CORONARY ARTERY DISEASE AND

STABLE
ANGINA
Melody L. Strattan, DO • Merrill Krolick,
DO, FACC,
FACP, FSCAI
BASICS
DESCRIPTION
• Coronary artery disease (CAD) refers to the atherosclerotic
narrowing of the
epicardial coronary arteries. It may manifest insidiously as
angina pectoris or
as an acute coronary syndrome (ACS).
• Stable angina is a chest discomfort due to
myocardial ischemia that occurs
predictably at a certain level of exertion or emotional
stress.
• The spectrum of ACS includes unstable angina (UA),
non–ST elevation
myocardial infarction (NSTEMI), and ST elevation myocardial
infarction
(STEMI). See separate chapters on these ACS.
• Definitions
– Typical angina: exhibits three classical characteristics:
(i) substernal chest
tightness, pressure, or heaviness that frequently radiates to
the jaw, back, or
arms and generally lasts from 2 to 15 minutes; (ii) occursin
a consistent
pattern at a certain level of myocardial oxygen demand
from exertion,
emotional stress,or increased sympathetic tone; and (iii) relieved
with rest
or sublingual nitroglycerin
– Atypical angina: exhibits two of the above typical
characteristics
– Noncardiac chest pain: exhibits =1 of the above typical
characteristics
– Anginal equivalent: Patients may present without
chest discomfort but with
nonspecific symptoms such as dyspnea, diaphoresis, fatigue,
belching,
nausea, light-headedness, or indigestion that occur with
exertion or stress.
– UA: anginal symptoms that arenew or changed in
character to become
more frequent, more severe, or both; it is considered an
ACS but does not
present with cardiac biomarkerelevation.
– NSTEMI: presents with cardiac biomarkerelevation.
Ischemic ECG
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changes may be present, but there is no ST segment
elevation.
– STEMI: defined by ST elevations on ECG and
elevated cardiac biomarkers;
generally caused by acute plaque rupture and complete
obstruction of the
culprit vessel
• Canadian Cardiovascular Society grading scale:
– Class I: Angina does not limit ordinary physical
activity, occurring only
with strenuous or prolongedexertion (7 to 8 metabolic
equivalents
[METs]).
– Class II: Angina causes slight limitation of ordinary
activity. It occurswhen
walking rapidly, uphill, or >2 blocks; climbing >1 flight of
stairs; or with
emotional stress (5 to 6 METs).
– Class III: Angina causes marked limitation of ordinary
physical activity. It
occurswhen walking one to two blocks or climbing one
flight of stairs (3 to
4 METs).
– Class IV: Angina occurswith any physical activity
and may occur at rest (1
to 2 METs).
Geriatric Considerations
• Elderly may present with atypical symptoms.
• Other physical limitationsmay delay recognition of
angina until it occurswith
minimal exertion or at rest.
• Maintain a high degree of suspicion during evaluation
of dyspnea and other
nonspecific complaints.
• Geriatric patients may be very sensitive to the side
effectsof medications used
to treat angina.
EPIDEMIOLOGY
• CAD is the leading cause of death for adults both in
the United States and
worldwide.
• CAD is responsible for about 30% of all deaths,
averaging 1 death every 40
seconds in the United States alone.
• Globalcost of CAD in 2010 was $863 billion.
• ~80% of CAD is preventable with a healthy lifestyle.
Incidence
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In the United States, the lifetime risk of a 40-year-old
developing CAD is 49%
for men and 32% for women.
Prevalence
In the United States, 17.6 million people carry a diagnosis of
CAD, while 10.2
million have angina pectoris (1).
ETIOLOGY AND PATHOPHYSIOLOGY
• Anginal symptoms occur during times of myocardial
ischemia caused by a
mismatch between coronary perfusion and myocardial oxygen
demand.
• Atherosclerotic narrowing of the coronary arteries is the
most common
etiology of angina, but it may also occur in those with
significantaortic
stenosis, pulmonary hypertension, hypertrophic
cardiomyopathy, coronary
spasm, or volume overload.
• Sensory nerves from the heart enter the spinal cord at
levels C7–T4, causing
diffusereferred pain/discomfort in the associated dermatomes.
RISKFACTORS
• Traditional risk factors: hypertension, ↓ HDL, ↑
low- LDL, smoking, diabetes,
premature CAD in first-degree relatives (men <55 years
old; women <65
years old), age (>45 for men, >55 for women).
