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Treatment of NSTEMI (Non-ST Elevation

Myocardial Infarction)

Article · March 2013

DOI: 10.1007/s40138-012-0006-y

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Curr Emerg Hosp Med Rep (2013) 1:18–28
DOI 10.1007/s40138-012-0006-y

ACUTE CORONARY SYNDROME (J HOLLANDER, SECTION EDITOR)

Treatment of NSTEMI (Non-ST Elevation Myocardial Infarction)

V. Anantharaman • Swee Han Lim

Published online: 24 January 2013

 Springer Science+Business Media New York 2013

Abstract Non-ST elevation myocardial infarction (NSTEMI) angina pectoris, acute myocardial infarction, heart failure
is a recognized diagnostic entity that has an unacceptable and sudden death. The first four of these are referred to as
mortality rate when it goes unrecognized. Following diagnosis, ‘‘acute coronary syndromes’’ (ACS). Though chest pain is
initial treatment with analgesics, nitrates and anti-platelet agents the commonest symptom in patients with ACS, the diag-
forms the initial approach. New anti-platelet agents such as nosis is contingent on the electrocardiogram (ECG), which
ticagrelor and prasugrel need to be clearly understood. Simul- identifies two groups of people, viz. those with persistent
taneously, risk stratification for ischaemia and bleeding of each ST-segment elevation of more than 20 min duration (ST-
such patient into mild, moderate and severe helps determine the elevation myocardial infarction or STEMI), and without
course of further treatment that will be provided to the patient. persistent ST-segment elevation (including patients with
The major decision is the need for and timing of early coronary persistent or transient ST-segment depression, T wave
angiography to determine the anatomy of the culprit vasculature inversions, flat T waves or pseudo-normalization of T
and the decision for coronary revascularization, either by the waves or no ECG changes at all), after a diagnosis of non-
percutaneous approach or coronary artery bypass grafting. It is at cardiac chest pain has been excluded. This paper will focus
this stage that the need for and type of anticoagulation will on this latter group of patients, especially those with non-
require decision making. Choices include fondaparinux, the ST elevation myocardial infarction (NSTEMI). The annual
heparins, bivalirudin and inhibitors of the coagulation cascade. incidence of NSTEMI varies significantly between coun-
tries, with a mean global annual incidence of about 3 per
Keywords Non-ST elevation myocardial infarction
1,000 population [1].
Cardiac biomarkers
Risk stratification
Clopidogrel

Ticagrelor
Percutaneous coronary intervention

Pathophysiology of Acute Coronary Syndromes

Introduction
The disease begins gradually with accumulation of ath-
Coronary artery disease (CAD), by far the commonest erosclerotic plaques in the coronary arteries until one of
variety of cardiovascular disease, includes a spectrum of these either ruptures or erodes at the luminal surface. The
conditions ranging from silent angina, stable and unstable acute thrombus formed over the diseased plaque may be
associated with coronary vasoconstriction and critical
reduction of blood flow to the distal myocardium. This may
be accompanied by endothelial dysfunction, accelerated
V. Anantharaman (&)
S. H. Lim atherothrombosis and further myocardial injury. NSTEMI
Department of Emergency Medicine, Singapore General
Hospital, Outram Road, Singapore 169608, Singapore lesions have lesser coronary stenosis with a thin overlying
e-mail: [email protected] fibroatheroma, a large plaque burden, small luminal cross-
S. H. Lim sectional area or some combination of these [2] than
e-mail: [email protected] STEMI lesions.

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Curr Emerg Hosp Med Rep (2013) 1:18–28 19

Diagnosis of NSTEMI failure may also demonstrate elevated troponin levels.

