Acute Coronary Syndromes-presentation

Acute Coronary Syndrome Chairman : Dr.Venkataramanappa Moderator : Dr. Vinay Presentor : Dr. Rahul.P.J

Acute coronary syndrome (ACS) :  is a set of signs and symptoms suggestive of sudden cardiac ischemia.  usually caused by disruption of atherosclerotic plaque in an epicardial coronary artery.

include:  Unstable Angina (UA)  Non-ST Segment Elevation Myocardial Infarction (NSTEMI), &  ST Segment Elevation Myocardial Infarction (STEMI), commonly referred to as a heart attack.

Spectrum of Acute Coronary Syndromes Presentation

No ST-Segment Elevation

ST-Segment Elevation +

+

In-Hospital

Unstable Angina

+

Non-Q-wave MI

(⊕ : positive cardiac biomarker)

+

Emergency Department

Ischemic Discomfort at Rest

Q-wave MI

• New Terminology in ACS Plaque Rupture

Old term

Stable Angina

Unstable Angina

New term Atherothrombosis

Non– Q-wave MI

STEMI

UA/NSTEMI

Daysweeks

Antithrombotic Therapy

Q-wave MI

Minuteshours

Thrombolysis Primary PCI

ACS, acute coronary syndrome; MI, myocardial infarction; UA, unstable angina; NSTEMI, non–ST-segment elevation myocardial infarction; STEMI, ST-segment elevation myocardial infarction; PCI, percutaneous coronary intervention. Cannon CP. J Thromb Thrombolysis. 1995;2:205-218.

 ACS should be distinguished from stable angina,develops during exertion and resolves at rest. In contrast ,unstable angina- occurs suddenly, often at rest or with minimal exertion, or at lesser degrees of exertion than the individual's previous angina ("crescendo angina").  New onset angina is also considered unstable angina, since it suggests a new pathophysiologic process in the coronary artery.

Angina • Chest pain and related symptoms which are caused by inadequate blood flow and oxygen supply to the myocardial cells of the heart.

Unstable Angina • Symptoms of angina at rest • New onset of exertional angina • Increase in severity of previously “stable” angina

NSTEMI • Similar to UA except that ischemia is severe enough to cause myocardial damage resulting in the release of cardiac enzymes

Who’s at risk ? • Classical: Male > Females until age 60 • Gender Difference • Symptom Presentation: – Males – primarily chest discomfort – Females » » » »

Shortness of Breath 55% Weakness 52% Fatigue 40% No Chest Pain 40%

• Risk Factors Gender Cigarette smoking Cholesterol – LDL Hypertension Diabetes – vascular disease more than blood sugar level Activity level Stress

PATHOPHYSIOLOGY  Decrease in O2 supply &/ increase myocardial O2 demand, superimposed on coronary obstruction.  4 pathophysiological processes contribute to this(a) plaque rupture/erosion with superimposed non occlusive thrombus. (b) dynamic obstruction {eg: coronary spasm} (c) progressive mechanical obstruction. (d) secondary to other systemic conditions{ anaemia}

AMONG UA/ NSTEMI    

5% - left main vessel stenosis 15%- 3 vessel CAD 30%- 2 vessel disease 40%- single vessel disease 10%- no critical coronary stenosis

Unstable Angina pathogenesis • Plaque disruption • Acute thrombosis • Vasoconstriction

 Plaque disruption – Passive plaque disruption soft plaque with high concentration of cholesteryl esters and a thin fibrous cap – Active plaque disruption macrophage-rich area with enzymes that may degrade and weaken the fibrous cap; predisposing it to rupture  Acute Thrombosis -- Vulnerable plaque disrupted plaque with ulceration occurring in 2/3 of unstable patients exposed lipid-rich core abundant in cholesteryl ester-highly thrombogenic --Systemic Hypercoagulable State disrupted plaque with erosion occurring in 1/3 of unstable patients  Vasoconstriction --the culprit lesion in response to arterial damage/plaque disruption --area of dysfunctional endothelium near the culprit lesion --platelet-dependent and thrombin-dependent vasoconstriction, -- --mediated by serotonin &

Process of resolution – spontaneous thrombolysis – vasoconstriction resolution – presence of collateral circulation

