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CHAPTER 2 Coronary Artery Disease
improves survival in patients with STEMI when administered within 12 hours
of symptom onset.
19
Primary PCI is the recommended reperfusion therapy over fi brinolysis if per-
formed by an experienced team within 120 minutes of fi rst medical contact.
24
In
the National Registry of Myocardial Infarction, which compared primary PCI to
fi brinolytic therapy, PCI was associated with 37 percent lower mortality at high-
volume interventional centers.
19
At facilities without PCI capability, patients
with STEMI may be treated with fi brinolytic therapy if not contraindicated or
transferred to a facility with PCI capability.
24,35
All hospitals participating in the
care of patients with STEMI must record and monitor delay times and work to
achieve the following quality targets:
• First medical contact to fi rst ECG, 10 minutes or less
• First medical contact to reperfusion therapy:
• For fi brinolysis, 30 minutes or less (“door to needle”)
• For primary PCI, 90 minutes or less (60 minutes or less if the patient pres-
ents within 120 minutes of symptom onset or directly to a PCI-capable
hospital [“door to balloon”])
24
Fibrinolytic drugs approved for the treatment are streptokinase, alteplase,
reteplase, and tenecteplase (Table 2.4).
19,24,35
The main absolute contraindica-
tions to thrombolytic therapy are any prior intracranial hemorrhage, known
structural cerebral vascular or malignant intracranial lesion, ischemic stroke
within 3 months, intracranial or intraspinal surgery within 2 months, suspected
aortic dissection, active bleeding or diathesis, signifi cant closed-head or facial
trauma within 3 months, severe uncontrolled hypertension, and, for streptoki-
nase, prior treatment with streptokinase within the previous 6 months.
24
Management of STEMI
Patients undergoing primary PCI should receive a combination of aspirin and
a P2Y12 inhibitor, as early as possible before angiography, and a parenteral
anticoagulant. The preferred P2Y12 inhibitors are ticagrelor or prasugrel.
They have been shown to be superior to clopidogrel in large outcome trials.
43
Anticoagulant options for primary PCI include unfractionated heparin (UFH),
enoxaparin, and bivalirudin. Use of fondaparinux in the context of primary PCI
was associated with potential harm in the OASIS-6 trial and is therefore not
recommended. The existing data suggest that if bivalirudin is chosen as the
anticoagulant, there is no benefi t of routine addition of GP IIb/IIIa blockers, and
a strategy of bivalirudin alone leads to lower bleeding rates and reduced mor-
tality. If UFH or enoxaparin is chosen as the anticoagulant, the role of routine
use of GP IIb/IIIa blockers remains contentious.
30,32
In patients undergoing fi brinolytic therapy there is a good case for the rou-
tine use of clopidogrel as an adjunct to lytic therapy. Prasugrel and ticagre-
lor have not been studied as adjuncts to fi brinolysis and should not be given.
Parenteral anticoagulation has been used extensively during and after fi brinoly-
sis and should preferably be given until revascularization or at least 48 hours or
for the duration of hospital stay, up to 8 days. Enoxaparin was associated with a
reduction in the risk of death and reinfarction at 30 days when compared with
a weight-adjusted UFH dose, but at the cost of a signifi cant increase in non-
cerebral bleeding complications. Finally, fondaparinux was shown in the large
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CHAPTER 2 Coronary Artery Disease
Table 2.4 Guideline Recommendations and Level of Evidence for Antithrombotics in Non-ST-Elevation ACS by Management
Strategy and for Antithrombotics in STEMI by Management Strategy
NSTEMI Therapy ACC/AHA 2012 ESC 2011 ACCP 2008/12
Initial Conservative Clopidogrel
Prasugrel
Ticagrelor
GP IIb/IIIa
UFH
LMWH
Fondaparinux
Bivalirudin
Class I (LOE: B)
No Recommendation
