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Heart Attacks: Killers in Disguise!
W. Frank Peacock, MD, FACEPVice Chief, Emergency DepartmentThe Cleveland Clinic
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Agenda What is an Acute Coronary Syndrome?
(a heart attack)
Why do you care?
– CAD is the number one killer in Scotland
Who gets ACS?
– What are the symptoms?
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Agenda
When should you go to the hospital?
– why you should go to the hospital?
How do we diagnosis it?
What happens if your diagnosed with it?
What can be done to prevent getting this?
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How does the heart work?
Its just a pump, right?
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Its also a gland
Myocardial injury Fall in LV performance
Activation of RAAS, SNS, ET,and others
Myocardial toxicityPeripheral vasoconstrictionHemodynamic alterations
Remodeling andprogressive
worsening ofLV function Heart failure symptomsMorbidity and mortality
ANPBNP
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Epidemiology of CHD in the US Single most frequent cause of death
– 656,000 deaths in 2002– 1 of every 5 deaths
Incidence– Each year, 1.2 million Americans will have a new or
recurrent coronary event, and >40% will die as a result– 700,000 events will be first attacks; 500,000 will
be recurrences
Prevalence– 13 million Americans have a history of CHD
(acute MI, other acute ischemic (coronary) heart disease, angina pectoris, atherosclerotic cardiovascular disease, and all other forms of heart disease)
CHD = coronary heart disease; MI = myocardial infarction.American Heart Association. Heart Disease and Stroke Statistics—2005 Update; 2005.
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Epidemiology of CHD Scotland
Single most frequent cause of death Incidence Prevalence
CHD = coronary heart disease; MI = myocardial infarction.American Heart Association. Heart Disease and Stroke Statistics—2005 Update; 2005.
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Risk for CHD Increases With Additional Risk Factors: INTERHEART Study
Yusuf S, et al. Lancet. 2004;364:937-952.
512
256
128
64
32
16
8
4
2
1Smk(1)
DM(2)
HTN(3)
ApoB/A1(4)
1+2+3 All 4 +Obes +PS All RFs
Od
ds
rati
o (
99%
Cl)
PS = psychosocial
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INTERHEART: Impact on CV Risk of Multiple Risk Factors (Smoking, Lipids, Hypertension, Diabetes, Abdominal Obesity, Diet,
↓Physical Activity, Alcohol, Psychosocial*)
Yusuf S, et al. Lancet. 2004;364:937-952.
Od
ds
Rat
io f
or
1st
MI
(99%
CI)
64
512
16
1
2
256
128
32
8
4
Smk(1)
DM(2)
HTN(3)
ApoB-ApoA1
(4)
1+2+3 All 4 All 4+ Obes
All 4+ Ps
All riskfactors
Smk = smokingDM = diabetesHTN = hypertensionObes = abdominal obesityPs = psychosocial factors
– Large int’l case-control study– 15,152 cases– 14,820 controls– 52 countries– Follow-up: 4 years
.*eg, stress, depressionNote: odds ratio plotted on a doubling scale.
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What does an ACS feel like?
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Symptoms of CAD
NONE……..– Sudden Cardiac Death
Chest Pain– Usually a pressure
Not seconds Anginal equivalents
– Jaw or shoulder pain– Nausea & vomiting– Shortness of breath– Weak & dizzy– Diaphoresis
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Symptoms of Heart Attack
Classicpresentation
Chest pressure– Elephant
Sweating Nausea/vomiting Radiation of pain Shortness of
breath
Anginal equivalents
Jaw/shoulder pain Nausea & vomiting Shortness of
breath Weak & dizzy Diaphoresis
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Who gets “Equivalents”?
