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Coronary Artery Disease

Occluded of the coronary artery
Partial
Total
1 coronary artery and branches
Blood flow

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Left Coronary Artery

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Right Coronary Artery

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Global Burden of Cardiovascular

Disease
In 2002 : CVD contributed to
approximately a third of all global
deaths (17 million). 80% of burden is
in low and middle income countries.
By 2020 : CHD and Stroke will
become the leading cause of death
and disability worldwide. Mortality for
CVD will increase to 20 million.
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Worldwide Statistics
Each year:
> 4 million patients are admitted with
unstable angina and acute MI
> 900,000 patients undergo PTCA
with or without stent

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Risk Factors for cardiovascular

disease
Modifiable :
- Smoking
- Dyslipidemia (Raised LDL-C, Low
HDL-C, Raised triglycerides)
- Raised Blood pressure
- Diabetes melitus
- Obesity
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Risk factors for cardiovascular

disease
Non-Modifiable :
- Personal History of CVD
- Family History of CVD
- Age
- Gender

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Family History
Premature CHD
Men (first degree) < 55 years.
Women (first degree) <65 years.

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Serum lipids and lipoproteins:

risk factors for coronary heart
disease
Lipid/Lipoprotein

Effect on coronary heart disease

risk if level is:
Decreased
Increased

Total cholesterol
LDL-cholesterol
HDL-cholesterol
Triglycerides

LDL= low-density lipoprotein; HDL=high-density lipoprotein

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Shaper et al (1985)

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CORONARY ARTERY DISEASE

1. Stable angina pectoris
2. Acute Coronary Syndrome
A. Unstable angina pectoris
B. Q wave acute myocardial
infarction : -NSTEMI
-STEMI
C. Non Q wave AMI : -NSTEMI
-STEMI
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STABLE ANGINA PECTORIS

Stable angina is a clinical syndrome
characterized by discomfort in the
chest, jaw, shoulder, back or arms,
typically elicited by exertion or
emotional stress and relieved by rest
or nitroglycerin. Less typically,
discomfort may occur in the
epigastric area.
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Diagnosis of stable angina

Clinical assesment
Laboratory test
Specific cardiac investigations

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History
Features of the history important in
risk stratification include current
smoking, increasing age, prior MI,
symptoms of heart failure, and the
pattern of occurance(recent onset or
progressive), and severity of angina,
particularly if unresponsive to
therapy.
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Physical examination
Patient with (suspected) angina
pectoris should be focused on
identification or exclusion of causal
or associated conditions or
precipitating factors and on risk
stratification.

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LABORATORY TEST
Fasting plasma glucose and lipid
profile (TC,HDL,LDL,TG) should be
evaluated in all patients with stable
angina, to establish the patients risk
profile and ascertain the need for
treatment. A full blood count and
serum creatinine are also indicated
in all patients.
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LABORATORY TEST
Futher laboratory testing, including
OGTT, cholesterol subfractions
(ApoA, ApoB), hemocysteine, Lpa,
NT-BNP, haemostatic abnormalities
and markers of inflammation such as
hsCRP, may a role in selected
patients.
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LABORATORY TEST
Measurement of markers of
myocardial damage such as troponin,
should be measured if evaluation
suggests clinical instability or acute
coronary syndrome.
Thyroid function should be tested if
dysfunction suspected clinically.
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Chest X-ray
Should be requesed only in patients
with suspected heart failure, valvular
disease or pulmonary disease.
The presence of cardiomegaly,
pulmonary congestion, atrial
enlargement and cardiac
calcifications have been related to
prognosis.
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ECG
All patient with suspected angina
pectoris based upon symptoms
should have a resting 12 lead ECG
Resting ECG abnormalities, ST
depression, Q waves, left anterior
hemiblock and left bundle-branch
block, are associated with an adverse
prognosis in stable angina.
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Normal conduction wave from an

electrocardiogram
Voltage (mV)
R

1.0
0.5

P
0
Q
-0.5

S
200

400

600

Time (ms)

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Ischemia & Infarction

Types of ST-segment depression
UPSLOPING very nonspecific for the diagnosis of
ischemia. Associated with a lot of false positive
exercise tests.