Class I (LOE: B)
Class IIa (LOE: A)
Class I (LOE: A)
Class I (LOE: A)
Class I (LOE: B)
Not Recommended
Class I (LOE: A)
No Recommendation
Class I (LOE: B)
Class III(LOE: A)
Class I (LOE: C)
Class I (LOE:B)
Class I (LOE:A)
No Recommendation
Grade 1A
No Recommendation
Grade 1B
Grade 2B
Grade 1A
Grade 1B
Grade 1A
No Recommendation
Early Invasive Clopidogrel
Prasugrel
Ticagrelor
GP IIb/IIIa
UFH
LMWH
Fondaparinux
Bivalirudin
Class I (LOE: A/B)
Class I (LOE: B)
Class I (LOE: B)
Class I (LOE: A/B)
Class I (LOE: A)
Class I (LOE: A)
Class I (LOE: B)
Class I (LOE: B)
Class I (LOE: B)
Class I (LOE: B)
Class I (LOE: B)
Class I (LOE: B)
Class I (LOE: C)
Class I (LOE: B)
Class I (LOE: B)
Class I (LOE: B)
Grade 1A
Grade 1B
Grade 1B
Grade 1A
Grade 1B
Grade 1B
Grade 1B
Grade 2B
(continued)
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CHAPTER 2 Coronary Artery Disease
STEMI ACC/AHA 2013 ESC 2012 ACCP 2008/12
Primary fi brinolytic Clopidogrel
Prasugrel
Ticagrelor
GP IIb/IIIa
UFH
LMWH
Foundaparinux
Bivalirudin
Class I (LOE: A)
No recommendation
No recommendation
No recommendation
Class I (LOE: C)
Class I (LOE: A)
Class I (LOE: B)
Not recommended
Class I (LOE:A)
Not recommended
Not recommended
Not recommended
Class I (LOE: C)
Class I (LOE: A)
Class IIa (LOE:B)
Not recommended
Grade 1 A
No recommendation
No recommendation
Grade 2B
Grade 1
Grade 1B
Grade 1B
Not recommended
Primary PCI Clopidogrel
Prasugrel
Ticagrelor
GP IIb/IIIa
UFH
LMWH
Fondaparinux
Bivalirudin
Class I (LOE: B)
Class I (LOE: B)
Class I (LOE:B)
Class IIa (LOE:A/B)
Class I (LOE: C)
No recommendation
Not recommended
Class I (LOE: B)
Class I (LOE:C)
Class I (LOE:B)
Class I (LOE:B)
Class IIa (LOE:B/C)
Class I (LOE:C)
Class IIb (LOE: B)
Not recommended
Class I (LOE: B)
Grade 1A
Grade 1B
Grade 1B
Grade 1B
Grade 1C
Grade 2A
Not recommended
No recommendation
ACC, American College of Cardiology; ACCP, American College of Chest Physicians; AHA, American Heart Association; ESC, European Society of Cardiology; LMWH, low-molecular-weight heparin;
LOE, level of evidence; UFH, unfractionated heparin.
Adapted from reference 41.
Table 2.4 Continued
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CHAPTER 2 Coronary Artery Disease
OASIS-6 trial to be superior to placebo or UFH in preventing death and rein-
farction, especially in patients who received streptokinase. Bivalirudin has not
been studied with fi brin-specifi c agents. Tenecteplase, aspirin, enoxaparin, and
clopidogrel are the antithrombotic combination that has been most extensively
studied as part of a pharmacoinvasive strategy (Tables 2.4 and 2.5).
19,24,33,35
Future directions in CAD
Various clinical issues of the management of patients with stable coronary dis-
ease are being addressed in many ongoing clinical trials. In the International Study
of Comparative Health Effectiveness with Medical and Invasive Approaches
(ISCHEMIA),
15
investigators are scheduled to enroll 8,000 patients with high-
risk noninvasive vascular testing results to a strategy of OMT (with coronary
angiography and revascularization when clinically indicated) or to a strategy
of revascularization. The results of this trial probably will determine the treat-
ment strategy for patients with high-risk myocardial imaging (stress perfusion
or echocardiographic) test results, by testing for differences in the composite
end point of time to fi rst occurrence of cardiovascular death or nonfatal MI.
46
The use of hematopoietic stem cells to boost bone marrow function and blood
vessel formation has been tested in the phase II Autologous Cellular Therapy
CD34—Chronic Myocardial Ischemia (ACT34-CMI) trial and in phase III, Effi cacy
and Safety of Targeted Intramyocardial Delivery of Auto CD34
+
Stem Cells for
Improving Exercise Capacity in Subjects With Refractory Angina (RENEW).
47
Finally, among the emerging platforms for CAD biomarkers discovery, perhaps
none has garnered more recent attention than proteomics and metabolomics.
