ISCHEMIC HEART DISEASE

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

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  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
Effects of Ischemia:
>> further minor decreases in the stenotic orifice area >>
myocardial ischemia - Inadequate perfusion >> decreased myocardial tissue O2
- Segmental atherosclerotic narrowing of ECAs occurs most tension = transient disturbance in mechanical, biochemical,
commonly due to a plaque >> subject to rupture or erosion of and electrical functions of the myocardium
the cap - 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
Exposure of
phosphates, i.e., ATP & creatine phosphate
plaque contents with blood leads to = platelet
o Impaired cell membrane function:
activation/aggregation + activated coagulation cascade
 Leading to deposition of fibrin strands  leakage of K+
 Formation of thrombus  Uptake of Na+ by myocytes
 Result: reduce coronary blood flow >>> myocardial  Increase in cytosolic Ca2+
ischemia sx
- Critical obstructions in vessels (ie., left main coronary artery; - Severity and duration of the imbalance in r/t damage
proximal left anterior descending coronary artery) are reversibility:
particularly hazardous o ≤20 min for total occlusion in the absence of collaterals =
- Collateral vessels develop if chronic severe narrowing + reversible
myocardial ischemia o >20 min = permanent, with subsequent myocardial
o May provide sufficient blood flow at rest but not during necrosis
conditions of increased demands - ECG changes:
- When progressive worsening of stenosis occurs: o Repolarization abnormalities
o Manifested by angina or ECG changes  Transient T-wave inversion = nontransmural,
o ECG = ST-segment deviation intramyocardial ischemia
o Sx are precipitated by: increases in MVO2 caused by  Transient ST-segment depression = patchy
subendocardial ischemia
physical activity, emotional stress, and/or tachycardia
 ST-segment elevation = severe transmural
- Changes that can upset O2 supply-demand balance leading to
ischemia.
myocardial ischemia:
o Electrical instability
o caliber of the stenosed coronary artery due to physiologic
 >> isolated ventricular premature beats
vasomotion
 >> ventricular tachycardia or v-fib
o loss of endothelial control of
o pathologic spasm (Prinzmetal’s angina)
Asymptomatic VS Symptomatic IHD
o small platelet-rich plugs
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 o may also be precipitated by unfamiliar tasks, a heavy
plaques & previously unrecognized obstructions meal or exposure to cold
- Coronary artery calcifications (CAC) may be seen on CT o Exertional angina: Typically relieved 1-5min by slowing
images of the heart, down activity and rapidly by rest & sublingual
- Postmortem exam of pts with such obstructions who are nitroglycerin
asympt often shows macroscopic scars 2ry to myocardial - Sharp, fleeting chest pain or a prolonged, dull ache localized
infarction in regions supplied by diseased coronary arteries, w/ to the left submammary area is rarely due to myocardial
or w/o collateral circulation. ischemia.
- ~25% of patients who survive acute myocardial infarction may - Anginal “equivalents”:
not come to medical attention, and these patients have the o sx of myocardial ischemia other than angina.
same adverse prognosis as do those who present with the o Ie: dyspnea, nausea, fatigue, and faintness
classic clinical picture of acute myocardial infarction o more common in the elderly & diabetic patients
- Sudden death may be unheralded; a common presenting - Additional information to obtain:
manifestation of IHD o Suspected IHD =
- Patients with IHD also can present with cardiomegaly & HF  Hx of angina with less exertion than in the past
2ry to ischemic damage of the LV myocardium w/o sx before  occurring at rest, or awakening the patient from
the development of HF = “ischemic cardiomyopathy” sleep
 family hx of premature IHD (<55 yrs in first-deg
Symptomatic IHD male relatives; <65 in female relatives)
- Characterized by chest discomfort due to either angina o Examined for PAD, stroke, or transient ischemic attacks
pectoris or acute myocardial infarction
o Risk factors = presence of DM, hyperlipidemia, HTN,
- Patient may exhibit a stable or progressive course, revert to the
cigarette smoking, and other risk factors for coronary
asymptomatic stage, or die suddenly.
atherosclerosis
- Factors increasing likelihood of hemodynamically significant
CAD: advanced age, male sex, the postmenopausal state; risk
factors for atherosclerosis

