ACUTE CORONARY SYNDROME (A CASE DISCUSSION)

BY

Dr Ijaz Hussain MBBS , MCPS, MRCGP, Dip Avn Med

Prince Sultan Military Medical CityRiyadh

Case Presentation

• Patient’s Name: Mohammad Al Shahrani• Age: 63 Yrs• Sex: ♂• Nationality: Saudi• Resident of al Oainah

Chief Complaints

• Mohammad al Shahrani was brought in the AnE with Brief History of :– Chest Pain– Diaphoresis– Collapse

• History of Present Illness:– Patient had an out door BBQ party – While coming back he exerted to pack-up and kept lifting

heavy luggage etc.– Since last abt 15 minutes he had been c/o chest

“discomfort”. Family rushed to the hospital as he collapsed.

• Past History: Known Case if IHD: had undergone cardiac cath one year and a half.

Initial Work-up

• Although the patient was in distress but his vital parameters were stable and as following:– B.P: 153/ 86 mm Hg– Pulse: 66 per min– Temp 36.2 ̊C– SPO2 99 %– Reflo: 7.6 mmol/dl

• ECG: – St Elevation in II, III, aVf– Reciprocal Changes in aVL, V1 and V2

ECG TRACING

Initial Work-up in PSMMC

• Cardiac Enzymes Enzyme 18.11.2012 19.11.2012 Ref Range

– Ck 144 651 {50-190 u/L}– Ck MB - 93 {0- 24 u/L }– AST 32 82 {2.0- 37 u/L}– LDH 530 495 {135-255 u/L}

• Troponine T Level– 18.11.2012 0.007 1.1 {0.1 ng/ml }– 19.11.2012 1.540

• FBC NAD • Renal Functions NAD• CxR NAD

DISCHARGE SUMMARY•Final Diagnosis:

– Diabetes ; Hypertension ; IHD e Hx of PCI in Asir 4 Yrs ago

•History:– Pt is 63 yrs old saudi male with Dx as above. Presented

in A’nE with C/O acute onset chest pain of few hrs duration with no SOB, Orthopnoea, Paraxysmol Nocturnal dyspnoea or Palpitaion.

•Physical Examination: – Chest clear, CVA Ex S1+S2+0 ; Abdomen soft lax ; CNS

intact ; B.P was normal

•Investigation Results: – Showed ST elevation in Inf leads with still having pain

DISCHARGE SUMMARY• Hosp Course & Mngmnt: Pt was taken directly from A’nE to

cath Lab. Shown tight mid RCA lesion ,with aspiration of thrombosis. Echo was done which shown slight irregularity. Pt was kept under observation for 24 hrs. Was discharged in a good condition, with no complaints and was doing fine.

• Drugs on Discharge: – Aspirin 81 mg 1xTab PO OD– Plavix 75 mg 1xTab PO OD– Prindopril 2.5 mg 1xTab PO OD – Isordil 20 mg 1xTab PO OD– Lipitor 40 mg 1xTab PO OD– Lasix20 mg 1xTab PO OD– Pantoperazole 40 mg 1xTab PO OD

• Future Plan: Pt was given an appt 24/52 to be seen in OPD

Case Discussion

•Heart is capable of pumping blood to every cell in the body in under one minute

•During the course of the day, your heart will beat approx 100,000 times driving 2,000 gallons of oxygen-rich blood through 60,000 miles of blood vessels.

DEFINITION

Myocardial infarction, commonly known as a heart attack, is the irreversible necrosis of heart muscle secondary to prolonged ischemia. This usually results from an imbalance in oxygen supply and demand, which is most often caused by plaque rupture with thrombus formation in a coronary vessel, resulting in an acute reduction of blood supply to a portion of the myocardium.

