ACUTE CORONARY SYNDROMES
Transcript of ACUTE CORONARY SYNDROMES
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ACUTE CORONARY SYNDROMES
Roby Rakhit BSc MD FRCP
Consultant Cardiologist Royal Free hospital
Honorary Senior Lecturer, UCL
Advanced Medicine, Manchester, 20th June 2016
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Age- and Sex-Adjusted Incidence Rates of
Acute Myocardial Infarction, 1999 to 2008,
n=46,086 Yeh RW et al. N Engl J Med 2010;362:2155-2165
Incidence of ACS US & UK
Fig 1 Age standardised event rates of acute
myocardial infarction by sex and type of event,
2002-10, England n=840,175
Kate Smolina et al. BMJ 2012;344:bmj.d8059
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Fig 2 Age standardised 30 day overall and case fatality rates for admissions to hospital (%) for acute
myocardial infarction by sex, 2002-10, England.
Kate Smolina et al. BMJ 2012;344:bmj.d8059
Prognosis after ACS UK
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STEMI prognosis in the era of PPCI…
Unadjusted 30-day mortality 2011-2014:
•8.1% overall (n= 72,688)
•7.2% (n= 63,408) patients admitted directly to ‘primary PCI interventional centre’
•14.3% (n= 9,261) patients admitted to ‘primary PCI non-interventional centre ’
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Universal definition of myocardial infarction (Thygesen K Circ 2012:16;2020-35
• Myocardial infarction should be used when there is evidence of myocardial necrosis in a clinical setting consistent with myocardial ischaemia. Under these conditions any one of the following criteria meets the diagnosis of myocardial infarction:
• Detection of rise and/or fall of cardiac biomarkers (preferably troponin) with at least one value above the 99th percentile of the upper reference limit (URL) together with myocardial ischaemia with at least one of the following
– Symptoms of ischaemia
– ECG changes of new ischaemia (new ST-T changes or new LBBB)
– Development of pathological Q waves on the ECG
– Imaging evidence of loss of viable myocardium or new regional wall motion abnormality
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Cardiac Troponins • Components of myocardial contractile apparatus encoded
by distinct genes
• Not detectable in healthy subjects
• Highly specific immunoassays
• False positives: PE, myocarditis, LVF, renal failure
• Troponin I (Antman et al, n=1404)
42 day mortality > 0.4ng/ml 3.7%
< 0.4ng/ml 1.0%
• Troponin T (GUSTO IIA, n=855)
30 day mortality > 0.1ng/ml 11.8%
< 0.1ng/ml 3.9%
• Troponin T (FRISC, n=437)
5 month mortality 0.2 ng/ml 13%
0.2 -0.06 ng/ml 9%
< 0.06 ng/ml 5%
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Implications of Hs Troponin assays
• Higher negative predictive value for MI
• Earlier detection of MI
• Increase in detection of MI and reduction in diagnosis of unstable angina
• >90% PPV for detection of MI if 5 fold increase
• 50-60% PPV for MI if 3 fold increase
• > 99th percentile differs between hsTropT and I
– hsTropT >14 ng/L
– hsTrop I >24 ng/L
• hsTrop I male >34
• HsTrop I female >16
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0 h/3 h rule-out algorithm of non-ST-elevation acute coronary syndromes
using high-sensitivity cardiac troponin assays.
Authors/Task Force Members et al. Eur Heart J
2015;eurheartj.ehv320
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0 h/1 h rule-in and rule-out algorithms using high-sensitivity cardiac troponins (hs-cTn) assays
in patients presenting with suspected non-ST-elevation myocardial infarction (NSTEMI) to the
emergency department. 0 h and 1 h refer to the time from first blood test.