HORIZONTAL likely associated with ischemia.

DOWNSLOPING almost certainly associated with an

ischemic myocardium

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ECG STRESS TESTING

In the majority of patients the
exercise ECG is the initial test of
choice to diagnosis coronary
disease and risk stratify.

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ECG STRESS TESTING

DIAGNOSIS OF CAD. ST segment
depression during exercise is used to
define a positive test.
Sensitivity and spesificity are 68% and
77% respectively.
Exercise ECG testing is not of diagnosis
value in presence of LBBB, paced rhythm
and WPW syndrome.
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ECG STRESS TESTING

Result are less reliable in patients
with an abnormal resting ECG in the
presence of LVH, electrolyte
imbalance, intraventricular
conduction abnormalities and during
use of digitalis.
Exercise ECG testing is also less
sensitive and specific in women.
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STRESS TESTING IN
COMBINATION WITH IMAGING
Exercise testing with
echocardiograpy
Single Photon Emission Computed
Tomography (SPECT)
Stress Cardiac magnetic Resonance
(CMR)

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OTHER INVESTIGATIONS
ECHOCARDIOGRAPHY AT REST
ELECTRON BEAM CT and MULTISLICE CT.
MAGNETIC RESONANCE (MR)
ARTERIOGRAPHY
CORONARY ANGIOGRAPHY.

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CORONARY ARTERIOGRAPHY
Providing reliable anatomical
information to identify the presence
or absence of coronary lumen
stenosis, define therapeutic options
(suitability of medical treatment or
myocardial revascularization) and
determine prognosis.
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TREATMENT
Aims of treatment.
A. Improve prognosis by preventing
myocardial infarction and death
B. Minimize or abolish symptoms.

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Non-pharmacological
Advice should be given for the
management of an acute attack, i.e. to
rest, at least briefly, from the activity that
provoked the angina and the use of
sublingual nitrate for acute relief of
symptoms.
Need to seek medical advice if angina
persist >10-20 minutes after rest and/or is
not relieved by sublingual nitrates.
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Non-Pharmalogical
Stop cigarette smoking
Mediterranean diet, with vegetables,
fruit, fish and poultry being the
mainstays.
Weight reduction diet --- Overweight
Alcohol in moderation may be
beneficial, but excessive
consumption is harmful
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Non-Pharmacological
Fish oil rich in omega-3 fatty acids (n-3
polyunsaturated fatty acids) are
recommended at least once weekly
Physical activity within the patients
limitation should be encouraged.
Concomitant disorders such as diabetes
and hypertension should be managed
appropriately.
Sexual intercouse may trigger angina.
Nitroglycerine prior to intercourse may be
helpful.
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Pharmacological therapy
Antitrombotic drugs. Antiplatelet therapy
to prevent coronary trombosis is
indicated. Low dose aspirin (75-100 mg) is
the drug of choise in most cases.
Aspirin allergic --- clopidogrel
Aspirin + clopidogrel --- post stenting or
after ACS
History of GI bleeding --- aspirin + proton
pum inhibitor
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Pharmacological therapy
Anticoagulant drugs (warfarin or
thrombin inhibitors), which are
combined with aspirin in certain high
risk patients, such as post MI, are
not indicated in the general stable
angina pectoris without a separate
indication such as atrial fibrillation
for example.
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Pharmacological therapy

Lipid lowering drugs

ACE inhibitors
Beta-blockers
Antianginal drugs : beta-blockers,
calcium antagonist and organic
nitrates

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Coronary artery bypass surgery