DEFINITION

Myocardial infarction is considered part of a spectrum referred to as acute coronary syndrome (ACS). The ACS continuum representing ongoing myocardial ischemia or injury consists of unstable angina, non–ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI). Patients with ischemic discomfort may or may not have ST-segment or T-wave changes denoted on the electrocardiogram (ECG). ST elevations seen on the ECG reflect active and ongoing transmural myocardial injury

Types

•STEMI : OR New Onset LBBB

•NSTEMI : ECG MAY SHOW ST-DEPRESSION,T-WAVE INVERSION, NON-SPECIFIC CHANGES OR NORMAL (NON-Q WAVE MI OR SUBENDOCARDIAL MI)

•UA: ANGINA OF INCREASING FREQUENCY OR SEVERITY, OCCURS ON MIN; EXERTION OR AT REST. ASSOCIATED WITH INCREASED RISK OF MI

ACUTE MI

Clinical Spectrum of Acute Coronary Syndromes

Evidence of necrosis None Positive Positive

ECG earlyST-segment depression

and/orT-wave inversion

ST-segment elevation

ECG late No Q No Q Q develops

Stable anginaStable angina UnstableUnstableanginaangina

Non-STE MINon-STE MI STE MISTE MI

ST-segment depression

and/or T-wave inversion

Unstable Angina STEMI N-STEMIN-STEMI

Non occlusive thrombus

Non specific ECG

Normal cardiac enzymes

Occluding thrombus sufficient to cause tissue damage & mild myocardial necrosis

ST depression +/- T wave inversion on ECG

Elevated cardiac enzymes

Complete thrombus occlusion

ST elevations on ECG or new LBBB

Elevated cardiac enzymes

More severe symptoms

EPIDEMIOLOGY OF ACS

Single largest cause of deathSingle largest cause of death 515,204 US deaths in 2000515,204 US deaths in 2000 1 in every 5 US deaths1 in every 5 US deaths

IncidenceIncidence 1,100,000 Americans will have a new or recurrent 1,100,000 Americans will have a new or recurrent

coronary attack each year and about 45% will die*coronary attack each year and about 45% will die* 550,000 new cases of angina per year550,000 new cases of angina per year

PrevalencePrevalence 12,900,000 with a history of MI, angina, or both12,900,000 with a history of MI, angina, or both

INCIDENCE IN UK=5/1000/ANNUM FOR STEMIINCIDENCE IN UK=5/1000/ANNUM FOR STEMI

PATHOPHYSIOLOGY

Understanding Myocardial Ischemia

Imbalance

Understanding Myocardial Ischemia

Dec O2 supply Inc. Demand

INCREASED CARDIAC OUTPUT….. (THYROTOXICOSIS)

MYOCARDIAL HYPERTROPHY (AS,HTN)

PATHOPHYSIOLOGY

• RUPTURE OR EROSION OF THE FIBROUS CAP OF A CORONARY ARTERY PLAQUE.

• PLATELETS AGGREGATION AND ADHESION.• LOCALIZED

THROMBOSIS.VASOCONSTRICTION.• DISTAL THROMBUS EMBOLIZATION.• THROMBUS FORMATION AND

VASOCONSTRICTION PRODUCED BY PLT RELEASE OF SEROTONIN & THROMBOXANE A2, RESULT IN MYOCARDIAL ISCHEMIA DUE TO REDUCTION OF CORONARY BLOOD FLOW.

Plaque Rupture, Thrombosis, and MicroembolizationPlaque Rupture, Thrombosis, and Microembolization

Quiescent plaqueQuiescent plaque

Platelet-thrombin micro-emboliPlatelet-thrombin micro-emboliPlaquePlaque rupturerupture

