Acute Coronary Syndrome SDMH 2016 - PowerPoint Presentation

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Acute Coronary Syndrome

SDMH 2016

Objectives

To review the definition the current definition acute myocardial infarction

To briefly review the benefits of the various treatments available for

ACS

To review the current management guidelines for STEACS and NSTEACS

Kristian Thygesen et al. Circulation. 2012;126:2020-2035

Copyright © American Heart Association, Inc. All rights reserved.

Definition of Acute Myocardial Infarction

Diagnostic definitions not necessarily directly translatable to clinical syndromes

Need rapid diagnostic criteria to select those for clinical interventions

STEMI vs NSTEMI (NSTEACS)

STE representative large vessel insufficiency BUT not necessarily Type I MINSTEMI may be Type I or Type 2



ST Elevation MI

Presence of STE indicates high likelihood of coronary artery occlusion

Can be rapidly diagnosed >70% cases on initial 12 lead on presentation

Indicated to be present with ischemic symptoms >20mins duration with presence of ECG changes

Presence of ’new’ LBBB controversial – ‘evolving’ likely better method of

DxSTEMI able to be diagnosed in presence existing LBBB (or paced) by use of Sgarbossa criteria – 90% Sn and Sp

Non-STE MI

Much more difficult to quantify due to Type 1 vs Type 2 MI criteria.

Requires typical rise and fall >20% of cardiac biomarker

In ED, ECG deflections most likely to give clue to ACS

Evolving/dynamic changes more diagnostic5-10% of ACS will have

normal ECG in EDT wave inversion may be considered to be evidence of myocardial ischaemia if:At least 1 mm deepPresent in ≥ 2 continuous leads that have dominant R waves (R/S ratio > 1)

ST depression ≥ 1 mm is more specific and conveys a worse prognosis.ST depression ≥ 2 mm in ≥ 3 leads is associated with a high probability of NSTEMI and predicts significant mortality (35% mortality at 30 days).ST depression due to subendocardial ischaemia is usually widespread — typically present in leads I, II, V4-6 and a variable number of additional leads.Always consider possibility that ST depression may be reciprocal change, or reflect LMCA occlusion

Features less specific for ischaemia –ST depression < 0.5 mmT wave inversion < 1 mmT wave flatteningUpsloping ST depressionTWI is a normal variation in leada III, aVR and V1

Treatment modalities

Oxygen, nitrates and morphine

Antiplatelet therapies

Anticoagulants

B-blockadeReperfusion strategies

Oxygen, nitrates, morphine

Oxygen

No proven benefit

Small studies suggesting increased biomarker release, ?increased infarct size with high flow O2.

Now contra-indicated

in absence of pre-existing hypoxiaGTN Effective analgesic agentPotentially more effective for NSTEACS than STEMIIV route more effective than SL, but close BP monitoring requiredCaution required with Inferior STEMI, with RV involvement

Opioid analgesia – morphine/fentanylTraditional analgesia.Questions over histamine release with morphineAll narcotics slow gastric emptying –questions over interference with oral therapiesNone of these therapies shown to have any effect on mortality or morbidity

Antiplatelet agents

Aspirin

Rapid inhibition of thromboxane A2. Rapid oral absorption

Large body of evidence supporting benefit, both historically and contemporary.

Reduction in incidence of death, recurrent MI and stroke of 5%, NNT 21

ICH rates offset by ischemic stroke reduction – no significant bleeding risk!Level IA recommendation for use in all ACS presentations – 300mg stat then 100-150mg dailyClopidogrel, Prasugrel, TicagrelorAct by inhibition of P2Y12 receptor. Well supported with evidence of effect in combination with aspirin, but with increased bleeding risk

Clopidogrel – 3.2% benefit, 0.5% bleed riskPrasugrel – 5.7% benefit (PCI), 1.2% bleed riskTicagrelor – 5.3% benefit(PCI), 1% bleed riskClopidogrel agent of choice in fibrinolysis strategy. Ticagrelor or prasugrel

preferred if PCI planned.Prasugrel higher bleeding rate in >75yrs ageAll agents should be reconsidered if CABG considered highly likely; requires delay of surgery >5 days

