The function of the heart is to circulate blood

throughout the body by:

Pumping blood through the lungs removes carbon dioxide

and refreshes the blood with oxygen
The oxygenated blood is pumped to the body to provide
oxygen and nutrients and to remove waste products.
The coronary arteries are the blood vessels that supply blood
and oxygen to the heart muscle.

Blood Supply To The Heart

2 coronary arteries branch
from the main aorta just
above the aortic valve. No
larger than drinking straws,
they divide and encircle the
heart to cover its surface
with a lacy network that
reminded physicians of a
slightly crooked crown
(coronary comes from the
Latin coronarius, belonging
to a crown or wreath). They
carry out about 130 gallons
of blood through the heart
muscle daily. (Clark, 119)

can, and
does, occur in almost any artery in the
body. But in the heart its effects can be
crucial. The body depends on a strong
pumping heart to circulate life-giving
blood, and this includes to the heart
muscle itself. If the coronary arteries
become blocked, the cardiac muscle
begins to fail, and so the blood circulation
decreases, which includes the circulation
to the heart muscle itself. (Thibodeau,
494)

Coronary Artery Disease

Coronary artery disease is one of the most common
and serious effects of aging. Fatty deposits build up
in blood vessel walls and narrow the passageway for
the movement of blood. The resulting condition,
called atherosclerosis often leads to eventual
blockage of the coronary arteries and a heart
attack.

Cardiovascular disease claimed 39.4 percent of all

deaths or 1 of every 2.5 deaths in the United States in
2000. CVD was about 60 percent of total mention
mortality. This means that of over 2,400,000 deaths
from all causes, CVD was listed as a primary or
contributing cause on about 1,415,000 death certificates.
(American Heart Disease)

IHD: Pathophysiology
Oxygen supply decreases due to :
a. Atherosclerotic plaque obstruction

< 50 % autoregulatory mech to preserve

coronary blood flow and ischemia
50-70 % autoregulatory mech may be
insufficient, angina with extreme exertion may
be developed
> 70 % autoregulatory mech cant
compensate, angina with minimal exertion ma
y be developed
> 80-85% autoregulatory mech is depleted,
rest angina may occur

IHD: Pathophysiology
b. Coronary Vasospasm : prinzmetal or
variant angina
c. Mixed atherosclerotic diseases and
coronary spasm
d. Platelet activation occurs in
response to
plaque formation, plaque rupture,
endothelial damage
which lead to thrombus formation,
unstable angina or acute MI

IHD: Pathophysiology
OTHER FACTORS:
Increased O2
demand

Tachycardia
Hypertension
Anxiety
LVH
Aortic stenosis
Hyperthyroidism
Exertion
Volume overload

Decreased O2
supply

Atherosclerosis
Hypoxemia
Anemia
LVH
Aortic stenosis

IHD: Clinical Manifestations

More common in men between 30-60 y.o.a.
Balance between men/women at >60 y.o.a.
Men often present with MI
Women often present with angina
May present as:

Chronic stable angina

Silent ischemia
Variant or Prinzmetals Angina
Acute Coronary Syndrome : unstable angina,
acute MI

Signs and Symptoms

Chest
Pain

None

Signs &
Symptoms

Shortness
Of Breath

Heart
Attack

None: This is referred to as silent

ischemia. Blood to your heart may
be restricted due to CAD, but you
dont feel any effects.
Chest pain: If your coronary
arteries cant supply enough
blood to meet the oxygen
demands of your heart, the result
may be chest pain called angina.
Shortness of breath: Some people
may not be aware they have CAD
until they develop symptoms of
congestive heart failure- extreme
fatigue with exertion, shortness
of breath and swelling in their
feet and ankles.
Heart attack: Results when an
artery to your heart muscle
becomes completely blocked and
the party of your heart muscles
fed by that artery dies.

