Acs Update

7/29/2019 Acs Update

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ACUTE CORONARY

SYNDROMESR MAHARAJ

EMERGENCY MEDICINE


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INTRODUCTION

Coronary Artery Disease leading cause of morbidity & mortality in

industrialised nations.

Although decrease in cardiovascular mortality still major cause of

morbidity & burden of disease.

South African perspective of cardiovascular disease:

A World in One Country - Yusuf et al

Epidemiological transitions of cardiovascular disease.


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HIGH RISK POPULATION FOR CAD/ACS:

INDIAN/WHITE/COLOURED

INCREASING rate in Black population lifestyle/socioeconomic

changes, urbanisation

GF Jooste stats: 23.8% of admissions to resus. unit for chest

pain/acs related (stats 1Jan 2009 28 Feb 2009) 150/628 entries.

In US 2004 1.56 million admissions for ACS 669 000 for

unstable angina, 896 000 for MI

Higher prevelance for NSTEMI.


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DEFINITIONS

CAD is a continuum of disease.

Angina -> unstable angina -> AMI -> sudden cardiac death

Acute coronary syndrome encompasses unstable angina, NSTEMI,STEMI

Stable angina transient episodic chest pain d/t myocardial

ischaemia, reproducible, frequency constant over time.usually

relieved with rest/NTG.

Classification of anginaCanadian Cardiovascular Societyclassification.


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Canadian Cardiovascular Association Classification of

Angina

CLASS 1 NO PAIN WITH ORDINARY PHYSICAL ACTIVITY

CLASS 2 SLIGHT LIMITATION OF PHYSICAL ACTIVITY

PAIN OCCURS WITH WALKING, CLIMBING

STAIRS,STRESS

CLASS 3 SEVERE LIMITATION OF DAILY ACTIVITY PAIN

OCCURS ON MINIMAL EXERTION

CLASS 4 UNABLE TO CONDUCT ANY ACTIVITY WITHOUT

PAIN, PAIN AT REST


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UNSTABLE ANGINA

Pain occurring at rest duration > 20min, within one week of first

visit

New onset angina ~ Class 2 severity, onset with last 2 months

Worsening of chest pain increase by at least 1 class, increases infrequency, duration

Angina becoming resistance to drugs that previously gave good

control.

NB! ECG normal, ST depression(>0.5mm), T wave changes


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ACUTE MYOCARDIAL INFARCTION

ECC/ACC DEFNrise and fall in cardiac enzymes with one or more

of the following:

Ischaemic type chest pain/symptoms

ECG changes ST changes, pathological Q waves Coronary artery intervention data

Pathological findings of an acute MI

NSTEMI = UNSTABLE ANGINA SYMPTOMS/FINDINGS +

POSITIVE CARDIAC ENZYMES

STEMI = ST ELEVATION ON ECG + SYMPTOMS


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WHY IS IT IMPORTANT TO RECOGNISE PATIENTS WITH

UNSTABLE ANGINA??

5 -17% suffer an MI within a week after admission.

3 -15% die within a year.


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ACS PATHOPHYSIOLOGY

Distruption of coronary artery

plaque -> platelet

activation/aggregation

/activation of coagulation

cascade -> endothelial

vasoconstriction ->intraluminal

thrombus/embolisation ->

obstruction -> ACS


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APPROACH

Identifying those with chest pain suggestive of IHD/ACS.

Thorough history required:

Character of pain

Onset and duration

Location and radiation

Aggravating and relieving factors

Autonomic symptoms

TYPICAL VS ATYPICAL HISTORY Failure to recognise symptoms other than chest pain -> approx 2 hr

delay in seeking medical attention


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CHARACTERISTICS OF TYPICAL ANGINAL CHEST PAIN

(ADAPTED FROM ROSENS, EMERGENCY MEDICINE)

CHARACTERISTIC SUGGESTIVE OF ANGINA LESS SUGGESTIVE OF

ANGINA

TYPE OF PAIN DULL

PRESSURE/CRUSHING

PAIN

SHARP/STABBING

DURATION 2-5 MIN,


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ATYPICAL PAIN

RISK FACTORS FOR DEVELOPING ATYPICAL PAIN:

