Diagnostic Testing in Cardiology

TABLE 2. lnterpretation of Stress Testing With exercise or dobutamine because of the potential for false
lmaging Results positive septal perfusion abnormalities.
Stress SPECT
Stress Echoc ardiographA
At Rest After Stressor tnterpretation Exercise stress echocardiography provides information on
Normal Normal Normal ischemia, hemodynamic significance of valvular abnormali-
Normal Perfusion defect Stress-induced ties, and pulmonary pressures during exercise. Exercise is
myocardial ischemia performed with supine or upright bicycle ergometry which
Perfusion Same perfusion lnfarct or hibernating allows for continuous imaging, or with a treadmill protocol,
defea defect myocardium which requires acquisition of poststress images within
Normal LV dilation Small or no distinct zone 90 seconds. The development of new wall motion abnormali-
of ischemia, possible
ties indicates ischemia in the visualized territory. Resting wall
balanced ischemia or
multivessel CAD motion abnormalities that do not improve at peak exercise
may indicate infarcted or hibernating myocardium (chronic
Stress Echocardiography
but potentially reversible ischemic dysfunction).
At Rest After Stressor lnterpretation
With pharmacologic stress echocardiography, dobu
Normal Normal Normal tamine is progressively infused (up to 40 pg/kg/min) to achieve
Normal Wall motion Stress-induced 85% of age predicted maximal heart rate. Atropine is adminis-
abnormality myocardial ischemia
tered ifthe target heart rate is not achieved. The sensitivity of
Regional wall Same regional lnfarct or hibernating stress echocardiography may be reduced in the setting of
motion wall motion myocardium
abnormalities abnormalities
baseline wall motion abnormalities, systolic dysfunction,
or single vessel disease.
Normal LV dilation Small or no distinct zone
of ischemia, possible
balanced ischemia or Myocardial Perfusion lmaging and Viability Testing
multivessel CAD Myocardial perfusion imaging (MPI), also known as nuclear
CAD = coronary artery disease; LV = left ventricular; SPECT = single photon
stress testing, uses dif'ferences in myocardial blood flow to
emission Cl detect ischemia. In SPECT MPI, a radiotracer is injected at rest
and at peak exercise/vasodilation, and the radiotracer is taken
later stage) systolic dysfunction, ECG changes, and lastly, up by the myocardium relative to blood flow. Rest images are
angina. The addition of imaging studies to stress testing compared with images obtained after stress. Perfusion defects
increases diagnostic sensitivity by detecting earlier signs of observed after stress indicate flor.r, limiting CAD (Figure 2).
and localizing ischemia.
Stress testing with imaging is indicated in patients with
an inability to exercise, baseline ECG abnormalities that limit
interpretation of the exercise ECG, or indeterminate findings
on the exercise ECG. Depending on the modality used, stress
testing with imaging compares wall motion, perfusion, and/
or metabolism at baseline and after stress (Table 2). Imaging
with SPECT, PET, or CMR can be used to detect reduced myo-
cardial perfusion as early evidence of ischemia. Systolic dys-
function, indicated by wall motion abnormalities during
stress, can be detected by echocardiography or CMR imaging.
Imaging choice should consider characteristics of the patient
and modalify as well as local availabilily and expertise (see
Table 1).
Exercise is preferred over pharmacologic stressors.
Dobutamine, like exercise, increases myocardial oxygen
demand and elicits ischemia because of insufficient perfusion
to the affected myocardium. Vasodilators, such as dipyrida-
mole, regadenoson, and adenosine, produce hyperemia and a F IGUR E 2. Selected images from a nuclear perfusion single-photon emission CI

flow disparity between myocardium supplied by unobstructed stress study. Normal perfusion is indicated by orange to white coloring, whereas poor
perfusion is indicated by purple to blue coloring. Short-axis views (/) of the heart with
vessels and myocardium supplied by stenotic vessels because
stres (top row) and alresl(boftom row) show a radiotracer defect in the septal, anterior,
of the inability of the distal vasculature to dilate further. In and inferior walls that is filled on the rest images. Long-axis views (8) demonstrate
patients with left bundle branch block undergoing myocardial anterior, apical, and inferior filling defects with stres (top row) that is perfused at rest
perfusion imaging, vasodilator induced stress is preferred to (bottom row). These findings are consistent with reversible myocardial ischemia.

7
Diagnostic Testing in Cardiology

TABLE 3. lnterpretation of Myocardial Viability Cardiouascular Magnetic Resononce lmaging

Study Results CMR imaging may be used with dobutamine to assess r,r'all
SPECT Viabitity Testing motion abnormalities or with vasodilators to assess perfusion.
lnitial Study Rest Study Interpretation It is commonll'performed to evaluate the degree of infarction.
(at Rest) Repeated After ViabiliR' can be determined by evaluating the extent of m1,o-
4-24 h (With cardial fibrosis within the left ventricle. Measures of right and
Thallium) left ventricular function can be obtained u'ith gating. CMR
Perfusion defect Perfusion defect Fixed defea: imaging is limited by operator expertise. length of tinte for
infara, no viability image acquisition. and availability.
Perfusion defect Reperfusion of Viable
area myocardium XEY POIilIS
PETViability Testing r Cardiac stress testing is best used in patients with an
intermediate pretest probability of coronary artery
Baseline Metabolism lnterpretation
disease.
Perfusion defea Metabolically Viable
active myocardium o Exercise ECG is the preferred stress test in patients who
Echocardiographic Viability Testing can exercise and have normal findings on a baseline
ECG, because exercise provides additional prognostic
Baseline Response to lnterpretation
Dobutamine
information on functional capacity and hemodynamic
response.
Wall motion Low dose: Biphasic response
abnormality improvement of indicates viable . Stress testing with imaging is indicated in patients with
function myocardium an inability to exercise, contraindications to exercise.
Higher dose: baseline ECG abnormalities that preclude interpretation
worsening of of exercise ECC results, or indeterminate findings on
function
exercise ECG.
SPECT = sing e photon emiss on CT