ANGINA
Transient discomfort in the:
-Chest
-Shoulder
-Arm
-Back
Aggravated by:
-Exertional stress
-Emotional stress
Relieved by:
-Nitroglycerin
-Rest

ANGINA: Clinical Characteristics

Quality
Pain/discomfort described as: heavy,
suffocating
Burning sensation
SOB
Gradual increase/decrease in intensity

Location
Near the sternum
Limited to left shoulder and arm

ANGINA: Clinical Characteristics

Radiation
Left shoulder and arm
Jaw
Occasionally right arm

Precipitating factors
Exercise, Cold environment, Eating,
Walking against wind or after large
meal, Emotional factors,

ANGINA: Clinical Characteristics

Duration
30 sec - 30 min

Response to nitroglycerine (NTG)

Pain relief within 45 sec - 5 min

High blood cholesterol

High blood pressure
Smoking
Obesity
Lack of physical activity

Risk Factors
Uncontrollable
Sex
Hereditary

Controllable
High blood
pressure

Race

High blood
cholesterol

Age

Smoking
Physical activity
Obesity
Diabetes
Stress and anger

Evaluation
Patients history
Lipid profile
BP & HR
Stress test
Treadmill test (TMT)
Dobutamine stress echocadiogram (DSE) :
ejection fraction, LV function abnormality
EKG
T-wave inversion
ST depression
ST elevation
Coronary angiogram (cardiac cath)

Blood tests: used to evaluate kidney and

thyroid function as well as to check
cholesterol levels and the presence of
anemia.
Chest X-ray: shows the size of your heart and
whether there is fluid build up around the
heart and lungs.
Echocardiogram: shows a graphic outline of
the hearts movement
Ejection fraction (EF): determines how well
your heart pumps with each beat.

Ischemic Coronary Syndromes

Acute Coronary Syndromes
Angina Pectoris
Unstable Angina
Acute Myocardial Injury
Acute Myocardial Infarction
Presentation with suspected ischemia
Non-diagnostic ECG
ST segment depression
ST segment elevation/New BBB

Ischemic Coronary Syndromes

Angina Pectoris
Acute pain, usually in the chest,
resulting from an increased
demand for oxygen and a
decreased ability to provide it
Usually due to a partially
occluded coronary artery or
vasospasm

Ischemic Coronary Syndromes

Angina Pectoris
Typical Presentation
Squeezing, Crushing, Heavy, Tight
Fist to chest = Levines sign

Pain/Discomfort may radiate to shoulders,

arms, neck, back, jaw or epigastrium
Usually lasts 3-5 min and rarely exceeds
15 min
Not changed by swallowing, coughing,
deep breathing or positional changes

Ischemic Coronary Syndromes

Angina Pectoris
Typical Presentation
Anxiety
Diaphoresis or clammy skin
Nausea, vomiting
Shortness of breath
Weakness
Palpitations
Syncope

Ischemic Coronary Syndromes

Angina Pectoris
Usually Provoked by:
Exercise
Eating
Emotion/Stress

Usually Relieved by:

Rest; Removal of provoking factor
Nitroglycerin

Ischemic Coronary Syndromes

Stable Angina Pectoris
Reasonably Predictable
frequency, onset, duration
Relief predictable with rest,
nitroglycerin

Ischemic Coronary Syndromes

Stable Angina Pectoris
Treatment Goals
Reduce myocardial oxygen demand
Improve myocardial oxygen suppl
Prophylaxis against recurrent episodes
Control and modify risk factors

Ischemic Coronary Syndromes

Stable Angina Pectoris
Treatment
Physical/Psychological rest
Position of comfort, sitting or supine
Oxygen
ECG Monitor
Assess the underlying rhythm

Nitroglycerin, 0.4 mg SL q 5 min as long as

BP > 90 mm Hg
Continue until pain relieved or contraindicated

The ABCs of Stable Angina

Ischemic Coronary Syndromes

Stable Angina Pectoris
Transport Considerations
Many persons stay home and treat
themselves
Treat first-time angina, unstable angina or
angina requiring more than 3 NTG (>15
min) as AMI
When in doubt, treat as AMI

Ischemic Coronary Syndromes

Stable Angina Pectoris
Variant Angina (Prinzmetals
Angina)
Occurs at rest
Episodes at regular times of day
Results from coronary vasospasms
Treated long term with calcium channel
blockers
May result in abnormal 12 lead ECG changes
that resolve with minimal treatment

