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CAT2 Valvular Diseases

After completing your assigned readings, can anyone answer the following questions related to the diagnosis and treatment of valvular diseases?

What are the key factors that determine when to proceed to aortic valve replacement for patients with aortic stenosis? What guided decision making relating to aortic surgery for acute and chronic aortic regurgitation?

Which patients with aortic stenosis should be considered for transcatheter therapies such as valvuloplasty or transcatheter aortic valve replacement?

What are the indications for surgery in patients with mitral stenosis? What are the goals of medical therapy for mitral regurgitation and when should patients be considered for mitral valve repair or replacement?

When should patients with mitral regurgitations be considered for transcatheter mitral valve procedures?

What are the objectives of treatment of pulmonic valve disease? When should patients be referred for surgery or transcatheter valve replacement?

What are the factors that determine medical versus surgical treatment of tricuspid stenosis or tricuspid regurgitation?

REPLY

  • AM

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SECTION 1
Cardiovascular Medicine

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CHAPTER 128
Acute Coronary Syndromes

Michael McDaniel, MD, FSCAI

Key Clinical Questions

What is the optimal care and management of patients with ST-segment elevation
myocardial infarction?

What is the optimal care and management of patients with non-ST segment
elevation acute coronary syndrome?

INTRODUCTION

The term acute coronary syndrome (ACS) refers to the spectrum clinical presentations
related to acute myocardial ischemia or infarction due to the abrupt reduction in coronary
blood flow. ACS is divided into ST-segment elevation myocardial infarctions (STEMIs) and
non-ST segment elevation acute coronary syndromes (NSTE-ACSs). The NSTE-ACS is
further subdivided on the basis of elevated cardiac biomarkers of myocardial necrosis.
Patients with elevated cardiac biomarkers are defined as non-ST segment elevation
myocardial infarction (NSTEMI) and those without elevated biomarkers are termed
unstable angina (UA).

This chapter will focus on the diagnosis, risk stratification, and treatment of patients
with ACS based on the American College of Cardiology Foundation and American Heart
Association (ACCF/AHA) practice guidelines for STEMI and NSTE-ACS. All guideline
recommendations will be cited in this chapter and referenced according the American

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College of Cardiology Foundation/American Heart Association classification scheme
(Table 128-1).

TABLE 128-1 ACCF/AHA Classification of Recommendations and Level of Evidence

Class I Class IIa Class IIb Class III
Benefit >>>
Risk
Procedure/Treatment
SHOULD be
performed/administered

Benefit >> Risk
Additional studies
with focused
objectives needed
IT IS REASONABLE
to perform
procedure/administer
treatment

Benefit ≥ Risk
Additional studies
with broad objectives
needed; Additional
registry data would
be helpful
Procedure/Treatment
MAY BE
CONSIDERED

Risk ≥ Benefit
No additional studies
needed
Procedure/Treatment
should NOT be
performed/administered
SINCE IT IS NOT
HELPFUL AND MAY BE
HARMFUL

Level A: Recommendation based on evidence from multiple randomized trials or meta-analyses
Level B: Recommendation based on evidence from a single randomized trial or non-
randomized studies
Level C: Recommendation based on expert opinion, case studies, or standard of care

From O’Gara PT, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction:
executive summary: a report of the American College of Cardiology Foundation/American Heart Association
Task Force on Practice Guidelines. J Am Coll Cardiol.2013;61(4):485-510.