Physical Examination
- 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:
STABLE ANGINA PECTORIS (Stable AnPe) o evaluate pulse contour at multiple locations
- Episodic clinical syndrome is due to transient myocardial
o ABI
ischemia
- Fundi = may reveal an increased light reflex and arteriovenous
- Males = 70% of all pts w/ AnPe; greater number w/ ages <50
nicking as evidence of HTN. T
yrs
- Cigarette smoking = signs of anemia, thyroid disease; nicotine
- Women = often atypical presentation
stains on fingertips
- Palpation: cardiac enlargement and abnormal contraction of
the cardiac impulse (LV dyskinesia).
History
- Auscultation
o can uncover arterial bruits
Chest pain/discomfort
- Typical pt w/ angina: man > 50yrs, woman >60yrs o S3 & S4
- Chest discomfort = described as heaviness, pressure, o if acute ischemia or previous infarction has impaired
squeezing, smothering, or choking; rarely frank pain papillary muscle function = apical systolic murmur due
- Location = to MR.
o typically places a hand over the sternum; Levine’s sign o signs are best appreciated in the left lateral decubitus
o rarely below umbilics or above mandible position.
- Duration = crescendo-decrescend; lasts 2–5 min o Exclude = Aortic stenosis, aortic regurgitation,
- Radiation = pulmonary HTN & hypertrophic cardiomyopathy; they
o shoulder and to both arms (esp the ulnar surfaces) may cause angina in the absence of coronary
o can arise in or radiate to the back atherosclerosis
o interscapular region - During an anginal attack = ischemia can cause transient LV
failure with S3 or S4, a dyskinetic cardiac apex, MR, and even
o root of the neck, jaw, teeth, and epigastrium
pulmonary edema.
o does not radiate to the trapezius muscles (pericarditis)
- Unlikely myocardial ischemia:
- Aggravation: exertion or emotion; recumbent pos o Tenderness of the chest wall
- Relief: usually at rest
o localization of the discomfort with a single fingertip on
- Timing:
the chest
o Nocturnal angina = may be due to episodic tachycardia,
o reproduction of the pain with palpation of the chest
diminished oxygenation during sleep, or expansion of the
intrathoracic blood volume that occurs in recumbency
o Usually occurs at a certain level of activity