Ischemic Coronary Syndromes

Unstable Angina
Prolonged chest pain/ischemic
symptoms or an atypical
presentation of angina without ECG or
laboratory evidence of AMI (Injury)
Usually associated with significant or
progressing occlusion of a coronary
artery or severe vasospasm
Considered Pre-infarction Angina

Ischemic Coronary Syndromes

Unstable Angina
May have Typical or Atypical Signs &
Symptoms
Atypical Presentation
Increased frequency or duration of
episodes
Onset with less exertion than normal
Increased severity of symptoms
Requires greater number of NTG tablets to
relieve symptoms

Ischemic Coronary Syndromes

Unstable Angina
Treatment same as Angina PLUS:
IV, NS (no dextrose), TKO
Some exceptions to restricting fluid

12 Lead ECG
Assess for RVI

Morphine sulfate, 2 - 4 mg q 5-15 min slow IV

titrated to pain relief and BP > 90
Aspirin, 160-325 mg PO
Chewed & swallowed if possible
Determine if hypersensitive to ASA

Ischemic Coronary Syndromes

Unstable Angina
Treatment
Metoprolol, 5 mg slow IV q 5 min to 15 mg total,
prn for HR/BP in absence of contraindications
In longer or interfacility transports, consider:
Nitroglycerin IV infusion, 10-20 mcg/min
Heparin
GP IIB/IIIA inhibitors

Thrombolytics Checklist (just in case)

Transport, destination?

Ischemic Coronary Syndromes

Acute Myocardial Injury
Presentation of Unstable Angina or
Acute Ischemia with potential for
myocardium salvage (penumbra)
Diagnostic evidence of Injury (ECG or
elevated Enzymes)
Does not necessarily imply necrosis of the
myocardium
Presentation, Signs and Symptoms are the same
as Acute MI

Ischemic Coronary Syndromes

Acute Myocardial Infarction (AMI)
Necrosis of myocardial tissue caused by a
lack of oxygenation and blood flow
resulting from an occluded coronary artery
Often also used to describe acute injury
when extent of necrosis is unknown but
imminent
Diagnostic evidence of injury is present
(elevated enzymes and possibly ECG)

Ischemic Coronary Syndromes

Acute Myocardial Infarction
(AMI)
Precipitating Factors
Coronary thrombosis (most common)
Coronary vasospasm
Microemboli
Severe Hypotension/Shock
Acute Hypoxia
Acute Volume Overload

Ischemic Coronary Syndromes

Acute Myocardial Infarction
(AMI)
Location, size of infarct and
severity depends on site of vessel
occlusion
majority involve left ventricle
LCA
anterior, septal, lateral

RCA
inferior, right ventricle

Ischemic Coronary Syndromes

Acute Myocardial Infarction
(AMI)
Often defined further as
subendocardial: involves only
subendocardial muscle
transmural: full thickness of ventricular
wall involved

Evolution of AMI
Anatomy of Plaque Disruption
Shoulder region
Lipid core
Media

Lumen

Lumen
Lipid core

Fibrous cap

Vulnerable Plaque
Thin, friable fibrous cap
separating substantial
thrombogenic lipid core
from blood

Stable Plaque
Thick fibrous cap
protecting thrombogenic
lipid core from blood
More luminal narrowing

Lumen could be well preserved

Ada pte d from Libby P . Circulat ion. 1995;9 1:2844- 2850, w ith permission.

Evolution of AMI
Plaque Rupture, Stenosis, and Thrombosis
Plaque rupture
intraplaque thrombus
Mural
thrombus
Occlusive
thrombosis

Total chronic
occlusion

Recanalized
lumen

Healed plaque
increased
stenosis

Healed plaque
decreased stenosis
Ada pte d from Davies MJ . In: Schla nt RC, Alexander RW, eds. The Heart, Arteries
and Ve ins. 8th ed. 1994:1 009-102 0, with permission.