Visualization of the Coronary Anatomy

Regions with fixed defects can indicate infarcted or hibernat Anatomic assessment of the epicardial coronary arteries can
ing myocardium, and viability assessment can help distin be performed with noninvasive coronary CTA or invasive lngi
guish between the two (Table 3). Gated images can provide an ography. Both tests require administration of contrast agents
assessment of left ventricular systolic function. and expose the patient to radiation. Abilit),to interpret CTA
SPECT imaging also can quantify the extent and severity can be limited in patients u'ith extensive calcification and
of disease. providing additional prognostic information. High small distal arteries.
risk features, such as multiple regions of hypoperfusion, In select symptomatic patients. CTA is another option fbr
reduction or lack ofaugmentation in poststress ejection frac ruling out CAD. ln the PROMISE trial. 10,000 symptomatic
tion, transient cavity dilatation, and wall motion abnormali patients suspected of having CAD were evaluated r.t,ith an ini
ties. are associated with a worse prognosis. tial strate$/ of either anatomic testing n'ith CTA or functional
Technetium based MPI has higher sensitivity and speci- testing. In patients n,ith an intermediate pretest probabilitl'of
ficity than thallium-based studies and provides belter image CAD, the composite cardiovascular event rate r\Ias lor,r' (<1'll,
quality. Technetium based agents bind to the mitochondria, per year) in both groups, and outcomes (death. ml,ocardial
allowing for delayed imaging. In contrast, thallium uptake infarction, hospitalization for unstable angina. or major proce
requires active metabolism, which can be useful in assessing dural complication) at 2 years did not differ betvreen groups.
myocardial viability. Coronary CTA also may play a role in the evaluation of
Cardiac PET provides excellent diagnostic and prognostic acute chest pain in the emergency department. CTA is appro
information for patients known or suspected to have CAD. PET priate in patients suspected of having an acute aortic syn
provides better temporal and spatial resolution than does drome or coronary embolism. CTA may be helpful in patients
SPECT, which is helpful in patients with obesity or nondiag- with low or intermediate likelihood of non ST elevation
nostic SPECT results. CT may be used with PET to provide acute coronary syndrome who have a lou, TIMI risk score.
information on the presence of coronary artery calcification. negatire troponin assay. or nonischemic findings on ECG. It
PET radiotracers have a short half'-life, resulting in lower radia also may be useful in patients with an equivocal diagnosis ol
tion exposure and necessitating the use of vasodilators. non ST elevation acute coronary s)'ndrome u'ho have an
Vasodilator stress allows for assessment of peak stress ejection equivocal initial troponin level or single troponin elevation
fraction, quantification of absolute myocardial blood flow and without further symptoms of acute coronary syndrome or in
evaluation of myocardial metabolism. The utility of PET in patients who have ischemic symptoms that resolved hours
cardiac patients is limited by availability of the technologz. before undergoing testing. Caref'ul consideration of patient

8
 Diagnostic Testing in Cardiology

f'actors is essential to avoid additional unnecessary testing, lmY P0t 1{r

potential harms, and unnecessary costs. . The absence of coronary artery calcification is associated
Invasive coronary angiography provides two dimensional with a low risk for cardiovascular events.
images of the coronary vessel Iumen through the injection of
nonionic contrast material using long, thin (<2-mm) catheters
percutaneously. The femoral or radial artery is used to obtain Risks of Diagnostic Testing for
arterial access, and radiation exposure is required. Invasive Coronary Artery Disease
angiography should be considered in highly symptomatic Cardiac diagnostic testing carries risks related to exerciser expo
patients with abnormal findings on stress testing, selected sure to pharmacologic stress testing agents, radiation, or contrast
patients with acute coronary syndrome, and patients with agents; and vascular access for invasive procedures. Additionally,
ischemic symptoms refractory to medical therapy. inappropriate initial testing may lead to unnecessary down-
FFR, when added to angiography or CTA, measures the stream testing with added physical and flnancial costs.
hemodynamic significance of a lesion and helps determine the There is a very small risk fbr myocardial infarction or
need for intervention. FFR is the ratio ofblood flow distal to death (1/2500 patients) with exercise stress testing. Absolute
the stenosis to blood flow proximal to the stenosis at maximal contraindications to exercise include unstable angina or acute
t'low. It is typically measured during cardiac catheterization myocardial inflarction, uncontrolled arrhythmias, decompen-
by placing a pressure wire across the stenosis and inducing sated heart failure, acute pulmonary embolism or deep venous
conditions of maximal hyperemia, usually with adenosine. thrombosis, acute pericarditis or myocarditis, acute aortic
lnstantaneous wave free ratio is a similar invasive functional dissection, and symptomatic severe aortic stenosis. Relative
assessment ofcoronary stenoses that does not utilize vasodila contraindications are left main coronary artery stenosis,
tor administration. FFR CT is an FDA approved noninvasive hypertrophic cardiomyopathy with severe obstruction, elec-
diagnostic test that provides both anatomic and functional trolyte abnormalities, high degree atrioventricular block, and
coronary data; it has higher specificity for the diagnosis of significant arrhythmias.
obstructive CAD than does CTA alone. FFR CT is performed Side effects of vasodilator stress agents (most commonly,
using computational fluid dynamics on CT derived data sets. adenosine and regadenoson) include chest pain, headache,
Limited availabiliff of FFR CT and potential delays in analysis and flushing. Atrioventricular block and bronchospasm also
affect its use in patients with acute symptoms. may occur. Theophylline may be given after testing to reverse
these effects. Vasodilator stress testing is contraindicated in
XEY POIl{I patients with reactive airways disease with active wheezing,
. Coronary angiography and CT angiography (ClA) pro- systolic blood pressure of less than 90 mm Hg, sick sinus syn
vide anatomic infbrmation regarding the extent and drome, or high degree atrioventricular block.
severity ofcoronary artery disease; however, the diag SPECT, PET, CAC scoring, coronary CTA. and coronary
nostic value of CTA may be limited in cases of extensive angiography all expose the patient to radiation. The level of
calcification. radiation exposure depends on the procedure, equipment,
choice ofradiopharmaceutical agent and dose, operator tech
Coronary Artery Calcium Scoring nique, and patient characteristics (e.g., body size).
Calcification of the coronary arteries is indicative ol ath- Contrast agents used in invasive angiography, coronary
erosclerosis and may be quantified with CT. Although CAC CTA, and CMR imaging also pose a risk to the patient. Rarely,
scoring provides infbrmation regarding the burden of dis CMR imaging that requires gadolinium contrast may cause
ease, it cannot determine the degree of obstruction. CAC nephrogenic systemic fibrosis in patients with end stage kid
measurement has been used for diagnosis and risk assess ney disease (see MKSAP 19 Nephrology). lodinated contrast
ment in both symptomatic and asymptomatic patients. material used in CT or angiography may result in acute kidney
Assessment ol CAC in asymptomatic patients should be injury. Microbubble contrast agents are used to enhance the
limited to those at intermediate cardiovascular risk and to endocardial borders in echocardiography and rarely can cause
select patients at borderline risk in whom CAC results may hypersensitivity reactions.
influence primary prevention therapy (see MKSAP 19 Coronary angiography can be complicated by vascular
Ceneral Internal Medicine l). CAC score also is incorpo- access problems, bleeding complications, coronary artery dis
rated in the MESA Risk Score to predict 10 year coronary section, aortic dissection, and plaque disruption or thrombus
heart disease risk (www.mesa nhlbi.org/MESACHDRisk/ leading to peripheral emboli, stroke, or myocardial infarction.
MesaRiskScore/RiskScore.aspx). Femoral artery access can be complicated by retroperitoneal
CAC scores are categorized as follows: 0, no disease; 1 to hemorrhage, which should be suspected in patients with
99. mild disease; 100 to 400, moderate disease; and greater hypotension, back or flank pain, and/or a drop in hemoglobin
than 400, severe disease. Normal reference values depend on level. Pseudoaneurysms at the arterial puncture sites occur
age, ethnicity, and sex. The absence ofCAC is associated with more commonly with f'emoral artery access and may manifest
a low risk for cardiovascular events. as a large hematoma or new bruit at the access site.

9
Diagnostic Testing in Cardiology

I(EV POITIT
o Vasodilator stress testing is contraindicated in patients
with reactive airways disease with active wheezing, sys
tolic blood pressure of less than 90 mm Hg, sick sinus
syndrome, or high degree atrioventricular block.