Women Diabetics Elderly Heart Transplant patients Patients who can’t
perceive/communicate well?– Drunk– Mentally ill
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EMS Transport
Onset of symptoms of
STEMI
9-1-1EMS
dispatch
EMS on-scene• Encourage 12-lead ECGs• Consider prehospital fibrinolytic
if capable and EMS-to-needle within 30 min
GOALS
PCIcapable
Not PCIcapable
Hospital fibrinolysis: door-to-needle within 30 min
EMS triage plan
Inter-hospitaltransfer
Golden hr = 1st 60 min Total ischemic time: within 120 min
Patient EMS Prehospital fibrinolysisEMS-to-needlewithin 30 min
EMS transportEMS-to-balloon within 90 min
Patient self-transport Hospital door-to-balloon
within 90 min
Dispatch1 min
5 min
8 min
Options for Transport of Patients With STEMI and Initial Reperfusion Treatment
Adapted with permission from Antman EM, et al. Available at: http://www.acc.org/clinical/guidelines/stemi/index.pdf.Accessed November 1, 2005.
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What happens in the Ambulance?
Paramedics take your history and perform a brief exam
IV Oxygen Put on the monitor May receive nitroglycerin under the tongue.
(tingle, get a H/A) Maybe: ECG, thrombolytic (clot dissolver)
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What happens when you get to
the hospital?
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ED Visits - US
130,000,000annually
6.24 Msuspected or actual
cardiac4.1 M
sent home non-cardiac
50,000 MIs
3.1 Mnon-cardiac
(50%)
10.4 M chest pain (8.0%)
1.2 MAMI
(20%)
1.5 MUA
(24%)
374,400sudden death
(6%)
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ST-segment Elevation
Spectrum of Acute Coronary Syndromes
Ischemic Discomfort at Rest
Unstable Angina (UA)
Non-Q-wave MI(NSTEMI)
Q-wave MI(STEMI)
No ST-segment Elevation
– + + + Cardiac Markers
Presentation
EmergencyDepartment
In-hospital6-24 hours
Adapted from Braunwald E, et al. Available at: http://www.acc.org/clinical/guidelines/unstable/unstable.pdf
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STEMI: Brief Physical Exam in the Emergency Department
Airway, Breathing, Circulation (ABC) Vital signs, general observation Presence or absence of jugular venous distension Pulmonary auscultation for rales Cardiac auscultation for murmurs or gallops Presence or absence of stroke Presence or absence of pulses Presence or absence of systemic hypoperfusion
(cool, clammy, pale/ashen)
Antman EM, et al. Available at: http://www.acc.org/clinical/guidelines/stemi/index.pdf. Accessed November 1, 2005.
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STEMI: Acute Medical TherapyGeneral treatment measures
Antman EM, et al. Available at: http://www.acc.org/clinical/guidelines/stemi/index.pdf. Accessed November 1, 2005.
Analgesics Nitrates Oxygen β-blockers (decrease heart rate)
Primary PCI or coronary thrombolysis(primary PCI preferred after 3 hours)
Aspirin (162-325 mg, acute dose) Heparin If PCI:
– Clopidogrel
– GP IIb/IIIa inhibitors
Infarct sizelimitation
Reperfusion
Antithrombotic and antiplatelet therapy
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Chest Pain on a Saturday morning
While the physician was examining the ECG, the patient became unconscious and the rhythm on the monitor changed…
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Chest Pain on a Saturday morning
12:01100J DC cardioversion, patient immediately in NSR
12:03Clot box brought to room and catheterization lab team notified
12:04IV line started, 325 mg aspirin chewed and metoprolol given
12:10Open cath table and staff available, heparin iv and
clopidogrel po given 12:19Patient’s stretcher rolls
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• Media campaign• Patient
education• Greater
use of 9-1-1
Methods of Speeding Time to
Reperfusion
• Prehospital ECG and
Prehospital Rx, if possible
• MI protocol• Critical pathway
• Quality improvement
program
• Bolus lytics • Dedicated PCI team
5 min < 30 minD-B ≤ 90 min
D-N ≤ 30 min
Patient Transport In-hospital Reperfusion
Goals of Reperfusion Therapy
Adapted with permission from: Antman EM, et al. Available at: http://www.acc.org/clinical/guidelines/stemi/index.pdf. Accessed November 1, 2005.