Diabetes, females, non white patients, elderly, dementia, no prior history ofMI

ATYPICAL SYMPTOMS:

GIT symptoms

Syncope SOB

Pleuritic/positional pain

Chest wall tenderness

No chest pain/symptoms

NRMI 2 STUDY MI without chest pain -> increased risk of death (23% vs9%)

More complications hypotension,heart failure, stroke

Delayed ED presentation, delayed intervention


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RISK STRATIFICATION IN ACS

Reasons :

Provides prognostic information

Determines treatment and level of intervention -> low risk patientsearly discharge, high risk -> admission to high care

Helps decongest the ED and make available medical resources tomore needy patients

Risk stratification should be ongoing at admission, 6-8 hrs, 24hrs,discharge


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TOOLS USED IN RISK STRATIFICATION

HISTORY

ECG

BIOCHEMICAL MARKERS


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ECG

First point of entry into ACS algorithm

Abnormal or normal

Neither 100% sensitive or 100% specific for AMI

Single ECG for AMI sensitivity of 60%, specificity 90%

Represents single point in timeneeds to be read in context

Normal ECG does not exclude ACS 1-6% proven to have AMI, 4%unstable angina


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GUIDELINES:

Initial 12 lead ECG goal door to ECG time 10min, read by

experienced doctor (Class 1 B)

If ECG not diagnostic/high suspicion of ACS serial ECGs initially

15 -30 min intervals (Class 1 B)

ECG adjuncts leads V7V9, RV 4 (Class 2a B)

Continuous 12 lead ECG monitoring reasonable alternative to serial

ECGs (Class 2a B)


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BIOCHEMICAL MARKERS

IDEAL MARKER:

High concentration in myocardium

Myocardium specific

Released early in injury

Proportionate to injury Non expensive testing

Troponins

CKMB Myoglobin

Other markers


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TROPONINS T/I

Troponin T vs I

both equivalent in diagnostic and prognostic abilities ( except in

renal failure Trop T less sensitive)

Elevation ~ 2hrs to 12hrs

~30 40% of ACS patients without ST elevation had normal

CKMB but elevated troponins on presentation

Meta-analysis (Heindereich et al) odds of death increased 3 to 8

fold with positive troponin


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Mortality at 42 days in troponin positive patients


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MYOGLOBIN

Rapid release within 2 hours

Not cardiac specific

Rule out for NSTEMI rather than rule in.

CKMB

Used in conjunction with troponinsUseful in diagnosing re-infarction


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MARKER CHANGE SCORES

2 hour delta CKMB mass

Aim to exclude MI within 6hrs of symptom onset

Determine changes in serum marker levels over certain timeintervalsdelta values

Increasing values while still within normal range suggestive of

ischaemia more rapid anti- ischaemic mxn.


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OTHER MARKERS

INDICATORS OF INFLAMMATION OR ACTIVATION OF

COAGULATION CASCADE:

Myeloperoxidase, soluble CD40 ligand, IL6, hsCRP, d dimer,

prothrombin fragment 1 & 2

Elevated before onset of irreversible injury

Lack specificity

Complex lab assays


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ISCHAEMIA MODIFIED ALBUMIN

Measured with albumin cobalt binding assay

In ischaemia -> decreased binding of albumin to cobalt

Increased with minutes of ischaemia elevated for 6-12hrs gone

by 24hrs

~90% negative predictive value Combined with myoglobin/CKMB/troponin increases diagnostic

sensitivity of ischaemia by 40%

Possible role for rule criteria in low risk patients

Positive IMA high risk patients more aggressive mxn

Positive in hypoxic disorders poor specificity in this setting


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Btype Natriuretic Peptide:

released from heart muscle in response to increased ventricular wall

stress.

Studies BNP not a specific marker but a strong predictor of ACS

especially in patients with chest pain, no ECG changes, nondiagnostic troponins.