ProcessPlaque formation

InflammationMultiple factors? Infection

Plaque Rupture? MacrophagesMetalloproteinases

ThrombosisPlatelet ActivationThrombin

ProcessPlaque formation

InflammationMultiple factors? Infection

Plaque Rupture? MacrophagesMetalloproteinases

ThrombosisPlatelet ActivationThrombin

MarkerCholesterolLDL

C-Reactive ProteinAdhesion MoleculesInterleukin 6, TNFsCD-40 ligand

MDA Modified LDL

D-dimer, Complement,Fibrinogen, Troponin, CRP, CD40L

MarkerCholesterolLDL

C-Reactive ProteinAdhesion MoleculesInterleukin 6, TNFsCD-40 ligand

MDA Modified LDL

D-dimer, Complement,Fibrinogen, Troponin, CRP, CD40L

Vulnerable plaqueVulnerable plaque

MacrophagesFoam Cells

Collagen platelet activation

TF TF ClottingClotting CascadeCascade

Lipid coreLipid core

Metalloproteinases

InflammationInflammation

Pathogenesis of Acute Coronary

Syndromes:The integral role of

plateletsPlaqueFissure or Rupture

PlateletAggregation

PlateletActivation

PlateletAdhesion

ThromboticOcclusion

Thrombus Formation and ACS

UA NQMI STE-MI

Plaque Disruption/Fissure/Erosion

Thrombus Formation

Non-ST-Segment Elevation Acute Coronary Syndrome (ACS)

ST-Segment Elevation Acute Coronary Syndrome (ACS)

Old Terminology:

NewTerminology:

RISK FACTORS

MODIFIABLE

NON-MODIFIABLE

RISK FACTORS

• AGE. • INCIDENCE INCREASES

WITH AGE.• RARE IN CHILDHOOD

EXCEPT IN FAMILIAL HYPERLIPIDEMIA.

• MALE GENDER.• MEN > PREMENUPAUSAL

WOMEN.• AFTER MENUPAUSE

INCIDENCE IS ALMOST SAME.

• REASON ??? LOSS OF PROTECTIVE EFFECT OF OESTROGEN~~~~

• FAMILY Hx OF IHD.

MODIFIABLE RISK FACTORS

•SMOKING•HYPERLIPIDEMIA•HTN•DM•LACK OF EXERCISE•BLOOD COAGULATION FACTORS•CRP•HOMOCYSTEINAEMIA•PERSONALITY•OBESITY•GOUT•SOFT WATER•DRUGS……OCP,COX-2 INHIBITORS•HEAVY ALCOHOL CONSUMPTION

DIAGNOSIS OF ACS

TYPICAL HISTORY ECG CHANGES INC CARDIAC ENZYMES

Focused History• Aid in diagnosis and

rule out other causes

– Palliative/Provocative factors

– Quality of discomfort– Radiation– Symptoms associated

with discomfort– Cardiac risk factors– Past medical history -

especially cardiac

• Reperfusion questions

– Timing of presentation

– ECG c/w STEMI – Contraindication to

fibrinolysis– Degree of STEMI

risk

SYMPTOMS

• ACUTE CENTRAL CHEST PAIN. • NAUSEA.• SWEATING.• DYSPNOEA.• PALPITATION.• SYNCOPE.• PULM;EDEMA.• EPIGASTRIC PAIN.• VOMITING.• POST-OP HYPOTENSION.• OLIGURIA. • ACUTE CONFUSIONAL STATE.• STROKE.• DIABETIC HYPERGLYCEMIC STATES.

BE-AWARE OF SILENT

SIGNS• DISTRESS.• ANXIETY.• PALLOR.• SWEATINESS.• TACHYCARDIA/BRADICARDIA• HYPO/HYPERTENSION• S4• SIGNS OF HEART FAILURE• PANSYSTOLIC MURMUR• LOW GRADE PYREXIA• PERICARDIAL FRICTION RUB• EDEMA

Clinical Presentation Substernal chest pain or pressure

(>20-30 min)• Localization or radiation to arms,

back, throat, jaw• Accompanying features

– Dyspnea– Nausea/vomiting– Diaphoresis– Weakness

• Atypical: syncope,

Targeted Physical Examination

– Vitals– Cardiovascula

r system– Respiratory

system– Abdomen– Neurological

status

Recognize factors that increase risk

•Hypotension•Tachycardia•Pulmonary rhales,

JVD, pulmonary edema

•New murmurs/heart sounds

•Diminished peripheral pulses

•Signs of stroke

DIFFERENTIAL DIAGNOSIS

ANGINAPERICARDITISMYOCARDITISAORTIC DISSECTIONPULMONARY EMBOLISMESOPHAGEAL REFLUX/SPASM

Differential Diagnosis

• CHEST PAIN HEAVY,GRIPPING,TIGHTNESS

• CENTRAL • RETROSTENAL• MAY RADIATE TO JAW/ARM• MAY PROVOKE SWEATING AND

FEAR• ASSOCIATED SOB• PROVOKED BY PHYSICAL

EXERTION,AFTER MEALS, IN COLD AND WINDY WEATHER

• AGGRAVATED BY ANGER AND EXCITEMENT

• FADES QUICKLY WITH REST OR NITROGLYCERINE.