• Nontraditional risk factors: obesity, sedentary lifestyle,
chronic inflammation,
abnormal ankle-brachial indices, renal disease
GENERALPREVENTION
• Smoking cessation
• Regular aerobic exercise program
• Weight loss for obese patients (goal BMI <25 kg/m
)
• BP control (goal <140/90 mm Hg; <150/90 mm
Hg for those =60 years old)
(2)
• Diabetes management
• Statin therapy for those with diabetes, known CAD, and
consider strongly for
10-year risk =7.5%
• Low-dose aspirinmay be considered in those with 10-
year risk =10%.
2
COMMONLY ASSOCIATED CONDITIONS
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Hyperlipidemia, peripheralvascular disease, cerebrovascular
disease,
hypertension, obesity, diabetes
 DIAGNOSIS
HISTORY
• Careful historyis important to elicit symptoms.
• Pain may be described with a clenched fist over the
center of the chest (Levine
sign).
• Discomfort is usually not affected by position or deep
inspiration.
• Episodes of angina aregenerally of the same character
and in the same
location.
• Recent decrease in level of physical activity may
be due to worsening anginal
symptoms.
• Dyspnea on exertion may present as the only
symptom. Atypical symptoms
aremore likely in women, the elderly, and diabetic patients.
• May present with symptoms similarto gastricreflux
or GI upset (indigestion,
nausea, diaphoresis)
PHYSICAL EXAM
• Normal physical exam does not exclude the diagnosis of
angina or CAD.
• Cardiac exam may reveal dysrhythmias, heart
murmurs indicative of valvular
disease, gallops, or signs of congestive heart failure.
• Evidence of peripheralvascular disease (diminished
pulses, bruits, abdominal
aortic aneurysm [AAA])
DIFFERENTIAL DIAGNOSIS
• Vascular: aortic dissection, pericarditis, myocarditis,
myocardial infarction
(MI)
• Pulmonary: pleuritis, pulmonary embolism,
pneumothorax
• Gastroesophageal: gastricreflux, esophageal spasm,
peptic ulcer
• Musculoskeletal: costochondritis, arthritis, muscle strain,
rib fracture
• Other: anxiety, psychosomatic, cocaine abuse
DIAGNOSTIC TESTS & INTERPRETATION
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Initial Tests (lab, imaging)
• Serial cardiac troponins to rule out MI in those
presenting with prolongedpain
or other symptoms compatible with MI.
• CBC, lipid profile, HgbA1c (1)[C]
• Basic metabolic panel to rule out electrolyte
abnormalitiesand assess renal
function
• ECG
– Should be routinely obtained unless there is a
noncardiac cause of the chest
pain (1)[C]
– Frequently unremarkable between anginal episodes;
may show signs of
myocardial ischemia during symptomatic episodes, evidence of
old MI
– Left bundle branch block or ventricular pacing
makesinterpretation
unreliable.
• Chest x-ray may exclude other causes of pain (1)
[C].
Follow-Up Tests & Special Considerations
• Goal is to detect possible high-risk coronary lesions,
where intervention
would improve long-term mortality or alleviate anginal
symptoms.
• Stress testingis most helpfulfor patients at intermediate
risk of heart disease.
– Exercise testingfor those who can physically exercise
(=5METS) (1)[A]
Standard exercise ECG for those with normal baseline
ECG
Exercise stress testingwith echo or perfusion imaging
for those with
abnormal baseline ECG or in premenopausal women
– In patients who cannot tolerate exercise, consider
pharmacologic stress
testing(1)[A].
• Echocardiogram shouldbe obtained in patients with a
new or loud (=III/VI)
murmur, evidence of MI, symptoms of heart failure, concern
for hypertrophic
cardiomyopathy or pericardial effusion, and in those with
new arrhythmias (1)
[A].
• Echocardiogram can be considered in patients with
hypertension or diabetes
and abnormal ECG (1).
• CT coronary angiography or cardiac MRI can be
considered as a
supplement/alternative to stress testingin patients with
continued symptoms
despite negative stress testing, inconclusive stress testing,
or need for better
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anatomic definition of disease (1)[A].
Diagnostic Procedures/Other
• Cardiac catheterization with coronary angiography is
the gold standard for
confirmation and delineation of coronary disease and
direction of
interventionaltherapy or surgery. It is indicated if noninvasive
testingsuggests
a high-risk lesion,or if patient fails to respond to
appropriate medical
management.