Evolution of AMI
Plaque Rupture and Thrombus Progression
Complete
occlusion

Lysis and residual

thrombus

Disease
progression

AMI
Lipid- Plaque
rich disruptio
plaque
n

Reocclusion

Unstable
angina
Thrombus

Partial (labile) occ lusion Recurrent pain

Ada pte d from Fus ter V. N Engl J Med. 199 2;326:2 42-250 , with perm iss ion.

Coronary Artery Without Evidence of

Plaque

Source: University of Utah WebPath

Coronary Artery with Significant

Plaque Formation
In addition
to reduced
Lumen
size, there
is also a
calcified
portion
(right side
of photo)

Source: University of Utah WebPath

Coronary Artery with Significant

Plaque Formation

Source: University of Utah WebPath

Rupture of Atheromatous Plaque

Results in Thrombus Formation

Rupture of Vulnerable plaques soft

lipid core is the initiating event in most
acute ischemic coronary events
Occlusion is dependent on clot formation
and and accompanying fibrinolysis
A thrombotic occlusion that is relatively
persistent (i.e., 2 to 4 hours or longer)
may result in acute myocardial infarction

Rupture of Atheromatous Plaque

Results in Thrombus Formation
Repeated thrombus formations may
further decrease the lumen size
Intermittent non-occlusive thrombus
formation results in Unstable Angina
Incomplete occlusion may also
result in MI possibly due to coronary
artery spasm

Coronary Artery With Plaque and

Thrombus Formation
A - Coronary
Artery crosssection
B - Lumen
C - Fissured
Plaque w/o
Cap
D - Acute
thrombus
Source: Emergency Cardiovascular Care Library (CD-ROM), American Heart Association, Dallas 1997

Plaque and Thrombus Formation

Resulting in Occlusion

Source: University of Utah WebPath

Coronary Artery Thrombus

The
external
anterior
view of the
heart
shows a
dark clot
formation
in this
artery
Source: University of Utah WebPath

Evolution of Infarction/Necrosis
Coronary Artery Occlusion:
The Evolution of Infarction
Progression of myocardial necrosis with time since occlusion
30 min

4h
Normal
myocardium

Normal
myocardium

At risk
myocardium,
ischemic but viable
Necrosis starting
subendocardially

6 - 12 h
Normal
myocardium

At risk
myocardium,
ischemic but viable

Necrosis extending
towards
subepicardium

Completed infarct
involving whole area
at risk

Ada pte d from Sa ltissi S , Mushahwar S S. Postgrad Med J. 1995;71 :534-54 1, with permission.

Ischemic Coronary Syndromes

Acute Myocardial Infarction (AMI)
Presentation
Similar to Angina but

Last longer
Not easily relieved with rest or NTG
Sx/Sx may be more severe (feeling of impending doom)
Pain often radiates to arms, neck, jaw, back, epigastrium

Some present atypically with complaints of only

weakness or shortness of breath
Dysrhythmias
Sudden Cardiac Death

Ischemic Coronary Syndromes

Acute Myocardial Infarction (AMI)
Presentation
10-20% have silent MI (no chest pain)
common in elderly, older women, diabetics

If adding chest pain to the patients list of Sx/Sx

completes a clear picture of AMI, then the patient is
having an AMI!!
Vital Signs and monitoring ECG leads DO NOT
provide DIAGNOSTIC evidence of AMI!!
Clinical diagnosis in absence of 12 Lead ECG or
Enzyme changes

Therapies
Goals for AMI Therapy
Shorten time to reperfusion

Preserve
LV function

Avoid heart failure

or cardiac shock

Limit
Infarct Size

REDUCE MORTALITY
IMPROVE OUTCOME

Yusuf, et al. Circulation. 199 0;82(suppl II):II-11 7-134.