Diagnostic Testing for Structural

Heart Disease
Diagnostic testing for structural heart disease should be consid
ered in patients with suggestive history and physical examina-
tion findings, such as a grade 316 or higher systolic murmur, a
late or holosystolic murmul a diastolic or continuous murmur,
or a murmur with accompanying symptoms. Repeat imaging is
indicated in patients with structural heart disease when there is
F IG U R E 3. Transesophageal echocardiogram showing an absence of thrombus
a change in the clinical presentation. tunctional status, or exam in the left atrial appendage (LAA). The transducer is posteraor t0 the heart, and the
ination findings; routine surveillance imaging is guided by left atrium (LA) and LAA (arow) are more easily seen than with transthoraci(
lesion severity (see Valvular Heart Disease). Imaging modalities echocardiography. LV = left ventricle.
to evaluate for structural heart disease are listed in Table 4.
The mainstay of noninvasive imaging fbr structural heart identifies cardiac amyloidosis due to misfolded transthyretin
abnormalities is transthoracic echocardiography (TTE). TTE proteins (ATTR), with a specificity greater than 99'1,.
evaluates right and left chamber size. thickness. and function. f,EY POIXIS
including wall motion. TTE also provides information on val . The mainstay of noninvasive imaging for structural
vular patholory (including endocarditis), diastolic function,
heart abnormalities is transthoracic echocardiography,
hemodynamics, and the pericardium. TTE can be used rt,ith
which is used to evaluate patients'*'ith valvular abnor
intravenous agitated saline contrast. normally cleared by the
malities. congenital heart disease. pericardial disease, or
pulmonary circulation, to document the presence of an intra-
ventricular dysfunction.
cardiac shunt. Dobutamine infusion during TTE may be used
in patients with low gradient aortic stenosis in the setting of
. ggm-Technetium pyrophosphate scintigraphy can be

reduced ejection fraction to help diflerentiate between severe used to differentiate between amyloid subtypes and guide
patient management.
aortic stenosis and pseud<lstenosis.
Transesophageal echocardiography (TEE) is commonly
used to evaluate for inf'ective endocarditis and its complica-
tions (e.g., abscess). TEE also may be used to better visualize
Diagnostic Testing for
valvular pathologr, particularly when surgical or percutaneous Cardiac Arrhythmias
intervention is plannedr to evaluate specilic structures that The initial study in patients llith palpitations. pres)'ncope. or
cannot be well visualized on TTE (e.g., prosthetic heart valves) syncope when an arrhythmia is suspected should be 12 lead
or in patients with poor transthoracic imaging; to ev:rlurrte resting ECG. The ECC may show evidence o1'preexcitation.
acute aortic abnormalities: and to rule out left atrial thrombus ectopic rhythms. atrioventricular block. or intraventricular
befbre cardioversion (Figure 3). TEE requires moderate seda conduction delay, providing insight into the cause of the
tion and placement of the probe in the distal esophagus and symptoms. Echocardiography should be perfbrmed in ptltients
stomach. Contraindications include esophageal strictures or suspected of having structural heart disease.
active esophageal varices. Esophageal injury. including perfb The intermittent and fleeting nature of'arrhllhmias can
ration and bleeding, is a potential complication. make diagnosis difficult. Diagnostic studies are selected on the
CMR imaging can be used for evaluation of myocardial basis of symptom frequency and the duration and timing of the
and pericardial disease, including inflammatory or infiltrative recording (Table 5). [f symptoms occur daill: a 2.1- or 1B hour
processes. CMR is particularly useful in diagnosing hyper ambulatory ECG monitor (Holter monitor) ma1'be used. Long
trophic cardiomyopathy when there is eccentric or apical term ambulatory ECC monitors can be worn fbr up to 30 days
hypertrophy that is diflicult to visualize on echocardiography. if symptoms are less fiequent. lntiequent s),mptomatic e\ents
Although cardiac amyloidosis can be diagnosed with may be captured $,ith an external patient triggered event
echocardiography or CMR imaging, 99m technetium pyro recorder if the event lasts long enough for the patient to trigger
phosphate scintigraphy (eetrlTc-PYP) has re emerged as a useful the device. A looping event recorder captures seleral seconds of
means fbr diflerentiating between amyloid subtypes, which the ECG signal befbre the device is triggered: it is useful for
guides patient management. eemTc PYP imaging specifically (Text continued on page 13)

10
 Diagnostic Testing in Cardiology

TABLE 4. Diagnostic Testing for Structural Heart Disease

Diagnostic Test Major lndications Advantages Limitations
Transthoracic Heart failure Accurate diagnosis of structural Operator-dependent data acquisition;
echocardiography heart disease and its severity interpretation requires expertise
Cardiomyopathy
Ouantitation of LV size . nd function, Variability in instrumentation
Valvular disease
pulmonary pressures, valve function,
lmage quality limits diagnosis in
Congenital heart disease and intracardiac shunts
some patients (COPD, large body
Pulmonary hypertension Widely available, portable, fast habitus)

Aortic disease May require microbubble contrast

agents
Pericardial disease
Transesophageal Endocarditis High-quality images, especially of Requires esophageal intubation,
echoca rd iog ra phy posterior cardiac structures typically with moderate sedation
Prosthetic valve dysfunction
Most accurate test for evaluation of
Evaluation of embolic source
endocarditis, prosthetic valves, and
Aortic disease left atrial thrombus
Left atrialthrombus

Th ree-dimensional Mitral valve disease lmproved tomographic imaging Adjunct to two-dimensional imaging
echocardiography
ASD (percutaneous ASD Used during cardiac procedures for Limited by availability and expertise
closure) device placement
Cardiac masses lmproved assessment of LV global/
regional systolic function
Radionuclide Evaluation of LV systolic Ouantitative EF measurements Radiation exposure
angiography (MUGA) function
Accurate for serial LVEF measurements Provides no data on other cardiac
(e.9., to evaluate for cardiotoxicity structures
from chemotherapy)
Cardiac catheterization Coronary artery disease Direct measurement of intracardiac lnvasive
(left and right) pressures, gradients, and shunts
Congenital heart disease Radiation and radiocontrast
Contrast angiography provides exposure
Valve assessment
visualization of complex cardiac
lmages are not tomographic, limiting
Shunt assessment anatomy
evaluation of complex three-
Allows percutaneous intervention dimensional anatomy
for structural heart disease
Coronary CT Coronary artery disease Visualization of complex cardiac Radiation and radiocontrast exposure
angiography anatomy
Coronary anatomy assessment lmage acquisition improved with
High-resolution tomographic images sinus rhythm and slower heart rate
Congenital heart disease
CMR imaging Congenital heart disease High-resolution tomographic Limited by availability and expertise
imaging and blood-flow data
Myocardial disease Patient claustrophobia
(infiltrative disease, Ouantitative RVvolume and EF
myocarditis, hypertrophic measurements May be contraindicated in patients
cardiomyopathy) with an older pacemakel lCD, or
No ionizing radiation or contrast other implanted devices
RV cardiomyopathy (ARVC) material
Certain gadolinium-based contrast
Ouantitation of LV mass and Enables three-dimensional agents are contraindicated in
function reconstruction of cardiac anatomy patients with CKD"
Sinus rhythm and slower heart rate are
needed for improved image quality
Chest CT with contrast Aortic disease High-resolution tomographic images Radiation and radiocontrast
exposure
Cardiac masses Enables three-d imensional
reconstruction of vascular structures
Pericardial disease
99m-Technetium Amyloid transthyretin (ATTR) High specificity for ATTR amyloidosis Radiation exposure
pyrophosphate cardiac amyloidosis
scintigraphy
ARVC = arrhythmogenic right ventricular cardiomyopathy; ASD = atrial septal defecU CKD = chronic kidney disease; CMR = cardiac magnetic resonance; EF = ejection fradion;