ANGINAPERICARDITISMYOCARDITISAORTIC DISSECTIONPULMONARY EMBOLISMESOPHAGEAL REFLUX/SPASM

Differential Diagnosis

• SHARP CENTRAL CHEST PAIN• EXACERBATED BY

MOVEMENT,RESPIRATION,AND LYING DOWN.

• RELIEVED BY SITTING FORWARD• MAY BE REFERRED TO NECK OR

SHOULDER• PERICARDIAL FRICTION RUB IN

THREE PHASES OF CARDIAC CYCLE– Atrial systole– Ventricular systole– Ventricular diastole

• BIPHASIC ‘TO AND FRO’ RUB• FEVER• LEUCOCYTOSIS• LYMPHOCYTOSIS• FEATURES OF PERICARDIAL

EFFUSION

ANGINA

PERICARDITISMYOCARDITISAORTIC DISSECTIONPULMONARY EMBOLISMESOPHAGEAL REFLUX/SPASM

Differential Diagnosis

• ASYMPTOMATIC • FATIGUE• PALPITATIONS• CHEST PAIN• DYSPNOEA• CCF• SOFT HEART SOUNDS• S3• TACHYCARDIA• PERICARDIAL FRICTION

RUB

ANGINAPERICARDITIS

MYOCARDITISAORTIC DISSECTIONPULMONARY EMBOLISMESOPHAGEAL REFLUX/SPASM

Differential Diagnosis

• SEVERE CENTRAL CHEST PAIN.

• RADIATES TO BACK.• SIGNS OF SHOCK• NEUROLOGICAL

SYMPTOMS• RENAL FAILURE• LOWER LIMB ISCHEMIA• VISCERAL ISCHEMIA

ANGINAPERICARDITISMYOCARDITIS

AORTIC DISSECTIONPULMONARY EMBOLISMESOPHAGEAL REFLUX/SPASM

Differential Diagnosis

PULMONARY EMBOLISM

SYMPTOMS •COUGH•UNEXPLAINED DYSPNOEA•PLEURITIC CHEST PAIN•HAEMOPTYSIS•DVT ~~~~~******•FEVER

SIGN •TACHYPNEA•TACHYCARDIA•SHOCKED•PALE•SWEATY•LOCALISED PLEURAL RUB•CREPTS•FEBRILE•HYPOTENSION•PERIPHERAL SHUTDOWN•RAISED JVP•RV HEAVE•GALLOP RHYTHM•WIDELY SPLIT S2

INVESTIGATIONS CXR------NORMAL,,,LINEAR ATELECTASIS,,BLUNTING OF CP ANGLE,,RAISED HEMIDIAPHRAGM,,,WEDGE-SHAPED PULM INFARCT,,

ECG-------NORMAL,,SINUS TACHY,,AF,,,,RV STRAIN,,,CBC-------PMN LEUCOCYTOSISESR-----RAISEDLDH-----RAISEDPL D-DIMERSV/Q SCANUS SCANECHOCARDIOGRAPHYSPIRAL CT SCANMRI

ANGINAPERICARDITISMYOCARDITISAORTIC DISSECTION

PULMONARY EMBOLISMESOPHAGEAL REFLUX/SPASM

ANGINAPERICARDITISMYOCARDITISAORTIC DISSECTIONPULMONARY EMBOLISM

ESOPHAGEAL REFLUX/ SPASM

20% OF THE PTS; ADMITTED INTO CCU HAVE GORD

Differential Diagnosis

ECG CHANGES

12-Lead ECG Variations in AMI and Angina

12-Lead ECG Variations in AMI and Angina

Baseline

Ischemia—tall or inverted T wave (infarct),ST segment may be depressed (angina)