EPIDEMIOLOGY & PATHOPHYSIOLOGY

ACS is common, with over 780,000 patients experiencing an ACS event every year in the
United States. Of these events, approximately 70% are classified as NSTE-ACS. ACS is
related to an acute imbalance of myocardial oxygen consumption and demand, usually
related to a sudden coronary artery obstruction. Autopsy studies suggest that most ACS
events are related to acute coronary thrombosis, with acute plaque rupture being the most
common etiology. The atherosclerosis at sites of plaque rupture is characterized by large
lipid-laden necrotic cores overlying a disrupted thin fibrous cap. The second most
common cause of acute coronary thrombosis is plaque erosion, characterized by
thrombus formation at an area of denuded endothelium. These plaques are characterized
by smaller plaques with less lipid necrotic core and thicker fibrous caps compared to
plaque rupture sites. Plaque erosion is actually the most common etiology of acute
coronary thrombosis in younger female patients, especially those who smoke tobacco.
More rare causes of coronary thrombosis are due to the calcified nodule which is not well
characterized and is mostly seen in the elderly, and cardioembolic etiologies which are
usually noted in distal coronary locations. Nonthrombotic sudden progressions in
coronary arteries may be related to acute intraplaque hemorrhage without thrombosis.
Rarely, acute coronary insufficiency may be caused by vasospasm, coronary arteritis, or
spontaneous dissection.

HISTORY AND PHYSICAL

The most common clinical presentation of ACS is new onset pressure-like chest pain that
occurs at rest (>10-20 minutes in duration) or with minimal activity. The pain is often

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retrosternal and can radiate to the arm (likelihood ratio [LR] 2.7), neck, or jaw and may be
associated with diaphoresis (LR 2.0), dyspnea, or nausea (LR 1.9). However, chest pain
can be absent in one-third of patients. Less common presentations of ACS include
syncope, abdominal pain, hypotension, pulmonary edema, or unexplained fatigue. While
older women and patients with diabetes most commonly present with typical symptoms
of ACS, atypical ACS presentations are most common in these patients. Symptoms that
are not characteristic of myocardial ischemia included pleuritic pain (LR 0.2), sharp or
stabbing pain localized to a single location (LR 0.3), pain reproduced by palpitation (LR
0.2-0.4), or brief episodes lasting only seconds. Risk factors for ACS include older age,
male sex, family history of coronary artery disease (CAD), peripheral arterial disease,
diabetes mellitus, renal insufficiency, and prior CAD. The differential diagnosis for ACS is
listed in Table 128-2.

TABLE 128-2 Differential Diagnosis for NSTE-ACS

Nonischemic Cardiovascular
• Aortic dissection
• Expanding aortic aneurysm
• Myocarditis
• Pericarditis
• Hypertrophic cardiomyopathy
• Pulmonary embolism
Pulmonary
• Pneumonia
• Pleuritis
• Pulmonary hypertension
• COPD
• Pneumothorax
Gastrointestinal
• Gastroesophageal reflux
• Esophageal spasm
• Esophagitis
• Esophageal hypersensitivity
• Peptic ulcer
• Pancreatitis
• Biliary obstruction
Musculoskeletal
• Cervical disk radiculopathy
• Costochondritis
• Rheumatic disease
• Trauma
Other etiologies
• Sickle cell crisis
• Herpes zoster

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• Depression and anxiety
• Drug intoxication
• Pheochromocytoma

Reprinted from Amsterdam EA, Wenger NK, Brindis RG, et al. 2014 AHA/ACC Guideline for the
Management of Patients with Non-ST-Elevation Acute Coronary Syndromes: a report of the American
College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll
Cardiol. 2014;64(24):e139-228 with permission from Elsevier, Inc.

The physical examination may be completely normal in many patients with ACS. Signs
and symptoms of new congestive heart failure, mitral regurgitation, and/or shock suggest
higher risk and usually require more emergent triage, treatment, and often invasive
therapies. Signs of low cardiac output may be suggested by tachycardia, cool extremities,
diaphoresis, confusion, and/or reduced urine output. Signs of congestive heart failure
include elevated jugular venous distension, pulmonary edema, audible S3, and/or lower
extremity edema.

ELECTROCARDIOGRAM

To rapidly identify STEMI, an electrocardiogram (ECG) should be performed within 10
minutes of arrival to the emergency department (ED) in all patients with signs and
symptoms of ACS (Class I, Level of Evidence [LOE] C). In addition, Emergency Medical
Service (EMS) personnel should perform a 12-lead ECG on site in all patients with
suspected ACS and transport patients with STEMI to percutaneous coronary intervention
(PCI)-capable facilities, where available.