Delayed or absence of resolution may lead to non-Q-wave or Q-wave myocardial infarction

The signs and symptoms may include: • chest pain • shortness of breath • nausea • vomiting • diaphoresis (sweating) • palpitations • anxiety or sense of impending doom • a feeling of being acutely ill

Chest Pain

vs. Discomfort

Quality: Heaviness Constriction Strangulation Burning Choking

Pressure Tightness Indigestion Aching

– Expanding from within Or just “an unpleasant sensation”

“Classic” Anginal chest pain! • • • •

Location: central chest Quality: squeezing, pressure, heaviness Radiation: arm(s), neck, jaw Associated symptoms: dyspnea, diaphoresis, nausea • Eliciting factors: exertion • Relieving factors: rest, nitroglycerin

Differential Diagnosis • Musculoskeletal • Gastrointestinal • Cardiac

• Psychiatric • Pulmonary • Other/unknown

Cardiovascular Chest Pain • Coronary Heart Disease – Stable angina pectoris – Unstable angina – Myocardial infarction

• Coronary Vasomotor Disease – Variant angina – Microvascular angina

• Pericarditis

• Myocarditis • Valvular Heart Disease – Aortic stenosis – Mitral stenosis – Hypertrophic cardiomyopathy

• Aortic Dissection • Postpericardiotomy

• Severity of Symptoms, not necessarily correlated with severity of illness.  Physical Appearance: • • • • • •

“Normal” Pallor cold, clammy skin pulse-strong weak or thready or absent regular or irregular Precordial palpitations

• Altered consciousness

• Examination- may be unremarkable. • If large area of myocardial ischaemia/large NSTEMI,a 3rd &/ 4th heart sound, bibasilar rales & sometimes hypotension, resembling findings of large STEMI. LABORATORY FINDINGS ELECTROCARDIOGRAMST segnent depression Trasient ST segment elevation T wave inversion CARDIAC BIOMARKERS• Elevated biomarkers of necrosis- CK-MB,troponins used 2 distinguish UA from NSTEMI • Performed at baseline, 4-6hrs & 12hrs

Risk Stratification Low Risk • new-onset exertional angina • minor chest pain during exercise • pain relieved promptly by nitroglycerine Management • can be managed safely as an outpatient (assuming close follow-up and rapid investigation)

Intermediate Risk • prolonged chest pain • diagnosis of rule-out MI Management • observe in the ER or Chest Pain Unit • monitor clinical status and ECG • obtain cardiac enzymes every 8 to 12 hours High Risk •recurrent chest pain • ST-segment change •hemodynamic compromise •elevation in cardiac enzymes Management •monitor in the Coronary Care Unit

Therapeutic Goals • Reduce myocardial ischemia • Control of symptoms • Prevention of MI and death Medical Management • Anti-ischemic therapy • Anti-thrombotic therapy

Medical Therapy • Anti-ischemic therapy – nitrates, beta blockers, calcium antagonists

• Anti-thrombotic therapy – Anti-platelet therapy • aspirin, ticlopidine, clopidogrel, GP IIb/IIIa inhibitors – Anti-coagulant therapy • heparin, low molecular weight heparin (LMWH), warfarin, hirudin, hirulog

Anti-ischemic Therapy • • • •

restrict activities morphine oxygen nitroglycerine – pain relief, prevent silent ischemia, control hypertension, improve ventricular dysfunction – nitrate free period recommended after the first 24-48 hours

• beta-blockers -- lowering angina threshold -- prevent ischemia and death after MI -- particularly useful during high sympathetic tone

• calcium antagonists -- particularly the rate-limiting agents -- nifedipine is not recommended without concomitant ß-blockade

Anti Thrombotic therapy Anti-platelet Therapy •

aspirin is the “gold standard” – irreversible inhibition of the cyclooxygenase pathway in platelets, blocking formation of thromboxane A2, and platelet aggregation. – in UA, ASPRIN reduced the risk of fatal or nonfatal MI by 71% during the acute phase, 60% at 3 months, and 52% at 2 years – bolus dose of 160-325 mg, followed by maintenance dose of 80-160 mg/d

• Thienopyridines -- Ticlopidine (Ticlid ) -- clopidogrel (Plavix ) { block platelet aggregation induced by ADP and the transformation of GP IIb/IIIa into its high affinity state }