Two main indications --- prognostic
and symptomatic
Prognostic benefit : reduction in
cardiac mortality
CABG has also been shown to
effectively reduce symptoms of
angina and ischemia in patients with
coronary disease.
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Better Prognosis with Coronary

artery bypass surgery
Significant stenosis of the left main
Significant proximal stenosis of the three
major coronary arteries
Significant stenosis of two major coronary
arteries, including high grade stenosis of
the proximal left anterior descending
coronary artery
Three vessel disease with impaired
ventricular function.
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Percutaneous coronary
intervention (PCI)
PCI may be considered an alternative to
CABG for relief of symptoms in almost all
cases
On available evidence, PCI compared to
medical therapy does not provide survival
benefit in stable angina, but PCI is more
often effective than medical treatment in
reducing events that impair quality of life
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Acute Coronary Syndrome

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PATOGENESIS

Fixed Coronary Obstruction

(Chronic Ischemic Heart Disease)

Unstable Plaque
7

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Occlusive Thrombus

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Kuliah PJK, 2004

Acute Coronary Syndrome

Ischemic Discomfort
Unstable Symptoms

No ST-segment
elevation

Unstable
angina

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History
Physical Exam

ST-segment
elevation

Non-Q
AMI

Q-Wave
AMI

ECG

Acute
Reperfusion

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Unstable Angina - Definition

angina at rest (> 20 minutes)
new-onset (< 2 months) exertional
angina (at least CCSC III in severity)
recent (< 2 months) acceleration of
angina (increase in severity of at
least one CCSC class to at least
CCSC class III)
Canadian Cardiovascular Society Classification
Agency for Health Care Policy Research - 1994

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CANADIAN CARDIOVASCULAR
SOCIETY FUNCTIONAL
CLASSIFICATION
CLASS I No angina with ordinary activity.
Angina with strenuous, rapid or prolonged
exertion.
CLASS II Slight limitation of ordinary
activity ; angina when walking up stairs
briskly, or walking on a cold or windy day.
CLASS III Marked limitation ; angina when
walking at normal pace up flight of stairs, or
walking 1-2 blocks distance.
CLASS IV Angina on minimal exertion or at
rest.
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Unstable Angina
precipitating factors
Inappropriate tachycardia
anemia, fever, hypoxia, tachyarrhythmias,
thyrotoxicosis
High afterload
aortic valve stenosis, LVH
High preload
high cardiac output, chamber dilatation
Inotropic state
sympathomimetic drugs, cocaine intoxication
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Unstable Angina
prognostic indicators
Presence of ST-T-wave changes with pain
Hemodynamic deterioration
pulmonary edema, new mitral regurgitation,
3rd heart sound, hypotension

Other predictors
left ventricular dysfunction, extensive CAD,
age, comorbid conditions (diabetes mellitus,
obstructive pulmonary disease, renal failure,
malignancy)
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Unstable Angina
pathogenesis
Plaque disruption
Acute thrombosis
Vasoconstriction

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Unstable Angina
Risk Stratification
Low Risk
new-onset exertional angina
minor chest pain during exercise
pain relieved promptly by nitroglycerine
Management
can be managed safely as an outpatient
(assuming close follow-up and rapid
investigation)
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Unstable Angina
Risk Stratification
Intermediate Risk
prolonged chest pain
diagnosis of rule-out MI
Management
observe in the ER or Chest Pain Unit
monitor clinical status and ECG
obtain cardiac enzymes (troponin T or I)
every 8 to 12 hours
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Unstable Angina
Risk Stratification
High Risk
recurrent chest pain
ST-segment change
hemodynamic compromise
elevation in cardiac enzymes
Management
monitor in the Coronary Care Unit
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Unstable Angina
Therapeutic Goals
Therapeutic Goals
Reduce myocardial ischemia
Control of symptoms
Prevention of MI and death
Medical Management
Anti-ischemic therapy
Anti-thrombotic therapy
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Unstable Angina
Medical Therapy
Anti-ischemic therapy
nitrates, beta blockers, calcium antagonists