STEMI is defined on ECG by new ST-elevation in at least two contiguous leads ≥2 mm
in leads V2-V3 or ≥1 mm in the other chest leads or limb leads. Abnormalities alone on the
EKG are insufficient to make a diagnosis of STEMI and the ECG must be interpreted in the
appropriate clinical context. While new left bundle branch block (LBBB) was once
considered as an STEMI equivalent, guidelines now recommend the LBBB in isolation
should not be considered diagnostic of acute myocardial infarction (AMI) and specific
ECG criteria have been proposed to diagnose STEMI in LBBB (Table 128-3). In addition,
ST depressions in V1-V4 may indicate posterior injury (Figure 128-1) and isolated ST-
elevation in aVR and/or V1 with diffuse ST depression may suggest acute left main or
proximal left anterior descending artery occlusion (Figure 128-2). Rarely, hyperacute T-
waves can be seen early in patients with STEMI. When the initial ECG is nondiagnostic
and the patient remains symptomatic, serial ECGs should be performed at 15 to 30 minute
intervals during the first hour or if symptoms recur (Class I, LOE C).

TABLE 128-3 ECG Criteria for Diagnosis of STEMI in the Setting of Left Bundle Branch
Block (Sgarbossa Criteria)

Criterion Odds Ratio (95% CI) Score
ST-elevation ≥1 mm and concordant with
QRS complex

25.2 (11.6-54.7) 5

ST-segment depression >1 mm in leads V1,
V2, or V3

6.0 (1.9-19.3) 3

ST-elevation >5 mm and discordant with
QRS complex

4.3 (1.8-10.6) 2

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A score >3 had a 98% specificity for acute myocardial infarction, but a score of 0 does
not rule out STEMI.

From O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of ST-
elevation myocardial infarction: a report of the American College of Cardiology Foundation/American
Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2013 29;61(4):e78-140.
Reprinted with permission from Elsevier, Inc.

Figure 128-1 EKG with and ST-depression in V1-V3 suggestive of acute posterior injury.
(Reproduced, by permission, from Knoop KE, et al eds. The Atlas of Emergency Medicine,
3rd ed. New York, NY: McGraw-Hill; 2010. ECG contributor: Ian D. Jones, MD.)

Figure 128-2 ST-elevation in aVR with diffuse ST depression consistent with acute left
main or very proximal left anterior descending artery occlusion.

The 12-lead ECG may suggest a diagnosis of NSTE-ACS, but is not required to make
the diagnosis. Horizontal or downsloping dynamic ST-segment depression is highly
suggestive of NSTE-ACS. In addition, significant deep precordial T-wave inversion (Wellen’s
sign) may suggest critical left anterior descending stenosis (Figure 128-3). More
nonspecific ST-T changes are less diagnostic. Significant Q-waves can suggest a prior
myocardial infarction (MI), but do not suggest ACS.

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Figure 128-3 Deep T-wave inversion in the precordial leads suggestive of ischemia in the
left anterior descending coronary artery (Wellen’s sign).

ST-SEGMENT ELEVATION MYOCARDIAL INFARCTION (STEMI)

MANAGEMENT OF STEMI AT PCI-CAPABLE HOSPITALS

All hospitals should develop coordinated regional approaches to STEMI care and
participation in programs such as Mission:Lifeline (American Heart Association’s Mission:
Lifeline: http://www.heart.org) and the D2B Alliance is recommended (Class I, LOE B).
These initiatives promote prehospital ECG to diagnose STEMI, EMS and ED activation of
cardiac catheterization labs (“cath labs”), single calls to central paging operator to
activate the cath team, cath lab staff arrival within 20 to 30 minutes of notification, and
timely data feedback to all members of the STEMI team.

Once the diagnosis of STEMI is made, the most important therapy for patients is
emergent revascularization within 90 minutes of first medical contact (FMC) (Class I, LOE
A). As such, it is preferred for patients to bypass the ED and present directly via EMS to the
cath lab when possible to optimize reperfusion times (Figure 128-4). Most patients
arriving by EMS with ACS will receive aspirin 325 mg by EMS personnel (Class I, LOE A).
Patients should also receive an unfractionated heparin (UFH) bolus (50-70 units/kg, max
5000 units) as soon as possible upon hospital arrival (Class I, LOE C). In addition, all
patients presenting with STEMI should receive a loading dose of an oral antiplatelet
P2Y12 antagonist as early as possible (Class I, LOE B). Presently, there are three options of
the oral antiplatelet P2Y12 antagonists: clopidogrel 600 mg, prasugrel 60 mg, and
ticagrelor 180 mg. Choosing between these agents will be discussed later in the Dual
Antiplatelet Therapy Section of Late Hospital & Hospital Discharge part of the chapter.