The recent introduction of highly-sensitive or ultrasen-
The diagnosis of NSTEMI requires the following: sitive troponin assays [3, 4, 5••, 6•, 7, 8, 9•] has allowed
earlier detection of myocardial damage in patients
1. History: Chest pain, the leading symptom, typically
presenting with chest pain. The addition of a second
presents as retrosternal discomfort, heaviness or pressure
sample of these newer assays 2–3 h after the first further
sometimes radiating to the left arm, neck or jaw, and
increases their sensitivity.
lasting several minutes or occasionally persistent. There
may be accompanying dyspnea, diaphoresis, nausea or Newer cardiac biomarkers [10••] are being tested in
vomiting and occasionally palpitations and syncope. clinical trials for their incremental value and cost-effec-
Atypical symptoms include epigastric discomfort, sharp tiveness. One promising example is Copeptin (C-terminal
chest pains, or increasing breathlessness and are more pro-vasopressin) which is released very early soon after
common in older patients (C75 years age), women, onset of symptoms [11–13, 14••, 15] and has demonstrated
diabetic patients, and those with uraemia or functional myocardial damage within an hour of symptom onset.
decline. Atypical symptoms can lead to under-diagnosis, Combinations of biomarkers may provide greater sensi-
hence requiring a high index of suspicion. The symptoms tivity for earlier diagnosis of NSTEMI.
may be aggravated by exertion and anaemia and relieved
by rest or taking of nitrates. Risk factors for NSTEMI are
Relief of Ischaemic Pain
similar to that for STEMI.
2. Physical Examination: This involves looking for com-
Pain relief is one of the most pressing needs of the patient. In
plications of CAD such as heart failure and arrhythmias,
acute coronary ischaemia, the increased heart rate, higher
precipitating conditions such as anaemia or thyroid
blood pressure or high preload result in decreased myocardial
problems or identifying non-ischaemic cardiac or non-
oxygen supply and increased myocardial oxygen demand.
cardiac causes of chest pain, such as pulmonary
This oxygen imbalance results in ischaemic pain. The objec-
embolism, aortic dissection, pneumothorax and others.
tive of anti-ischaemic drugs is to reverse these processes and
3. Electrocardiogram: Features on the ECG suggesting
secure pain relief. Drugs that have been demonstrated to
NSTEMI include ST-segment depression or transient
benefit symptoms and promote good outcomes are:
elevation and/or T-wave changes. However, the pres-
ence of a normal or inconclusive ECG at presentation Nitrates: Their venodilator effects decrease myocardial
does not exclude NSTEMI. Diagnosis may be enhanced oxygen demand by lowering myocardial preload and left
by comparing with previous ECGs, if available, or ventricular end-diastolic volume, and at the same time
repeat ECGs at 3–9 h after presentation or even at 24 h, increase myocardial oxygen supply by dilating coronary
at discharge, or immediately on symptom recurrence. arteries and increasing coronary collateral blood flow.
Occasionally changes may be picked up with additional Nitrate use favours lesser increase in cardiac biomarker
chest leads at V7–V9 and V3R–V6R. Transient bundle levels [16•]. When given intravenously, nitroglycerine
branch block during occurrence of symptoms signals allows titration of dose until symptom relief or occurrence
ongoing coronary ischaemia. of side effects. Caution is needed when administering
4. Cardiac Biomarkers: Elevation of cardiac markers is nitrates to patients on phosphodiesterase-5 inhibitors (e.g.,
crucial for a diagnosis of NSTEMI, distinguishing this sildenafil) because of likely severe vasodilatation and
from unstable angina. They have a role in risk stratifi- hypotension.
cation. The range of cardiac biomarkers becoming b-Blockers: While the CRUSADE registry [17] registered
available is growing. In addition to the traditional a significant 34 % reduction (3.9 vs 6.9 %, p \ 0.001) in
creatine kinase MB isoenzyme (CKMB) and myoglobins in-hospital mortality with acute b-blocker administration,
which are less specific for cardiac muscle damage, a systematic review conducted some years later [18•] did
troponins (both Trop-T and Trop-I) have been used as not demonstrate any such benefit if given within the first
standard biomarkers over the last few years. In NSTEMI 8 h of presentation. Current recommendation [19•]
patients, cardiac troponin elevation occurs from myo- includes introducing b-blockers within 24-h of diagnosis
cardial damage secondary to distal embolization of in those without signs of low-output heart failure or major
platelet-rich thrombi from the site of a ruptured or eroded risk factors for cardiogenic shock.
plaque. Troponins, when released into the circulation, Calcium Channel Blockers: These are for patients
usually rise at least 3 h after symptom onset. Other life- already on nitrates/b-blockers, those for whom b-block-
threatening causes of chest pain, e.g. dissecting aortic ers are contraindicated [20], and those with coronary
aneurysms, pulmonary embolism and patients with renal vasospasm.