Anti-thrombotic therapy
Anti-platelet therapy
aspirin, ticlopidine, clopidogrel,
GP IIb/IIIa inhibitors
Anti-coagulant therapy
heparin, low molecular weight heparin
(LMWH), warfarin, hirudin, hirulog
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Unstable Angina
Anti-ischemic Therapy

restrict activities
morphine
oxygen
nitroglycerine
pain relief, prevent silent ischemia, control
hypertension, improve ventricular dysfunction
nitrate free period recommended after the first
24-48 hours
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Unstable Angina
Anti-ischemic Therapy
beta-blockers
lowering angina threshold
prevent ischemia and death after MI
particularly useful during high sympathetic tone

calcium antagonists
particularly the rate-limiting agents
nifedipine is not recommended without
concomitant -blockade

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Unstable Angina
Anti-thrombotic Therapy
Thrombolytics are not indicated
lytic agents may stimulate the
thrombogenic process and result in
paradoxical aggravation of ischemia and
myocardial infarction

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TIMI IIIB Investigators

Circulation 1994; 89:1545-1556

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Unstable Angina
Anti-platelet Therapy
aspirin is the gold standard
irreversible inhibition of the cyclooxygenase
pathway in platelets, blocking formation of
thromboxane A2, and platelet aggregation
in AMI, ASA reduced the risk of death by 20-25%
in UA, ASA reduced the risk of fatal or nonfatal
MI by 71% during the acute phase, 60% at 3
months, and 52% at 2 years
bolus dose of 160-325 mg, followed by
maintenance dose of 80-160 mg/d

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Unstable Angina
Anti-platelet Therapy
Thienopyridines
ticlopidine
clopidogrel
block platelet aggregation induced by
ADP and the transformation of GP IIb/IIIa
into its high affinity state
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Unstable Angina
Anti-platelet Therapy
GP IIb/IIIa inhibitors
abciximab (monoclonal antibody)
eptifibatide (peptidic inhibitor)
lamifiban and tirofiban (non-peptides)
direct occupancy of the GP IIb/IIIa receptor by a
monoclonal antibody or by synthetic compounds
mimicking the RGD sequence for fibrinogen binding
prevents platelet aggregation
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Unstable Angina
Anti-coagulant Therapy
Heparin
recommendation is based on documented
efficacy in many trials of moderate size
meta-analyses (1,2) of six trials showed a
33% risk reduction in MI and death, but with
a two fold increase in major bleeding
titrate PTT to 2x the upper limits of normal

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1. Circulation 1994;89:81-88
2. JAMA 1996;276:811-815

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Unstable Angina
Anti-coagulant Therapy
Low-molecular-weight heparin
advantages over heparin:
better bio-availability
higher ratio (3:1) of anti-Xa to anti-IIa activity
longer anti-Xa activity, avoid rebound
induces less platelet activation
ease of use (subcutaneous - qd or bid)
no need for monitoring
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Unstable Angina
Coronary Interventions
TIMI 3B
early intervention vs conservative strategy
(coronary angiography within 24-48 hrs,
followed by angioplasty or bypass surgery)
1473 patients with UA or non-Q-wave MI
were randomized, there were no difference
between the groups in the rates of death or
MI at 1 year
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Circulation 1994;89:1545-1556

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Acute Myocardial Infarction

Myocardial Infarction if the rapid
development of myocardial necrosis
by a critical imbalance between
oxygen supply and demand to the
myocardium

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History
Chest Pain- anterior precordium
tightness
Pain may radiate to jaw, neck and
epigastrium
Dyspnea- angina equivalent, poor LV
function
Nausea/abdominal pain with
posterior MI
Anxiety
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History