•

GP IIb/IIIa inhibitors – abciximab (monoclonal antibody) – eptifibatide (peptidic inhibitor) – lamifiban and tirofiban (non-peptides) {direct occupancy of the GP IIb/IIIa receptor by a monoclonal antibody or by synthetic compounds mimicking the RGD sequence for fibrinogen binding prevents platelet aggregation }

Anti-coagulant Therapy • Heparin -- trials showed a 33% risk reduction in MI and death, but with a two fold increase in major bleeding – titrate PTT to 2x the upper limits of normal

•Low-molecular-weight heparin -- advantages over heparin: -- better bio-availability -- higher ratio (3:1) of anti-Xa to anti-IIa activity -- longer anti-Xa activity, avoid rebound -- induces less platelet activation -- ease of use (subcutaneous - qd or bid) -- no need for monitoring 1. Circulation 1994;89:81-88 2. JAMA 1996;276:811-815

Coronary Interventions – early intervention vs conservative strategy (coronary angiography within 24-48 hrs, followed by angioplasty {PCI} or bypass surgery {CABG} ) LONG TERM MANAGEMENT Risk factor modification, optimal wt :, diet Cessation of smokeing, daily exercise, BP control, tight control of hyperglycemia Lipid management Drugs { B-blockers, statins, ACE inhibitors etc} Circulation 1994;89:1545-1556

STEMI Acute, evolving or recent MI • Requires 1 of 2: 1. Typical rise and gradual fall (troponin) or more rapid rise and fall (CK-MB) of markers of myocardial necrosis with >= 1 of: - Symptoms - Q waves - ECG c/w ischemia - S/p coronary artery intervention 2. Pathologic findings of AMI

Symptoms of STEMI • Chest, epigastric, arm, wrist, jaw pain or discomfort w/ exertion or at rest • Pain-is deep & visceral {heavy, squeezing & crushing, stabbing or burning} IIar in charc: of angina pectoris; but more severe & lasts longer. • Associated sx: dsypnea, diaphoresis, nausea, vomiting, light-headedness,anxiety,weakness & sense of impending doom. • Other presentation-sudden loss of consciousness confusional state. • Substernal pain(>30min)+diaphoresis– strongly suggests STEMI

• O/E• 25% with ant: infarction—sympathetic sys: hyperactivity {tachycardia} • 50% of inf: infarction– parasympathetic hyperactivity{bradycardia &/hypotension} • Raise in temp upto 38’ C • Arterial press:-variable • PRECORDIUM-quite.. • Apical impulse- diff: 2 palpate. • S1-dec in intensity, S2-paradoxical splitting, Audible S3 & S4. • Trasient midsystolic/late systolic murmur in apical area {dysfunction of mitral valve apparatus}

Laboratory findings Electrocardiogram• ST segment elevation- in 2 or more contiguous leads {corresponding to wall supplied by epicardial artery}

• 75%- presence of Q waves • Gradually ST segment elevation dec: & T wave inversion develops • T wave inversion-persist 4 wks to mnths. • Q waves-persist 4 mnths to yrs,sometimes lifelong Cardiac markers• CK-rises within 4-8hrs,returns to normal by 4872hrs {lacks specificity for STEMI} • CK-MB{more specific}-rises 6-10hrs aft onset of infarc-tion,{in absence of reperfusion/thrombolysis},peaks-24hrs, & returns to normal- 36-72hrs

• Troponins{cTnT & cTnI}-rises 3-6hrs & peak24hrs,remain elevated for 7-10 days

• Myoglobin: for rapid diagnosis Biochemical Markers II

Biochemical Markers III Protein

Molecular mass (kD)

First Duration of detection detection

Sensit Specif ivity icity

Myoglobin

16

8–12 hours

+++

+

CK-MB

83

1–2 days

+++

+++

Troponin I

33

7–10 days

++++ ++++

Troponin T

38

7–14 days

++++ ++++

CK

96

1.5–2 hours 2–3 hours 3–4 hours 3–4 hours 4–6 hours

2–3 days

++

++

Non MI Causes of Troponin Elevation • • • • • •

Tachycardia PE w/ Right Vent: infarct Cardiac failure w/ myonecrosis Cardiac surgery Myocarditis Renal failure

Coronary Angiogram • Observer variability • Discordance btw severity of lesion and physiologic effects – Greater stenosis vs more unstable plaques?

