Coronary Artery Disease

Erwin Sukandi
Division of Cardiology
Department of Internal Medicine
Dr. Moh. Hoesin General Hospital
Coronary Artery
 Cardiovascular Disease

63,400,000 Americans have one or more forms

of heart or blood vessel disease

50% of all deaths are cardiovascular disease

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 Cardiovascular Disease
Acute Myocardial Infarction (Heart Attack) - leading
cause of death in U.S.

1.5 million Americans will have AMIs this year

Of these 0.5 million will die!
350,000 will die in first two hours!

Temple College EMS Program 4

 Classification
Coronary Artery
Disease

Asymptomatic Symptomatic

Stable Angina Acute Coronary

Syndrome

Unstable Non ST-Elevation ST-Elevation

Angina Myocardial Myocardial
Infarction Infarction
 Risk factors
High blood pressure (hypertension)
High blood cholesterol
Smoking
Obesity
Physical inactivity
Diabetes Controllable
Stress (?)
 Risk Factors (contd)

Gender
Heredity
Age
History of Premature CAD in the family

Uncontrollable
 Major Risk Factors:
The Big Three
Hypertension
High cholesterol All three increase risk
Diabetes Mellitus factor eight times

AND. we should add LACK OF EXERCISE

THE DEADLY QUARTET

Dyslipidemia
Diabetes Obesity
Hypertension
 Symptoms
Angina Pectoris
Substernal
Squeezing/Crushing/ Heaviness
May radiate to arms, shoulders,
jaw, upper back, upper abdomen
back
May be associated with
shortness of breath, nausea,
sweating

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 Stable CAD
Stable CAD is generally characterized by episodes
of reversible myocardial demand/supply
mismatch related to ischemia or hypoxia which
are usually inducible by exercise, emotion or
other stress and reproducible, but which may
also be occuring spontaneously

Stable CAD is most commonly caused by

atheromatous plaque that obstructs or gradually
narrows one or more of the epicardial coronary
arteries
Clinical Classification of Chest Pain
 Pretest Likelihood of CAD in Symptomatic Patients
According to Age and Sex* (Combined Diamond/Forrester
and CASS Data)

*Each value represents the percent with significant CAD on

catheterization.
 Prevalence of CAD (%) in Symptomatic
Patients According to Age and Sex

Typical angina Atypical angina Non anginal

chest pain
AGE Men Women Men Women Men Women

30-39 69.7 25.8 21.8 4.2 5.2 0.8

40-49 87.3 55.2 46.1 13.3 14.1 2.8

50-59 92.0 79.4 58.9 32.4 21.5 8.4

60-69 94.3 90.6 90.6 54.6 28.1 18.6

3 of 3 criteria 2 of 3 criteria 1 of 3 criteria

1) Retrosternal discomfort.2) Provoked by exercise or stress.3) Relieved by rest or NTG

Comparing Pretest Likelihood of CAD in Low-Risk
Symptomatic Patients With High-Risk Symptomatic
Patients (Duke Database)

Each value represents the percentage with significant CAD. The first is the percentage for a
low-risk, mid-decade patient without diabetes mellitus, smoking, or hyperlipidemia. The second
is that of a patient of the same age with diabetes mellitus, smoking, and hyperlipidemia. Both
high- and low-risk patients have normal resting ECGs. If ST-T-wave changes or Q waves had
been present, the likelihood of CAD would be higher in each entry of the table.
 The goals of therapy
Alleviate symptoms
Delay or prevent the progression of coronary
artery disease
Decrease the risk of adverse outcomes such as
death, heart failure, or myocardial infarction
 Comprehensive Management
1. Identification and treatment associated diseases that
can precipitate or worsen angina and ischemia
2. Reduction of coronary risk factors
3. Application of pharmacologic and nonpharmacologic
interventions for secondary prevention, with
particular attention directed to adjustments in
lifestyle
4. Pharmacologic management of angina
5. Revascularization by catheter-based percutaneous
coronary intervention (PCI) or by coronary artery
bepass grafting (CABG)
Reduction of Coronary Risk factors
Hypertension
Diabetes
Cigarette smoking
Mangement of dyslipidemia
Exercise
Obesity
Inflammation
Counceling and Changes in lifestyle
Medical Management of Patients with sCAD
Pharmacological treatments in sCAD patients
Pharmacological treatments in sCAD patients
(Cont.)
Treatment in patients with microvascular angina
 Acute Coronary Syndrome
Unstable Angina Pectoris (UAP)
Non ST segment Elevation Myocardial
Infarction (NSTEMI)
ST segment Elevation Myocardial
Infarction (STEMI)
 ACUTE CORONARY SYNDROMES
ETIOLOGY