"Group I gadolinium-based contrast agents are contraindicated in patients with end-stage kidney disease or estimated glomerular filtration rate less than 30 mUmin/1 .73 mr.
Group ll gadolinium-based contrast agents are not contraindicated in patients with CKD. There is insufficient data to malu u recommendation for group lll gadolinium_based
contrast agents in CKD.

11
Diagnostic Testing in Cardiology

TABTE 5. Diagnostic Testing for Suspected or Known Cardiac Arrhythmias

Diagnostic Test or Device lndications Advantages Limitations
Resting ECG lnitial diagnostic test in all 12-lead ECG recorded during Most arrhythmias are
patients the arrhythmia often identifies intermittent and not recorded
the specific arrhythmia on resting ECG
Continuous ambulatory ECG Short-term: Frequent (at least Records every beat for 24 h, Short-term: Not helpful when
(Holter monitor) daily) asymptomatic or 48 h, or up to 30 d for later arrhythmia occurs infrequently;
symptomatic arrhythmias for ana lysis ECG leads limit patient
24- and 4B-h monitors activities (24- and 48-h
Patient log allows correlation
monitors)
Long-term: lnfrequent with symptoms
asym ptomatic or sym ptomatic Long-term:Adhesive
Recorded data may be
arrhythmias for monitoring up attachment to chest; detection
transmitted to central
to30d of rhythm abnormalities that
monitoring service for rapid
are asymptomatic or not
notification
clinically significant
Exercise ECG Arrhyth mias provoked by Allows diagnosis of exercise- Physician supervision needed
exercise related arrhythmias during testing
Allows assessment of impact of Most arrhythmias are not
arrhythmia on blood pressure exercise related
and symptoms
Patient-triggered event I nfrequent symptomatic Small, pocket-sized recorder Symptomatic arrhyth mias must
recorder arrhythmias that last >1 '2 min is held to the chest when last long enough for patient to
symptoms are present activate the device
Recorded data may be Arrhythmia onset is not recorded
transmitted to central
Not use{ul for syncope or
monitoring service for rapid
extremely brief arrhythmias
notification
Looping event recorder lnfrequent, brief symptomatic Continuous ECG signal is ECG leads limit patient
(wearable) arrhythmias recorded (with the previous activities
30 s to 2 min saved)when the
Syncope patient activates the recording
Used for 1-4 wk in most cases

mode Device records only when

activated by patient
Arrhythmia onset is recorded
Looping event recorder Very i nfrequent asymptomatic Long-term continuous ECG lnvasive procedure with minor
(implantable) or symptomatic arrhythmias monitori ng with patient- ri sks
(e.g., infrequent syncope) triggered or heart rate-
Device is functionalfor 1 3 y
tri g gered episode stora ge
(device may need to be
Specific heart rate or ORS explanted)
parameters can be setto
initiate recording of data

Mobile cardiac outpatient Continuous outpatient ECG Auto-trig gered and patient- ECG leads limit patient
telemetry recording for precise triggered capture of arrhythmic activities unless a patch device
quantification or capture of events is used
rare arrhythmia
Up to 96 h of retrievable Resource intensive
memory
Some patch models connect
wirelessly to a mobile phone

Electrophysiology study lnducing, identifying, and Origin and mechanism of an lnvasive procedure with some
clarifying the mechanism o{ arrhythmia can be precisely risk
arrhythmia as well as potential defined
Some arrhythmias may not be
treatment (catheter a blation) inducible, particularly i{ the
Catheter ablation of the
abnormal heart rhythm or patient is sedated
implantation of a cardiac
electronic device (e.9.,
pacemaker or cardioverter-
defibrillator) may be
performed concomitantly

12
 Coronary Artery Disease

syncope or presyncope associated with arrhyhmias. An o Duration

implanted loop recorder may be warranted in patients with o Aggra\ating factors (exertion. anrietl'. meals)
very infiequent events. . Relieving factors
Exercise stress testing frequer.rtly is used in patients with
o Associated symptoms (shortness of breath. nausea. clil
suspected or known arrhythmia to evaluate for chronotropic
phoresis)
incompetence. ischemia, and exercise induced arrhy'thmia.
Most patients do not require invasive electrophysiologr Some demographic groups. including u'ot,'.tctt rti-tti

testing. Electrophysiology testing may be indicated in patients patients \\'ith diabetes mellitus. may present onll'u'itl-r iln l.licril
in rn hom the diagnosis remains indeterminate or in settings in s)'mptoms. including exertional d1'spnea. nausea. or e\aKqci-
which catheter based intenentions mav be needed to treat ated fatigue.
refractory arrhyhmias. The physical examin:rtion includes an eraluation oi tilt
cardiovascular system and a search for findings su&qcstills
I(EY POIlIT
conditions that mimic angina, including heart f.ailure. pr-rlmo
o The initial study in patients with palpitations, presyn- nary hypertension, valvular heart disease (particularll aortic
cope, or syncope when an arrhythmia is suspected stenosis), and hypertrophic cardiomyopathy
should be 12-lead resting ECG. The first step in diagnostic testing is to determine the pretcst
probability (or likelihood) of coronary artery diseasc' ((..\i))

Coronary Artery Disease (Table 6). A baseline resting ECG is required to eraiuate tbr ot'tg r

ing ischemia and to guide the choice of stress test (Figure +1.
Stress testing is most useful in patients $'ith an ir.rtemtedi.iic
Stable Angina Pectoris probabiliry* of CAD; houever. u'hen the pretest probabilir,\ ot'C.\i)
Diagnosis and Evaluation is high. testing may provide prognostic infbrmation. Other ctiirg
Stable angina pectoris is reproducible angina (discon.rfort or noses sl-rould be pursued in patiellts u'ith normal stress test finci
pressure of the chest, neck, or arms) of at least 2 months'dura
ings. lf stress testingyields abnormal results. additional er,aluation
tion that is precipitated by a stable level of exertion or emotional should be considered (see Diagnostic Testing in Cardiolog').
stress and is relieved with rest. Unstable angina is new onset
angina or angina occurring at a relatively low level of exefiion. I(EY POIf,TS
occurring at rest. or accelerating in fiequency or severity. r Stable angina is characterized by reproducible chest dis
Unstable angina is associated u,ith increased short term risk for comfbrt precipitated by exertion or emotional stress
acute myocardial infarction (Ml). without appreciable worsening over a period of at least
The evaluation of angina includes a focused history elicit 2 months.
ing information on the follort,ing anginal characteristics: o The initial evaluation of angina includes a locused his
o Qualit! tory eliciting qualiry location, radiation. and duration
o Location ofangina; aggravating and relieving factors; and associ
ated symptoms.
o Radiation

TABLE 6. Pretest Likelihood of Coronary Artery Disease in Symptomatic Patients According to Age and Sex'
Pretest Likelihood
Nonanginal Chest Painb Atypical Angina' Typical Anginad
Age (v) Men Women Men Women Men Women
30 39 4 2 34 12 76 26
40-49 13 3 51 22 8l 55
50-59 20 7 65 31 93 t3
60 69 27 14 72 51 94 B6

'Each value represents the percentage with s gnrficant coronary anery disease on catheterization.