Injury—elevated ST segment, T wave may invert

Infarction (Acute)—abnormal Q wave,ST segment may be elevated and T wavemay be inverted

Infarction (Age Unknown)—abnormal Q wave,ST segment and T wave returned to normal

ECG FINDINGS IN ACS

• NORMAL• ST-DEPRESSION• T-WAVE INVERSION• PERSISTANT ST-

ELEVATION OR• LBBB PATTERN

• REPEAT ECG WHEN PATIENT IS IN PAIN

• CONTINUOUS ST – SEGMENT MONITORING

ECG Assessment

ST Elevation or new LBBBST Elevation or new LBBBSTEMISTEMI

Non-specific ECGNon-specific ECGUnstable AnginaUnstable Angina

ST Depression or dynamicST Depression or dynamicT wave inversionsT wave inversions

NSTEMINSTEMI

TYPICAL ECG CHANGES IN

STEMI

Normal or non-diagnostic EKG

ST-Segment Elevation MI

New LBBB

QRS > 0.12 secL Axis deviation

Prominent R wave V1-V3Prominent S wave 1, aVL, V5-V6 with t-wave inversion

Case 13. A 53 year old man with 3 hours of "crushing" chest pain.

Interpretation

Acute inferior myocardial infarctionST elevation in the inferior leads II, III and aVF reciprocal ST depression in the anterior leads

Case 16. 51 yr old male with no prior cardiac history presents with mid-sternal chest discomfort

Questions 1. Is there ECG evidence of injury or ischemia? 2. Is this patient having an MI? If so, in what anatomic distribution?

Interpretation 1. YES2. YES, ANTEROSEPTAL

post thrombolysis ECG

                                                                                                             

post thrombolysis ECG

BIOCHEMICAL MARKERS

• TROP. I• TROP T• CK-MB• MYOBLOBIN

• FBC• S ELECTROLYTES• BGL• LIPID PROFILE• TRANSTHORACIC ECHO CARDIOGRAPHY (TTE)

OTHERBLOOD

INVESTIGATIONS

CARDIAC TROPONONSI T C

BIOCHEMICAL MARKERS

Cardiac Markers

• Troponin ( T, I)

– Very specific and more sensitive than CK

– Rises 4-8 hours after injury

– May remain elevated for up to two weeks

– Can provide prognostic information

– Troponin T may be elevated with renal dz, poly/dermatomyositis

• CK-MB isoenzyme

– Rises 4-6 hours after injury and peaks at 24 hours

– Remains elevated 36-48 hours

– Positive if CK/MB > 5% of total CK and 2 times normal

– Elevation can be predictive of mortality

– False positives with exercise, trauma, muscle dz,

MYOGLOBIN

RAPID DIAGNOSIS BUT

POOR SPECIFICITY

Troponins for Evaluation and Troponins for Evaluation and Management of ACSManagement of ACS

• Risk StratificatonRisk Stratificaton

• Sens/Spec > CKMBSens/Spec > CKMB

• Detect Recent MIDetect Recent MI

• Selection of RxSelection of Rx

• Detect ReperfusionDetect Reperfusion

• Low sens. early (< 6h)Low sens. early (< 6h)

• Repeat at 8-12 h if neg.Repeat at 8-12 h if neg.

• Limited ability to Limited ability to detect late minor reinfarctiondetect late minor reinfarction

AdvantagesAdvantages DisadvantagesDisadvantages

• Useful as single test to efficiently Dx NSTEMIUseful as single test to efficiently Dx NSTEMI

• Clinicians should familiarize themselves with Dx “cutoffs” in local labClinicians should familiarize themselves with Dx “cutoffs” in local lab

RecommendationRecommendation

Cardiac Markers

Initial Peak Normal

Myoglobin 1-4hr 6-7hr 24hr Nonspecific

CK-MB 3-12hr 24hr 48-72hrAlso elevated with Sk muscle

TroponinI 3-12hr 24hr 5-10d Highly sensitive/ specific

MANAGEMENT

Cardiac Care Goals

• Decrease amount of myocardial necrosis

• Preserve LV function

• Prevent major adverse cardiac events

• Treat life threatening complications

MANAGEMENT OF ACS

2 KEY QUESTIONS

IS THERE ST-SEGMENT ELEVATION?

