ISCHEMIC HEART DISEASE

FIGURE A.1
Definition & Etiology
- IHD is a condition in w/c there is an inadequate supply of
blood & O2 to portion of the myocardium
- Imbalance between myocardial O2 supply-demand
- Most common cause: Atherosclerotic disease of an epicardial
coronary artery
- Cardiac ischemia may also be the result of:
o increased demand (ie. increased HR; HTN)
o diminished blood volume (ie HoTN; shock)
o diminished oxygenation (ie. due to pneumonia or CHF)
o diminished O2-carrying capacity (ie. due to anemia or
carbon monoxide poisoning).
Epidemiology
- The most common, serious, chronic, life-threatening illness in
the US:
o 15.5 mil have IHD
o 3.4 mil aged ≥40 years have angina pectoris
- Assoc. w/ the emergence of IHD = Genetic factors, high-fat &
energy-rich diet, smoking, and a sedentary lifestyle
- In the US and Western Europe:
o Growing among low-income groups
o Primary prevention delayed the disease to later in life
- Powerful risk factors for IHD:
o Obesity; insulin resistance
o type 2 diabetes mellitus
-Coronary blood flow also can be limited by:
o spasm (Prinzmetal’s angina)
o arterial thrombi
o rarely, coronary emboli
o ostial narrowing due to aortitis
-Congenital abnormalities (ie., origin of the left anterior descending
coronary artery from the pulmonary artery) may cause
myocardial ischemia and infarction in infancy, but this cause is
very rare in adults
-Myocardial ischemia also can occur if:
o Increased MVO2 + limited coronary blood flow
o Ie. LVH due to aortic stenosis; can present w/ angina
-Severe anemia or presence of carboxyhemoglobin, rarely causes
myocardial ischemia by itself but may lower the threshold for
ischemia in patients with moderate coronary obstruction.
-Abnormal constriction/ failure of normal dilation of the coronary
resistance vessels also can cause ischemia; if (+) angina >>
“microvascular angina”
CORONARY ATHEROSCLEROSIS
Prevalence & Risk Factors
- Major site: epicardial coronary arteries (ECA)
- Major risk factors for atherosclerosis:
o high plasma LDL levels
o low plasma HDL levels
o cigarette smoking
o HTN; diabetes mellitus

Loss of these
Pathophysiology
defenses leads
- In a normal heart, myocardium controls the supply of O2-rich to:
blood to prevent under perfusion of myocytes Inappropriate
- Major determinants of myocardial O2 demand (MVO2) = HR, constriction
myocardia contractility, & wall stress
- Blood flows through the coronary arteries in a phasic Luminal thrombus
formation
fashion, majority occurs during diastole
- About 75% of the total coronary resistance to flow occurs Abnormal
across three sets of arteries: [w/ major determinant of coronary interactions
resistance found in R2 & R3] between blood
o Large epicardial arteries (Resistance 1 = R1) cells
o Prearteriolar vessels (R2)
o Arteriolar & intramyocardial capillary vessels (R3) - Functional
- Normal coronary circulation is dominated & controlled by the changes in the vascular milieu ultimately result in the
heart’s requirements for O2 subintimal collections of the ff w/c define the atherosclerotic
- Normally, intramyocardial resistance vessels demonstrate a plaque:
great capacity for dilation (R2 and R3 decrease). o Fat
o Ie: the O2 needs of heart during exercise and emotional o SMCs
stress affect coronary vascular resistance >> regulation o Fibroblasts
of o2 supply and substrate to the myocardium (metabolic o intercellular matrix
regulation) - “Vulnerable vessel” + “vulnerable blood” = state of
o Coronary resistance vessels adapt to physiologic hypercoagulability and hypofibrinolysis (ie in pts w/ DM)
alterations in BP to maintain coronary blood flow
(autoregulation)
- In atheroscleroisis: (see figure A.1)

Pathogenesis:
- Atherosclerosis:

Page 1 of 8
  develops at irregular rates in different segments of the
epicardial coronary tree
 leads eventually to segmental reductions in cross-sectional
area (i.e., plaque formation)
- Atherosclerotic plaques tend to develop at sites of increased
turbulence in coronary flow (ie., branch points)
- If stenosis reduces the diameter of an epicardial artery by 50%
= limited ability to increase flow to meet inc myocardial
demand.
- If diameter is reduced by ~80% >> reduced at-rest blood flow
>> further minor decreases in the stenotic orifice area >>
myocardial ischemia
- Segmental atherosclerotic narrowing of ECAs occurs most
commonly due to a plaque >> subject to rupture or erosion of
the cap
-
Exposure of
plaque contents with blood leads to = platelet
activation/aggregation + activated coagulation cascade
 Leading to deposition of fibrin strands
 Formation of thrombus
 Result: reduce coronary blood flow >>> myocardial
ischemia sx
- Critical obstructions in vessels (ie., left main coronary artery;
proximal left anterior descending coronary artery) are
particularly hazardous
- Collateral vessels develop if chronic severe narrowing +
myocardial ischemia
o May provide sufficient blood flow at rest but not during
conditions of increased demands
- When progressive worsening of stenosis occurs:
o Manifested by angina or ECG changes
o ECG = ST-segment deviation
o Sx are precipitated by: increases in MVO2 caused by
physical activity, emotional stress, and/or tachycardia
- Changes that can upset O2 supply-demand balance leading to
myocardial ischemia:
o caliber of the stenosed coronary artery due to physiologic
vasomotion
o loss of endothelial control of
o pathologic spasm (Prinzmetal’s angina)
o small platelet-rich plugs
Effects of Ischemia:
- Inadequate perfusion >> decreased myocardial tissue O2
tension = transient disturbance in mechanical, biochemical,
and electrical functions of the myocardium
- Usually causes nonuniform ischemia
- During ischemia, regional disturbances of ventricular
contractility cause: [w/c reduce myocardial pump)
o segmental hypokinesia; akinesia
o (severe cases) bulging (dyskinesia)
- Abrupt development of severe ischemia:
o As occurs w/ total/subtotal coronary occlusion
o Assoc. w/ almost instantaneous failure of normal muscle
relaxation and then contraction
- Poor perfusion of the subendocardium causes more intense
ischemia of this portion of the wall
- Ischemia of large portions of the ventricle:
o Causes transient left ventricular (LV) failure, and
o if the papillary muscle apparatus is involved = mitral
regurgitation can occur.
- When ischemia is transient = may be assoc. with angina
pectoris
- When ischemia is prolonged = can lead to myocardial necrosis
and scarring w/ or w/o acute myocardial infarction
- Mechanical disturbances during ischemia:
o If severe O2 deprivation: [normal myocardium
metabolizes FAs and glucose to CO2 & water]
 fatty acids cannot be oxidized
 glucose is converted to lactate
 intracellular pH is reduced
 reduced myocardial stores of high-energy
phosphates, i.e., ATP & creatine phosphate
o Impaired cell membrane function:
 leakage of K+
 Uptake of Na+ by myocytes
 Increase in cytosolic Ca2+
- Severity and duration of the imbalance in r/t damage
reversibility:
o ≤20 min for total occlusion in the absence of collaterals =
reversible
o >20 min = permanent, with subsequent myocardial
necrosis
- ECG changes:
o Repolarization abnormalities
 Transient T-wave inversion = nontransmural,
intramyocardial ischemia
 Transient ST-segment depression = patchy
subendocardial ischemia
 ST-segment elevation = severe transmural
ischemia.
o Electrical instability
 >> isolated ventricular premature beats
 >> ventricular tachycardia or v-fib
Asymptomatic VS Symptomatic IHD
Asymptomatic IHD
- Can begins before 20 y/o
- Exercise stress tests = shows silent myocardial ischemia
- Exercise-induced ECG changes not accompanied by angina
pectoris
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- Coronary angiographic studies = reveals coronary artery
plaques & previously unrecognized obstructions
- Coronary artery calcifications (CAC) may be seen on CT
images of the heart,