Authors/Task Force Members et al. Eur Heart J
2015;eurheartj.ehv320
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Acute Coronary syndromes
Unstable Angina NSTEACS STEMI
NSTEMI (Trop +) 75% 25%
- ST elevation
+ persistent ST elevation
ECG changes in NSTEACS:
ST depression Evidence of previous Q wave MI
normal LBBB
Transient ST elevation T wave inversion
Minor non-specific changes
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Pathophysiology • Plaque rupture/erosion/calcified nodule (Virmani JACC 2006)
• Platelet adhesion
• Thrombus formation ---> coronary occlusion
(1) Transient, intermittent and non-occlusive = UNSTABLE ANGINA
(2) Shortlasting, partly occlusive, spontaneous reperfusion = NSTEMI
(3) Prolonged and occlusive = STEMI
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NON-ST ELEVATION ACS = NSTEACS = NSTEMI/UNSTABLE ANGINA
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Natural History of NSTEACS
• NSTEACS precedes 50% of STEMI/ sudden cardiac death
• During first 30 days:
– Risk of death or STEMI is 10 % (GUSTO II)
– An additional 35 - 50% will experience recurrent ischaemia despite medical therapy (FRISC, TIMI IIIB, Klein)
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References:
Savonitto et al. JAMA. 1999;281:707.
Days from randomization
Mort
alit
y (
%)
180 0 20 40 60 80 100 160 0
6
8
10
2
4
120 140
% mortality at six months
T-wave inversion
3.4% (n=2,723)
ST-segment elevation
& depression
9.1% (n=1,769)
ST-segment depression
8.9% (n=4,263)
ST-segment elevation
6.8% (n=3,369)
Not all NSTEACS are the same… NSTEACS with ST depression has a 30% higher mortality at 6 months than STEMI (GUSTO IIb)
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ECG: RBBB and “posterior” ST depression
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GRACE – Global Registry of Acute Coronary
Events. Eagle KA, Lim MJ, Dabbous OH, et al. JAMA 2004;291:272–733.
• Multi-national registry of patients admitted with ACS at 94 hospitals in 14 countries (70,359 enrolled)
• Includes UA,STEMI,NSTEMI.
• The primary endpoint was all-cause mortality within 6 months of discharge.
• Nine predictors for the 6-month mortality were derived.
• Age per 10 year increase above 40.
• History of MI
• History of CHF
• Tachycardia
• Hypotension
• Elevated Creatinine.
• Elevated Cardiac Enzymes.
• ST depression
• Absence of in hospital PCI.
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Predicted 6-month mortality Risk of future adverse cardiovascular events
1.5% or below Lowest
> 1.5 to 3.0% Low
> 3.0 to 6.0% Intermediate
> 6.0 to 9.0% High
over 9.0% Highest
Risk categories derived from Myocardial Ischaemia National Audit Project (MINAP) database
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Very High Risk < 2hours
Mechanical complications of MI
Recurrent ST/T changes
Acute HF
High Risk < 24 hours
Positive Troponin
Recurrent ST/T changes
GRACE score >140
Intermediate Risk < 72 hours
Diabetes
CKD (eGFR <60)
EF <40% or congestive HF
Prior PCI or CABG
Early post MI angina
GRACE score >109 and <140
Low Risk
Any characteristics not mentioned above
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Timing of angiography: current clinical guidelines
NICE 2014 ESC 2015
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• 3031 patients randomised early <24hrs vs delayed <36hrs angiography (GRACE)
• Primary endpoint composite: death, new MI, stroke at 6 months
• Secondary end point: composite death, MI, refractory ischaemia, stroke, re-intervention at 6 months
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TIMACS trial May 2009 N Engl J Med 2009;360:2165-75.
Mehta SR, et al. N Engl J Med. 2009;360:2165-75.
High risk defined as GRACE risk >140
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How are we doing?
