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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?

3

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?

4

How does the heart work?

Its just a pump, right?

5

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

6

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

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

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