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Figure 128-4 Algorithm for evaluation and management of acute coronary syndrome for
PCI-capable hospitals. ACS, acute coronary syndromes; ASA, aspirin; CCU, coronary care
unit; CP, chest pain; ECG, electrocardiogram; Non-STE ACS, Non-ST segment elevation
acute coronary syndrome; NTG, nitroglycerin; PCI, percutaneous coronary intervention; PO,
Per Os; SL, sublingual; STEMI, ST-segment elevation myocardial infarction.

There is little benefit to intravenous (IV) glycoprotein IIb/IIIa inhibitors (GPIs) prior to
angiography in STEMI (Class IIb, B). However, GPIs are indicated in many patients during
and after PCI for STEMI as it blocks the final common pathway of platelet activation. While
a comprehensive review of the GPI trials is beyond the scope of this chapter, a few general
principals regarding GPIs deserve mention. GPIs provide very rapid inhibition of platelets,
much greater and faster than oral P2Y12 inhibitors. In addition, pooled studies suggest
that GPIs reduce recurrent 30-day unplanned revascularization and mortality in STEMI. In
a meta-analysis of 7414 patients from multiple randomized trials, patients undergoing PCI
for STEMI receiving GPIs have about a 25% relative decrease in mortality compared to no
GPI. However, GPIs are clearly associated with about a 50% relative increase in bleeding

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complications, especially with femoral access. This bleeding is attenuated but not
eliminated by radial access. Currently, there are three GPI agents available for clinical use.
There are two small molecule agents, eptifibatide and tirofiban, and one large molecule
agent abciximab. Randomized trials, registries, and meta-analyses suggest that the large
and small molecule GPI agents have similar efficacy and safety in patients undergoing
primary PCI. As such, the choice of GPI may be driven more by cost considerations.

Bivalirudin is a direct thrombin inhibitor that has been studied extensively in primary
PCI in STEMI, but its use is controversial given conflicting recent studies. In both the 3602
patient Harmonizing Outcomes with Revascularization and Stents in Acute Myocardial
Infarction (HORIZONS AMI) and the 2218 patient European Ambulance Acute Coronory
Syndrome angiography study (EUROMAX) trials, there were significantly less bleeding
complications in patients randomized to bivalirudin compared to the combination of UFH
and planned or provisional GPI. However, there was also significant more acute stent
thrombosis, and the bleeding reduction was attenuated in patients with radial access.
More recently, the benefits of bivalirudin compared to UFH alone have been questioned. In
the How Effective Are Antithrombotic Therapies in Primary PCI (HEAT PPCI) trial, 1812
patients with STEMI were randomized to bivalirudin or UFH, both with provisional use of
GPI. In this trial, there was no reduction of bleeding with the use of bivalirudin and actually
higher major cardiac events with bivalirudin. It should be noted however that the use of
provisional GPI was low and similar in both groups and most patients underwent PCI
using the radial approach. Given the significantly higher cost compared to UFH, it is
controversial if bivalirudin provides value compared to UFH, and further studies are
warranted to best define the optimal role of bivalirudin in STEMI.

The radial access is increasingly utilized in STEMI as this strategy decreases access-
site complications compared to PCI via femoral access (Class IIa, LOE A). In the 1001
patient Radial versus Femoral Randomized Investigation in ST Elevation Acute Coronary
Syndrome trial, patients randomized to radial access had lower bleeding at 30 days (7.8%
vs 12.2%, number needed to treat [NNT]23, P = 0.026) and cardiac mortality (5.2% vs 9.2%,
NNT25, P = 0.02) compared with patients randomized to femoral access. Similar findings
were noted in a meta-analysis of 5055 patients from 11 randomized trials in STEMI.