• 2-D picture of a 3-D problem – Diffuse disease may limit estimation of “abnormal segments”

• Missed lesions

Prehospital Chest Pain Evaluation and Treatment Prehospital EMS providers should administer 162 to 325 mg of aspirin (chewed) to chest pain patients suspected of having STEMI unless contraindicated or already taken by the patient. Although some trials have used enteric-coated aspirin for initial dosing, more rapid buccal absorption occurs with non–enteric-coated formulations.

ED Evaluation of Patients With STEMI Brief Physical Examination in the ED 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 7. Presence or absence of pulses 8. Presence or absence of systemic hypoperfusion (cool, clammy, pale, ashen)

ED Evaluation of Patients With STEMI Differential Diagnosis of STEMI: Life-Threatening Aortic dissection

Tension pneumothorax

Pulmonary embolus

Boerhaave syndrome

Perforating ulcer

(esophageal rupture with mediastinitis)

ED Evaluation of Patients With STEMI Differential Diagnosis of STEMI: Other Cardiovascular and Nonischemic Pericarditis Atypical angina Early repolarization Wolff-Parkinson-White syndrome Deeply inverted T-waves suggestive of a central nervous system lesion or apical hypertrophic cardiomyopathy

LV hypertrophy with strain Brugada syndrome Myocarditis Hyperkalemia Bundle-branch blocks Vasospastic angina Hypertrophic cardiomyopathy

ED Evaluation of Patients With STEMI Differential Diagnosis of STEMI: Other Noncardiac Gastroesophageal reflux (GERD) and spasm

Cervical disc or neuropathic pain

Chest-wall pain

Biliary or pancreatic pain

Pleurisy

Somatization and psychogenic pain disorder

Peptic ulcer disease Panic attack

Electrocardiogram

If the initial ECG is not diagnostic of STEMI, serial ECGs or continuous ST-segment monitoring should be performed in the patient who remains symptomatic or if there is high clinical suspicion for STEMI.

Electrocardiogram Show 12-lead ECG results to emergency physician within 10 minutes of ED arrival in all patients with chest discomfort (or anginal equivalent) or other symptoms of STEMI. In patients with inferior STEMI, ECG leads should also be obtained to screen for right ventricular infarction.

Laboratory Examinations Laboratory examinations should be performed as part of the management of STEMI patients, 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

Biomarkers of Cardiac Damage Cardiac-specific troponins should be used as the optimum biomarkers for the evaluation of patients with STEMI who have coexistent skeletal muscle injury. For patients with ST elevation on the 12-lead ECG and symptoms of STEMI, reperfusion therapy should be initiated as soon as possible and is not contingent on a biomarker assay.

Imaging Patients with STEMI should have a portable chest X-ray, but this should not delay implementation of reperfusion therapy (unless a potential contraindication is suspected, such as aortic dissection). Imaging studies such as a high quality portable chest X-ray, transthoracic and/or transesophageal echocardiography, and a contrast chest CT scan or an MRI scan should be used for differentiating STEMI from aortic dissection in patients for whom this distinction is initially unclear.

Oxygen

Supplemental oxygen should be administered to patients with arterial oxygen desaturation (SaO2 < 90%). It is reasonable to administer supplemental oxygen to all patients with uncomplicated STEMI during the first 6 hours.

Nitroglycerin Patients with ongoing ischemic discomfort should receive sublingual NTG (0.4 mg) every 5 minutes for a total of 3 doses, after which an assessment should be made about the need for intravenous NTG.

Intravenous NTG is indicated for relief of ongoing ischemic discomfort that responds to nitrate therapy, control of hypertension, or management of pulmonary congestion.

Nitroglycerin 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) or • suspected RV infarction. Nitrates should not be administered to patients who have received a phosphodiesterase inhibitor for erectile dysfunction within the last 24 hours (48 hours for tadalafil).

Analgesia

Morphine sulfate (2 to 4 mg intravenously with increments of 2 to 8 mg intravenously repeated at 5 to 15 minute intervals) is the analgesic of choice for management of pain associated with STEMI.