• Significant CAD is defined as =50% stenosis of the
left main coronary artery
or =70% stenosis of other major coronary arteries by
angiography.
• Borderline lesions may be assessed with a
pressure wire. Fractional flow
reserve (FFR) of =0.8 demonstrates a hemodynamically
significantlesion.
 TREATMENT
GENERALMEASURES
• BP control goal: <140/90 mm Hg for most, exceptin
elderly(2)[A]. Selected
high-risk nondiabetic patients may benefit from a systolic
blood pressure
target of <120 mmHg(3)[B].
• Smoking cessation goal: complete cessation, no
exposure to secondhand
smokeor e-cigarettes
• Physical activity goal: 30 to 60 minutes of moderate
aerobic activity, at least 5
(preferably 7) days/week
• Weight management goal: BMI 18.5 to 24.9 kg/m
2
; waist circumference <35
inches (women) or <40 inches (men)
• Glycemic control in diabetics: Avoid hypoglycemic
episodes.
MEDICATION
First Line
• ß-Blockers: decrease myocardial oxygen demand by
lowering heart rate, BP,
and contractility
– Improve mortality in patients with MI or heart failure,
and shouldbe used
as initial therapy (1)[A]
– Can improve symptoms of angina
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– Metoprolol (25to 400 mg daily [succinate] or divided
BID [tartrate]) or
carvedilol (3.125 to 25 mg BID). Adjust doses according to clinical
response. Maintain resting heart rate 50 to 60 bpm.
– Side effectsbradycardia, fatigue, and sexual dysfunction
• Calcium channel blockers (CCBs): cause arterial
vasodilation, decreased
myocardial oxygen demand, and improved coronary blood
flow. Similar
effectiveness to ß-blockers; may be used instead of, or in
addition to ßblockers (1)[A]. Only long-acting CCBs should
be used:
– Dihydropyridine CCBs: nifedipine (30to 90 mg/day),
amlodipine (5 to 10
mg/day), or felodipine (2.5 to 10 mg/day): vasodilators
– Nondihydropyridine CCBs: diltiazem (120 to 480 mg/day)
or verapamil
(120 to 480 mg/day) also have negative inotropic effects;
shouldnot be
used in those with EF <40%. Side effectsinclude constipation
and
peripheraledema. The nondihydropyridine CCBs may also
cause
bradycardia or precipitate heart failure in those with
significantsystolic
dysfunction (ejection fraction <40%).
• Nitrates: dilate systemic veins and arteries (including
coronary vessels) and
cause decreased preload. At higher doses,they decrease BP
and thus increase
myocardial flow.
– Sublingual nitroglycerin (0.4 mg every 5 minutes for 2
to 3 doses) may be
used for acute anginal episodes (1)[A].
– Long-acting nitrates such as isosorbide mononitrate
(30to 240 mg daily
[extended release]) can be used for angina prophylaxis.
– Side effectsinclude headache and hypotension but tend
to improve with
continued usage.
– Contraindicated with concomitant PDE-5inhibitor use
• Lipid-lowering agents:
– High-intensity statin therapy is indicated for all patients
with CAD
regardless of lipid levels (4)[A].
– Statin therapy shouldalso be encouraged for those with
high CAD risk.
– Atorvastatin (20to 80 mg/day) and rosuvastatin (10to
40 mg/day) arehighintensity statins.
– Statins reduce risk of MI and revascularization
need. Side effectsinclude
myalgias, transaminitis, rhabdomyolysis (rare), and impaired
glucose
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tolerance.
– Ezetimibemay be added to statin therapy, although
evidence for improved
clinical outcomes remains weak.
– PCSK-9 inhibitors can further reduce LDL levels and
arein clinical trials to
determinetheir benefit in reducing cardiovascular events.
• Antiplatelets: decrease risk of thrombosis
– Aspirin (75to 162 mg/day) decreases risk of first
MI and reduces adverse
cardiovascular eventsin those with stable angina (1)[A].
– Clopidogrel (75mg/day) may be used in patients with
contraindications to
aspirin(1)[A].
– Dual antiplatelet therapy with aspirin+ clopidogrel,
prasugrel,or ticagrelor
is indicated after MI or percutaneous coronary intervention
(PCI) (use
prasugrel only after PCI).