MANAGEMENT OF STEMI AT NON-PCI-CAPABLE HOSPITALS

Not all patients with STEMI present to hospitals that can perform primary PCI. These
patients should be transferred to a PCI-capable hospital for primary PCI if this transport
can occur rapidly and achieve revascularization at the receiving hospital with FMC-to-
device time less than120 minutes (Class I, LOE B). If this time goal cannot be met,
fibrinolytic therapy is recommended in the absence of contraindications within 30 minutes
of hospital arrival (Class I, LOE B). Fibrin-specific agents (Tenecteplase, Reteplase, and
Alteplase) are preferred over non-fibrin-specific agents (Streptokinase). Absolute and
relative contraindications to fibrinolytic therapy are listed in Table 128-4. In addition,
patients presenting with cardiogenic shock, high bleeding risk, or presentations >3 to 4
hours after symptom onset should usually be transported to a PCI-capable hospital
regardless of transport times.

TABLE 128-4 Contraindications to Fibrinolysis in STEMI

Absolute Contraindications
• Prior intracranial hemorrhage

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• Structural cerebral vascular lesions
• Malignant intracranial neoplasm
• Ischemic stroke within 3 mo
• Suspected aortic dissection
• Active bleeding
• Significant closed-head or facial trauma within 3 mo
• Intracranial or intraspinal surgery within 2 mo
• Severe uncontrolled hypertensions unresponsive to therapy
Relative Contraindications
• Significant hypertension (SBP >180 mm Hg or DBP >110 mm Hg)
• History of ischemic stroke >3 mo
• Dementia
• Prolonged CPR >10 min
• Major surgery within 3 wk
• Recent internal bleeding within 2-4 wk
• Noncompressible vascular punctures
• Pregnancy
• Active peptic ulcer
• Oral anticoagulant therapy

All patients who receive fibrinolysis should also receive aspirin 325 mg PO loading
dose, clopidogrel 300 mg PO loading dose, and unfractionated heparin bolus and infusion.
In addition, all patients should be transferred emergently to a PCI-capable hospital for
urgent/emergent angiography as part of either a rescue PCI strategy (for failed lysis) or a
pharmocoinvasive strategy as both strategies have been shown to improve outcomes
compared to conservative management strategies.

COMATOSE PATIENTS WITH OUT-OF-HOSPITAL CARDIAC ARREST

Comatose patients with out-of-hospital cardiac arrest (OHCA) due to ventricular fibrillation
(VF) or pulseless ventricular tachycardia (VT) with return of spontaneous circulation
(ROSC) deserve special mention. These patients have about a 10-fold increase in mortality
compared to STEMI patients without cardiac arrest. Survival is optimized when CPR and
defibrillation are initiated early. Importantly, the neurologic exam should not be used in the
acute setting to predict future neurologic recovery or survival. While patients with longer
pulseless times, unwitnessed arrests, and longer CPR durations have worse neurologic
outcomes, there are no absolute predictors in the acute setting of neurologic recovery with
intervention. As such, the neurologic status should not solely be used to guide decisions
about invasive procedures in the acute setting.

Immediate angiography and PCI should be strongly considered for all comatose
patients with OHCA and ROSC with STEMI on initial ECG (Class I, LOE B). In addition,
targeted temperature management (TTM) should be started as soon as possible to target
32°C to 34°C for 12 to 24 hours (Class I, LOE B). Two randomized trials have reported
improved neurologic survival when TTM was initiated before or at the time of PCI, and the
combination of early angiography/intervention and TTM is associated with the highest
survival and neurologic recovery. More recently, other randomized clinical trials of TTM in

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postresuscitated patients have found equally impressive survival rates, whether cooled to
33°C versus 36°C or whether initiated in the field or after arrival at the hospital. Several
methods for hypothermia are available, but there are insufficient data to recommend one
technique over another and local expertise should guide decisions between external
cooling pads, intravascular cooling, cooling blankets, and ice packs. Of note, iced saline
should rarely be used as the volume may precipitate pulmonary edema in patients at risk
for heart failure and this can lead to more rapid fluctuations in body temperature.