Nausea with and without vomiting

Diaphoresis or sweating
Syncope or near syncope
Elderly present - fatigue, syncope or
weakness
As many as half of MI are clinically
silent
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Physical
- Hypertension
- Hypotension
- Acute valvular dysfunction may be
present
- Rales
- Neck vein distention
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Physical
Third heart sound may be present
A fourth heart sound poor LV
compliance
Dysrhythmias
Low grade fever

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Causes
Most frequent cause is rupture of an
atherosclerotic lesion within coronary
wall with subsequent spasm and
thrombus formation
Coronary artery vasospasm
Ventricular hypertrophy
Hypoxia
Coronary artery emboli
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Causes

Cocaine
Coronary anomalies
Aortic dissection
Pediatrics Kawasaki disease,
Takayasu arteritis
Increased afterload which increases
myocardial demand
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Differentials

Acute coronary syndrome

Anxiety
Aortic stenosis
Asthma
Cholecystitis and biliary colic
Cholethiasis
COPD
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Differentials

Aortic Dissection
Endocarditis
Esophagitis
Shock
Myocarditis
Pericarditis
Pulmonary embolism
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Mechanisms of Myocardial
damage
The severity of an MI is dependent of
three factors
The level of the occlusion in the
coronary
The length of time of the occlusion
The presence or absence of
collateral circulation
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Electrocardiogram
A normal ECG does not exclude ACS
High probability include ST segment
elevation in two contiguous leads or
presence of q waves
Intermediate probability ST
depression
T wave inversions are less specific
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Ischemia & Infarction

Acute anterior MI

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Cardiac Biomarkers
Cardiac biomarkers are protein
molecules released into the blood
stream from damaged heart muscle
Since ECG can be inconclusive ,
biomarkers are frequently used to
evaluate for myocardial injury
These biomarkers have a
characteristic rise and fall pattern
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Troponin T and I
These isoforms are very specific for
cardiac injury
Preferred markers for detecting
myocardial cell injury
Rise 2-6 hours after injury
Peak in 12-16 hours
Stay elevated for 5-14 days
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Creatinine Kinase ( CK-MB)

Creatinine Kinase is found in heart
muscle (MB), skeletal muscle (MM),
and brain (BB)
Increased in over 90% of myocardial
infraction
However, it can be increased in muscle
trauma, physical exertion, post-op,
convulsions, and other conditions
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Creatine Kinase (MB)

Time sequence after myocardial infarction
Begins to rise 4-6 hours
Peaks 24 hours
returns to normal in 2 days
MB2 released from heart muscle and
converted to MB1.
A level of MB2 > or = 1 and a ratio of
MB2/MB1 > 1.5 indicates myocardial injury

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Myoglobin
Damage to skeletal or cardiac muscle
release myoglobin into circulation
Time sequence after infarction
Rises fast 2hours
Peaks at 6-8 hours
Returns to normal in 20-36 hours
Have false positives with skeletal
muscle injury and renal failure
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Ischemia & Infarction

Biomarkers in an MI:

Multiples of the AMI cutoff Limit

50

Myoglobin

20

Cardiac Troponin
CK-MB

10

Cardiac Troponin after unstable angina

5
2

AMI decision limit

Upper normal limit

0

Days after MI Onset

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CBC
CBC is indicated if anemia is
suspected as precipitant
Leukocytosis may be observed within
several hours after myocardial injury
and returns returns to levels within
the reference range within one week
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Chemistry Profile
Potassium and magnesium levels
should be monitored and corrected
Creatinine levels must be considered
before using contrast dye for
coronary angiography and
percutanous revascularization
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C-reactive Protein (CRP)

C- reactive protein is a marker of
acute inflammation
Patients without evidence of
myocardial necrosis but with
elevated CRP are at increased risk of
an event
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Chest X-Ray
Chest radiography may provide
clues to an alternative diagnosis
( aortic dissection or pneumothorax)
Chest radiography also reveals
complications of myocardial
infarction such as heart failure
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Echocardiography
Use 2-dimentional and M mode
echocardiography when evaluating
overall ventricular function and wall
motion abnormalities
Echocardiography can also identify
complications of MI ( eg. Valvular or
pericardial effusion, VSD)
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Therapy