"Nonanglnal chest pain has one or none of the components of typical angrna.

'Atypical angl na has two of the three components of typica I angi na.

Reproduced with permission from F hn SD, Gardin JM, Abrams J, et al; Amer can College of Cardiology Foundat on.2A12 ACCF/ANNACP/AATS/PCNAJSCA /STS gu oelrne i.ri

College of Cardiology Foundation and the Amelcan Hean Association, lnc. Published by Elsevier lnc. Ail rights reserued.

13
Coronary Artery Disease

Cardiovascular symptoms

Calculate pretest probability (likelihood) of CAD

Low lntermediate" Highb

No additional testing ECG normal and Medical therapy

able to exercise? for CAD

Yes No

ECG abnormal and

Exercise ECG
able to exercise?
. No response to
Markedly Yes No therapy
positiye test o Lifestyle-limiting
symptoms
. Progression to
Exercise MPl, exercise Pharmacologic MPl, unstable angina
echocardiography, or pharmacologic
coronary CT angiography echocardiography, or
coronary CT angiography

Markedly Markedly
positive test positive test
Coronary angiography

Stress lest Criteria for Markedly Positive Test Result

Exercise ECG Significant ST-segment J at low workload, ST-segment 1, hypotension
Exercise/pharmacologic MPI TID or lung intake of thallium, ischemia in >2 vascular distributions, EF <35%
Exercise/pharmacologic echocardiography EF <3596 at rest, ischemia in >2 vascular distributions, fall in EF with stress
Coronary CT angiography Significant stenosis (>70% in a major epicardial coronary artery)

FIGURE 4, Diagnosisof coronaryarterdisease.CAD=coronararterydisease; EF=ejectionfraction; MPI =myocardial perfusionimaging;TlD=transientischemicdilation.

'lntermediate pretesl probabi ity {likelihood) is variably delined as between 1 0% and 90% 0r belween 25"kail75"k.

General Approach to Treatment of alternative. Neither prasugrel nor ticagrelor has been studied
Stable Angina Pectoris in the context of stable angina, and their role in managing this
All patients with angina should receive guideline-directed condition remains to be established.
medical therapy comprising risk factor modification (regular Lipid-lowering therapy, targeting LDL cholesterol in par-
physical activity, weight loss, tobacco cessation, and dietary ticular, reduces the risk for vascular events and progression of
changes), cardioprotective medications to prevent thrombosis and underlying CAD. Statin therapy remains a cornerstone of sec
limit atherosclerotic progression, and antianginal medications to ondary prevention because it has been shown to reduce the
improve frurctional capacity through reduced cardiac workload risk for MI, death, and stroke. High intensity statin therapy
and/or increased myocardial oxygen delivery (Figure 5 and
(atorvastatin, 40-80 mg/d, or rosuvastatin, 20-40 mg/d)
Figure 6). Blood pressure control (with a goal of <130/80 mm Hg) decreases the LDL cholesterol level by 50'7, or more and is pre

and diabetes management should be emphasized. f'erred to moderate intensity therapy fbr secondary preven
tion, as higher statin dosing and the resultant lower LDL
Cardioprotective Medications cholesterol have been associated with graded improvement in
Aspirin reduces the risk for Ml and cardiovascular death in outcomes. In patients with statin intolerance (e.g., those who
patients with stable angina. Guidelines recommend low dose develop significant myalgia) or inadequate LDL cholesterol
aspirin (75 762 mg/d) for secondary prevention because it is as reduction with statin therapy, it is reasonable to address LDL
effective as high-dose aspirin (325 mgid) in preventing MI and cholesterol with nonstatin medications, especially ezetimibe
confers a lower bleeding risk. In aspirin intolerant patients, or proprotein convertase subtilisin/kexin type 9 (PCSKg)
clopidogrel, a platelet P2Yr2 receptor inhibitor, is an acceptable inhibitors. The addition of icosapent ethyl to statin therapy

14
 Coronary Artery Disease

HbAr. level >5.7%?

BMI :35 kg/m'??
eGFR>45 oGFR <45
mUminl 1.7 3 m2 mU minJ 1 -l 3 m2

level
27

risk and F.sing TG >150 mgy'dL

(1.69 mmol/L)?
risk?
LDL-C rcmains
Ml? >70 mmol/L)? BPstill >130/80 Shared
No Yes mm Hg?

LDI--C rcmains
.70mg,/dL(1,81 mmoYLP

FIGURE 5. Guideline-directedmedical therapyforpatientswithstableischemicheartdisease(SIHD).ACC=AmericanCollegeof Cardiology; ACEI =ACEinhibitor; AHA=

American HeartAssociation; ARB =angiotensin receptor blocker; BB = p-blocker; BID=twice daily; BP = blood pressurei CPAP= continuous positive airway pressure; eGFR =
estimated glomerular filtration rate; GLP-1 = glucagon-like peptide 1; HbA,, = hemoglobin A1.; LDL-C = LDI- cholesterol; Ml = myocardial infarction; PCSK9 = proprotein
convertase subtilisin/kexin type 9; SG[T2 = sodium-glucose cotransporter 2; TG = triglycerides.

Guidelino-directed medical ther.py heart

disease
o pBlocker (if not prescribed previously)
r Sublingual nitroglycorin as needed for angina

Continued symptoms

Continued symptoms and impaired quality of life

. Optimize long-acting and blocker

. Consider renolazine
Continued symptoms and impaired quality of life

Refer ior coronary angiography F IG Un E 6. Management of stable angina pectoris.

pfl = parcutaneous coronary intervention.