While there is not a consensus to the optimal management of patients with OHCA due
to VF/VT with ROSC without ST-elevations on ECG, most of the studies also support early
angiography, PCI, and TTM for these patients as up to 25% to 30% of these patients will
have culprit lesions at angiography despite a normal ECG. However, given the greater
heterogeneity of these patients, consultation should be undertaken with interventional
cardiology prior to cath lab activation for these patients.

PRACTICE POINT

STEMI
Rapid ECG with interpretation is recommended prehospital by EMS or within 10
minutes of arrival to the hospital to rapidly identify patients with STEMI and optimize
reperfusion times.
When the initial ECG is nondiagnostic and the patient remains symptomatic, serial
ECGs should be performed at 15- to 30-minute intervals during the first hour or if
symptoms recur.
Left Bundle Branch Block in isolation should not be considered diagnostic of acute
myocardial infarction and specific ECG criteria have been proposed to diagnose
STEMI in LBBB (Table 128-3).
All patients with STEMI should receive an aspirin loading dose (325 mg),
unfractionated heparin bolus (50-70 units/kg, max 5000 units), and a P2Y12 inhibitor
loading dose prior to or at the time of angiography.
Primary PCI is recommended within 90 minutes of first medical contact for PCI-
capable hospitals.
Transfer for primary PCI from a non-PCI-capable hospital is recommended when the
first medical contract to device time (balloon or aspiration catheter) can be
accomplished within 120 minutes. When this is not possible, fibrinolysis is preferred
within 30 minutes of hospital arrival.
The optimal use of glycoprotein IIb/IIIa inhibitors and Bivalirudin in STEMI remains
controversial. When GPIs are used, they should usually be deferred until angiography
is performed.
Most comatose patients with out-of-hospital cardiac arrest due to VT/VF and return of
spontaneous circulation should undergo emergent angiography and targeted
temperature management.

NON-ST SEGMENT ELEVATION ACUTE CORONARY SYNDROMES (NSTE-ACS)
MORPHINE, OXYGEN, NITROGLYCERIN, AND ASPIRIN

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“MONA” (Morphine, Oxygen, Nitroglycerin, and Aspirin) has been part of the classic
teaching for patients with ACS for decades. However, aside from aspirin, there are now
reasons to caution the routine use of these other agents in ACS.

Morphine should probably be avoided in most patients with active angina as it can
mask ongoing ischemia or infarction in patients who may benefit from emergent
revascularization, and its use has been downgraded in recent guidelines (Class IIb, LOE B)
based on observational studies suggesting an association with adverse events and
morphine use in ACS. While this may be related to the fact that sicker patients get
morphine, morphine may mask the pain of ongoing infarction resulting in delays in
revascularization and larger infarctions. Furthermore, morphine may impair the absorption
of the oral antiplatelet agents. For most patients with active angina despite IV
nitroglycerin, urgent coronary angiography should be considered instead of morphine.

Supplemental oxygen therapy is recommended only in patients with ACS and arterial
oxygen saturation less than 90% or in respiratory distress (Class I, LOE C). The benefits of
routine oxygen use without hypoxia have never been demonstrated, and some studies
suggest that oxygen therapy may actually increase vascular resistance, reduce coronary
flow, and result in larger infarctions. Furthermore, in a pooled Cochrane analysis of 430
patients from four randomized trials demonstrated a twofold higher risk of death in
patients with AMI treated with oxygen. Taken together, routine oxygen therapy is probably
not necessary in most patients with ACS unless hypoxia is present.

Nitrates are endothelium-independent vasodilators that relieve angina by decreasing
cardiac preload and reducing ventricular wall tension. Sublingual (SL) nitroglycerin is
recommended for patients with active angina (Class I, LOE C). If the angina continues
despite 3 SL nitroglycerin, IV nitroglycerin should be given and titrated until chest pain free
or limited by side effects such as hypotension or headache (Class I, LOE B). While
nitroglycerin is effective at reducing the symptoms of angina, randomized trials have
never demonstrated improved morbidity or mortality outcomes with nitrates. In addition,
nitroglycerin should be avoided in patients with hypotension, right ventricular infarctions,
and recent phosphodiesterase inhibitor-5 (sildenafil, vardenafil, or tadalafil) use due to risk
of significant hypotension (Class III, LOE B).