Atherosclerotic plaque rupture *

inflammation
thrombosis
Vasospasm
Dissection
Decreased oxygen delivery (e.g.
anemia,hypotension)

Increased oxygen consumption (e.g. sepsis,

thyrotoxicosis)
 ACUTE CORONARY SYNDROMES
PATHOPHYSIOLOGY
atheromatous plaque with a large, soft lipid rich core
enveloped eccentrically within the coronary intima
contained on the luminal surface by a thin fibrous
cap

core possesses lipid laden monocytes and macrophages

that produce large amounts of tissue factor, a potent
procoagulant

rupture occurs at the shoulder (the junction of the

plaque and normal endothelium)
 ACUTE CORONARY SYNDROMES
PATHOPHYSIOLOGY
exposed tissue factor complexes with factor VIIa which in turn
promotes generation of factor Xa and the production of large
amounts of thrombin

circulating platelets are activated by exposure to collagen, von

Willebrand factor, thrombin

adenosine diphosphate, thromboxane A2 and prostacyclins,

released by damaged endothelium, contribute to platelet
activation and induce vasospasm
 ACUTE CORONARY SYNDROMES
PATHOPHYSIOLOGY

activated platelets bind to one another by cross-linking

fibrinogen to their surface glycoprotein receptors

the activation, adhesion and aggregation of platelets and the

activation of the clotting cascade results in an occlusive
thrombus

thrombus may partially or fully occlude a vessel lumen

precipitating myocardial ischemia +/- necrosis
ACUTE CORONARY SYNDROMES
 Symptoms
Great anxiety/Fear
Fixation of the body
Pale, ashen, or livid face
Dyspnea (SOB) may be associated
Nausea
Diaphoresis
BP usually up during attack
Dysrhythmia may be present
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 Diagnosis

Cardiac Chest pain

ECG changes
Elevated Cardiac enzymes
 THE ELECTROCARDIOGRAM
12 lead EKG
Cornerstone of initial evaluation
Within 10 minutes of presentation
Previous EKG tracings
Compare
Serial EKGs
Essential
THE ELECTROCARDIOGRAM
1. ST segment elevation 2mm (2 contiguous leads),
new LBBB, true posterior ischemia
STEMI

2. ST depression >1mm, marked symmetrical T wave

inversions >2 mm, dynamic ST-T changes with
pain
UA/NSTEMI LIKELY

3. Non-diagnostic or normal ECG

ACS LESS LIKELY
RISK STRATIFY
 THE ELECTROCARDIOGRAM
INFARCT LOCATION

II, III, AVF : Inferior

V1 - V4 : Anteroseptal
I, aVL : High lateral
I, aVL, V5-V6 : Lateral
I,aVL, V1-V6 : Extensive anterior
V1-V2 tall R, ST depression : True posterior
 ELECTROCARDIOGRAM
Extensive anterior infarction
ELECTROCARDIOGRAM
Inferior infarction
 Cardiac Enzyme Marker

Cardiac Initial Mean time Time to

enzyme elevation to peak return to
Marker after AMI elevations baseline
Myoglobin 1-4hr 6-7hr 18-24hr
CTnI 3-12hr 10-24hr 3-10 day
CTnT 3-12hr 12-48hr 5-14 day

CKMB 4-12 hr 10-24hr 2-3day

TCK 2-6 hr 4.7hr(3-5) 72hr(50-96)
 KILLIP SCORE
SEVERITY CLASS LV FUNCTION IN AMI

I No crackles, no S3

IIa Crackles < 50 % lung fields,

no S3
IIb Crackles < 50 % lung fields,
S3 present
III Crackles > 50 % lung fields,
pulmonary edema
IV Cardiogenic Shock
Management of ACS
 AGENTS USED IN ACS

WHY

WHEN

HOW

PRECAUTIONS
 THE EVIDENCE
Level of Evidence Grading

A Well designed, randomized,

controlled trials OR meta-analyses
involving large number of patients

B Smaller radomized trials OR reviews

of observational, retrospective or
nonrandomized trials

C Expert consensus, primary

nonrandomized OR observational
data
 THE EVIDENCE
Class I Evidence or general agreement that
a specific procedure or treatmetn is
useful and effective
Class II Conflicting evidence or divergence of
opinion about the utility or efficacy of
a procedure or treatment