Aspirin

Aspirin should be chewed by patients who have not taken aspirin before presentation with STEMI. The initial dose should be 162 mg to 325 mg

Although some trials have used enteric-coated aspirin for initial dosing, more rapid buccal absorption occurs with non–enteric-coated formulations.

Beta-Blockers Oral beta-blocker therapy should be administered promptly to those patients without a contraindication, irrespective of concomitant fibrinolytic therapy or performance of primary PCI.

It is reasonable to administer intravenous betablockers promptly to STEMI patients without contraindications, especially if a tachyarrhythmia or hypertension is present.

Reperfusion •

Given the current literature, it is not possible to say definitively that a particular reperfusion approach is superior for all pts, in all clinical settings, at all times of day

• The main point is that some type of reperfusion therapy should be selected for all appropriate pts with suspected STEMI • The appropriate & timely use of some reperfusion therapy is likely more important than the choice of therapy

Treatment Delayed is Treatment Denied

Symptom Recognition

Call to Medical System

PreHospital

ED

Cath Lab

Increasing Loss of Myocytes Delay in Initiation of Reperfusion Therapy

Contraindications and Cautions for Fibrinolysis in STEMI • Any prior intracranial hemorrhage • Known structural cerebral vascular lesion Absolute (e.g., arteriovenous malformation) Contraindications • Known malignant intracranial neoplasm (primary or metastatic) • Ischemic stroke within 3 months EXCEPT acute ischemic stroke within 3 hours • Suspected aortic dissection • Active bleeding/ bleeding diathesis

• Sig: closed head/ facial trauma{within 3 mths NOTE: Age restriction for fibrinolysis has been removed compared with prior guidelines.

Contraindications and Cautions for Fibrinolysis in STEMI Relative • History of chronic, severe, poorly controlled Contraindications hypertension • Severe uncontrolled hypertension on presentation (SBP > 180 mm Hg or DBP > 110 mm Hg) • History of prior ischemic stroke greater than 3 months, dementia, or known intracranial pathology not covered in contraindications • Traumatic or prolonged (> 10 minutes) CPR or major surgery (< 3 weeks)

Contraindications and Cautions for Fibrinolysis in STEMI Relative • Recent (< 2 to 4 weeks) internal bleeding Contraindications • 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: the higher the INR, the higher the risk of bleeding

Fibrinolysis Fibrinolytic therapy should not be administered to asymptomatic patients whose initial symptoms of STEMI began more than 24 hours earlier. Fibrinolytic therapy should not be administered to patients whose 12-lead ECG shows only STsegment depression, except if a true posterior MI is suspected.

Primary PCI for STEMI: Specific Considerations It is reasonable to perform primary PCI for patients with onset of symptoms within the prior 12 to 24 hours and 1 or more of the following: a. Severe CHF b. Hemodynamic or electrical instability c. Persistent ischemic symptoms.

Rescue PCI Rescue PCI is reasonable for selected patients 75 years or older with ST elevation or LBBB or who develop shock within 36 hours of MI and are suitable for revascularization that can be performed within 18 hours of shock. It is reasonable to perform rescue PCI for patients with one or more of the following: a. Hemodynamic or electrical instability b. Persistent ischemic symptoms.

PCI After Fibrinolysis In patients whose anatomy is suitable, PCI should be performed for the following: Objective evidence of recurrent MI Moderate or severe spontaneous/provocable myocardial ischemia during recovery from STEMI Cardiogenic shock or hemodynamic instability.

Ancillary Therapy to Reperfusion Unfractionated heparin (UFH) should be given intravenously in:  Patients undergoing PCI or surgical revascularization  After alteplase, reteplase, tenecteplase  After streptokinase, anistreplase, urokinase in patients at high risk for systemic emboli.

Aspirin

A daily dose of aspirin (initial dose of 162 to 325 mg orally; maintenance dose of 75 to 162 mg) should be given indefinitely after STEMI to all patients without a true aspirin allergy.

Thienopyridines In patients for whom PCI is planned, clopidogrel should be started and continued: • ≥ 1 month after bare-metal stent • ≥ 3 months after sirolimus-eluting stent • ≥ 6 months after paclitaxel-eluting stent • Up to 12 months in absence of high risk for bleeding.