- Postmortem exam of pts with such obstructions who are
asympt often shows macroscopic scars 2ry to myocardial
infarction in regions supplied by diseased coronary arteries, w/
or w/o collateral circulation.
- ~25% of patients who survive acute myocardial infarction may
not come to medical attention, and these patients have the
same adverse prognosis as do those who present with the
classic clinical picture of acute myocardial infarction
- Sudden death may be unheralded; a common presenting
manifestation of IHD
- Patients with IHD also can present with cardiomegaly & HF
2ry to ischemic damage of the LV myocardium w/o sx before
the development of HF = “ischemic cardiomyopathy”
Symptomatic IHD
- Characterized by chest discomfort due to either angina
pectoris or acute myocardial infarction
- Patient may exhibit a stable or progressive course, revert to the
asymptomatic stage, or die suddenly.
Physical Examination
STABLE ANGINA PECTORIS (Stable AnPe)
- Episodic clinical syndrome is due to transient myocardial
ischemia
- Males = 70% of all pts w/ AnPe; greater number w/ ages <50
yrs
- Women = often atypical presentation
History
Chest pain/discomfort
- Typical pt w/ angina: man > 50yrs, woman >60yrs
- Chest discomfort = described as heaviness, pressure,
squeezing, smothering, or choking; rarely frank pain
- Location =
o typically places a hand over the sternum; Levine’s sign
o rarely below umbilics or above mandible
- Duration = crescendo-decrescend; lasts 2–5 min
- Radiation =
o shoulder and to both arms (esp the ulnar surfaces)
o can arise in or radiate to the back
o interscapular region
o root of the neck, jaw, teeth, and epigastrium
o does not radiate to the trapezius muscles (pericarditis)
- Aggravation: exertion or emotion; recumbent pos
- Relief: usually at rest
- Timing:
o Nocturnal angina = may be due to episodic tachycardia,
diminished oxygenation during sleep, or expansion of the
intrathoracic blood volume that occurs in recumbency
o Usually occurs at a certain level of activity
o may also be precipitated by unfamiliar tasks, a heavy
meal or exposure to cold
o Exertional angina: Typically relieved 1-5min by slowing
down activity and rapidly by rest & sublingual
nitroglycerin
- Sharp, fleeting chest pain or a prolonged, dull ache localized
to the left submammary area is rarely due to myocardial
ischemia.
- Anginal “equivalents”:
o sx of myocardial ischemia other than angina.
o Ie: dyspnea, nausea, fatigue, and faintness
o more common in the elderly & diabetic patients
- Additional information to obtain:
o Suspected IHD =
 Hx of angina with less exertion than in the past
 occurring at rest, or awakening the patient from
sleep
 family hx of premature IHD (<55 yrs in first-deg
male relatives; <65 in female relatives)
o Examined for PAD, stroke, or transient ischemic attacks
o Risk factors = presence of DM, hyperlipidemia, HTN,
cigarette smoking, and other risk factors for coronary
atherosclerosis
- Factors increasing likelihood of hemodynamically significant
CAD: advanced age, male sex, the postmenopausal state; risk
factors for atherosclerosis
- PE is often normal in asympt pts
- Evidences of atherosclerotic disease:
o abdominal aortic aneurysm
o carotid arterial bruits
o diminished arterial pulses in lower extremities
o xanthelasmas and xanthomas
- Evidences for PAD:
o evaluate pulse contour at multiple locations
o ABI
- Fundi = may reveal an increased light reflex and arteriovenous
nicking as evidence of HTN. T
- Cigarette smoking = signs of anemia, thyroid disease; nicotine
stains on fingertips
- Palpation: cardiac enlargement and abnormal contraction of
the cardiac impulse (LV dyskinesia).
- Auscultation
o can uncover arterial bruits
o S3 & S4
o if acute ischemia or previous infarction has impaired
papillary muscle function = apical systolic murmur due
to MR.
o signs are best appreciated in the left lateral decubitus
position.
o Exclude = Aortic stenosis, aortic regurgitation,
pulmonary HTN & hypertrophic cardiomyopathy; they
may cause angina in the absence of coronary
atherosclerosis
- During an anginal attack = ischemia can cause transient LV
failure with S3 or S4, a dyskinetic cardiac apex, MR, and even