Anticoagulants

Unfractionated Heparin

Potentiates anti-thrombin III activity, some anti-

Xa

inhibtion

Half life ~ 10-20min IVReduces risk death, recurrent MI by 4.3% (NNTB 23)Increased bleeding risk 1.5% (NNTH 65)Bolus dose 60 U /kg (max 4000U) , then infused 12-15U/Kg/hrLevel 1A recommendation for routine use in high risk ACS

Low Molecular Weight HeparinActivity is anti-Xa based4-5 hr half life, primarily renal excretionNo dose modification required until CrCL <30ml/minBenefits, bleeding risk same as for UFHFor non-reperfusion strategy, dose is 1mg/kg

bd SCFor reperfusion, dose of 30mg IV followed by SC dose recommendedIf age >75, recommended to NOT bolus and reduce dosing to 0.75mg/kg bd

Beta Blockers

Previously proven to be beneficial in studies

pre-dating reperfusion therapies

1% absolute mortality benefit in this time period

Thought to assist my reducing wall stress and ‘fixing’ tachycardia by early IV useRecommendation – commence when stable, and LV function thought suitable for administration

COMMIT trial 200545000 participants with STEMI1 trial arm compared IV metoprolol with placeboFound that use reduced subsequent risk VF and re-infarction, BUT early use increased incidence of cardiogenic shockOverall effect neutral on mortality

Reperfusion therapies

Primary aim of reperfusion is to re-establish flow to ischemic myocardium as soon as possible

Greatest benefit –

Anterior STEMI;

Age <75;

Reperfusion within first hourDrop in efficacy after 4 hrs. No benefit after 12 hrs.Also beneficial in patients with; Resolved chest pain if has otherwise fulfilled STEMI criteria; Persisting ongoing pain over 12 hrs; Out of hospital cardiac arrest if ECG changes present after ROSC

Reperfusion options

Alteplase

/

Reteplase

/Tenecteplase

Widespread, easy to distribute (pre-hospital)Acts by activating plasmin to degrade fibrinTNK – activity period ~ 20 mins. Deranges clotting factors for hrs. afterwardsSignificant exclusions to ensure safe useRequires adjunctive heparinisation Mortality benefit 4% (NNT 25) Bleeding risk 2%

Exclusion criteria – Systolic >180 mmHg or Diastolic >110 mmHg

Any hx. ICH, Cerebral aneurysm, AVM, Cerebral MalignancyCVA/TIA last 3 monthsMajor trauma or surgery (incl. eye) in last 6 weeksGI or GU bleeding last 6 weeksBleeding diathesis – hemophilia or medication (warfarin, NOACS)Non-compressible vascular punctureProlonged CPR

Pregnant or post partum 2 weeks

Reperfusion strategies

Percutaneous Coronary Intervention

Requires Cath. Lab infrastructure

Avoids problems with fibrinolysis related bleeding

Higher success rate with restoration of flow acutelyMortality benefit 5.5-6% NNT (16-18) Bleeding risk 1%

Choice of strategy….

PCI outperforms Fibrinolysis for in-hospital reperfusion

Transfer from non-PCI site to PCI site shown to improve mortality, recurrent MI and stoke by ~ 1% each

Mortality advantage of PCI diminishes with increasing delay to procedure

‘Break-even’ point shown to be 121 minutes by analysis Fibrinolysis vs PCI outcomes

Very early administration (eg pre-hospital) of fibrinolysis may further narrow differences in outcomeIndications for PCIPCI available in <90 minutes from presentation to PCI capable site, or <120 minutes in non-capable sitePt demonstrating haemodynamic instability and/or cardiogenic shock (ideally with CABG back-up)

Fibrinolysis contra-indicatedLate presentationFailure of fibrinolysis (<50% resolution of ST segments, or persisting pain 60-90 minutes post fibrinolysis) – ‘rescue-plasty’Indication for FibrinolysisUnable to access PCI lab in reasonable time frameVery early access to fibrinolytic

Contrast anaphylaxis

NSTEACS

R

eperfusion not shown to be beneficial in reducing

mortality

Benefit effect to PCI 4.9%, but all related to reduction in recurrent ischemiaBenefit seems limited to non-invasive interventions , with PCI within 48 hrs recommended for low-intermediate risk patients