II a Weight of evidence or opinion is in

favour of utility-efficacy

II b Utility-efficacy is less well

established by evidence or opinion

Class III Evidence or general agreement that

a specific procedure or treatment is
neither useful n effective and may be
harmful
 AGENTS USED IN ACUTE CORONAY SYNDROMES
OXYGEN
Level C evidence

WHY
Increase supply to ischemic tissue
WHEN
Suspect ACS
HOW
Start with nasal cannula at 4L/min
PRECAUTIONS
COPD
 AGENTS USED IN ACUTE CORONAY SYNDROMES
ASPIRIN
Class I, Level A evidence

WHY
Mortality reduction
Blocks synthesis of thromboxane A2
Inhibits platelet aggregation
Relaxes arterial tone
WHEN
Suspected ACS
HOW
160 mg chewed slowly, then 81-325 mg daily or pr
CONTRAINDICATION
True allergy
No GI tract !
 AGENTS USED IN ACUTE CORONAY SYNDROMES
NITROGLYCERINE
Level C evidence
Does not reduce mortality
WHY
Decreases ischemic pain
Venodilation/decreased preload
Dilates coronary arteries (eliminates vasospasm)
Increases coronary collateral flow
WHEN
Ischemic chest pain
For 24-48 hr after AMI
Recurrent pain
Hypertension
CHF
 AGENTS USED IN ACUTE CORONAY SYNDROMES
NITROGLYCERINE
HOW
Sublingual
Tablets: 0.3mg q 5 minutes
Spray: 0.4 mg q 5 minutes
IV Infusion
Start 10-20 mcg/min
Increase by 5-10 mcg/min q5-10 minutes
PRECAUTIONS
Avoid hypotension
Extreme caution with RV infarction
Interaction with sildenafil (Viagra)
 AGENTS USED IN ACUTE CORONAY SYNDROMES
MORPHINE
WHY Level C evidence

Reduce ischemic pain

Reduce anxiety
Reduce extension
Reduction of sympathetic tone and oxygen demands
WHEN
Ongoing pain of infarction
Acute pulmonary edema
SBP > 90 mmHg
 AGENTS USED IN ACUTE CORONAY SYNDROMES
MORPHINE
HOW
Small increments IV
5 mg prn, to eliminate pain
PRECAUTIONS
Allergy
Nausea and vomiting
Hypotension
Respiratory depression
 MANAGEMENT NSTEMI ACS

PRESENTATION TREATMENT
Prolonged/recurrent pain ASA
>2mm ST depression Clopidogrel
Positive cardiac markers Unfractionated Heparin/LMWH
Hemodynamic instability Eptifibatide
Refractory ischemia Urgent coronary angiography
Urgent revascularization

Can. J Cardiol. 18(11), 2002

 MANAGEMENT STEMI

Urgent reperfusion:

FIBRINOLYSIS
Streptokinase
Tenecteplase (TNK-tPA)
Reteplase (rPA)
Alteplase (tPA)
PERCUTANEOUS CORONARY INTERVENTION (PCI)
Coronary Artery Bypass Grafting (CABG)
 CONTRAINDICATIONS TO THROMBOLYSIS

CONTRAINDICATIONS
ABSOLUTE:
Lack of clear indications
Active internal bleeding
Recent trauma, major surgery, internal bleeding (within
2weeks)
Suspected aortic dissection
Pericarditis
Previous hemorrhagic stroke
Other strokes within one year
Known intracranial neoplasm
 CONTRAINDICATIONS TO THROMBOLYSIS

RELATIVE:
Recent trauma, major surgery, internal bleeding (2-4 weeks)
Severe uncontrolled hypertension (> 180/110 mmHg)
Current use of anticoagulants (INR > 2-3)
Intracerebral pathology (other than stroke)
Known bleeding diathesis
Active peptic ulcer disease
Pregnancy
Noncompressible vascular punctures
Known hypersensitivity to agent
Age > 75 years
Prolonged (> 10 minutes) traumatic CPR
Percutaneous Coronary Intervention
(PCI)
Percutaneous Coronary Intervention
(PCI)
Percutaneous Coronary Intervention
(PCI)
CABG
THANK YOU !!!