No Recommendations based on tihn SD, GardinJM,AbramsJ, etal; Ameri6n College of Gr

Coronary anatomy suitable for PCI diology toundation. 201 2 ACCF/AHA/ACP/MTS/PCNA/sCAI/SIS guideline for the diagnosis
or surgical rcvascularization? and management 0f patients with stable isdemi( heaft disease: a reportof theAmelicn
College olGrdiology toundation/Ameilcn HeartlssodationTask Force 0n PndiceGuide-
Yes lines, and the American College of Physicians,American Association forTholacic Sutgery,
Preventive Grdiovas.ular Nu6esfusociation, Society for GrdiovascularAngiography and
lnteoentions, and Sodety ol lhoracic Surgeons. J Am Coll Grdiol. 201 2;60:e44-e1 64.
IPMID: 231821251 doi:10.1016/ija(c2012.07.013

15
L
Coronary Artery Disease

provides further risk reduction in high risk patients with sublingual nitrates should be prescribed for acute reliel of
ll,pertriglyceridemia. Management of statin and nonstatin angina. Long acting nitrates, including isosorbide mononitrate
lipicl lowering therapies is discussed in MKSAP 19 General or dinitrate and nitroglycerin patch formulations. provide
lntern:rl Medicine 1. constant vasodilation. A nitrate free intenal of B to 12 hours.
ACE inhibitor therapy is indicated for stable angina if generalll' at night. is needed to avoid derelopment ol nitrate
there is concomitant diabetes. chronic kidney disease. left tolerance and reduced efficacy. Side effects include headache.
ventricular (LV) dysfunction (ejection fraction <40')1,), heart flushing, and hypotension. Because ofthe risk for h1'potension.
lirilure, or history of MI. In these populations. ACE inhibitors concurrent use ofnitrates and phosphodiesterase 5 inhibitors
have additional benefits unrelated to CAD, including presen'a (e.g.. sildenafil) is contraindicated.
tion of kidney function and improvement in LV function. Ranolazine reduces wall tension and myocardial oxlgen
Angiotensin receptor blockers (ARBs) may be used as an alter consumption through inhibition of the late sodium current
nativc to ACE inhibitors, although combination therapy is not and subsequent prevention of calcium overload. resulting in
indic:rted given the associated increase in ad'r,erse erents reduced angina and increased exercise time. Ranolazine has a
without clinical benefit. modest QT prolonging effect but no proarrhlthmic effects.
The QT interval should be monitored n'ith co administration
Antianginal Medications ofother QT-prolonging drugs, and dose reduction is indicated
p I3krckers relieve angina by reducing heart rate, myocardial in patients receiving moderate inhibitors olcltochrome P '150
contractility, and blood pressure. resulting in reduced myocar 3A,1 (CYP3A4), such as verapamil and diltiazem. Ranolazine
di:rl oxygen demand. They are recommended as first-line ther should not be used in combination r,r'ith strong CYP3A4 inhib
ilpv in patients with stable angina. All B-blockers are equally itors (clarithromycin, itraconazole. ketoconazole, severaI HIV
efTicacious in reducing angina. and the choice of p blocker medications) because of resultant increases in ranolazine
rr-ray depend on concomitant medical conditions (LV dysfunc serum levels.
tion, kidnev dysfunction. lung disease, or significant hyper
tension). Dosage should be titrated to achieve a resting heart
f,rY POTf,TS

rate between 55/min and 60/min. B-Blockers should be used o All patients with coronary artery disease should be
n,ith caution in patients taking nondihydropyridine calcium counseled on lifestyle modification. blood pressure
channel blockers (verapamil, diltiazem) because of additive control, and management of diabetes mellitus.
neqrrtive inotropic and chronotropic effects. Caution also o First-line therapy for stable angina includes aspirin.
shoulcl be exercised in the setting of significant conduction statin therapy, and p-blocker therapy.
disease or LV dysfunction. B, Selective p blockers. such as o inhibitor therapy is indicated for stable angina with
ACE
n-retoprolol. are preferred in patients with significant lung concomitant left ventricular dysfunction, heart failure.
clisease to avoid worsening respiratory flunction. In patients
diabetes mellitus, chronic kidney disease. or history of
n'ith reduced LV function. metoprolol succinate, bisoprolol. myocardial infarction.
anit canreclilol are associated with reduced long term mortal
itll Side eflects include fatigue. lethargl sleep disturbances.
irnd impotence. Coronary Revascularization
Calcium channel blockers improve myocardial oxygen Decision to Revascularize
delivery through coronary vasodilation and reduction in Patients with angina refractory to medical therapy or mark
corr)nrrry vilscular resistance while also decreasing myocardial edly abnormal stress testing or coronary CT angiography
oxlrgen consumption through antihypertensive and negative results should be considered for invasive coronary angiogra
inotropic etTects. These agents can be useful when symptoms phy (see Figure 4). The risks. benefits. and alternatives to
persist despite B blocker therapy or when p blockers are not angiography should be discussed along u'ith potential findings
tolerated. Shoft-acting dihydropyridine formulations. such as and therapeutic options. The primary goals of revasculariza
short acting nifedipine, should be avoided because they can tion in stable syndromes are to lessen angina and improve
p:rradoxically worsen angina by acutely lowering blood pres- quality ollife. In contrast, in unstable or acute presentations as
sure. resulting in reflex tachycardia and increased myocardial lvell as in stable patients \\,ith high-risk anatomic or clinical
oxygen demand. Nondihydropyridine calcium channel block f'eatures (left main CAD, large ischemic burden. and or heart
er-s shonld not be used in patients with LV dysfunction because failure). revascularization is indicated for prer,ention of future
ot'the increased adverse events associated with their negative events and improved survival.
chronotropic and inotropic effects. Revascularization targets are identified based on ana
Nitrates improve myocardial oxygen delivery through cor tomic and functional physiotogic characteristics associated
onary vasodilation and reduce oxygen demand by reducing with myocardial ischemia. Techniques such as fractional flolv
prelold, thereby reducing ventricular wall stress. The benefi reserve and instantaneous wave free ratio provide information
cja I etfbcts may be offset by reflex tachycardia unless combined on the f'unctional hemodynamic significance of indeterminate
n,itlr F blockers or calcium channel blockers. Short acting lesions identified on angiographic imaging (see Diagnostic