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20 Curr Emerg Hosp Med Rep (2013) 1:18–28

Angiotensin Converting Enzyme (ACE) Inhibitors: Oral on the extent of the abnormality. The HEART score is
ACE inhibitors (if not contraindicated) may be given the sum of these five factors.
within 24 h of presentation for NSTEMI patients with
Some scoring systems for bleeding risk that may be used
pulmonary venous congestion or left ventricular ejection
in the early assessment of NSTEMI include:
fraction (LVEF) B40 % or in the absence of hypoten-
sion. If ACE inhibitors are contraindicated, an angio- • Can Rapid risk stratification of Unstable angina patients
tensin receptor blocker (such as losartan, telmisartan or Suppress ADverse outcomes with Early (CRUSADE
valsartan) may be used [21]. implementation of the ACC/AHA guidelines) bleeding
Morphine: Data from the CRUSADE registry [22] score [31] which considers baseline patient character-
demonstrated higher mortality in patients requiring istics (female sex, history of diabetes, peripheral
morphine. While this may have been owing to a higher vascular disease), admission clinical variables (heart
level of pain in such patients, the use of intravenous rate, systolic blood pressure, signs of CHF), and
morphine in NSTEMI would be mainly for those with admission laboratory values (hematocrit, calculated
chest pain refractory to nitrates and presuming other creatinine clearance) to estimate the patient’s likelihood
anti-anginal therapy is also underway. of having an in-hospital major bleed event.
• Acute Catheterization and Urgent Intervention Triage
strategY (ACUITY) [32], an integer-based risk score
Risk Stratification in NSTEMI that includes age, gender, serum creatinine levels, white
cell count, anaemia, clinical presentation and use of
The objective of risk stratification in patients with NSTE- antithrombotic medications, with weightage given to
MI is to identify those at high risk for further ischemic different levels of these seven variables.
events or adverse outcomes. The initial assessment is to
With such available stratification systems, risks may be
detect patients at immediate high risk. Subsequent evalu-
categorized into one of three groups with predicted six-
ation is to identifying patients who will benefit from an
monthly mortality, viz. low (0–3.0 %), intermediate
early invasive strategy at 4–48 h and, finally, at predicting
(3.0–6.0 %) and high-risk (9.0 % and above) [33••].
who are at increased risk after discharge [23••].
Primary criteria for high-risk categorization includes rele-
On diagnosis of NSTEMI, a decision is required on the
vant rise or fall in cardiac biomarker levels, and/or dynamic
level of acute ischaemic and bleeding risk for the patient
ST- or T-wave changes. Secondary criteria include diabetes
(high, intermediate or low). Such risk determinations aid
mellitus, renal insufficiency (with eGFR of less than 60 mL/
decision making on available treatment options. Some
min/1.73 m2), left ventricular ejection fraction B40 %,
common or promising risk stratification scoring systems
early post-infarction angina, recent percutaneous coronary
[24] are:
intervention (PCI) procedures, prior coronary artery bypass
• Thrombolysis in Myocardial Infarction (TIMI) score grafting and intermediate to high risk stratification scores.
[25, 26] includes age C65 years, C3 CAD risk factors
(high cholesterol, family history, hypertension, diabetes
mellitus, smoking), prior CAD, aspirin in the past Early Management of NSTEMI
7 days, at least two angina-related events in the
previous 24 h, ST-segment deviation and elevated Risk-level determination allows one to offer advice regard-
cardiac biomarkers (CKMB or troponin). ing a variety of treatment procedures, viz. need for a variety
of anti-platelet agents, glycoprotein IIb/IIIa inhibitors
• Global Registry of Acute Coronary Events (GRACE)
(GP23I) and anticoagulants, and allow rational discussion of
Score [27], which uses age, heart rate, systolic blood
a choice of early invasive versus conservative management.
pressure, creatinine level, Killip class, cardiac arrest at
Figure 1 below outlines a schema for such decision making.
admission, elevated cardiac markers and ST segment
deviation.
• Platelet glycoprotein IIb/IIIa in unstable angina: recep- Antiplatelet Therapy
tor suppression using integrilin therapy (PURSUIT)
[28, 29] scoring uses age (as a decade), gender, Measures to reduce the dominant role of platelet activation
symptomatic class within the last 6 weeks, presence and aggregation in the formation and propagation of an
of heart failure symptoms, and ST depression on ECG. arterial thrombus, form a major therapeutic objective in the
• History, ECG, age, risk factors and troponin (HEART) management of these patients. Antiplatelet agents should
[30] scores begin with zero, one or two points, depending be administered once the diagnosis of NSTEMI is likely