pulmonary edema.
- Unlikely myocardial ischemia:
o Tenderness of the chest wall
o localization of the discomfort with a single fingertip on
the chest
o reproduction of the pain with palpation of the chest
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- A protuberant abdomen = may have metabolic syndrome;
increased risk for atherosclerosis
- Urinalysis: for evidences ofDM & renal disease
- CBC; Hct; Hb
- Lipid profile: cholesterol—total, LDL, HDL—and TGs
- Glucose: HgbA1C
- Creatinine
- Thyroid function test
- CXR: To show consequences of IHD (ie. cardiac enlargement,
ventricular aneurysm, or signs of HF)
- CRP: if elevated (0-3mg/dL); an independent risk factor for
IHD; can be used in:
o Decision for initiation of hypolipidemic tx
o Can reclassify risk of IDH in pts in the “intermediate”
category
- There may be signs of old myocardial infarction (MI)
- Repolarization abnormalities (nonspecific)
o ST-segment and T-wave changes
o LVH; disturbances of cardiac rhythm = may be
contributing factors to episodes of angina in pts in whom
IHD has developed as a consequence of conventional risk
factors.
o Intraventricular conduction
Electrocardiographic
- Most widely used test for dx of IHD & estimation of risk &
prognosis; sensitivity is 75%
- Involves recording of the 12-lead ECG before, during, and
after exercise (ie treadmill)
- Exercise duration is usually symptom-limited; discontinued if
ssx are present:
o chest discomfort; severe SOB
o dizziness, severe fatigue
o ST-segment flat or downsloping (>0.1mV from baseline)
depression or total of >0.2 mV (2 mm); lasts for >0.08 s
o fall in SBP >10 mmHg
o development of a ventricular tachyarrhythmia
o Target HR is 85% of maximal predicted HR for age and
sex
- Positive result on exercise indicates that:
o the likelihood of CAD is 98% in males who are >50
years with a hx of typical angina pectoris and who
develop chest discomfort during the test.
o likelihood decreases if the patient has atypical or no chest
pain by hx and/or during the test.
- False-positive tests is significantly increased in:
Laboratory Examination
o asymptomatic men age <40
o premenopausal women with no risk factors for premature
atherosclerosis
o pts taking cardioactive drugs (ie digitalis; antiarrhythmic
o those with intraventricular conduction disturbances
o those w/ resting ST-segment and T-wave abnormalities,
ventricular hypertrophy
o pts w/ abnormal serum K+ levels
o Obstructive disease limited to the circumflex coronary
artery
- Equipment for resuscitation should be available
- Contraindications to exercise stress testing:
o rest angina within 48 h
o unstable rhythm
o severe aortic stenosis
o acute myocarditis
o uncontrolled HF; severe pulmonary HTN
o active infective endocarditis
- Normal response to test: progressive HR & BP inc
- What suggests severe IHD:
o Development of angina
o severe (>0.2 mV) ST-segment depression at a low
workload, i.e., before completion of stage II of the Bruce
protocol
o ST-segment depression >5min after exercise
Cardiac Imaging
- Info gained from exercise test can be enhanced by stress
myocardial radionuclide perfusion imaging
- Uses IV thallium-201 or 99m-technetium sestamibi during
exercise stress
- Images obtained immediately after cessation of exercise to
detect regional ischemia
- If pt can’t exercise (due to PVD or Musculoskeletal
disease;exertional
Electrocardiogram dyspnea; deconditioning) = IV
pharmacologic challenge is used
o Ie: dipyridamole or adenosine can be given to create a
coronary “steal” by temporarily increasing flow in
nondiseased segments of coronary arteries
o Ie: graded incremental infusion of dobutamine may be
administered to increase MVO2
- Echocardiography:
o To assess LV fxn in pts w/:
 chronic stable angina pectoris (CSAP)
 history of a prior MI; pathologic Q waves
Stress Testing clinical evidence of HF
o 2D echo: assess both global and regional wall motion
abnormalities of LV that are transient due to ischemia
o Stress echo: (exercise or dobutamine):
 may cause regional akinesis or dyskinesis not
present at rest
 more sensitive than exercise ECG in dx of IHD
- Cardiac magnetic resonance (CMR) stress testing:
o alternative to radionuclide, PET, or echo stress imaging
o performed with dobutamine infusion;
o can be used to assess wall motion abnormalities
accompanying ischemia, as well as myocardial
perfusion
o used to provide more complete ventricular evaluation
using multislice MRI studies
- CT application: measure of the presence of coronary
atherosclerosis
Page 4 of 8
 Coronary Arteriography
- Outlines the lumina of the coronary arteries; used to detect or
exclude serious coronary obstruction
- Does not provide info about arterial wall; severe
atherosclerosis encroaching in lumen may be undetected
- Atherosclerosis:
o Plaques scattered throughout coronary tree
Prognosis
o Occurs frequently at branch points; progressive growth in
intima & media of an EC artery
- Indication:
o Severely symptomatic pts w/ CSAP; considered for
revascularization, i.e., PCI or CABG
o Pts w/ troublesome sx & diagnostic difficulties; to
confirm or rule out the dx of IHD
o Pts w/ known or possible angina pectoris who have
survived cardiac arrest
o Pts w/ angina or evidence of ischemia on noninvasive
testing with clinical or lab evidence of ventricular
dysfunction
o Pts judged to be at high risk of sustaining coronary
events, regardless of presence or severity of sx
 Chest discomfort suggestive of angina pectoris but
neg/nondiagnostic stress test; requires definitive dx
 Frequent hospital admission for a suspected ACS;
dx not established
 Pts w/ careers involving safety of others (ie pilots,
police, firefighters); w/ questionable sx or
suspicious/positive noninvasive test
 Pts w/ aortic stenosis or hypertrophic
cardiomyopathy & angina
 Male >45yrs & females >55 yrs who are to undergo
cardiac operation; may or may not have sx of
myocardial ischemia
 Pts after MI
 Pts w/ angina who have high risk of coronary
events, regardless of severity
 Pts in whom coronary spasm or nonatherosclerotic
cause of myocardial ischemia (ie coronary artery
anomaly, Kawasaki disease) is suspected
- Alternatives: CT angiography & CMR angiography
- Prognostic indicators:
o Age
o LV functional state
o Location + severity of coronary artery narrowing
o severity or activity of myocardial ischemia
- Conditions indicating inc risk of adverse coronary events:
o Angina pectoris of recent onset
o Unstable angina
o Early post-MI angina, angina unresponsive/poorly
responsive to medical therapy
o Angina accompanied congestive HF sx
o Physical signs of HF
o Episodes of pulmonary edema
o Transient S3
o MR
o Echo: cardiac enlargement & reduced EF (<0.40)
- Signs during noninvasive testing indicates a high risk for
coronary events:
o inability to exercise for 6 min, i.e., stage II (Bruce
protocol) of the exercise test
o strongly positive exercise test showing onset of
myocardial ischemia at low workloads
 ≥0.1 mV ST-segment depression before
completion of stage II
 ≥0.2 mV ST-segment depression at any stage
 ST-segment depression for >5 min after the
cessation of exercise
 decline in systolic pressure >10 mmHg during
exercise
 development of ventricular tachyarrhythmias
during exercise
o the development of large or multiple perfusion defects
o increased lung uptake during stress radioisotope
perfusion imaging
o decrease in LV EF during exercise
- Poor prognosis on cardiac catheterization: elevated LV end-
diastolic pressure & ventricular vol + rEF
- Obstructive lesions of the L main (>50% luminal diameter) or
L anterior descending coronary artery proximal to the origin of
the first septal artery are assoc. w/ a greater risk than are
lesions of the R or left circumflex coronary artery
- Atherosclerotic plaques in ECA + fissuring/filling defects =
increased risk
- With any degree of obstructive CAD, mortality is greatly
increased when LV function is impaired
Treatment
Explanation & Reassurance
- Offer results of clinical trials showing improved outcomes
- A planned program of rehabilitation
Identification & Treatment of Aggravating Conditions
- LVH, aortic valve disease, and hypertrophic cardiomyopathy
may cause/contribute to angina and should be excluded or
treated.
Page 5 of 8
- Obesity, HTN, and hyperthyroidism should be treated
aggressively to reduce frequency and severity of anginal
episodes.