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Current pathway for NSTEACS for patients presenting to hospitals with angiogram only facilities
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Facilitating access for high risk NSTEACS
Koganti & Rakhit BMJ Open in press
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NSTEACS KEY MESSAGES
• Risk assessment (GRACE) is important in all NSTEACS presentation
• High risk NSTEACS with ST depression has a greater risk compared with ST elevation alone
• hsTrop assays allow rapid rule out of ACS using either 3 hr or 1 hr algorithms
• Angiography should be offered within 24 hours for patients at high clinical risk and <72 hours for intermediate risk patients
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ST ELEVATION MI = STEMI
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STEMI THE TRAINCRASH....
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“Time Is Muscle” The Wavefront of Necrosis
CM Gibson 2002
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Acute Inferior MI
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Meta-analysis of 23 randomised trials 7739 patients: 4-6 week data Keeley EC, Boura JA, Grines CL The Lancet 2003;361:13-20
0%
2%
4%
6%
8%
10%
12%
14%
Death Exc.Shock Non-fatal MI CVA Combined
PCI
Lysis
P=0.0002 P=0.0003 P<0.0001 P=0.0004 P<0.0001
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Association of door-to-balloon time and mortality in patients admitted to hospital with ST elevation myocardial infarction: national cohort study Rathore SS BMJ 2009
ACC national CVD registry 2005-2006 n=43801
120min
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Fig. 3. Log-rank analysis showing better survival in the HAC group.
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ST–Segment-Elevation Myocardial Infarction Patients
Randomized to a Pharmaco-Invasive Strategy or Primary
Percutaneous Coronary Intervention (STREAM)
Sinnaeve P et al 2014 Circulation 130(14):1139-1145 Copyright © American Heart Association, Inc. All rights reserved.
1:1 randomisation Immediate PCI vs Tenecteplase and then PCI (if PCI not deliverable within 60min)
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Do I treat culprit only or culprit and bystander disease in STEMI?
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14% reduction cardiac death,MI, repeat revascularisation
50% reduction cardiac death,MI, repeat revascularisation
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STEMI KEY MESSAGES
• PPCI, ideally direct access to a HAC, is the gold standard treatment for STEMI and should be delivered within 120min of symptom onset
• If PPCI cannot be timely delivered facilitation with fibrinolytic therapy and PCI after is an alternative
• Radial access is preferred to femoral
• Complete revascularisation should be performed either at the time of PCI or as a in-hospital staged procedure
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ANTI-THROMBOTIC MEDICATION
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Mechanism of platelet activation and site of action of platelet inhibitors
Story R Heart 2011
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Agent Class Mode Onset Offset/ withdrawbefore surgery
Dose Caution Trials Indication
Aspirin COX inhibitor Irreversible <60min 10 days 300mg then 75mg od 1 year
True allergy GI bleeding
All ACS
Clopidogrel Thienopyridine Irreversible 2-4 hrs 10 days/ 5 days
300-600 Then 75mg od 1 year
CURE
All ACS
Prasugrel Thienopyridine Irreversible 30min
10 days/ 7 days
60mg Then 10mg od 1 year
Previous CVA, >75years
TRITON TIMI -38
Stent thrombosis After angio and prior to PCI
Ticagrelor Cyclopentyl- triazolopyrimidine
Reversible 30min 3-4 days/ 5 days
180mg then 90mg BD 1 year
Bradycardia, dyspnoea
PLATO
All ACS
Cangrelor IV only
Stabilised ATP analogue
Reversible 2-3 min
1-2hrs /1 hr
Bolus 30ug/kg and infusion 4ug/kg/min
CHAMPION PHOENIX (VS ASPIRIN & CLOPID)
ALL ACS
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Anti-platelet therapy in ACS NSTEACS • 1 year aspirin & clopidogrel (CURE) • Prolonged clopid (2.5yrs) vs 1 yr
associated with reduced recurrent MI but increased bleeding (DAPT)
• Prasugrel/aspirin superior to clopid/aspirin (TRITON TIMI 38)
• Ticagrelor/aspirin superior than clopid/asp (PLATO)
STEMI • Ticagrelor or Prasugrel 1 year superior
to clopidogrel • Prasugrel not for >75years
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Heparins
• Unfractionated
- combined with aspirin given for 48hrs of benefit
c.f aspirin alone
• LMWT heparin (eg enoxaparin, daltaparin)
- as effective as unfractionated heparin (FRIC)
- superior to unfractionated heparin (ESSENCE,TIMIIIB)
- prolonged Rx (3/12) not superior to short term Rx (FRISC II)
- recommended length of Rx 2-8 days
• Factor Xa Fondaparinux in NSTEACS (OASIS5) and STEMI (OASIS6)
– Non-inferior to enoxaparin
– Given up to 8 days (mean 6 days)
– 50% reduction in bleeding compared to enoxaparin
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Factor Xa Inhibitors and ACS (ATLAS ACS 2 TIMI 51)
• Concept that thrombin
generation persists > 6 months after MI
• Warfarin is associated with MI reduction by 44% in ACS meta-analyses
• Could prolonged Factor Xa inhibition with Rivaroxaban reduce recurrent thrombotic events?