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Curr Emerg Hosp Med Rep (2013) 1:18–28 21

or definite. Three classes of antiplatelet agents will be Ticlopidine

discussed, viz. aspirin, P2Y12 receptor antagonists and
glycoprotein IIb/IIIa receptor antagonists. Ticlopidine, the first of this group to be used is an adeno-
sine diphosphate (ADP) receptor antagonist. Originally
Aspirin used in patients not tolerating aspirin and later tried in
patients requiring dual antiplatelet therapy, reports of
Aspirin (between 150 and 325 mg per oral) should be increased risk of thrombotic thrombocytopenic purpura
administered [34–41] as soon as possible after presentation, (TTP) and neutropenia led to its relative non-use and
provided no contraindications (e.g., allergy, active bleeding, replacement by clopidogrel. Ticlopidine is usually given
current peptic ulceration, recent neurosurgery or haemor- orally in 250 mg doses twice daily. It is contraindicated in
rhagic stroke) [42] exist to its use. Aspirin should be con- patients with bleeding disorders, active bleeding and severe
tinued indefinitely at a daily maintenance dose of liver disease, and needs to be reviewed in those with renal
75–150 mg. Aspirin therapy reduces the risk of a vascular or hepatic impairment, geriatric patients (increased sensi-
event. Efficacy is not increased with higher maintenance tivity), pregnancy, lactation, children, neutropenia and
doses, which carry a greater risk of gastrointestinal intoler- TTP. It may be used in patients allergic to clopidogrel.
ance. The drug should be offered to all patients with
NSTEMI, unless contraindicated. Clopidogrel

P2Y12 Receptor Inhibitors Clopidogrel, a pro-drug activated in the liver by the

CYP2C19 isoenzyme of cytochrome P450, irreversibly
The thienopyridines were the first group of P2Y12 receptor inhibits the P2Y12 subtype of ADP receptor and also blocks
inhibitors used in NSTEMI. activation of the glycoprotein IIb/IIIa pathway. Platelet

Fig. 1 Schema for early management of NSTEMI

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22 Curr Emerg Hosp Med Rep (2013) 1:18–28