Also positive in heart failure, PE, atrial arrythmias, renal failure

Pregnancy Associated Plasma Protein A (PAPP-A):

Released when plaque ruptures

Predictor of ischaemia


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HEART FATTY ACID BINDING PROTEIN (HF ABP)

Identifies AMI


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2007 ACC/AHA guidelines: Cardiac biomarkers measured in all patients with suspicion of ACS

(Class 1 B)

Troponin preferred marker( Class 1 B)

If troponin negative within 6 hours of onset, repeat 8-12hours

later(Class 1 B) Remeasuring of positive biomarkers to determine infarctsize/necrosis (Class 2a B)

Patients presenting within 6 hours of symptom onset myoglobin inconjunction with troponin measured (Class 2b B)

2hr delta CKMB/Delta troponin considered in


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RISK STRATIFICATION MODELS


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TIMI RISK SCOREincrease in mortality with increasing score ~40%

all cause mortality at 14 days for patients requiring urgent

revascularisation


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WHICH MODEL IS MOST APPROPRIATE??

2007 ACS/AHA GUIDELINES:

Risk stratification models useful in decision making with regard to

treatment options ( Class 2a B)

TIMI vs GRACE vs PURSUIT

PURSUIT & GRACE risk scores allow better discrimination of in

hospital and 1 year mortality in patients compared to TIMI. (Andrew

et al, Risk scores for risk stratification in ACS )

Whats appropriate in our setting???


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MANAGEMENT ALGORITHM


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MANAGEMENT UPDATE

2007ACS/AHA GUIDELINES:

Rapid catergorisation of patient (Class 1 C)

Possible ACS, non diagnostic ECG/biomarkers observed in facility

with cardiac monitoring (Class 1 C)

Alternative to in patient treatment: for those with 12hr ECG/markers

negative stress ECG in 72hrs (Class 1 C)

Giving precautionary treatment for those for OPD stress (Class 1 B)


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INITIAL INVASIVE

VS

INITIAL CONSERVATIVE STRATEGY

CLASS 1 RECOMMENDATIONS:

Early invasive strategy for refractory angina, hemodynamicinstability (LOE B)

Early invasive strategy for stabilised patients with elevated risk forclinical events.

High risk factors include: Recurrent angina, ischaemia at rest or minimal activity

Elevated troponins

New ST depression

Signs of heart failure/worsening mitral regurg.

Ventricular tachycardia

Prior CABG

PCI in last 6 months

High TIMI/GRACE scores

LVEF < 40%


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CLASS 2b

May opt for initial conservative strategy in stabilised high risk

patients dependent on patient/physician preference (LOE B)

CLASS 3 Invasive strategy -not recommended in patients with multiple co

morbidities, low risk patients, patients not consenting.(LOE C)


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UA/NSTEMIPHARMACOTHERAPY UPDATE

GENERAL:

IV B Blockers downgraded from Class 1 to 2a recommendation.

(COMMIT Trial)

Oral B Blockers in first 24hrs still Class 1 but not used in signs of

heart failure, cardiogenic shock and reactive airway disease.(LOE B)

MORPHINE downgraded from Class 1 to 2a findings from

CRUSADE Registry


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NSTEMI- PHARMACOTHERAPY UPDATE

ANTIPLATELET THERAPY:

CLASS 1 RECOMMENDATION

Aspirin to all patients as soon as possible and continued (if no C/I) (LOE A)

Initial dose 162 -325mg

Maintenance 75 -162mg

No added benefit from higher doses except post stenting

Clopidogrel for those allergic to aspirin or major GI bleeding (LOE A)

For initial invasive strategy aspirin + clopidogrel or IV glycoprotein 2b/3atherapy (LOE A)

Abciximab if no delay in angiography/PCI, eptifibatide/tirofiban if delayedangiography(LOE B)


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CLASS 2a

In patients managed conservatively who develop recurrent

ischaemia on clopidogrel/ASA/Anticoagulant can add

glycoprotein inhibitor. (LOE C)

Invasive strategy can use clopidogrel + glycoprotein

inhibitors(LOE C)

CLASS 2b

In patients managed conservatively can add glycoprotein inhibitortherapy, in addition to aspirin & anticoagulant (LOE B)


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CLASS 3

ABCIXIMAB should not be given if PCI not planned (LOE A)


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For initial conservative strategy:

Aspirin + Clopidogrel + anticoagulant administered for 1

month(LOE A), continued ideally up to 1 year(LOE B)

If initial conservative strategy selected but patient has recurrentischaemic symptoms/heart failure/arrythmias diagnostic

angiography recommended. Clopidogrel or Glycoprotein 2b/3a

inhibitors should be added before angiography.