Schroder R. e t al. J Am Coll Cardiol. 1995;2 6:1657- 1664

Resolve
ST-segment
elevation

Ischemic Coronary Syndromes

Acute Myocardial Infarction
(AMI)
Treatment Goals
Decrease myocardial oxygen demand
Remove physical/psychological stressors
Relieve pain
Reduce workload of the heart (BP, HR)

Inhibit further clot formation

Rapid identification/diagnosis
Transport for reperfusion therapy

Ischemic Coronary Syndromes

Acute Myocardial Infarction (AMI)
Treatment same as Angina PLUS:
IV, NS, large bore

TKO with some exceptions

No dextrose containing solutions
Fluid boluses appropriate in some cases
2nd line if time permits
Minimize number of attempts

12 Lead ECG
Diagnostic evidence of AMI present
Assess for RVI

Ischemic Coronary Syndromes

Acute Myocardial Infarction
(AMI)
Treatment
Morphine sulfate, 2 - 4 mg q 5-15 min slow IV
Maintain BP > ~ 90 mm Hg
Titrated to Pain relief
Reduce PVR and workload on the heart

Aspirin, 160-325 mg PO
Chewed & swallowed if possible
Determine if hypersensitive to ASA

MONA greets all patients

Ischemic Coronary Syndromes

Acute Myocardial Infarction
(AMI)
Treatment
Metoprolol, 5 mg slow IV q 5 min to 15 mg total,
prn for HR/BP in absence of contraindications
In longer or interfacility transports, consider:
Nitroglycerin IV infusion
Heparin

Thrombolytics Checklist
Exclusions for thrombolysis

Ischemic Coronary Syndromes

Acute Myocardial Infarction
(AMI)
Treatment
Transport for reperfusion therapy;
Destination?
Thrombolysis vs Coronary Artery Catheterization
For patients with associated pulmonary edema,
hypotension or cardiogenic shock, consider
transport to facility with capability of
angiography & revascularization

Considerations for Fibrinolytics

Acute Ischemic Syndromes:
Diagnostic Considerations
Thrombolytics are not appropriate in all acute ischemic
syndromes
Not all acute ischemic syndromes are AMIs
ST-segment elevation suggests thrombic occlusion
and need for immediate reperfusion
No proven benefit of thrombolytic therapy in patients
without ST-segment elevation
Patients with ST-segment depression and/or T-wave
inversion are currently not candidates for thrombolytic
therapy

Contraindications for Fibrinolytics

Lack of diagnostic 12
Lead ECG changes
Chest pain < 20 min or
> 12 hours
Not oriented, can not
cooperate
History of stroke or TIA
Known bleeding
disorder
Active internal bleeding
in past 2-4 weeks

Surgery or trauma in
past 3 weeks
Terminal illness
Jaundice, hepatitis,
kidney failure
Use of anticoagulants
Systolic BP < 180 mm
Hg
Diastolic BP < 110
mm Hg

Ischemic Coronary Syndromes

Ischemic and injured tissue have reduced blood flow

but may be salvaged. The area of the Penumbra may
be viable for several hours after onset of occlusion.
Source: Emergency Cardiovascular Care Library (CD-ROM), American Heart Association, Dallas, 1997

Ischemic Coronary Syndromes

Sudden Cardiac Death (SCD or SCA)
Sudden, unexpected biologic death presumably
resulting from cardiovascular disease
Most common rhythm of SCA is Ventricular
Fibrillation
May be primary or secondary VF
Chain of Survival is the greatest determinant of
outcome
Treatment based on ECG rhythm & arrest events

Time is
Muscle!!!

 Many people are able to manage

coronary artery disease with
lifestyle changes and medications.
Other people with severe coronary
artery disease may need
angioplasty or surgery.

Treatment (continued)
1) Stenting
a stent is introduced into a blood vessel on a balloon
catheter and advanced into the blocked area of the artery
the balloon is then inflated and causes the stent to expand
until it fits the inner wall of the vessel, conforming to
contours as needed
the balloon is then deflated and drawn back
The stent stays in place permanently, holding the vessel
open and improving the flow of blood.

Treatment
(continued)

2) Angioplasty
a balloon catheter is passed through the guiding catheter to the
area near the narrowing. A guide wire inside the balloon catheter is
then advanced through the artery until the tip is beyond the
narrowing.
the angioplasty catheter is moved over the guide wire until the
balloon is within the narrowed segment.
balloon is inflated, compressing the plaque against the artery wall
once plaque has been compressed and the artery has been
sufficiently opened, the balloon catheter will be deflated and
removed.