All patients with ACS should receive nonenteric-coated ASA of 325 mg as soon as
possible followed by 81 mg daily maintenance dose (Class I, LOE A). Aspirin is a mainstay
of ACS therapy, results in thromboxane A2 inhibition via irreversible COX-inhibition, and
results in approximately 30% to 45% relative reductions in death and recurrent myocardial
infarction across a large spectrum of ACS. Enteric-coated aspirin should be avoided in the
early setting of ACS due to delayed absorption.

SERIAL TROPONIN ANALYSIS

Increasingly, a troponin-only biomarker strategy (without ordering creatine kinase [CK] and
creatine kinase myocardial enzyme [CK-MB] fraction) is used for the evaluation of AMI in
NSTE-ACS. Although damaged cardiac myocytes release several biomarkers, troponins are
preferred based on their superior sensitivity and specificity. Cardiac troponin will rise
within 2 to 4 hours of symptom onset and will remain elevated for several days. Shorter
intervals of serial troponin measurements (such as 0, 3, and 6 hours) more rapidly
diagnose and/or rule out AMI (Class I, LOE A). Contemporary sensitive troponin assays
now permit earlier serial sampling (in 3 hours vs previous 8 hours) for earlier detection and
treatment of AMI. Furthermore, a negative troponin value 6 hours from presentation
essentially excludes the diagnosis of AMI (unless recurrent symptoms), leading to earlier
diagnostic testing or hospital discharge. It is important for physicians to be aware of the

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troponin assay used in their local hospital, as troponin measures >6 hours from onset may
be required with less sensitive older assays. In addition, testing at longer intervals is
required (up to 24 hours) if information about infarct size is required.

There is very little value to using other cardiac biomarkers in addition to troponin, as
they are both less sensitive and less specific. Furthermore, moderate-sized registries
suggest that the addition of CK-MB adds no additional diagnostic information compared
to troponin alone. With contemporary troponin assays, CK-MB and myoglobin are not
useful in the diagnosis of ACS and the current guidelines recommend against their use
(Class III, LOE A). Importantly, elevated troponin values alone are insufficient to make a
diagnosis of NSTEMI and should be evaluated in the appropriate clinical context. There
are many reasons other than ACS for elevated troponin values (Table 128-5).

TABLE 128-5 Causes of Elevated Cardiac Troponin Values Due to Myocardial Injury

Injury related to primary myocardial ischemia
Plaque rupture
Intraluminal coronary artery thrombus formation
Injury related to supply/demand imbalance
Tachy-/bradyarrhythmias
Aortic dissection or severe aortic valve disease
Hypertrophic cardiomyopathy
Cardiogenic, hypovolemic, or septic shock
Severe respiratory failure
Severe anemia
Hypertension
Coronary spasm
Coronary embolism or vasculitis
Coronary endothelial dysfunction
Injury not related to myocardial ischemia
Cardiac contusion, surgery, ablation, pacing, or defibrillator shocks
Rhabdomyolysis with cardiac involvement
Myocarditis
Cardiotoxic agents, like anthracyclines
Multifactorial or indeterminate myocardial injury
Heart failure stress (Takotsubo)
Pulmonary embolism or pulmonary hypertension
Sepsis
Renal failure
Severe acute neurological diseases, such as stroke or subarachnoid hemorrhage
Infiltrative diseases, like amyloidosis or sarcoidosis
Strenuous exercise

Modified by permission from Thygesen K. Third Universal Definition of Myocardial Infarction. JACC.
2012;60(16):1586 (table 1). Elsevier Inc.

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EARLY HOSPITAL TRIAGE IN NSTE-ACS

Patients with possible or definite NSTE-ACS represent a broad population with various
levels of risk. Of patients presenting to the ED with possible ACS, less than 25% will be
diagnosed with UA or AMI. However, on the opposite end, up to 5% of patients with ACS
are inappropriately discharged from the hospital without appropriate diagnostic workup.
To address these …

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