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ANTICOAGULANT THERAPY

CLASS 1

Anticoagulant therapy should be added as soon as possible

For patients undergoing angiography/PCI enoxaparin/UFH (LOE

A) of Bivalirudin/ fondaparinux (LOE B)

For conservative strategy: enaxaparin, UFH (LOE A), fondaparinux

For patients with increased risk of bleeding with conservative

strategy fondaparinux


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CLASS 2a

Enoxaparin /fondaparinux vs UFH

Enoxaparin/fondaparinux preferred except in those undergoing

CABG within 24hrs (LOE B)


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ADDITIONAL MANAGEMENT

STRESS TEST should be performed for those managed

conservatively.

If stress test positive/ high risk needs diagnostic

angiography(Class 1 LOE A)

If classed as low risk

need to continue aspirin indefinitely ( LOE A)

Clopidogrel for at least 1 month(LOE A), ideally up to 1 year(LOE B)


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UA/NSTEMI ALGORITHM- INVASIVE STRATEGY


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UA/NSTEMI ALGORITHMCONSERVATIVE STRATEGY


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STEMI

PHARMACOLOGICAL UPDATE:

ANALGESIA changes from 2004 guidelines

MORPHINE: still remains Class 1 C for STEMI, titrated doses

NSAIDS/COX 2 INHIBITORS: those on it should have it

discontinued ( increased risk of mortality, re infarction, heart failure,

myocardial rupture) Class 1 C

NSAIDS should not be administered in hospital for MI (Class 3)


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BETA BLOCKERS

Modified recommendation

Oral Beta Blockers should be initiated in first24rs, if no contra-

indications (heart failure, risk of cardiogenic shock) Class 1 B

Patients with early contraindications -> re- evaluated later forpossible use

Role of IV B blockers used in hypertensive patients with STEMI

Class 2a B

Class 3 LOE A IV B blockers should not be administrated to

patients with heart failure, risk of cardiogenic shock


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No major changes to reperfusion strategies.

Emphasis on decreasing ischaemic time.

Increase use of prehospital 12 lead ECG emphasised.

In PCI capable hospital door to PCI time 90 min (Class 1 A)

In non PCI capable hospital door to needle time 30 min or timeous

transfer to PCI capable hospital. (Class 1 B)


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REPERFUSION STRATEGY


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FIBRINOLYTICS

AVAILABLE FIBRINOLYTICS: STREPTOKINASE 1.5mu infusion over 30min (1hourACLS)

rtPA accelerated infusion over 1.5hrs

- 15mg IV bolus, 0.75mg/kg over 30 min, 0.5mg/kg over 1hr

ANISTREPLASE 30 U IV over 5 min

TENECTEPLASE 30 TO 50 MG

RETEPLASE 10 U IV bolus, ffd. 10U IV after 30 min

WHICH FIBRINOLYTIC TO USE???

GISSI 2 trial tPA vs Streptokinase , no difference in mortality, marginallyhigher stroke rate with tPA (1.3% vs 1%)

GUSTO 1 trial early vessel patency post infract assoc. with better survival.

Accl. tPA/heparin cf comb. Streptokinase/tPA/heprain cf strep with IV vsS/C heparin

Outcome better flow rates with accl. tPA -> lower mortality rates


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ASSENT 2 TRIAL tenecteplase vs aTPA

- tenecteplase was equally or minimally more

effective, especially in those presenting > 4hrs after symptom onset.