inhibition is evident 2 h after a single dose of oral clopi- inhibitors, including PPIs, or loss-of-function variants of
dogrel. Patients with a variant allele for the CYP2C19 the CYP2C19 gene; nor by reduced ABCB1 function [52].
isoenzyme have lower levels of active metabolite and are The recommended loading dose is 60 mg orally adminis-
1.5–3.5 times more likely to die or have complications than tered not later than 1 h once coronary anatomy is defined
those with the high-functioning allele [43–45]. Poor and a decision made to proceed with PCI. Maintenance
metabolizers apparently make up to about 14 % of the therapy is 10 mg daily for at least 12 months. Prasugrel has
patients and are at high risk of treatment failure. The Food a lower incidence of cardiovascular death, non-fatal myo-
and Drug Administration (FDA) [46] has placed a warning cardial infarction and stroke when compared to clopidogrel
on clopidogrel to make doctors and patients aware of this. [53] owing to a significant risk reduction for myocardial
Serious adverse drug reactions associated with clopi- infarction and lesser stent thrombosis. However, life-
dogrel include severe neutropenia, TTP and hemorrhage threatening bleeding has been noted, especially in patients
(gastrointestinal and cerebral). Use of NSAIDs is discour- with a history of cerebrovascular accidents. Greater benefit
aged in those taking clopidogrel, owing to increased risk of without increased risk of bleeding is observed in diabetic
gastrointestinal bleeding. Other side effects include diar- patients. There is no apparent net clinical benefit in patients
rhea and rash. [75 years of age and in those with body weight \60 kg.
Clopidogrel interacts with many drugs, especially proton
pump inhibitors (PPIs) (except possibly pantoprazole), phe-
nytoin, tamoxifen, tolbutamide, warfarin, heparin, enoxapa- Ticagrelor
rin, anistreplase, dipyridamole, streptokinase, ticlopidine and
urokinase. In November 2009, the FDA announced that This is a cyclopentyl-triazolo-pyrimidine and reversibly
clopidogrel should be used with caution in patients on PPIs binds to the P2Y12 inhibitor with a plasma half-life of 12 h.
such as omeprazole and esomeprazole [47]. The degree of P2Y12 inhibition depends mainly on the
Clopidogrel is currently the commonest used P2Y12 plasma ticagrelor level. The onset of action is rapid com-
receptor inhibitor in patients presenting with NSTEMI. The pared with clopidogrel. Offset of action is also quicker with
recommended loading dose is uncertain, especially in those faster recovery of platelet function and shorter duration of
undergoing PCI. The benefit of higher-dose clopidogrel effect. Ticagrelor increases levels of drugs metabolized
loading is offset by an increase in major bleeding [48]. through CYP3A, such as simvastatin. Moderate CYP3A
Current United States guidelines recommend higher-dose inhibitors such as diltiazem increase levels and lengthen
(600 mg loading, 150 mg daily for 6 days and then 75 mg duration of ticagrelor effect.
daily for 12 months) than the lower dose of 300 mg In the PLATO trial [54], ticagrelor (180 mg loading
loading and 75 mg daily thereafter for those undergoing dose and 90 mg twice daily for up to 12 months) reduced
PCI, because of reduction in myocardial (re)infarction death from vascular causes, MI, or stroke to 9.8 % from
and cardiovascular death at these higher doses in the 11.7 % in the clopidogrel group (HR 0.84; 95 % CI
CURRENT–OASIS 7 Trial [48, 49•] and in stent throm- 0.77–0.92; p = 0.001). Stent thrombosis was reduced from
bosis. For those who had a prior loading dose of 300 mg, a 1.9 to 1.3 % (p = 0.01) and total mortality from 5.9 to
supplementary dose of 300 mg is suggested. Doses for 4.5 % (p = 0.001). Ticagrelor also reduced early and late
patients aged 75 years and above has not been established. mortality following CABG from 9.7 to 4.7 % (HR 0.49; CI
Clopidogrel therapy may be initiated early, such as at the 0.32–0.77; p = 0.01). Adverse effects include dyspnea
emergency department or even earlier, or delayed until just (usually transient, occurring within the first week and
after cardiac catheterisation when coronary anatomy can be occasionally persisting until cessation of treatment [54, 55,
defined and a decision made on whether revascularisation is 56•, 57]) without any deterioration in cardiac or pulmonary
appropriate. The advantage of early treatment is the potential function, increased frequency of ventricular pauses, and
to reduce ischaemic events. The disadvantage is the potential asymptomatic increases in uric acid [54, 58, 59]. Caution
for increased bleeding in patients who subsequently may is advised in patients with either advanced sinoatrial dis-
require early CABG [50]. The delayed approach avoids the ease or second- or third-degree atrioventricular block,
increased bleeding risk. Current consensus is to go for early unless already treated by permanent pacemaker. The
initiation of higher-dose clopidogrel. mechanism for the dyspnoea and ventricular pauses rem-
ains uncertain.
Prasugrel
Glycoprotein IIb/IIIa Inhibitors
Prasugrel is chemically similar to and produces more rapid
and consistent platelet inhibition than clopidogrel [51]. GP23I have not demonstrated any reduction in MI or death
Response to prasugrel is not affected significantly by CYP rates when used in purely medically managed patients

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Curr Emerg Hosp Med Rep (2013) 1:18–28 23