Adaptation of Activity
- Rational programming of activity
- Encourage patients to reduce their energy reqs in the morning,
immediately after meals, and in cold or inclement weather
- It may be necessary to recommend a change in employment or
residence to avoid physical stress
- Physical conditioning to improve exercise tolerance
o Isotonic exercises within pt’s limits/threshold
o Do not exceed 80% of HR assoc. w/ ischemia

Treatment of risk factors

Obesity:
- Diet low in saturated & trans-unsaturated fatty acids
- Reduced calorie intake
- Emphasize weight loss & regular exercise in pts w/ DM or
metabolic syndrome

Cigarette smoking:
- Smoking cessation

Hypertension:
- Antihypertensive drugs
- DASH diet
- Less sodium intake

Diabetes Mellitus:
- Aggressive control of dyslipidemia (target LDL <70mg/dL)
- Control of HTN (target BP 120/80 mmHg)

Dyslipidemia:
- Diet low in saturated and trans-unsaturated fatty acids,
exercise, and weight loss
- HMG-CoA reductase inhibitors (statins)
o Lowers LDL-c(25–50%)
o Raise HDL -c(5–9%)
o Lowers triglycerides (5–30%).
- Fibrates or niacin can be used to raise HDL c & and lower
triglycerides
- Medication compliance with the health-promoting behaviors
listed above

Risk Reduction in Women with IHD

- When cholesterol lowering, beta blockers after MI, and CABG
are applied in the appropriate patient groups, women benefit to
the same degree as men

Drug therapy

(Read more in the Pharmacology Notes)

Drugs Indications/Comments A/E &
Contraindications
Nitrates Causes include systemic
venodilation w/ reduction in LV
end-diastolic volume and
pressure.
Most commonly admin. Via
sublingual (0.4 or 0.6 mg) due to
rapid & complete absorption.
Taken to relieve angina or
~5mins before activities likely to
cause angina

Long-acting Can be swallowed, chewed, or Different prep. or admin.

nitrates via transdermal patch/paste during the daytime should be
Therapeutic level up to 24hr tried only to prevent
To minimize the effects of nitrate discomfort while avoiding s/e