Treatment (continued)
3) Bypass surgery
healthy blood vessel is removed from leg, arm or chest
blood vessel is used to create new blood flow path in your heart
the bypass graft enables blood to reach your heart by flowing
around (bypassing)
the blocked portion
of the diseased
artery. The increased
blood flow reduces
angina and the risk
of heart attack.

Get regular medical checkups.

Control your blood pressure.
Check your cholesterol.
Dont smoke.
Exercise regularly.
Maintain a healthy weight.
Eat a heart-healthy diet.
Manage stress.

Complication
Cardiomyopathy / Congestive
heart failure
Cardiac Arrthymia
Death

Anti-Anginal and Ant-Ischemic

Pharmacotherapy
Nitrates
Beta-blockers
Calcium-channel blockers
Goals of therapy:
Reduce symptoms of ischemia
Maintain or improve physical function
and quality of life

Nitrates
Mechanism of Action:
Metabolized to endogenous EDRF (nitric
oxide) which increase cGMP
smooth
muscle relaxation & vasodilation

Antianginal effect
Venodilation
decrease preload
(venous return), ventricular wall stress and
O2 demand
Coronary vasodilation improves blood flow
to the myocardium and relieves vasospasm

Nitrates: Clinical Effectiveness

SL NTG or NTG spray are
recommended for immediate relief of
angina
Relieves acute attacks and can be used
prophylactically prior to planned
exercise
All patients with angina should have RX for
SL NTG and education regarding its use

Nitrate-free period: 8-12 hours to

avoid tolerance

Nitrates: Clinical Effectiveness

Long-acting nitrates: initial therapy for
decreasing symptoms if BBs are
contraindicated or not tolerated
Long-acting nitrates: effective in
combination with BBs and CCBs
All long-acting nitrates: equally effective
Differ in dosing, ease of administration,
kinetics, and patient preference

Nitrates
Adverse Effects
Nitrate tolerance
Reflex tachycardia
:*combine with
drugs controlling HR
Headache
Most common,
usually subsides after
few days

Dizziness, presyncope
Worse with alcohol

Contraindications
Aortic valve
stenosis
Hypertrophic
obstructive
cardiomyopathy

Patient education

Beta-Blockers
Mechanism of action
Antagonize effect of catecholamine
by blocking beta receptor
reduce BP, HR and contractility
Decrease myocardial oxygen demand
Negative Inotropic

Beta-Blockers: Clinical Effectiveness

Decrease mortality in patients with h/o MI
1st-line therapy in the absence of
contraindications
Limit HR during exercise and delay or even
prevent the onset of angina during exercise
Target HR: 55-60 BPM or <50 in severe
angina
As effective as CCBs for angina
ISA is a potential disadvatage

Beta-Blockers
Adverse Effects

Bradycardia
Hypotension
Fatigue
Sexual
dysfunction

Contraindications
Absolute
HR<50 BPM, heart
block : AV block,
severe LV failure,
acute HF,
vasospastic angina

Relative
Asthma, COPD,
severe depression,
PVD, DM,
dyslipidemia

Beta-Blockers
Withdrawal symptom from
abruptly discontinuing therapy
AMI
Sudden death

Dose should be tapered over a

period of 2 weeks, if therapy is to b
e discharged.

Calcium-Channel Blockers
Mechanism of Action
Block calcium entry into myocardial and smooth
muscle cells=variable negative inotropic effects

Increases myocardial O2 supply by coronary

vasodilation -all agents
Decreases myocardial O2 demand by
reduce after load and preload- all agents
reduce heart contraction and HR- non DHP
group

Diltiazem/Verapamil Vs.
Dihydropyridines

Diltiazem and Verapamil (non-DHP)

Decrease AV-node conduction and can
decrease HR

Dihydropyridines: Amlodipine,
Nifedipine
No effect on AV-node conduction and
may result in reflex tachycardia

