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e196 Circulation August 14, 2007
2. Continue enoxaparin for duration of hospitalization, up to 8 d,
if given before diagnostic angiography. (Level of Evidence: A)
3. Continue fondaparinux for duration of hospitalization, up to 8
d, if given before diagnostic angiography. (Level of Evidence: B)
4. Either discontinue bivalirudin or continue at a dose of 0.25 mg
per kg per h for up to 72 h at the physician’s discretion, if given
before diagnostic angiography. (Level of Evidence: B)
6. For UA/NSTEMI patients in whom a conservative strategy is selected
and who do not undergo angiography or stress testing, the
instructions noted below should be followed (Fig. 8; Box K):
a. Continue ASA indefinitely. (Level of Evidence: A)
b. Continue clopidogrel for at least 1 month (Level of Evidence: A)
and ideally up to 1 year. (Level of Evidence: B)
c. Discontinue IV GP IIb/IIIa inhibitor if started previously. (Level of
Evidence: A)
d. Continue UFH for 48 h or administer enoxaparin or fondaparinux
for the duration of hospitalization, up to 8 d, and then
discontinue anticoagulant therapy. (Level of Evidence: A)
7. For UA/NSTEMI patients in whom an initial conservative strategy is
selected and in whom no subsequent features appear that would
necessitate diagnostic angiography (recurrent symptoms/ischemia,
HF, or serious arrhythmias), LVEF should be measured. (Level
of Evidence: B) (Fig. 8; Box L)
CLASS IIa
1. For UA/NSTEMI patients in whom PCI is selected as a postangiography
management strategy, it is reasonable to omit administration
of an intravenous GP IIb/IIIa antagonist if bivalirudin was
selected as the anticoagulant and at least 300 mg of clopidogrel
was administered at least 6 h earlier. (Level of Evidence: B) (Fig. 9)
2. If LVEF is less than or equal to 0.40, it is reasonable to perform
diagnostic angiography. (Level of Evidence: B) (Fig. 8; Box M)
3. If LVEF is greater than 0.40, it is reasonable to perform a stress test.
(Level of Evidence: B) (Fig. 8; Box N)
CLASS IIb
For UA/NSTEMI patients in whom PCI is selected as a postangiography
management strategy, it may be reasonable to omit an intravenous GP
IIb/IIIa inhibitor if not started before diagnostic angiography for
troponin-negative patients without other clinical or angiographic highrisk
features. (Level of Evidence: C)
CLASS III
Intravenous fibrinolytic therapy is not indicated in patients without
acute ST-segment elevation, a true posterior MI, or a presumed new left
bundle-branch block. (Level of Evidence: A)
Antithrombotic therapy is essential to modify the disease
process and its progression to death, MI, or recurrent MI in
the majority of patients who have ACS due to thrombosis on
a plaque. A combination of ASA, an anticoagulant, and
additional antiplatelet therapy represents the most effective
therapy. The intensity of treatment is tailored to individual
risk, and triple-antithrombotic treatment is used in patients
with continuing ischemia or with other high-risk features and
in patients oriented to an early invasive strategy (Table 11;
Figs. 7, 8, and 9). Table 13 shows the recommended doses of
the various agents. A problematic group of patients are those
who present with UA/NSTEMI but who are therapeutically
anticoagulated with warfarin. In such patients, clinical judg-
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ment is needed with respect to initiation of the antiplatelet and
anticoagulant therapy recommended in this section. A general
guide is not to initiate anticoagulant therapy until the international
normalized ratio (INR) is less than 2.0. However,
antiplatelet therapy should be initiated even in patients therapeutically
anticoagulated with warfarin, especially if an invasive
strategy is planned and implantation of a stent is anticipated. In
situations where the INR is supratherapeutic, the bleeding risk
is unacceptably high, or urgent surgical treatment is necessary,
reversal of the anticoagulant effect of warfarin may be considered
with either vitamin K or fresh-frozen plasma as deemed
clinically appropriate on the basis of physician judgment.
3.2.4. Antiplatelet Agents and Trials (Aspirin,
Ticlopidine, Clopidogrel)
3.2.4.1. ASPIRIN
Some of the strongest evidence available about the longterm
prognostic effects of therapy in patients with coronary
disease pertains to ASA (363). By irreversibly inhibiting
COX-1 within platelets, ASA prevents the formation of
thromboxane A2, thereby diminishing platelet aggregation
promoted by this pathway but not by others. This platelet
inhibition is the plausible mechanism for the clinical benefit
of ASA, both because it is fully present with low doses of
ASA and because platelets represent one of the principal
participants in thrombus formation after plaque disruption.
Alternative or additional mechanisms of action for ASA are
possible, such as an anti-inflammatory effect (364), but they
are unlikely to be important at the low doses of ASA that
are effective in UA/NSTEMI. Among all clinical investigations
with ASA, trials in UA/NSTEMI have consistently
documented a striking benefit of ASA compared with
placebo independent of the differences in study design, such
as time of entry after the acute phase, duration of follow-up,
and dose used (365–368) (Fig. 10).
No trial has directly compared the efficacy of different
doses of ASA in patients who present with UA/NSTEMI;
however, information can be gleaned from a collaborative
meta-analysis of randomized trials of antiplatelet therapy for
prevention of death, MI, and stroke in high-risk patients
(i.e., acute or previous vascular disease or other predisposing
conditions) (375). This collaborative meta-analysis pooled
data from 195 trials involving more than 143,000 patients
and demonstrated a 22% reduction in the odds of vascular
death, MI, or stroke with antiplatelet therapy across a broad
spectrum of clinical presentations that included patients
presenting with UA/NSTEMI. Indirect comparisons of the
proportional effects of different doses of ASA ranging from
less than 75 mg to up to 1500 mg daily showed similar
reductions in the odds of vascular events with doses between
75 and 1500 mg daily; when less than 75 mg was administered
daily, the proportional benefit of ASA was reduced
by at least one half compared with the higher doses. An
analysis from the CURE trial suggested that there was no
difference in the rate of thrombotic events according to ASA
dose, but there was a dose-dependent increase in bleeding in