Coronary Artery Disease

By: Huson Amin

cardiovascular disease and

coronary heart disease
cardiovascular disease ( CVD, heart and
circulatory disease)
all diseases of the heart and blood vessels
(e.g stroke, congenital heart defects, valvular
heart disease, peripheral arterial disease)

coronary heart disease (CHD, ischaemic

heart disease)
disease of the coronary arteries due to
atherosclerosis

the coronary arteries

atherosclerosis
Atheroma

Artery wall

Blood within
the artery

Atheroma
(fatty deposits)
building up

Fat deposits develop,

restricting blood flow
through the artery

coronary artery with

atheroma
Coronary Artery
with atherosclerosis
Coronary Artery

Atheroma

atheroma
Atheroma (fatty layer)

Cross Section

Longitudinal Section

angina and heart attack

angina
narrowed coronary
artery
tightness or ache in
the chest,
breathlessness, sick
feeling, dizziness
comes on with
exertion or emotion
goes away with rest
- usually 2-10 mins

heart attack
due to sudden
blockage of the
coronary artery
chest pain like a
band, indigestion,
breathlessness,
sickness, looking pale
comes on at any time
doesnt go away - if still
there in 15 minutes call
999

clarifying some terms

Heart failure
the pumping action of the heart is less efficient,
possibly caused by raised blood pressure, heart
attack, or valve defect

Heart attack (myocardial infarction)

a coronary artery is suddenly blocked by a blood clot

Cardiac arrest
the heart stops beating when it quivers or fibrillates
causing the person to collapse

Stroke
an artery leading to the brain is suddenly blocked with
a blood clot or a bleed

main risk factors for

coronary heart disease

smoking
inactivity
obesity and overweight
high blood pressure
raised blood cholesterol
diabetes
family history of coronary heart disease
excessive alcohol intake

SIGNS & SYMPTOMS

Chest pain (Angina pectoris)
Myocardial infarction
Diaphoresis
Ecg changes
Dysarrithmias
Chest heaviness
Dyspnea
Fatigue

ANGINA PECTORIS
Angina pectoris is a clinical syndrome
usually characterised by paroxysms of
pain or pressure of anterior [Link]
cause is usually insufficient blood flow

TYPES
Stable angina
Predictable consistent pain that occurs in
exertion and is relieved by rest
Unstable angina
Also called preinfarction angina
Symptoms occur frequently and last longer than
stable angina
Pain may occur at rest

 Variant angina
Also called prinzmentals angina.
Pain at rest with reversible ST segment
elevation thought to be caused by
coronary artery vasospasm
Microvascular angina
Patient have chest pain but do not seem
to have any blockage in coronary artery
The pain may be due to tiny vessels that
feed heart,arm and neck are not working
properly

 Silent ischemia
Objective evidence of ischemia (such as
electrocardiographic changes with a stress
test) but patient report no symptoms

ANGINA PAIN FEATURES

Squeezing burning tightening aching
across chest usually starting behing
breast bone.
The often spread to
neck,jaw,arms,shoulders,throat,back,or
even teeth
Attack of stable angina last for 1 5
minutes

Stable CAD
Acute Coronary Syndromes
Unstable angina

Non-ST Elevation MI
(Non-Q-wave MI)

ST-Elevation MI
(Q-wave MI)

The continuum of acute coronary syndromes ranges from unstable

angina, through non-ST-elevation myocardial infarction (also referred
to as non-Q-wave myocardial infarction [MI]), to ST-elevation MI (also
referred to as Q-wave MI).

Triggers to Plaque Rupture

Inflammatory
cytokines

Vulnerable
Plaque

Plaque Rupture

Physical Stress

Emotional
Stress

Causes of Acute Coronary

Syndromes
Atherosclerosis with superimposed thrombus
Vasculitic syndromes
Coronary emboli (e.g., from endocarditis, artificial valves)
Congenital anomalies of the coronary arteries
Coronary trauma or aneurysm
Severe coronary artery spasm (primary or cocaine-induced)
Increased blood viscosity (e.g., polycythemia vera,
thrombocytosis)
Significantly increased myocardial oxygen demand (e.g.,
aortic stenosis)

Unstable Angina
Prior stable angina

in:

Frequency
Duration
Intensity

Angina at rest previously

only on provocation
New onset angina

Acute Myocardial Infarction

History and exam
EKG changes
Serum markers

Symptoms
Pain
Sympathetic response
Parasympathetic response
Inflammatory response

Pressure
Burning (hot)
Chest/arms/jaw/back

Sweats
Tachycardia
Cool, clammy skin

Nausea
Vomiting
Weak

Mild fever

Other

Dyspnea
Asymptomatic

Physical Findings
Inspection
BP

- often increase anterior MI

- often decrease inferior MI

HR

- often increase anterior MI

- often decrease inferior MI

Diagnosis of ACS
Unstable Angina

Myocardial Infarction
NSTEMI

Typical symptoms

STEMI

Crescendo, rest, or new

Prolonged crushing chest pain, more

onset severe angina

severe and wider radiation than usual angina

Serum biomarkers

No

Yes

Yes

ECG initial findings

ST depression and/or

ST depression and/

ST elevation (and Q

T wave inversion

or T wave inversion

waves later)

NSTEMI, non-ST-elevation myocardial infarction (MI); STEMI, ST-elevation MI

Lilly. Pathophysiology of Heart Disease, 4th Ed. Lippincott Williams, 2007. Page 182