IS THERE A RISE IN TROPONINS?

1 2

RIGHT ANSWER LEADS TO SUCCESSFULMANAGEMENT

Acute Management

• Initial evaluation & stabilization

• Efficient risk stratification

• Focused cardiac care

ACS RISK CRITERIA

Low Risk ACS

No intermediate or high risk factors

<10 minutes rest pain

Non-diagnostic ECG

Non-elevated cardiac markers

Age < 70 years

• ASA• CLOPIDOGRAL• BETA-BLOCKER• NITRATES

•LOW RISK ACS

• ELEVATED TROPS.• DYNAMIC ST OR T WAVE

CHANGES.• DM• RENAL DYSFUNCTION• REDUCED LVF• EARLY POST-INFARCTION

ANGINA.• PCI WITHIN 6 M• PREVIOUS CABG

ACS RISK CRITERIA

EARLY <72 HOURS> CORONARY ANGIOGRAPHY.+ INTERVENTION

HIGH RISK ACS• PTS WITH PERSISTENT

OR RECURRENT ANGINA.

• ST CHANGES > 2MM• OR DEEP NEGATIVE T

WAVE CHANGES.• CLINICAL SIGNS OF

HEAR FAILURE.• HAEMODYNAMIC

INSTABILITY.• LIFE THREATENING

ARRHYTHMIAS (VT,VF)

URGENT CORONARY ANGIOGRAPHY

ACS RISK CRITERIA

Chest pain suggestive of ischemia

– 12 lead ECG

– Obtain initial cardiac enzymes

– electrolytes, cbc lipids, bun/cr, glucose, coags

– CXR

Immediate assessment within 10 Minutes

Establish Establish diagnosisdiagnosis

Read ECGRead ECG Identify Identify

complicationcomplicationss

Assess for Assess for reperfusionreperfusion

Initial labsInitial labsand testsand tests

Emergent Emergent carecare

History & History & PhysicalPhysical

IV accessIV access Cardiac Cardiac

monitoringmonitoring OxygenOxygen AspirinAspirin NitratesNitrates

ONSET OF SYMPYOMS

EMS ARRIVAL PRE-HOSP

ECG

HOSP ARRIVAL

REPERFUSION

REPERFUSION GOALS

EMS-TO-DRUGS

EMS-TO-BALLOON

SYMPTOM ONSET –TO-REPERFUSION

<30 MIN

<90 MIN

<120 MIN

INCREASING LOSS OF MYOCYTES

STEMIEARLY MEDICAL MANAGEMENT• ARRANGE EMERGENCY AMBULANCE• ASPIRIN 300MG.• GTN S/L. 0.3-1 MG.----REPEAT• OXYGEN 2-4 L/M• ANALGESIA IV DIAMORPHINE 2.5-5MG+

METOCLOPRAMIDE 10 MG.(NOT IM ~~~RISK OF BLEEDING WITH THROMBOLYSIS.

• BETA-BLOCKER (IF NO C/I ) FOR ONGOING CHEST PAIN,HTN,TACHYCARDIA

• IF PRIMARY PCI AVAILABLE GIVE GP11b/111a INHIBITOR.

• ALTERNATIVELY GIVE THROMBOLYSIS.

PRE-HOSPITAL TREATMENT INCLUDING THROMBOLYSIS CAN BE GIVEN BY TRAINED HEALTHCARE PROFESSIONAL UNDER GUIDELINES

IN-HOSPITAL MANAGEMENT OF ACS IN STEMI

• THROMBOLYSIS OR PRIMARY ANGIOPLASTY.

• BETA-BLOCKER (ATENOLOL 5MG IV).– CONTRAINDICATION IN ASTHMATICS

• ACE-INHIBITORS.– CONSIDER (LISINOPRIL 2.5 MG) IN ALL

NORMOTENSIVE PATIENTS WITHIN 24 HRS OF ACUTE MI ESPECIALLY IF THERE IS EVIDENCE OF HEART FAILURE OR ECHO EVIDENCE OF LV DYSFUNCTION.