Page 6 of 8
 tolerance, min dose used at a min
of 8hr each day kept free of the
drug
B-Blocker Reduces MVO2 by inhibiting
increases in HR, BP, and
myocardial contractility caused
by adrenergic activation.
Can reduce mortality and
reinfarction rates in patients after
MI.
Since sudden dis-continuation
can intensify ischemia, the doses
should be tapered over 2 weeks.
B-blockers with relative β1-
receptor specificity
(ie .metoprolol and atenolol )
may be preferable in pts w/ mild
bronchial obstruction and insulin
requiring DM.
CCB Coronary vasodilators that
produce variable and dose-
dependent reductions in MVO2,
contractility, & arterial pressure.
Indicated when B-blockers are
contraindicated, poorly tolerated,
or ineffective.
Variant (Prinzmetal’s) angina
responds particularly well to
CCBs
such as headache and
dizziness.
Relative contra-indications
include asthma and reversible
airway obstruction in patients
with chronic lung disease,
AV conduction disturbances,
severe bradycardia,
Raynaud’s phenomenon, and
a hx of mental depression.
S/E: fatigue, reduced
exercise tolerance,
nightmares, impotence, cold
extremities, intermittent
claudication bradycardia
Do not combine Verapamil
w/ B-blockers due to a/e on
HR and contractility.
Diltiazem + B-blockers in
patients with normal
ventricular fxn & no
conduction problems.
Amlodipine + B-blockers =
complementary actions on
coronary blood supply and
MVO2
Amlodipine + 2nd gen
dihydro CCBs = potent
vasodilators for tx of angina
& HTN
- Ranolazine, a piperazine derivative, may be useful for patients
with chronic angina despite standard medical therapy; Dose of
500–1000 mg orally BID
- NSAID use in patients with IHD may be assoc. with a small
but finite increased risk of MI and mortality; generally should
be avoided in IHD patients; if required for sx relief, coadmin
aspirin in the lowest dose required for the shortest period of
time.
- Nicorandil 20 mg PO BID = for prevention of angina.
- Ivabradine (2.5–7.5 mg PO BID) is a specific sinus node
inhibiting agent that may be helpful for preventing CV events
in patients with IHD who have a resting HR ≥70 bpm (alone
or in combo with a beta blocker) and LV systolic dysfunction.
Angina & Heart Failure
- Transient LV failure with angina can be controlled by the use
of nitrates.
- Treatment of congestive heart failure with an ACE inhibitor, a
diuretic, and digoxin
- Nocturnal angina often can be relieved by the treatment of
heart failure.
- The combination of congestive heart failure and angina in
patients with IHD usually indicates a poor prognosis and
warrants serious consideration of cardiac catheterization and
coronary revascularization.

Avoid short-acting dihydro

CCBs due to risk of
precipitating infarction, esp
w/out co-admin of B-
blockers
Antiplatelet Aspirin = 75 to 325 mg PO/d
Clopidogrel (300–600 mg
loading and 75 mg/d)
Prasugrel and ticagrelor have
been shown to be more effective
than clopidogrel for prevention
of ischemic events after
placement of a stent for ACS, but
inc risk of bleeding.

Initial therapy: Beta blockers or CCBs?

- B-blockers have been shown to improve life expectancy after
acute MI = preferable in patients with angina and a damaged
LV
- CCBs are indicated in patients with the following:
o inadequate responsiveness to the combo of B-blockers +
nitrates; many of these patients do well with a B-blocker +
CCBs
o Adverse reactions to B-blockers such as depression, sexual
disturbances, and fatigue
o Angina and a hx of asthma or COPD
o Sick-sinus syndrome or significant AV conduction
disturbances
o Prinzmetal’s angina
o Symptomatic PAD

Other Therapies:
- ACE-Is benefits most evident and are widely used in the tx of:
o survivors of MI
o pts w/ HTN or chronic IHD ie. angina pectoris
o at high risk of vascular diseases such as diabetes
o in IHD pts at inc risk, especially if DM or LV dysfunction
is present
o Pts who has not achieved adequate control of BP and LDL-
c on beta-blockers & statin
- Routine admin of ACE-Is to IHD pts who have normal LV
function and have achieved BP and LDL goals on other
therapies does not reduce the incidence of events and therefore
is not cost-effective.

Page 7 of 8
References

Page 8 of 8