Fibrinolysis combined with glycoprotein 2b/3a inhibitors no overalladvantage (ASSENT 3, GUSTO 5 trials)


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RESCUE PCI: CLASS 1 LOE B angiography with +/- PCI in patients (


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ANTICOAGULANT ADJUNCTS

NEW RECOMMENDATIONS:

CLASS 1

Patients undergoing fibrinolysis should be kept on anticoagulants for

atleast 48 hrs and preferably the duration of hospital stay. LOE A

Anti coagulants with proven efficacy:

Unfractionated Heparin - keeping aPTT 1.5 2 sec above control

(LOE C)

Enoxaparin (Clexane) initial dosage of 30mg IV bolus ffd by

1mg/kg 12hrly, caution in renal impairment (LOE A) Fondaparinux 2.5mg IV, ffd by 2.5mg dly S/C maintenance for

duration of hospitalisation (LOE B)


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ANTICOAGULANTS

CLASS 2a recommendation to use anticoagulants in STEMI without

reperfusion.

UFH (LOE B)

LMWH (LOE C)

Fondaparinux (LOE B)


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THIENOPYRIDINES

CLASS I

CLOPIDOGREL now recommended in all STEMI patients in

addition to aspirin, whether undergoing reperfusion or not. Dosage

75mg daily(LOE A)

Duration -14 days (LOE B)

CLASS 2 A

In patients < 75yrs Clopidogrel 300mg loading dose

recommended(LOE C)

Long term maintenance therapy should be considered, 75mg dly for 1year (LOE C)


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SECONDARY PREVENTION

INCREASED FOCUS ON SECONDARY PREVENTION:

SMOKING CESSATION

DIET MODIFICATION/WT CONTROL

BP CONTROL

LIPID MANAGEMENT

EXERCISE

DIABETES MANAGEMENT


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Despite good reperfusion strategies approx. 1/3 of patientsworldwide miss out.

Attributed to delayed presentation, atypical presentation,

complicated disease presentation, older age

SYMPTOMS OF INFARCT BUT NO ESTABILISHED ECG

CHANGES - keep in mind aortic dissection, GIT disease, other

chest pathology


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CONCLUSION

With increase burden of CVD, and lack of health resources riskstratification becomes important.

Emphasis should also be placed on primary &secondary prevention

of ACS.

Early intervention helps prevent complications, decreases morbidity

& mortality

The way forward fully equipped CHEST PAIN OBSERVATIONUNIT


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REFERENCES

EDITORS MARX ET AL, ROSENS EMERGENCY MEDICINE: CONCEPTS AND CLINICALPRACTICE, 6TH EDITION

PAUL PD ET AL, KEY ARTICLES IN MANAGEMENT OF ACS & PCI -2007 UPDATE,PHARMACOTHERAPY 2007:27(12), 1722 -1750

WHITE HD, DEFINING THE LIMITS OF ACS, CARDIOLOGY AT THE LIMITS IV, EDITORS:

OPIE LH, YELLON DM

YUSUF S, THE GLOBAL EPIDEMIC OF ATHEROSCLEROTIC CARDIOVASCULAR DISEASE,CARDIOLOGY AT THE LIMITS IV, EDITORS: OPIE LH, YELLON DM

FOX KA, MANAGEMENT OF ACS: AN UPDATE, HEART.2004 JUNE, 90(6):698 -706

ANDERSON ET AL, ACC/AHA 2007 GUIDELINES FOR MXN OF U/A,NSTEMI EXECUTIVESUMMARY DOWNLOADED content.onlinejacc.org

SIX AJ ET AL, CHEST PAIN IN THE ER: VALUE OF THE HEART SCORE, NETH. HEART J.2008 JUNE,16(6):191 -196


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ANTMAN EM ET AL, 2007 FOCUSSED UPDATE OF ACC/AHA 2004 GUIDELINES FOR MAXNOF PATIENTS WITH STEMI, DOWNLOADED http://circ.ahajournals.org

McCANN CJ ET AL, NOVEL BIOMARKERS IN EARLY DIAGNOSIS OF AMI COMPARED WITH

CARDIAC TROPONIN T, EUROPEAN HEART JOURNAL 2008,29(23): 2843 -2850

KING III SB ET AL, 2007 FOCUSSED UPDATE OF ACC..FOR PCI, JOURNAL OF

AMERICAN COLLEGE OF CARDIOLOGY, VOL 51, NO 2, 2008
http://circ.ahajournals.org/http://circ.ahajournals.org/

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