MANAGEMENT OF AMITHRMBOLYSIS

• EFFECTIVE IN REDUCING MORTALITY.

• GREATEST BENEFIT IF GIVEN <12 H OF ONSET OF PAIN.

• BEST TIME <60MIN (BHF)

• ST Elevation>2mm IN 2 OR MORE CHEST LEADS. OR

• ST elevation>1mm IN 2 OR MORE LIMB LEADS. OR

• POSTERIOR INFARCTION (DOMINANT R WAVES & ST DEPRESSION IN V1-V3)

• NEW ONSET OF LBBB

INDICATIONS(PRESENTATION WITHIN 12 H)

• HAEMORRHAGIC STROKE OR STROKE OF UNKNOWN ORIGIN AT ANY TIME

• ISCHEMIC STROKE IN PRECEDING 6 MONTHS

• CNS DAMAGE OR NEOPLASM• RECENT MAJOR TRAUMA/SURGERY/HEAD

INJURY/ WITHIN PRECEDING 3 WEEKS• GI BLEEDING WITHIN LAST MONTH• KNOWN BLEEDING DISORDER• AORTIC DISSECTION

THRMBOLYSIS CONTRAINDICATIONS

• H/O SEVERE HTN (SBP >180 mmHg.)• PREGNANCY OR <1 WEEK POSTPARTUM• ORAL ANTICOAGULANT THERAPY.• NON-COMPRESSIBLE PUNCTURES.• TRAUMATIC RESUSSITATION• ADVANCED LIVER DISEASE• TRANSIENT ISCHEMIC ATTACK IN

PRECEDING 6 MONTHS.

THRMBOLYSIS RELATIVE CONTRAINDICATIONS

SIDE-EFFECTS OF THROMBOLYTICS

• NAUSEA• VOMITING• BLEEDING• REPERFUSION ARRHYTHMIA• RECURRENT ISCHEMIA• ANGINA• CEREBRAL EDEMA• PULM EDEMA• HYPOTENSION• FEVER • CONVULSIONS• ALLERGIC REACTIONS----RASH, FLUSHING,UVEITIS • ANAPHYLAXIS • GB SYNDROME

ACUTE MANAGENT OF N-STEMI)

• ADMIT TO CCU• MONITOR CLOSELY• O2: • ANALGESIA: MORPHINE 2.5-5mg +METOCLOPRAMIDE 10 mg. IV

• NITRATES:GTN SPRAY OR S/L TABS• ASPIRIN: 300mgPO

• BETA-BLOCKER: METOPROLOL 50-100mg/8H OR ATENOLOL 50-100mg/24H

• IF B-BLOCKER IS CI THEN GIVE RATE LIMITING Ca; Channel ANTAGONIST.

• VERAPAMIL 80-120 mg/8H PO » OR

• DILTIAZEM 60-120 mg/8H PO

DON’T USE VERAPAMIL AND

B-BLOCKER TOGATHERCAN CAUSE ASYSTOLE

• LMW HEPARIN• ENOXAPARIN 1mg/kg SC/12h

• Or• Dalteparin 120u/kg/12h sc

• Alternatively :unfractionated heparin 5000u iv bolus then IVI infusion @0.25 UNITS/KG/H.

• Check APTT 6-hourly.• Alter IVI rate to maintain APTT @ 1.5-2.5 times

control.

• Nitrates IV if pain continues• GTN 50mg in 50 ml 0.9%saline @2-10ml/h titrate to

pain and maintain SBP >100mmHg.

• Record ECG while in pain.

ACUTE MANAGENT OF N-STEMI)Cont…..

ACUTE MANAGENT OF ACS WITHOUT ST-SEGMENT ELEVATION

(NSTEMI) CONTD:

• May be discharged if a repeat troponin (>12h) is negative.

• Treat medically.

• Arrange further investigations:• Stress test• angiography

LOW Risk Pts.

•No further pain•Flat or inverted T-waves or normal ECG•Negative Troponins

POST-MI DRUG THERAPY• ASA 75-100MG./D• A BETA-BLOCKER TO MAINTAIN HR <60/MIN.