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0
2
4
6
8
10
12
0 60 120 180 240 300 360
Ischemic time (min)
1 ye
ar m
ort
alit
y (%
)
0
2
4
6
8
10
12
0 60 120 180 240 300 360
Ischemic time (min)
1 ye
ar m
ort
alit
y (%
)Time from Symptom Onset to Treatment Predicts 1 Year Mortality—Primary PCI
The relative risk of 1 year mortality increases by 7.5% for each 30 minute delay.
De Luca G, et al. Circulation. 2004;109:1223-1225.
Y=2.86 (± 1.45) + 0.0045X1 + 0.000043X2
P<.001
Roughly 1% every 3 minutes
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25Boersma E, et al. Lancet.1996;348:771
Meta-analysis of 50,246 Patients in Lytic Trials
(Juice to squeeze)
0
Ab
solu
te b
enef
itp
er 1
000
trea
ted
pat
ien
ts
0
20
40
60
80
3 6 9 12 15 18 21 24Time to Treatment
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Primary PCI vs Thrombolysis in STEMI: Meta-analysis (23 RCTs, N=7739)
Adapted with permission from Keeley EC, et al. Lancet. 2003;361:13-20.
PCI
Thrombolytictherapy
0
5
10
25
15
20
Fre
qu
ency
(%
)
Short-term Outcomes(4-6 weeks)
Death
P=.0002
NonfatalMI
P<.0001
RecurrentIschemia
P<.0001
Hemor-rhagicStroke
P<.0001
MajorBleed
P=.032
Death, Nonfatal
Reinfarction,or Stroke
P<.0001
Bonferroni correction6 variables: p <0.0083
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What if the ECG is not diagnostic?
(As it is in >95%)
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Blood Markers
Necrosis– Something has to die
Strain– Natriuretic peptides
Other– Inflammation– Plaque rupture– Ischemia changes the blood
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All NecrosisAll Ischemia Some Ischemia, Some Necrosis
ACS Sequence and Timing
Pla
qu
e R
up
ture
On
set o
f Pain
ED
Pre
sen
tatio
n
Dis
ch
arg
e0-12 to
0 hrs12 to24 hrs Time
Am
ou
nt o
f T
issu
e
IMA
cTn
Ischemia
Muscle death
Ventricular OverloadBNPBNP
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30
01020
30405060
7080
0 2 4 6 8 12 18 24 32 48 72
Hours After Onset of MI
CKMB
Myoglobin
TnI
Appearance of necrosis markers
Hospital arrival
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Disease vs Events?
Time
Oxygen
Oxygen supply diminishes with disease progression
Oxygen demand changesdaily and during life
Ischemia occurs when O2 demand exceeds supply
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What is in the future?
New better markers
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Human Serum Albumin (HSA) isa circulating protein in blood with a metal binding site at the N-terminus.
What is IMA?
Bar Or et al, European Journal of Biochemistry, 2001
The N-terminus is altered during an ischemic event, resulting in Ischemia Modified Albumin (IMA™). IMA is unable to bind metals at the N-terminus.
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Chest Pain at Presentation
25% ACS
35% Rule Out
40% Grey Zone
EP Protocol with good NPV ischemia marker
12% ACS
13% Rule Out
75% Grey Zone
Current EP Protocol
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What if the markers are all negative?
(And they are in >90%)
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If It Moves, Even Below Your Hospital’s Cutpoint, It Is Bad
Marker Comparator OR for 30 day MACE
95% CI
ing Tn
vs. stable Troponin
2.25 1.42-3.55
ing Tn 3.04 1.94-4.75
ing CKMB
vs. stable CKMB
0.67 0.48-0.95
ing CKMB 0.96 0.57-1.60
Logistic regression models showing the odds ratios for predicting ACS
MACE: MI, revascularization (PCI or CABG), or positive testing (>70% stenosis at
catheterization, [+] MPI or non-invasive stress testing) within 30 days of index visit.
N=2,188
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All this testing… What’s the end result?