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- A protuberant abdomen = may have metabolic syndrome; o the likelihood of CAD is 98% in males who are >50
increased risk for atherosclerosis 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:
- Urinalysis: for evidences ofDM & renal disease o Development of angina
- CBC; Hct; Hb o severe (>0.2 mV) ST-segment depression at a low
- Lipid profile: cholesterol—total, LDL, HDL—and TGs workload, i.e., before completion of stage II of the Bruce
- Glucose: HgbA1C protocol
- Creatinine o ST-segment depression >5min after exercise
- Thyroid function test
- CXR: To show consequences of IHD (ie. cardiac enlargement, Cardiac Imaging
ventricular aneurysm, or signs of HF) - Info gained from exercise test can be enhanced by stress
- CRP: if elevated (0-3mg/dL); an independent risk factor for myocardial radionuclide perfusion imaging
IHD; can be used in: - Uses IV thallium-201 or 99m-technetium sestamibi during
o Decision for initiation of hypolipidemic tx exercise stress
o Can reclassify risk of IDH in pts in the “intermediate” - Images obtained immediately after cessation of exercise to
category detect regional ischemia
- If pt can’t exercise (due to PVD or Musculoskeletal
disease;exertional
Electrocardiogram dyspnea; deconditioning) = IV
pharmacologic challenge is used
- There may be signs of old myocardial infarction (MI) o Ie: dipyridamole or adenosine can be given to create a
- Repolarization abnormalities (nonspecific) coronary “steal” by temporarily increasing flow in
o ST-segment and T-wave changes nondiseased segments of coronary arteries
o LVH; disturbances of cardiac rhythm = may be o Ie: graded incremental infusion of dobutamine may be
contributing factors to episodes of angina in pts in whom administered to increase MVO2
IHD has developed as a consequence of conventional risk - Echocardiography:
factors. o To assess LV fxn in pts w/:
o Intraventricular conduction  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
Electrocardiographic abnormalities of LV that are transient due to ischemia
- Most widely used test for dx of IHD & estimation of risk & o Stress echo: (exercise or dobutamine):
prognosis; sensitivity is 75%  may cause regional akinesis or dyskinesis not
- Involves recording of the 12-lead ECG before, during, and present at rest
after exercise (ie treadmill)  more sensitive than exercise ECG in dx of IHD
- Exercise duration is usually symptom-limited; discontinued if - Cardiac magnetic resonance (CMR) stress testing:
ssx are present: o alternative to radionuclide, PET, or echo stress imaging
o chest discomfort; severe SOB o performed with dobutamine infusion;
o dizziness, severe fatigue o can be used to assess wall motion abnormalities
o ST-segment flat or downsloping (>0.1mV from baseline) accompanying ischemia, as well as myocardial
depression or total of >0.2 mV (2 mm); lasts for >0.08 s perfusion
o fall in SBP >10 mmHg o used to provide more complete ventricular evaluation
o development of a ventricular tachyarrhythmia using multislice MRI studies
o Target HR is 85% of maximal predicted HR for age and - CT application: measure of the presence of coronary
sex atherosclerosis
- Positive result on exercise indicates that:

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 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 - Prognostic indicators:
- Indication: o Age
o Severely symptomatic pts w/ CSAP; considered for o LV functional state
revascularization, i.e., PCI or CABG o Location + severity of coronary artery narrowing
o Pts w/ troublesome sx & diagnostic difficulties; to o severity or activity of myocardial ischemia
confirm or rule out the dx of IHD - Conditions indicating inc risk of adverse coronary events:
o Pts w/ known or possible angina pectoris who have o Angina pectoris of recent onset
survived cardiac arrest o Unstable angina
o Pts w/ angina or evidence of ischemia on noninvasive o Early post-MI angina, angina unresponsive/poorly
testing with clinical or lab evidence of ventricular responsive to medical therapy
dysfunction o Angina accompanied congestive HF sx
o Pts judged to be at high risk of sustaining coronary o Physical signs of HF
events, regardless of presence or severity of sx o Episodes of pulmonary edema
 Chest discomfort suggestive of angina pectoris but o Transient S3
neg/nondiagnostic stress test; requires definitive dx o MR
 Frequent hospital admission for a suspected ACS; o Echo: cardiac enlargement & reduced EF (<0.40)
dx not established
- Signs during noninvasive testing indicates a high risk for
 Pts w/ careers involving safety of others (ie pilots,
coronary events:
police, firefighters); w/ questionable sx or
o inability to exercise for 6 min, i.e., stage II (Bruce
suspicious/positive noninvasive test
protocol) of the exercise test
 Pts w/ aortic stenosis or hypertrophic
o strongly positive exercise test showing onset of
cardiomyopathy & angina
myocardial ischemia at low workloads
 Male >45yrs & females >55 yrs who are to undergo
 ≥0.1 mV ST-segment depression before
cardiac operation; may or may not have sx of
completion of stage II
myocardial ischemia
 ≥0.2 mV ST-segment depression at any stage
 Pts after MI
 ST-segment depression for >5 min after the
 Pts w/ angina who have high risk of coronary
cessation of exercise
events, regardless of severity
 decline in systolic pressure >10 mmHg during
 Pts in whom coronary spasm or nonatherosclerotic
exercise
cause of myocardial ischemia (ie coronary artery
 development of ventricular tachyarrhythmias
anomaly, Kawasaki disease) is suspected
during exercise
- Alternatives: CT angiography & CMR angiography
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.

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- 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

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

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.

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References

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