16
t

Coronary Artery Disease

Testing in Cardiologz), reducing both unnecessary stenting Although guidelines define minimum DAPT duration, the
and the need for urgent revascularization. optimal duration should be individualized according to the
patient's risks for thrombotic and bleeding complications.
Percutaneous Coronary Intervention In patients requiring oral anticoagulation for atrial fibril
Percutaneous coronary intervention (PCI) comprises several lation, warfarin or a direct oral anticoagulant (preferred) plus
different catheter based techniques to improve coronary clopidogrel can be considered without aspirin, often after 2 to
blood flow by relieving coronary obstruction. Following early 4 weeks of triple therapy. In patients with a mechanical valve
\ experience with balloon angioplasty and bare metal stenting, prosthesis, warfarin plus clopidogrel therapy is reasonable;
I
most PCI procedures currently involve second generation direct oral anticoagulants are contraindicated in these patients.
drug eluting stent placement, which reduces the risk fbr in In patients undergoing CABG for stable CAD, DAPT for
stent restenosis compared with bare metal stenting. 12 months may be reasonable to improve the patency ol vein
PCI is indicated to relieve symptoms in patients with grafts.
medically refractory angina, those unable to tolerate optimal
t( EY P0lltT5
L medical therapy, and those with high risk features on nonin
vasive testing. PCI has not been shown to be superior to o The primary goals of revascularization in stable ischemic
L
guideline directed medical therapy in reducing the risk for syndromes are to lessen angina and improve quality of
death or MI in patients with stable angina with or without life.
diabetes. o Percutaneous coronary intervention may alleviate
angina symptoms but does not decrease mortality or
!
Coronary Artery Bypass Graft Surgery risk for myocardial infarction in patients with stable
Coronary artery bypass grafting (CABG) with optimal medi angina.
cal therapy is generally recommended for patients with . In patients with stable angina who require revasculari
multivessel CAD because it results in decreased recurrence zation, coronary artery bypass graft revascularization is
of'angina, lower rates of MI, and fewer repeat revasculariza generally preferred to percutaneous coronary interven
tion procedures compared with PCI or medical therapy tion in those with left main or three-vessel coronary
alone, especially when arterial (internal mammary artery)
artery disease or multivessel coronary artery disease plus
conduits are utilized. CABC is associated with improved diabetes mellitus.
survival in patients lvith left main or three vessel CAD and
is indicated in those with multivessel disease and diabetes.
. Ten-year survival is improved in patients with coronary
artery disease and severe left ventricular dysfunction
CABG also improves 10 year survival compared with medi
who undergo coronary artery bypass grafting compared
cal therapy alone in patients with severe LV dysfunction.
with those who receive medical therapy.
Although myocardial viability is associated with improved
survival and ventricular recovery following revasculariz:r . In patients with stable angina who undergo percutane-
tion in patients with LV dysfunction, the role of viability ous coronary intervention, dual antiplatelet therapy
testing before revascularization has not been established as should be continued for at least 1 month after bare
a predictor of outcome. metal stent placement and at least 6 months after drug
eluting stent placement.
After Revascularization
Aspirin is recommended indef initely after revascularization.
't'he addition of a P2Y,, inhibitor to aspirin (dual antiplatelet Acute Coronary Syndromes
therapy [DAPT]) is indicated to reduce risk fbr stent thrombo General Considerations
sis and remote ischemic events. DAPT duration depends on An acute coronary syndrome (ACS) results from acute or sub
clinical considerations, including patient presentation and acute plaque rupture or erosion and coronary blood flow
bleeding and ischemic risks. impairment, manilesting as acute onset chest pain or an
ln patients treated with bare metal stent placement, a angina equivalent, often without a clear precipitant. The spec-
minimum of 1 month of DAPT is recommended. Current trum of ACS is further characterized by the presence of serum
guidelines recommend treating patients with stable angina biomarkers of myocardial injury (elevated troponin T or I).
with DAPT for at least 6 months without interruption after Mycicardial injury or MI may be related to an atherothrombotic
drug eluting stent placement, with the option to continue event (type 1) or demand/supply mismatch (type 2) (Figure 7).
therapy for a longer duration in those with a high risk for ST elevation Ml (STEMI) is differentiated from non
thrombosis related complications (e.g., depressed LV func ST elevation acute coronary syndrome (NSTE ACS) by findings
tion, saphenous vein graft stenting, and diabetes) and a favora on ECG (Figure 8). The hallmark ECG features of STEMI are
ble bleeding profile. In patients at high risk for bleeding, ST segment elevation of at least 1 mm in two or more contigu
current evidence supports 3 months of DAPT followed by ous limb or chest leads, although ST segment elevation in
lif'elong antiplatelet monotherapy as a reasonable strategz. leads V, and V" must be at least 2 mm in men and at least

17
Coronary Artery Disease

Elevated Cardiac Troponin Value(s) >9fth percentile URL

Troponin rise and/or fall Troponin level stable'

With acute Without acute

ischemiab ischemiab

Acute myocardial Acute myocardial Chronic

infaraion injury myocardial injury

Oxygen supply
Atherosclerosis
and demand
+ thrombosis
imbalance

Type 1 Ml: triggers Type 2 Ml: examples Examples Examples

o Plaque rupture . Severe hypertension o Acute heart failure o Structural heart disease
. Plaque erosion o Sustained tachyarrhythmia . Myocarditis o Chronic kidney disease

FIGURE 7. Amodel{orinterpreting myocardial injur. lschemicthresholdsvarsubstantially in relationtothe magnitudeofthestressorandtheextentofunderlying cardiac

disease. Ml= myocardial infarction; URL= upper reference limit.

'Stable denotes <20% variation of trop0nin values in the appropriate clin cal rontext.

blschemia denotes
signs and/0r symptoms of clinical myocardial ischemia.

@201 I The European Society of Cardiology; American College ol Cardioloqy Foundati0n; American Heart I6s0ciation, lnc ; and lhe World Heart Federation.

1.5 mm in women for diagnosis. Posterior MI typically mani bundle branch block may be considered a STEMI equivalent
fests as ST segment depression greater than 2 mm in the ante and potentially reflects an acute left anterior descending artery
rior leads (V, through V1) with tall R waves, often with occlusion or extensive injury.
ST segment elevation in the inferior or lateral leads and NSTE-ACS is categorized according to the presence ofbio
ST-segment elevation in posterior leads V, through Vr. New markers of cardiac injury (troponin T or l) in the serum. Non-
ST elevation MI is defined as a biomarker positive presentation

Acute coronary syndrome that does not meet criteria for STEMI. Unstable angina is charac-
(STEMI and NSTE-ACS) terized by new or worsening angina, with or without ECG
changes, and without detectable levels of cardiac injury markers.

Sl-Elevation Myocardial t nfarction

ST-segment elevation Nonspecific ECG changes
ST-segment depression Recognition
T-wave inversion STEMI typically involves coronary plaque mpture causing
platelet adhesion, activation, and aggregation and acute
thrombotic occlusion. The sudden transmural myocardial
STEMI NSTE-ACS ischemia manifests as ST-segment elevation and signifies the
need for rapid initiation ofreperfusion therapy (Figure 9).
Although the presentation of STEMI is olten dramatic and
Elevated cardiac
clear, several diagnoses can mimic STEML Acute pericarditis
Normal cardiac
troponin levels troponin levels presents with acute chest pain and ST-segment elevation sugges-
tive of STEMI. Distinguishing features may include pleuritic or
positional pain and diffuse or localized concave ST-segment ele
NSTEMI Unstable angina vation with corresponding PR segment depression (Frgure lO).
F IGUR E 8, Diagnosis of acute coronary syndromes. NSTE-ACS = non-Sl-elevation Pericarditis and myopericarditis resulting from viral infections
acute coronary syndrome; NSIEMI = non-ST-elevation myocardial infarction; or autoimmune conditions can cause cardiac enzyme release,
SIEMI = SI'elevation myocardial infarction. further confusing the clinical picture and necessitating a

18
 Coronary Artery Disease

STEMI

Evaluate:
1. Time from onset of symptoms"
2. High-risk featuresb
3. Time to device therapy with PCI
4. Risks of thrombolytic therapy (contraindications)

lnitiate medical therapy: aspirin,

p-blocker, nitrates, anticoagulant

PCI-capable facility Non-PCl-capable facility

Transfer for primary PCI'

Administer P2Yl, inhibitord Thrombolytic therapy

glycoprotein llb/llla inhibitor (goal s30 min from arrival)'
=
Administer clopidogrel
(300-mg loading dose)

PCI (FMC-to-device goal: <90

min for primary PCI)

Thrombolytic failure Successful reperfusion

Long-term medical therapy:
aspirin, P-blocker, ACE inhibitor,
high-intensity statin,
P2Y,, inhibitor Emergent transfer Urgent transfer for
for rescue PCI elective coronary
angiography and
possible PCll

FIGURE 9. Managementof ST-elevationmyocardial infarction(SIEI\41).Fl\4C=firstmedicalcontact; PCI =percutaneousc0r0naryintervention.