• Randomised trial of 2.5mg BD vs 5mg BD vs placebo in addition to standard DAPT (aspirin & clopidogrel) for 2 years
Incidence of the Primary Efficacy Endpoint
The primary efficacy endpoint consists of cardiovascular death, myocardial infarction
(MI), or stroke. Data are presented for the rivaroxaban doses combined compared with
placebo. CI = confidence interval; HR = hazard ratio; ITT = intention-to-treat; mITT =
modified ITT.
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What about warfarin: WOEST trial warf & clopid vs warf/asp/clopid n= 573 1:1 randomisation De Wilde Lancet 2013
0
5
10
15
20
25
30
35
40
45
50
TIMI
Minimal
TIMI Minor TIMI Major Any TIMI
bleeding
Doubletherapygroup
Tripletherapygroup
0
1
2
3
4
5
6
7
8
9
Death MI TVR Stroke ST
Doubletherapy group
Triple therapygroup
P < 0.001 except TIMI major p=ns
P ns for all
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Antithrombotic strategies in patients with non-ST-elevation acute coronary
syndromes (NSTE-ACS) and non-valvular atrial fibrillation.
Marco Roffi et al. Eur Heart J 2016;37:267-315
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ANTI-THROMBOTIC MEDICATION: KEY MESSAGES • Aspirin together with a novel P2Y12 inhibitor should
be given for 1 year after ACS
• Fondaparinux is the preferred LMWT in view of lower bleeding risk
• Prolonged treatment with low dose Rivaroxaban may play a role in reducing recurrent events in addition to clopidogrel/aspirin (not Ticagrelor)
• Clopidogrel and warfarin (without aspirin) can be used safely after coronary stenting in ACS
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Can we identify the vulnerable patient?
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PROSPECT trial Stone GW eta l NEJM 2011:364;226-235
• 700 patients with ACS
• 3 vessel coronary imaging (IVUS)
• 3 year follow up of recurrent events
• Lesion characteristics independently predicting events
– Thin cap fibroatheroma
– Plaque burden >70%
– Minimum luminal area <4mm2
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PROSPECT: MACE M
AC
E (
%)
Time in Years
0 1 2 3
All
Culprit lesion (CL) related
Non culprit lesion (NCL) related
Indeterminate
0
5
10
15
20
25
Number at risk
20.4%
12.9%
11.6%
2.7%
13.2%
7.9%
6.4%
0.9%
18.1%
11.4%
9.4%
1.9%
ALL 697 557 506 480
CL related 697 590 543 518
NCL related 697 595 553 521
Indeterminate 697 634 604 583
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Summary • Management of ACS has transformed over
recent years driven by: – Earlier diagnosis
– Better risk stratification
– Early angiography and revascularisation
– Improved anti-thrombotic medication
– Better outcomes
• Future horizons – Identifying vulnerable patients
– Optimising secondary prevention to stop recurrent events
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THANK YOU