(METOPROLOL 50MG BID)• ACE-INHIBITORS (RAMIPRIL 2.5MG BID TITRATED TO

MAX TOLERATED OR TARGET DOSE)• IF INTOLERANT OF ACE-INH USE ARB (VALSARTAN

20MG BID)• STATINS(SIMVASTATIN 20-80MG/D)• CLOPIDOGREL 75MG/D FOR 9-12 MONTHS.(FOR

MODERATE – HIGH RISK Pts. WITH NST- ACS• GTN SPRAY FOR SYMPTOMATIC RELIEF OF ANGINA • ALDOSTERONE ANTAGONIST(EPLERENONE 25MG/D

FOR REDUCED EF AND HF PTS

SUBSEQUENT MANAGEMENT IN ACS

CONTD;• ADDRESS MODIFIABLE RISK FACTORS.

– DISCOURAGE SMOKING– ENCOURAGE EXERCISE 20-30MIN/DAY– DIAGNOSE AND TREAT DM,HTN &

HYPERLIPIDEMIA– ENCOURAGE TO CONSUME >7 GRAMS OF

OMEGA 3 FATTY ACIDS/WEEK FROM OILY FISH OR >1 GRAM/D OF OMEGA -3-ACID ETHYL ESTERS.

– WEIGHT REDUCTION

SUBSEQUENT MANAGEMENT IN ACSCONTD;

GENERAL ADVICE

• DISCHARGE FROM HOSPITAL AFTER 5-7 DAYS IF UNCOMPLICATED.

• MAY RETURN TO WORK AFTER 2 MONTHS.• FOLLOWING OCCUPATIONS SHOULD NOT BE

RESTARTED POST-MI.– AIRLINE PILOTS– AIR-TRAFFIC CONTROLLERS– DIVERS

SUBSEQUENT MANAGEMENT IN ACSGENERAL ADVICE CONTD;

• DRIVERS OF HEAVY GOODS VEHICLES AND PUBLIC SERVICE MAY BE PERMITTED TO RETURN TO WORK IF MEET CERTAIN CRITERIA.

• LIGHTER JOB PREFERRED AGAINST HEAVY MANUAL LABOUR.

• DIET: – HIGH IN OILY FISH LOW IN SATURATED FATS– FRUITS– VEGETABLES– FIBRE

• EXERCISE:REGULAR DAILY EXERCISE.• SEX: AVOID INTERCOURSE FOR 1 MONTH.• TRAVEL: AVOID AIR TRAVEL FOR 2 MONTHS.• F/U REVIEW AT 5 WKS POST-MI: IF ANGINA RECURS

CONSIDER FOR ANGIOGRAPHY.• REVIEW AT 3 MONTHS : CHECK LIPIDS

MANAGEMENT OF AMI

ECG

O2 IV ACCESS TAKE LABS

BRIEF ASSESSMENT

ASPIRIN 300 MG

GTN S/L 2 PUFFS OR 1 TAB.

MORPHINE 2.5-5mg IV +METOCLOPRAMIDE

10mG

THROMBOLYSIS

BETA-BLOCKER

CXR

CONSIDER GLUCOSE,INSULIN,& POTASSIUM INFUSION FOR DM PTs.

CONT;MEDICATION EXCEPT Ca;CHANNEL ANTAGONIST (UNLESS SPECIFIC INDICATIONS)

CONSIDER DVT PROPHYLAXIS

SUMMARY

• ACS includes UA, NSTEMI, and STEMI

• Management guideline focus– Immediate assessment/intervention

(MONA+BAH)– Risk stratification (UA/NSTEMI vs. STEMI)– RAPID reperfusion for STEMI (PCI vs.

Thrombolytics)– Conservative vs Invasive therapy for UA/NSTEMI

• Aggressive attention to secondary prevention initiatives for ACS patients

• Beta blocker, ASA, ACE-I, Statin

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Copyright ©2007 American College of Cardiology Foundation. Restrictions may apply.

Anderson, J. L. et al. J Am Coll Cardiol 2007;50:e1-e157

Timing of Release of Various Biomarkers After Acute Myocardial Infarction