RISK STRATIFICATION AND MEDICAL MANAGEMENT OF STEMI Dr . Ranjith MP 14-11-2011
Mar 29, 2015
RISK STRATIFICATION AND MEDICAL
MANAGEMENT OF STEMI
Dr . Ranjith MP
14-11-2011
OUTLINE
Definition of MI
Risk stratification
Medical management
REVISED DEFINITION 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;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 necrosis with at least one of the following:a) Ischemic symptomsb) ECG changes indicative of new ischemia (new ST elevation or
new/presumed to be new LBBB)c) Development of pathological Q waves in the ECGd) Imaging e/o new loss of viable myocardium or new RWMA
2. Pathologic findings of an acute MI
REVISED DEFINITION 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;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.
REVISED DEFINITION 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;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.
Risk stratification of STEMI
Risk stratification of STEMI
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
Risk Stratification
Occurs in several stages
Initial presentation
In-hospital course (CCU, intermediate CU)
At the time of hospital discharge
Acute Phase Risk Stratification:
Prior angina pectoris
Prior MI Female gender Hypertension History of CHF Hyperlipidemia Diabetes
ECG Criteria Markedly elevated
cardiac enzymes Elevated BUN Complications
VSR/PMD-ruptureMyocardial rupture
Acute Phase Risk Stratification:Electrocardiographic features
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
Acute Phase Risk Stratification:Importance of LV dysfunction
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
Risk Scores
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 . . .
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, 102:2031-2037)
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, 102:2031-2037)
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 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)
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)
GRACE RISK SCORE
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
Risk Stratification at Hospital Discharge
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)
Post MI Management:Pre-discharge TMT
Sub maximal protocolTarget workload =5 METS, 70 % MPHR or symptom
limited
Predictors 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.
Post MI Management-Phases:Convalescence
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
MEDICAL MANAGEMENT
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
EMS Transport
Onset of symptoms of STEMI
EMSDispatc
h
EMS on-scene• Encourage 12-lead ECGs.• Consider prehospital fibrinolytic
if capable and EMS-to-needle within 30 min.
GOALS
PCIcapable
Not PCIcapable
Hospital fibrinolysis: Door-to-Needle within 30 min.
EMS Triage Plan
Inter-HospitalTransfer
Golden Hour = first 60 min.Total ischemic time: within 120 min.
Patient EMS Prehospital fibrinolysisEMS-to-needlewithin 30 min.
EMS transportEMS-to-balloon within 90
min.Patient self-transport Hospital door-to-balloon
within 90 min.
Dispatch
1 min.
5 min.
8 min.
Options for Transport of Patients With STEMI and Initial Reperfusion
Treatment
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 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 hrMedical contact-to-balloon or door-to-balloon more
than90 min
Invasive strategy preferred
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 shockKillip class ≥ 3
Contraindications to fibrinolysis
Late presentation (> 3 hr)
Diagnosis of STEMI is in doubt
Initial Recognition and Management in the Emergency
Department
1. Airway, Breathing, Circulation (ABC)2. Vital signs, general observation3. Presence or absence of jugular venous
distension4. Pulmonary auscultation for rales5. Cardiac auscultation for murmurs and
gallops6. Presence or absence of stroke
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
0 1 2 3 4 5 6 78
Cardiac troponin-no reperfusion
Days After Onset of STEMI
Mul
tiple
s of
the
URL
Upper reference limit1
2
5
10
20
50
URL = 99th %tile of Reference Control Group
100
Cardiac troponin-reperfusion
CKMB- reperfusion
CKMB- no reperfusion
Cardiac Biomarkers in STEMI
Control of cardiac pain
Pain contribute to the heightened sympathetic activity
Typically accomplished with combination of nitrates, analgesics, oxygen and β-blockers
OxygenArterial oxygen desaturation (SaO2 < 90%) Class I(B)
Uncomplicated STEMI during the first 6 hours Class II(A)
Control of cardiac pain 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 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 baseline severe bradycardia (< 50 bpm) tachycardia (> 100 bpm) suspected RV infarction. who have received a phosphodiesterase
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)
REPERFUTION THERAPY
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
Importance of time to reperfusion in patients undergoing fibrinolysis
(National Cardiovascular Data Registry )
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)
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 hours Suspected aortic dissectionActive 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.
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 bleeding Noncompressible vascular punctures For streptokinase/anistreplase: prior exposure (> 5 days ago)
or prior allergic reaction to these agentsPregnancy, Active peptic ulcer Current use of anticoagulants
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.)
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)
CHOICE OF FIBRINOLYTICS
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
Late fibrinolysis
LATE and EMERAS trials
Fibrinolytics between 12 and 24 hours
No mortality benefit
Increases risk of cardiac rupture
Assessment of Reperfusion after fibrinolysis
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)
TIMI grading system Flow in the IRA angiographically
Gd. 0, compl. Occlussion
Gd. 1, some penetration
Gd.2, entire vessel withImpaired flow
Gd.3, entire vessel withNormal flow
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
Anticoagulant therapy
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.
Anticoagulant therapyConsensus
Antiplatelets 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)
Thienopyridines 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
Thienopyridines 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)
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.
Beta-Blockers 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)
Beta-Blockers
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.
Beta-Blockers
Inhibitors of the RAAS
Favorable impact on ventricular remodeling, improvement in hemodynamics, and reductions in congestive heart failure
Angiotensin-converting enzyme inhibitors
Angiotensin II receptor blockers
Aldosterone blockade
ACE inhibitors on mortality after MI- from long-term trials.
ACE inhibitors on mortality after MI- from short-term trials.
Angiotensin II receptor blockersVALIANT TRIAL-Mortality
Angiotensin II receptor blockers
VALIANT TRIAL-MACE
Aldosterone blockade
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
Calcium Channel Antagonists
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
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)
Physical activity
In the absence of complications patients need not be confined to bed for more than 12 hours
Progression of activity should be individualized
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
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 or The patient has a large anterior infarction
whether or not a thrombus is visualized echocardiographically
Post MI myocardial rupture 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
Cardiac arrhythmias in MICATEGORY 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/defibrillation
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
Cardiac arrhythmias in MI
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 supraventricular tachycardia
Reduce ventricular rate; restore sinus rhythm
Vagal maneuvers; verapamil, cardiac glycosides, beta-adrenergic blockers; cardioversion; rapid atrial pacing
Cardiac arrhythmias in MICATEGORY ARRHYTHMIA OBJECTIVE OF TREATMENT THERAPEUTIC
OPTIONS
Bradyarrhythmias 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
Ventricular Septal Rupture (VSR),
RUPTURE OF VENTRICULAR FREE WALL
PAPILLARY MUSCLE RUPTURE
Post MI Management-Phases:Convalescence
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)
Indications for Angiography
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
Secondary Prevention and Long Term Management
LIFE-STYLE MODIFICATION
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
Secondary Prevention and Long Term Management
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:
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.
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
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)
Potential Cumulative Impact of 2° Prevention Treatments
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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