'lf )4 hours have elapsed since symptom 0nset, PCI is prefered.

bHigh.risk features, such as cardioqenic shock and heart failure, favor PCl.

'F[,4C.to.device ("doorto balloon") goal for patients beinq transle(ed for primary PCI is as soon as possible and <1 20 minutes.

dP2Yr2 inhibitore: dopidogrel, prasugrel,

ticagrelor.

within 30 minltes 0l h0spital presentati0n ("door to needle time') as a systems goal unless thrombolytic therapy is contraindicated.

thrombolytic therapy administration but is ideally performed within 24 hours.

CIR 0h013e3182742r{6

thorough history physical examination, and careful study of Patients with accelerated hyper-tension, significant LV
the ECG and biomarker release patterns. hypertrophy, and cardiomyopathies may present with chest
Acute aortic syndromes can cause ST-segment elevation if pain and elevated cardiac troponin levels caused by elevated
I the dissection involves the left or right coronary artery and is LV filling pressures or wall tension with associated subendo-
L
due to transmural myocardial ischemia. Early recognition is cardial ischemia. The ECG findings are often abnormal in these
i essential for this surgical emergency. Diagnostic clues to aortic patients. LV hypertrophy induced ECG changes may look
i

L dissection include differential blood pressures in the upper similar to ST segment elevation injury currents; however,
I extremities, tearing quality of pain with radiation to the back, these changes are tlpically concave in appearance. Comparison
I and mediastinal widening on chest radiograph. with previous ECG findings is helpful in identifying acute
I

Severe hypercalcemia may result in ST segment elevation changes.

t
L

that mimics ACS; however, other findings include a short QT Patients with supraventricular tachycardias, which may
t interval and flattened T waves. dramatically increase the rate pressure product, often present
I

t
I 19
t
i
Coronary Artery Disease

with chest pain, ST-segment depression, and elevated cardiac Primarg Percutaneous Coronary Interuention
enzyme levels, even if no CAD is present. PPCI refers to the process by which an emergency medical
provider activates a team of clinicians to initiate emergent
Reperfusion coronary angiography and PCI in patients with STEMI. The
Prompt reperfusion with primary PCI (PPCD or thrombolytic goal time from first medical contact until PPCI is 9O minutes
therapy is indicated in all patients with STEMI who do not or less. Because rates of achieving vessel patenry are higher
have limited life expectancy from other nonreversible disease and more reliable with PPCI than with thrombolysis, PPCI is
(see Figure 9). Short times to repedusion are correlated with the preferred method of treating STEMI when the patient pre-
improved outcome regardless of reperfusion strates/. sents to a PCl-capable hospital or can be transferred from an

20
 Coronary Artery Disease

TABLE 7. P2Y.2 lnhibitors Used in the Treatment of Patients With CAD Undergoing PCI
Drug lndications Loading Dose Maintenance Dose Adverse Effects Contraindications
Clopidogrel Stable CAD treated with 300-600 mg 75 mg/d I ncreased Known allergy to the
PCI bleeding risk drug
ACS
Ticagrelor ACS 180 mg 90 mg twice daily" lncreased Known allergy to the
bleeding risk, drug
\ dyspnea
Prasugrel ACS treated with PClb 60 mg 10 mg/d' lncreased Known allergy to
bleeding risk the drug, previous
transient ischemic
attack/stroked, age
>-75 y

ACS = acute coronary syndrome; CAD = coronary aa(ery disease; PCI = percutaneous coronary ntervent on.

Ticagrelor should be used with aspirin, 81 mg/d.

"Prasugrel should not be loaded "upstream" (before catheterization).

' Prasugrel, 5 mg/d, shou ld be consrdered for those weighi ng less than 60 k9 (1 32 lb).

aftack or stroke

ir.rdex hospital to a PCI capable center quickly (time from first h-rtracerebral hemorrhage is catastrophic, occurring in approx
medical contact to PPCI of <120 minutes). Although the initial imately l'1, of patients. Relative and absolute contraindications
fbcus of PPCI is on quickly restoring flow to the acutely to thrombolytic therapy are listed in Table 8.
occluded artery there is a demonstrable reduction in cardio ln addition to thrombolytic therapy, all patients without
vasclllar death and MI end points associated with complete a specific contraindication should receive a loading dose of
revascularization compared with culprit only PCI in patients aspirin (162 325 mg) as well as intravenous unfractionated
with multivessel disease. The relative benefit associated with heparin, enoxaparin, or fbndaparinux. Clopidogrel loading
timing of PCI of nonculprit vessels during the same procedure (300 mg orally) has been demonstrated to increase rates of
or within a short interval after PCI of the infarct related vessel vessel patency and is also recommended in this setting.
is not established. Prompt transfer to a PCI capable center following throm
Patients undergoing PPCI should receive aspirin (t0Z :ZS mg). bolytic therapy (for possible rescue PCI) is reasonable when
intravenous unfractionated heparin (with or without glyco this option is available. The ECG should be monitored at 60 to
protein IIb/llla blockade) or bivalirudin, and loading doses of 90 minutes to confirm reperfusion, reflected by at least 50'7,
additional antiplatelet drugs (P2Yu inhibitors) prior to or upon improvement in maximal ST segment elevation. One quarter
arrival in the catheterization laboratory (Table 7). to one third of patients do not achieve reperfusion, particu
larly with delayed presentation. Rescue PCI is associated with
Thrombolytic Therapy improved outcomes compared with conservative management
'lhrombolytic therapy is recommended for patients with in cases of failed reperfusion. Comnary angiography is recom
STEMI when symptom onset is within 12 hours and PPCI is not mended in all patients before discharge, even after successful
available within 120 minutes of first medical contact. If symp thrombolysis.
tcrnrs began 12 to 24 hours befbre presentation and there is
XEY POIilIS
evidence of hemodynamic instability or significant myocar
. When available in a timely manner, primary percutane-
dium at risk (such as with anterior MI), thrombolytic therapy
ous coronary intervention is preferred to thromboly'tic
should be considered if timely transfer for PPCI (the pref,erred
therapy for the treatment of ST elevation myocardial
strategy) is not available. Thrombolytic therapy is most
inlarction.
eftective within the first 3 to 6 hours from symptom onset,
after which time fibrin cross linking renders the clot rela r If primary percutaneous coronary intervention (PCI) is
tively resistant to lysis. When compared with streptokinase, not available within 120 minutes of first medical con
r.rewer fibrin specific thrombolytic agents (alteplase, reteplase, tact, patients with ST elevation myocardial infarction
tenecteplase) are associated with improved infarct artery should receive thrombolytic therapy and be transferred
patency and fewer allergic reactions, although they are more urgently to a PCl-capable center.
costly and have not lowered the risk tbr intracerebral hemor
rhage (0.5'){, 0.97,). Complications of STEMI
Although thrombolytic therapy is potentially life saving, Arrhythmias are common in the peri infarct setting. Atrial
it carries significant risks, primarily related to bleeding. fibrillation, which aftects up to 20'X, of patients with STEMl,

21