not subjected to coronary revascularization procedures. In UFH is proven to reduce the rate of death and MI in
patients who had undergone PCI [60••], if GP23Is were multiple trials [65], especially when given in combi-
maintained during the procedure, significant cardiovascular nation with aspirin, though with some increased risk of
benefit was observed. There was generally an increase in bleeding. When invasive procedures such as PCI are
bleeding complications, though not intracranial haemor- performed the usual dose given is 70–100 IU/kg body
rhage. The recommendations for use of these agents would weight, or 50–60 IU/kg if used in combination with a
be as follows: GP IIb/IIIa inhibitor [66]. Dosing should be guided by
measurements of activated clotting times (ACT). UFH
1. Not routinely before coronary angiography if the
use should be terminated after removal of the arterial
decision is for an invasive treatment strategy [61].
sheath. LMWHs, however, can be administered sub-
2. Not for patients on dual anti-platelet therapy if for
cutaneously at a dose of 1 mg/kg every 12 h for at least
conservative management, unless the risk of bleeding
2 days until clinical stabilization. The arterial sheath
is low [60••, 61].
should be removed at least 8 h following a dose of
3. In high-risk patients eptifibatide or tirofiban may be
enoxaparin with the subsequent dose another 8 h after
added to those on aspirin alone or on dual anti-platelet
sheath removal. Treatment may be continued for up to
therapy prior to angiography if there is ongoing
8 days. LMWH can be administered without the use of
ischaemia and the risk of bleeding is low [61, 62].
anti-factor Xa monitoring, except in patients with renal
4. They may be withheld until after angiography, when
failure or obesity. Efficacy rates have generally been
the procedure demonstrates the presence of thrombi
similar with both UFH and LMWH while lower
and the extent of the disease is clear, biomarker levels
bleeding rates have been noted with the LMWHs
are elevated, and there has already been concurrent
[67, 68]. Crossover of heparins in the same patient is
treatment with a P2Y12 inhibitor and a relative lack of
usually not recommended.
factors that contribute to serious bleeding [63, 64].
b. Direct inhibitors of thrombin, e.g., bivalirudin. Biva-
lirudin directly inhibits thrombin by specifically bind-
ing both to the catalytic site and the anion-binding
exosite of circulating and clot-bound thrombin [69]. It
Anti-coagulant Therapy
is to be administered at a dose of 0.1 mg/kg IV bolus
followed by an infusion at 0.25 mg/kg/h until the PCI
Since the initiating event in a myocardial infarction is the
procedure is completed. Trials have demonstrated a
formation of a thrombus, reducing pro-thrombotic events
similar efficacy endpoint when compared to heparins,
would assist in minimizing propagation of the clot formed.
both given with GP IIB/IIIa inhibitors [32, 70–72] with
In addition to platelet inhibition, processes that counteract
significant reduction in major bleeding [73].
conversion of prothrombin to thrombin would naturally
c. Direct inhibitors of factor Xa such as apixaban,
decrease the conversion of fibrinogen to fibrin [65, 66].
rivaroxaban and otamixaban: while apixaban and
Together, these two processes may be expected to further
rivaroxaban have been used mainly for management
inhibit thrombus formation in a coronary vessel. Therefore,
of deep vein thrombosis, otamixaban, an investigational
anticoagulation is recommended for all patients presenting
anti-factor Xa compound, in intermediate dosages, has
with NSTEMI, in addition to dual anti-platelet therapy.
been found, in initial studies [74] to offer substantial
Selection of anticoagulants should be based on subsequent
reduction in major coronary complications such as
ischaemic bleeding risk profile. Such anticoagulation
death and myocardial infarction in patients presenting
should be maintained at least until hospital discharge.
with NSTEMI, with similar bleeding rate when com-
Discontinuation of anticoagulant should be considered
pared to a combination of UFH and eptifibatide.
after completion of an invasive procedure, unless otherwise
d. Indirect inhibitors of factor Xa such as fondaparinux:
contra-indicated. During anticoagulation, gastric protection
this is a synthetic, highly sulfated pentasaccharide, with
should be considered, especially with PPIs, since the com-
a sequence derived from the minimal antithrombin (AT)
monest spontaneous bleed in such patients is gastrointestinal.
binding region of heparin. Fondaparinux binds to AT
Anti-platelet agents, on the other hand, need to be continued
with a higher affinity than the native pentasaccharide of
for at least a further 12 months, even without PCI.
UFH or low molecular weight heparin, and causes a
Anti-coagulants can be divided into a few groups
conformational change in AT that significantly
depending on their mode of action:
increases the ability of AT to inactivate factor Xa.
a. Heparins, such as unfractionated heparin (UFH) and Fondaparinux is licensed in Europe for treatment of
low-molecular weight heparins (LMWH) have been NSTEMI in patients for whom invasive management is
used in patients with NSTEMI for more than a decade. not indicated within 2 h of diagnosis. Administration of

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24 Curr Emerg Hosp Med Rep (2013) 1:18–28

the drug is recommended [75, 76, 77•] as soon as cardiac events and major bleeding. Following initial relief of
possible following diagnosis and continued for up to symptoms and haemodynamic optimization, further man-
8 days or hospital discharge, whichever occurs earlier. agement revolves around measures to decrease thrombus
Fondaparinux is not yet recommended in patients for propagation and re-open significantly blocked coronary
whom urgent PCI is indicated. vessels, if any. Future areas of NSTEMI management will
include more aggressive imaging modalities to define cor-
onary anatomy safely for earlier definitive treatment options.
Coronary Revascularization in NSTEMI Disclosure No potential conflict of interest relevant to this article
were reported.
The primary mechanism for occurrence of symptoms is
coronary artery blockage. Various grades of patients con-
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