Thienopyridines

In patients taking clopidogrel in whom CABG is planned, the drug should be withheld for at least 5 days, and preferably for 7 days, unless the urgency for revascularization outweighs the risk of excessive bleeding.

Glycoprotein IIb/IIIa Inhibitors It is reasonable to start treatment with abciximab as early as possible before primary PCI (with or without stenting) in patients with STEMI. Treatment with tirofiban or eptifibatide may be considered before primary PCI (with or without stenting) in patients with STEMI.

Other Pharmacological Measures Inhibition of the renin -angiotensin -aldosterone system

Angiotensin converting enzyme (ACE) inhibitors Angiotensin receptor blockers (ARB) Aldosterone blockers Glucose control Magnesium Calcium channel blockers

Strict Glucose Control During STEMI An insulin infusion to normalize blood glucose is recommended for patients and complicated courses. It is reasonable to administer an insulin infusion to normalize blood glucose even in patients with an uncomplicated course.

Secondary Prevention and Long Term Management Goals Smoking Goal: Complete Cessation

Recommendations • Assess tobacco use. • Strongly encourage patient and family to stop smoking and to avoid secondhand smoke. • Provide counseling, pharmacological therapy (including nicotine replacement and bupropion), and formal smoking cessation programs as appropriate.

Secondary Prevention and Long Term Management Goals Blood pressure control: Goal: < 140/90 mm Hg or <130/80 mm Hg if chronic kidney disease or diabetes

Recommendations If blood pressure is 120/80 mm Hg or greater: • Initiate lifestyle modification (weight control, physical activity, alcohol moderation, moderate sodium restriction, and emphasis on fruits, vegetables, and lowfat dairy products) in all patients.

If blood pressure is 140/90 mm Hg or greater or 130/80 mm Hg or greater for individuals with chronic kidney disease or diabetes: • Add blood pressure-reducing medications, emphasizing the use of beta-blockers and inhibitors of the renin-angiotensin-aldosterone system.

Secondary Prevention and Long Term Management Goals Physical activity: Minimum goal: 30 minutes 3 to 4 days per week; Optimal daily

Recommendations • Assess risk, preferably with exercise test, to guide prescription. • Encourage minimum of 30 to 60 minutes of activity, preferably daily but at least 3 or 4 times weekly (walking, jogging, cycling, or other aerobic activity) supplemented by an increase in daily lifestyle activities (e.g., walking breaks at work, gardening, household work). • Cardiac rehabilitation programs are recommended for patients with STEMI.

Secondary Prevention and Long Term Management Goals Lipid management: (TG less than 200 mg/dL) Primary goal: LDL-C << than 100 mg/dL

Recommendations • 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: 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.

Secondary Prevention and Long Term Management Goals

Recommendations

Antiplatelet • In the absence of contraindications, start aspirin agents/ 75 to 162 mg/d and continue indefinitely. anticoagulants

• If aspirin is contraindicated, consider clopidogrel 75 mg/day or warfarin. • Manage warfarin to INR 2.5 to 3.5 in postSTEMI patients when clinically indicated or for those not able to take aspirin or clopidogrel.

Secondary Prevention and Long Term Management Goals ReninAngiotensinAldosterone System Blockers

Recommendations ACE inhibitors in all patients indefinitely; start early in stable, high-risk patients (ant. MI, previous MI, Killip class ≥ 2 [S3 gallop, rales, radiographic CHF], LVEF < 0.40). Angiotensin receptor blockers in patients who are intolerant of ACE inhibitors and with either clinical or radiological signs of heart failure or LVEF < 0.40. Aldosterone blockade in patients without significant renal dysfunction or hyperkalemia who are already receiving therapeutic doses of an ACE inhibitor, have LVEF ≤ 0.40, and have either diabetes or heart failure.

Secondary Prevention and Long Term Management

Goals BetaBlockers

Recommendations Start in all patients. Continue indefinitely. Observe usual contraindications.

Cardiac Rehabilitation

Cardiac rehabilitation/secondary prevention programs, when available, are recommended for patients with STEMI, particularly those with multiple modifiable risk factors and/or those moderate- to high-risk patients in whom supervised exercise training is warranted.

THANK U