs of heart failure  evidence of a low output state  increased risk for cardiogenic shock  other relative contraindications (PR interval > 0.24 S. 2nd or 3rd degree AV block, or reactive airway disease)
  • 44.  Favorable 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.
  • 45.  Favorable impact on ventricular remodeling, improvement in hemodynamics, and reductions in congestive heart failure Angiotensin-converting enzyme inhibitors Angiotensin II receptor blockers Aldosterone blockade
  • 46.  EPHESUS 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
  • 47.  Immediate-release preparation of nifedipine increased risk of in-hospital mortality  Verapamil & 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
  • 48.  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)
  • 49.  In the absence of complications patients need not be confined to bed for more than 12 hours  Progression of activity should be individualized
  • 50.  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
  • 51.  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 or  The patient has a large anterior infarction whether or not a thrombus is visualized echocardiographically
  • 52.  More in older patients, women , hypertensive  More frequently in the left than right ventricle  1 day and 3 weeks, most commonly 1 to 4 days  Near the junction of infarct and normal muscle  Most often in patients without previous infarcts  Fibrinolytic therapy more than PCI
  • 53. CATEGORY ARRHYTHMIA OBJECTIVE OF TREATMENT THERAPEUTIC OPTIONS Electrical instability Ventricular premature beats Correction of electrolyte deficits and increased sympathetic tone Potassium and magnesium solutions, beta blocker Ventricular tachycardia Prophylaxis against ventricular fibrillation, restoration of hemodynamic stability Antiarrhythmic agents; cardioversion/defibrillatio n Ventricular fibrillation Urgent reversion to sinus rhythm Defibrillation; bretylium tosylate Accelerated idioventricular rhythm Observation unless hemodynamic function is compromised Increase sinus rate (atropine, atrial pacing); antiarrhythmic agents Nonparoxysmal atrioventricular junctional tachycardia Search for precipitating causes (e.g., digitalis intoxication); suppress arrhythmia only if hemodynamic function is compromised Atrial overdrive pacing; antiarrhythmic agents; cardioversion relatively contraindicated if digitalis intoxication present
  • 54. CATEGORY ARRHYTHMIA OBJECTIVE OF TREATMENT THERAPEUTIC OPTIONS Pump failure, excessive sympathetic stimulation Sinus tachycardia Reduce heart rate to diminish myocardial oxygen demands Antipyretics; analgesics; consider beta blocker unless congestive heart failure present; treat latter if present with anticongestive measures (diuretics, afterload reduction) Atrial fibrillation and/or atrial flutter Reduce ventricular rate; restore sinus rhythm Verapamil, digitalis glycosides; anticongestive measures (diuretics, afterload reduction); cardioversion; rapid atrial pacing (for atrial flutter) Paroxysmal supraventricul ar tachycardia Reduce ventricular rate; restore sinus rhythm Vagal maneuvers; verapamil, cardiac glycosides, beta- adrenergic blockers; cardioversion; rapid atrial pacing
  • 55. CATEGORY ARRHYTHMIA OBJECTIVE OF TREATMENT THERAPEUTIC OPTIONS Bradyarrhyth mias and conduction disturbances Sinus bradycardia Acceleration of heart rate only if hemodynamic function is compromised Atropine; atrial pacing Junctional escape rhythm Acceleration of sinus rate only if loss of atrial “kick” causes hemodynamic compromise Atropine; atrial pacing Atrioventricular block and intraventricular block Insertion of pacemaker
  • 56. At time of discharge patient should be on:  ASA unless contra-indication  Clopidogrel if PCI/NSTEMI (duration minimum1 year)  Longer duration of clopidogrel if DES in critical location or complex lesion  -blocker unless contra-indication  ACE inhibitor for CHF or LV dysfunction  All for vascular protection?  Statin for LDL to < 70mg%(minimum 50% reduction)
  • 57.  High Risk  extensive ECG changes  anterior/ infero-posterior/ prior MI  Residual ischaemia  post MI angina  positive TMT/ perfusion scan  non-Q MI  ischaemia at a distance  Complicated MI  CHF/ flash pulmonary edema  shock  heart block  RBBB  sustained ventricular arrhythmias  Anxiety/ physical labor/ young age
  • 58.  Smoking Goal: Complete Cessation  With in 2yrs risk of nonfatal MI falls to normal  Blood pressure control:  Goal: < 140/90 mm Hg or <130/80 mm Hg if chronic kidney disease or diabetes  Physical activity:  Minimum goal: 30 minutes 3 to 4 days per week; Optimal daily
  • 59.  Weight management:  Goal: BMI 18.5 to 24.9 kg/m2  Waist 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:
  • 60.  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.
  • 61.  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
  • 62.  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)
  • 63. RRR 2yr Event Rate None 8% ASA 25% 6%  -Blockers 25% 4.5% Lipid lowering 30% 3.0% ACE- inhibitors 25% 2.3% ( Yusuf, S. Two decades of progress in preventing vascular disease. Lancet 2002; 360: 2-3). Cumulative relative risk reduction if all four drugs are used is about 75%

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