The identifi cation of new biomarkers of coronary artery diseases will depend
on the complementary power of genetics, transcriptional profi ling, proteomics
and metabolomics.
48
Taken together, these new lines of research discovery for
patients with symptomatic coronary disease will help to evolve the diagnosis and
management of these patients in an effort to better control patient symptoms
and further improve short-term and long-term outcomes.
Table 2.5 Dosing of Antithrombotic Therapies for the Treatment
of Acute Coronary Syndromes
Drug Class Dose Comments
Aspirin
Aspirin
• Initial dose 160–325 mg, then
75–325 mg daily for both
STEMI and NSTEMI
Indefi nitely
Platelet P2Y12
Inhibitors
Recommend for up to
12 months for patients with
STEMI and NSTEMI, regardless
of whether PCI is performed
Clopidogrel
• Loading dose: 300–600 mg,
then 75 mg/day
There may be an interaction of
proton pump inhibitors with
clopidogrel treatment so caution
is recommendation is using this
concomitant medication.
(continued)
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CHAPTER 2 Coronary Artery Disease
Drug Class Dose Comments
Prasugrel
• Loading dose: 60 mg, then
10 mg/day
There are no recom mendations
for treatment with prasugrel before
PCI and no recommendations
for use in patients who do not
undergo PCI
Ticagrelor
• Loading dose: 180 mg,
then 90 mg twice a day
The recommended maintenance
dose of Aspirin to be used with
ticagrelor is 81 mg daily
Glycoprotein IIb-
IIIa Inhibitors
STEMI: to support
reperfusion with primary
PCI in conjunction with
UFH or bivalirudin, in
selected patients, or in
High-risk UA/NSTEMI
patients
Abciximab
• 0.25 mg/kg IV bolus, then
0.125 mcg/kg/min (maximum
10 mcg/min)
Duration:12 hrs
Eptifi batide
• 180 mg/kg bolus followed
10 mins later by second IV
bolus of 180 mg/kg, then
2.0 mg/kg/ min, started after
fi rst bolus
Duration: 18–24 hours
In patients with CrCl <50 mL/min,
reduce infusion by 50%
Avoid in patients on hemodialysis
Tirofi ban
• STEMI: 25 mcg/kg IV bolus,
then 0.15 mcg/kg/min
• UA/NSTEMI:
• Before angiography:0.4 mcg/
kg/min IV for 30 mins then
0.1 mcg/kg/min IV for 12–24
hours (PRISM-PLUS)
• Adjunct to PCI: 10 mcg/kg/
min IV bolus over 3 minutes
immediately prior to PCI
plus 0.15 mcg/kg/min IV for
18–24 hours (RESTORE/
TACTICS)
Duration: 12–24 hours
In patients with CrCl < 30 mL/min,
reduce infusion by 50%
Avoid in patients on hemodialysis
Anti-Coagulants
Unfractionated
heparin
(NSTEMI)
• 60 U/kg IV bolus then 12 U/ kg
IV infusion adjusted to
achieve an activated partial
thromboplastin time of
50–70 secs
(STEMI)
• PCI with GPIIb/IIIa: 50–70 U/kg
bolus IV > Intermittent bolus
to achieve activated clotting
time of 200–250 secs
• PCI without GPIIb/IIIa: 70–100
U/kg IV > Intermittent bolus to
achieve activated clotting time
of 250–300 sec
Duration: 2–5 days, discontinue
after successful PCI
Discontinue after successful PCI
Discontinue after successful PCI
Table 2.5 Continued
(continued)
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CHAPTER 2 Coronary Artery Disease
Drug Class Dose Comments
• Use with fi brinolysis: IV bolus
of 60 U/kg (maximum 4000 U)
followed by an infusion of 12
U/kg/h (maximum 1000 U)
initially, adjusted to maintain
aPTT at 1.5 to 2.0 times
control (approximately 50
to 70 s) for 48 h or until
revascularization.