Calcium-Channel Blockers:
Clinical Effectiveness

Good choice for Prinzmetals angina

Monotherapy with short acting DHP is
generally avoided due to reflex
tachycardia
Equally as effective as BBs: initial
therapy when BBs are contraindicated
or if intolerable side effects to BBs
Effective in combination with BBs
when monotherapy is not successful

Calcium-Channel Blockers
Adverse Effects

Reflex tachycardia
Headache/flushing
Peripheral edema
Gingival
hyperplasia (N)
Hypotension
Bradycardia (D/V)
Constipation (V)

Contraindications
Heart Failure (D/V)
Bradycardia, heart
block ,AV block:
(D/V only)
CHF exarceration
(D/V)

Combination Therapy
Beta-blockers often combined with
nitrates or dihydropyridine CCBs
Diltiazem or verapamil often
combined with nitrates
Rarely used with beta-blockers but
some patients may benefit: monitor
heart rate

Combination therapy more

effective than either agent alone

Pharmacotherapy to Prevent
MI and Death
Antiplatelet Agents
Lipid-lowering Therapy
ACEIs

Pharmacotherapy to Prevent
MI and Death
Antiplatelet agents
Aspirin
81-325 mg daily is indicated for all patients
lacking contraindications / EC reduce GI irritation

Clopidogrel (Plavix)
75 mg daily for patients unable to take aspirin
Avoid: ticlopidine and dipyridamole

Ticlopidine
250 mg bid with food

Pharmacotherapy to Prevent
MI and Death
Lipid-lowering therapy

All patients with documented or

suspected CAD and LDL cholesterol
>130mg/dl Primary target LDL
<100mg/dl
1% decrease in TC = 2% decrease in
coronary risk
Statins reduce risk for ischemic
events ~30%

Pharmacotherapy to Prevent
MI and Death

Angiotensin Converting Enzyme

Inhibitors
All patients with CAD who also have
diabetes and/or LV systolic
dysfunction
All patients with CAD or other
vascular disease (Class IIa-level B)

Patient Education
Take an active role!
Educated patients are happier patients
Poor adherence = poor outcomes
Multi-disciplinary approach is strongly
encouraged by ACC/AHA

Unproven or harmful treatments

HRT for reducing CV risk in PM
women
Vitamin C and E supplementation
Chelation therapy
Garlic

Variant or Prinzmetals Angina

Nitrates are the mainstay of treating acute coronary artery
spasms
Calcium channel antagonists are the agents of choice for
variant angina
Beta-blockers should be avoided in vasospastic angina
Combination therapy with CCAs + nitrates or two CCAs from
different classes may be effective if monotherapy is not
effective.
All patients should be treated for acute attacks and maintained
on prophylactic treatment for 6-12 months following an initial
episode

Coronary Intervention
PTCA (percutaneous transluminal
coronary angioplasty)
CABG (Coronary Artery Bypass
Graft)

QUICK REVIEW
BBs: decrease oxygen demand
Nitrates: decrease oxygen demand and
increase oxygen supply
CCBs: decrease oxygen demand and
increase oxygen supply-D/V vs. DHP
Preventive therapy : ASA, lipid lowering
agents, ACEIs
ABCDE

QUICK REVIEW
LG is a 59 y.o. male with a PMH of HTN, mild
asthma, HL and CAD. Allergy: NKA. Current
meds include: lisinopril 10 mg QD, lovastatin 20
mg QD, atenolol 100 mg QD, albuterol inhaler
PRN, 0.4 mg NTG SL prn. BP=128/76;
pulse=60.
Since increasing the dose of
atenolol, he has noticed an increase in the use
of his albuterol. His anginal symptoms are well
controlled with his current regimen. Dr. Johnson
would like to know your assessment and
recommendations regarding LGs current
therapy.

QUICK REVIEW
A) Continue current therapy as there are no
other therapeutic options
B) Add isosorbide dinitrate 10 mg TID and
aspirin 81 mg QD
C) Gradually taper atenolol over the course of 12 weeks and add diltiazem CR 120 mg QD and
aspirin 81 mg QD
D) Add steroid inhaler due to increased use of
albuterol
E) Gradually taper atenolol over the course of 12 weeks and add isosorbide mononitrate ER 30
mg daily