Most (88%) of the time, its negative– You go home
18% of the time, something is positive– ECG IMMEDIATE Cath lab– Marker URGENT Cath lab– Stress test Semi-elective Cath lab
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What happens in the Cath Lab?
Define the anatomy– Acutely closed vessel fix it– Chronically closed vessel nothing– Stenotic vessel: have options
~50%; either medicine or angioplasty works
>70%; most get angioplasty
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Scotland Epidemiology
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Prevalence of coronary heart disease in Scotland: Scottish Heart Health Study.
10,359 men and women aged 40-59 years from 22 districts in the Scottish Heart Health Study– Described the prevalence rates of coronary heart disease
in Scotland in 1984-1986 and their relation to the geographical variation in mortality in these districts.
Coronary heart disease in Scotland was the highest reported to the WHO from 1984-86– Angina was more common in men (5.5%) than in women
(3.9%)– A history of MI was 3 times more common in men than
women – Angina correlated well with mortality from coronary heart
disease
Br Heart J. 1990 Nov;64(5):295-8
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2001: The good news
The Cardiovascular Epidemiology Unit at the University of Dundee celebrated its 20th anniversary with a 40 % decline in coronary mortality rate
The steep decline in coronary mortality in Scotland mirrors the pattern in the rest of Britain.
Improvement is a combination of: Heightened awareness of health issues Improved diet and more exercise Improvement in treatments.
Scotland's record on heart disease is much improved– Russia now has the highest coronary mortality rate.
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2003 British Women's Heart and Health Study
4286 Women– 20% MI, angina, HF, CVA, PVD. – 50% HTN, 12% smoked, 25% obese– 50% w/ total cholesterol > 6.5 mmol/l, only 3% had low HDL
Age adjusted CVD prevalence– highest in Scotland: 25.0% (21.5% to 28.8%)– lowest in S. England: 15.4% (13.5% to 17.6%). – Woman in Scotland are 1.53 times more likely to have CVD
Of women with CVD– 12% are smokers, 1/3 had uncontrolled HTN, 1/3 were obese– 90% had a cholesterol > 5 mmol/l. – Only 41% were taking antiplatelet drugs and 22% were taking
a statin.
Journal of Epidemiology and Community Health 2003;57:134-140
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In Scotland
Coronary Heart Disease– one of the leading causes of death
10,331 deaths in 2005– Scotland has one of the highest death
rates from CHD in the western world – Due to
high rates of smoking poor diet deprivation
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In the year ending March 31 2006
Scottish hospitals 48,962 hospital discharges for CHD
16,320 were for AMI(heart attack)
CHD discharges represented around 4% of all acute hospital discharges.
NHSScotland carried out2,319 Coronary Artery Bypass Grafts 5,803 angioplasties17,065 angiographies
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http://www.isdscotland
CHD mortality is strongly related to age. 0-44 year olds is 4.1 per 100,000 75+, the rate is 1682.1 per 100,000
The incidence of CHD is higher in men, elderly and deprived areas of Scotland
Smoking being overweight raised blood pressure raised level of cholesterol
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Cost of Cardiovascular Disease in the UK
CVD cost the UK £29.1 billion in 2004– (exceeds the GDP of Kuwait)– 29% (£8.5 billion) was due to Coronary Heart Disease– 27% (£8.0 billion) Cerebrovascular Disease
CVD Cost break down– 60% health care– 23% productivity losses– 17% informal care-related costs
Conclusions:
CVD is a leading public health problem in the UK measured by the economic burden of disease.
Heart 2006;92:1384-1389
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Small changes in UK cardiovascular risk factors could halve CHD mortality
The UK called for a 40% reduction in CVD mortality by 2010. Potential reductions from the year 2000, were calculated for:
– Continuation of recent risk factor trends ~10,685 fewer CAD deaths in 2010 than in 2000
– Modest additional reductions in cholesterol and smoking ~51,270 fewer deaths Optimistic changes in obesity, DM, and physical
activity, would have relatively small effects.
Journal of Clinical Epidemiology 58 (2005) 733–740