Duration: 48 hours after fi brinolysis
Enoxaparin
• If age <75 y: 30 mg IV bolus,
followed in 15 min by 1 mg/
kg subcutaneously every 12
h (maximum 100 mg for the
fi rst 2 doses)
• If age ≥ 75 y: no bolus, 0.75
mg/kg subcutaneously every
12 h (maximum 75 mg for the
fi rst 2 doses)
• Regardless of age, if CrCl
<30 mL/min: 1 mg/kg
subcutaneously every 24 h
• Duration of hospitalization
(up to 8 days); discontinue after
successful PCI
• Contraindicated if Contraindicated
if CrCl <30 mL/min
Foundaparinux
•
2.5 mg SC daily • Duration of hospitalization
(up to 8 days)
• Contraindicated if CrCl <30
mL/min
• Not recommended as sole
anticoagulant for primary PCI
Bivalirudin
• Loading dose: 0.75 mg/kg IV
bolus, then 1.75 mg/kg/hr
infusion with or without prior
treatment with unfractionated
heparin
• Duration: Up to 72 hours;
discharge after successful PCI
• An additional bolus of 0.3 mg/kg
can be given if needed.
• Reduce infusion to 1 mg/kg/h
with estimated CrCl <30 mL/min
• Preferred over UFH with GP
IIb/IIIa receptor antagonist in
patients at high risk of bleeding
Fibrinolytics
Alteplase
• 15 mg IV bolus
• 0.75 mg/kg over 30 min
(up to 50 mg) then
• 0.5 mg/kg over 60 min IV
(up to 35 mg)
Use a concomitant anticoagulant –
either UFH or enoxaparin
Reteplase
• Two 10 unit boluses, given
30 mins apart
Use a concomitant anticoagulant –
either UFH or enoxaparin
Tenecteplase
• Single IV bolus:
30 mg if <60 kg
35 mg if 60 to <70 kg
40 mg if 70 to <80 kg
45 mg if 80 to <90 kg
50 mg if ≥ 90 kg
Use a concomitant anticoagulant –
either UFH or enoxaparin
Streptokinase
• 1.5 million units given over
30–60 mins
Concomitant anticoagulant is not
required
Table 2.5 Continued
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CHAPTER 2 Coronary Artery Disease
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CHAPTER 2 Coronary Artery Disease
33. Kushner FG, Hand M, Smith SC Jr, et al. 2009 f ocused updates: ACC/AHA guide-
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2012; 163 (5): 844–850 .e1.
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Chapter 3
Valvular Heart Disease
Patrick Collier and Brian Griffi n
Introduction
The present chapter reviews the importance of atherothrombosis in clinical
practice with specifi c regard to valvular heart disease. Particular attention is
focused on the important overlap that exists between aortic stenosis (the most
common valvular lesion encountered among elderly patients) and atheroscle-
rosis. In addition, the thrombotic risks associated with valvular heart disease
are discussed. Finally, as the number of surgical cases of heart valve disease
is expected to triple by 2050 (and to exceed 1 million worldwide cases annu-
ally) the emerging technology of transcatheter aortic valve replacement merits
special attention.
1
Shared etiologies of aortic stenosis
and atherosclerosis
Aortic stenosis and atherosclerosis are common diseases whose prevalence
increases with age; they frequently occur as comorbid pathologies.
2
Indeed,
it has been reported that up to 40 percent of patients with aortic stenosis
had at least one epicardial coronary artery stenosis of more than 70 percent.
3
However, rather than just a simple overlap between two common disease
entities, an emerging literature now suggests the possibility of a common eti-
ology between nonrheumatic aortic stenosis and atherosclerosis.
4,5
A shared
importance for risk factors traditionally associated with atherosclerosis has
been demonstrated to apply to the development and progression of calcifi c
degenerative aortic valve disease, which itself strongly correlates with future
cardiovascular events.
2,6
This hypothesis has also been driven by the fact that
many histological similarities have been found between the early lesions of aor-
tic stenosis and coronary plaque—namely that both are initiated by endothelial
dysfunction, both involve local activation of fi bro-infl ammatory pathways, and
both are chronic self-propagating pathologies.
7
Atherosclerotic risk factors have repeatedly been shown to be associated
with aortic stenosis, including older age, male sex, hypertension, waist circum-
ference, smoking, diabetes, and hyperlipidemia.
8,9
Furthermore, the gradient in
the association of cardiovascular risk factors with the severity of valve thick-
ening and calcifi cation suggests that they may even be causally implied in the
pathogenesis of the disease.
9
In atherosclerosis and aortic stenosis, these risk
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