Lilly. Pathophysiology of Heart Disease, 4th Ed. Lippincott Williams, 2007. Page 182

Serum Markers of
Myocardial Infarction
Myocardial necrosis causes sarcolemma
disruption
Intracellular macromolecules are released
Can be measured by serial blood testing
Pattern and level of rise correlates with
timing and size of MI

Cardiac-Specific Troponins
Regulatory protein that controls interaction
between actin & myosin
3 subunits: TnC, I, T

Skeletal &
cardiac muscle

Unique cardiac troponins I and T exist - absent in

serum of healthy people
Powerful marker of myocyte damage
Rise at 3-4 hours post-MI, peak 18-36 hrs,
decline slowly 10-14 days

Creatinine Kinase
Enzyme that converts ADP to ATP
Found in many tissues: heart, brain, skeletal
muscle, kidney, etc.
Can be elevated after injury to any of these
tissues
3 isoenzymes:

- CK-MM
- CK-MB
- CK-BB

CPK-MB
Makes up 1-3% of skeletal CK
Makes up much higher % of cardiac CK
Rises 4-8 hours after MI, peaks by 24 hours
Returns to normal in 48-72 hours

Treatment of Acute
Coronary Syndromes:
STE vs. Non STE

Treatment of Acute Coronary

Syndromes
Anti-ischemic therapies

-blocker
Nitrates
+/- Calcium channel blocker

General measures:

Pain control (morphine)

Supplemental O2 if needed

Antithrombotic therapies
Antiplatelet agents:

Anticoagulants (use one):

Adjunctive therapies:

Aspirin
Clopidogrel (or prasugrel)

LMWH (enoxaparin)
Unfractionated intravenous heparin
Fondaparinux
Bivalirudin (should be used in ACS
patient only if undergoing PCI)

Statin
Angiotensin converting-enzyme inhibitor

Treatment of Acute Coronary

Syndromes
ST-Elevation
(STEMI)

Non-ST-Elevation
(UA and NSTEMI)

Emergent PCI available

within 90 min?

Risk Assessment
(e.g., GRACE Score)

No
Fibrinolytic
Therapy

(e.g., tPA)

Yes
Primary PCI

Low
Conservative
Strategy
(Proceed to cardiac cath
only if recurrent angina
or predischarge
stress test is markedly
positive)

High
Invasive
Strategy
(Cardiac cath
leading to
PCI or CABG)

Nitrates
Reduce ischemia (not mortality)
Venodilation:

R heart return

Coronary vasodilation
Usually given SL then IV

Beta Blockers

Sympathetic drive; HR & BP

O2 demand

Shear stress

Sudden death, death, recurrent MI

Non Dihydropyridine
Calcium Channel Blockers

Heart rate

Vasodilate
Relieve ischemia, not mortality
Dont give in patients with sx/signs
of heart failure

Non - STE ACS:

Conservative vs. Early
Invasive Approach

Early Invasive
Urgent catheterization performed after
initial medical Rx
Allows rapid identification & Rx of
critical CAD
More PCI/CABG

Acute Treatment: STE MI

Reperfusion: Thrombolysis vs. PTCA
ASA
O2
Beta blockers
Nitrates
ACE inhibitors
Morphine
Anticoagulants

Additional Rx: STE MI

Maintain vessel patency
Restore balance between 02 supply
and demand
Relieve chest pain
Prevent complications

Aspirin
Reduces mortality & reinfarction
Give immediately on presentation
and daily thereafter
If aspirin allergy, use clopidogrel

Heparin
Give 1-2 days IV after PCI or lysis with tPA, rPA,
or TNK-tPA NOT SK
Also if:

Atrial fibrillation

LV thrombus

New anterior MI with large wall motion change

All others: SQ heparin while at bed rest to

prevent DVT

- Blockers

Risk arrhythmia, reinfarction, rupture,

death

Give IV, then orally unless contraindication

exists (asthma, hypotension, significant
bradycardia)

Nitrates
Reduce pain/ischemia
Relieve pain
Reduce pulmonary congestion in
heart failure

ACE - Inhibitors
Limit adverse LV remodeling

Heart failure/death

MI

Benefit additive ASA, BB

Esp. benefit anterior MI and/or LV
dysfunction

Statins
Reduce reinfarction, death
More benefit when started early
Give if LDL cholesterol is > 100

Acute MI: Complications

Recurrent ischemic/reinfarction
Arrhythmias
Myocardial dysfunction
Mechanical complications
Pericarditis
Thromboembolism

Complications of MI
Myocardial Infarction
Ventricular
thrombus
Embolism

Contractility

Cardiogenic
shock
Ischemia

Electrical
instability
Arrhythmias

Tissue
necrosis

Pericardial
inflammation
Pericarditis

Hypotension

Coronary
perfusion
pressure

Papillary Ventricular Ventricular

muscle
septal
rupture
infarction/
defect
ischemia
Mitral
regurgitation
Congestive
heart failure

Cardiac
tamponade

Standard Discharge Rx

3 to 5 day length of stay

ASA; clopidogrel
Beta blocker
ACE for CHF; LVEF < 40%, perhaps all
Warfarin as noted
Cardiac Rehab
PRN Nitrates
Exercise prescription
Low fat diet
Smoking Cessation
Statin if LDL cholesterol > 100 mg/dl