• Angiotensin-converting enzyme inhibitors (ACEIs): act on
the reninangiotensin-aldosterone system to reduce BP and
afterload. They also have
effectson cardiac remodeling after MI.
– ACEIs such as lisinopril (5 to 40 mg/day) and enalapril
(2.5 to 20 mg BID)
have been shown to reduce both cardiovascular death and
MI in patients
with CAD and left ventricular systolic dysfunction (1)[A].
– Angiotensin receptor blockers such as candesartan (4 to
32 mg daily) may
be used in patients intolerant to ACEIs.
– Side effectsinclude cough (ACEIs only), hyperkalemia,
and angioedema.
SecondLine
Ranolazine (500 to 1,000 mg BID) decreases calcium
overload in myocytes,
acting as an antianginal/anti-ischemic agent.
• Does not affect heart rate or BP
• Use as adjunctive therapy when symptoms persist
despite optimal doses of
other antianginals
• Side effectscan include nausea, constipation,
dizziness,QT prolongation, and
headache.
SURGERY/OTHER PROCEDURES
• Revascularization shouldbe considered when noninvasive
testingsuggests a
high-risk lesion.It can also be performed if optimal
medical therapy is
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inadequate to control symptoms.
• PCI with balloon angioplasty and/or stent placement
(with drug-eluting or
bare-metal stent) is performed for significantlesions.
Additionaltechniques
include laser therapy and atherectomy.
• PCI does not decrease mortality or risk of MI versus
aggressive medical
management in those with stable angina.
• Coronary artery bypass graft (CABG) is preferred over
PCI for those with
severe left main coronary stenosis, significantlesions in =3
major coronary
arteries, and for lesions not amenable to PCI.
COMPLEMENTARY & ALTERNATIVE MEDICINE
Relaxation/stress reduction therapy for angina
ADMISSION, INPATIENT, AND NURSING
CONSIDERATIONS
Inpatient evaluation of patients with changes in anginal
symptoms representing
UA (anACS)
ONGOING CARE
FOLLOW-UP RECOMMENDATIONS
• Lifestyle modifications shouldbe aggressively stressed at
every visit.
• Patients shouldbe followed clinically; routine stress
testingis not necessary
for asymptomatic patients.
Patient Monitoring
Frequent follow-up after initial event: every 4 to 6 months in
first year and then
1 to 2 times peryear.
DIET
• Reduced intake of trans-fattyacids (1)[C]
• Adherence to dietary modification for comorbid
conditions (diabetes, heart
failure, hypertension)
PROGNOSIS
Variable; depends on severity of symptoms, extent of CAD,
and left ventricular
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function
COMPLICATIONS
ACS, arrhythmia, cardiac arrest, heart failure
REFERENCES
1. Fihn SD, Gardin JM, Abrams J, et al. 2012
ACCF/AHA/ACP/AATS/PCNA/SCAI/STS guideline for the
diagnosis and
management of patients with stable ischemic heart disease. J
Am Coll
Cardiol. 2012;60(24):e44–e164.
2. JamesPA, Oparil S, Carter BL, et al. 2014 Evidence-
based guideline for the
management of high blood pressure in adults:report from the
panel members
appointed to the Eighth Joint National Committee (JNC 8).
JAMA.
2014;311(5):507–520.
3. Wright JT Jr, Williamson JD, Whelton PK, et al. A
randomized trial of
intensive versusstandard blood-pressure control. N Engl J
Med.
2015;373(22):2103–2116.
4. Stone NJ, Robinson JG, Lichtenstein AH, et al. 2013
ACC/AHAguideline on
the treatment of blood cholesterol to reduce atherosclerotic
cardiovascular
risk in adults.Circulation. 2014;129(25 Suppl 2):S1–S45.
SEE ALSO
Algorithm: Chest Pain/Acute Coronary Syndrome
CODES
ICD10
• I25.119 Athscl heart disease of native cor art w unsp
ang pctrs
• I25.118 Athscl heart disease of native cor art w oth ang
pctrs
• I20.9 Angina pectoris, unspecified
CLINICAL PEARLS
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• Maximize antianginal therapy: combine ß-blockers,
CCBs, and nitrates as
tolerated, and high-intensity statin therapy.
• Lifestyle changes and optimal medical therapy must
be emphasized to prevent
progression of atherosclerosis and to control contributing
risk factors.