The goals of therapy in AMI

are the expedient
restoration of normal
coronary flow and the
maximum salvage of
functional myocardium
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Antiplatelet Agents
Aspirin at lease 160mg immediately
Interferes with function of
cyclooxygenase and inhibits the
formation of thromboxane
ASA alone has one of the greatest
impact on the reduction of MI mortality.
Clopidogrel, ticlopidine, have not been
shown in any large scal trail to be
superior to Aspirin in acute MI
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Supplemental Oxygen
Because MI impairs the circulatory
function of the heart, oxygen
extraction by the heart and other
tissues may be diminished
Supplemental oxygen should be
administered to patient with symptoms
and or signs of pulmonary edema or
pulse oximetry readings less than 90%.
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Nitrates
IV nitrates to all patients with MI and
congestive heart failure, persistent
ischemia, hypertension, or large
anterior wall MI
Primary benefit vasodilator effect
Metabolized to nitric oxide in the
vascular endothelium, relaxes
endothelium
Vasodilatation reduces myocardial
oxygen demand and preload and
afterload
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Beta-blockers
Recommended within 12 hours of MI
symptoms and continued indefinitely
Reduces Myocardial mortality by
decreasing arrythmogenic death
Decrease the rate and force of
myocardial contraction and
decreases overall oxygen demand
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Unfractionated heparin
Forms a chemical complex with
antithrombin III inactivates both free
thrombin and factor Xa
Recommended in patients with MI
who undergo PTCA or fibrinolytic
therapy with alteplase

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Low-molecular weight heparin

Direct activity against factors Xa and
IIa
Proven to be effective in treating ACS
that are characterized by unstable
angina or non ST- elevation MI
Their fixed doses are easy to
administer and laboratory testing to
measure their therapeutic effect is not
necessary makes them attractive
alternative of un-fractionated heparin
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Thrombolytics
Indicated with MI and ST segment
elevation greater than 0.1mV in 2
contiguous ECG leads, or new onset
LBBB, who present less than 12 hours
but not more than 24 hours after
symptom onset
The most critical variable in achieving
successful fibrinolysis is time form
symptom onset to drug administration
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Thrombolytics
As a class the plasminogen activators
have been shown to restore coronary
blood flow in 50-80% of patients
Contraindication active intracranial
bleeding, CVA 2months, CNS neoplasm,
HTN, coagulopathy
Retaplase slightly higher angiographic
patency but did not translate into survival
benefit
Intracranial bleed risk major drawback
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Glycoprotein IIb/IIIa
Antagonists
Potent inhibitors of platelet
aggregation
Use during PCI and in patients with
high risk features ACS have been
shown to reduce the composite end
points of death, reinfraction and the
need for target lesion
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Surgical Revascularization
Emergent or surgical
revascularization in setting of failed
PTCA in patients with hemodynamic
instability and coronary anatomy
amendable to surgical grafting
Also indicated of mechanical
complications of MI including VSD,
free wall rupture, or acute MR
Carries a higher risk of perioperative
mortality than elective CABG
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Lipid Management
All post MI patients should be on
AMA step II diet ( < 7% of calories
from saturated fats)
Post MI patients with LDL > 100
mg/dl are recommended to be on
drug therapy to try to lower levels to
<100 mg/dl
Recent data indicate that all MI
patients should be on statin therapy,
regardless of lipid levels or diet
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Long term Medications

Most oral medications instituted in the
hospital at the time of MI are
continued long term
Aspirin, beta blockers and statin are
continued indefinitely
ACEI indefinitely in patients with CHF,
ejection fraction <.40, hypertension,
or diabetes
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T H AN K YO U

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