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  Acute Coronary Syndrome

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john



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PostSubject: Acute Coronary Syndrome    Wed Jun 22, 2011 9:03 am

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Acute Coronary Syndrome
Background

Acute coronary syndrome (ACS) refers to a spectrum of clinical presentations
ranging from those for ST-segment elevation myocardial infarction
(STEMI) to presentations found in non–ST-segment elevation myocardial
infarction (NSTEMI) or in unstable angina. In terms of pathology, ACS is
almost always associated with rupture of an atherosclerotic plaque and
partial or complete thrombosis of the infarct-related artery. (See
Etiology.) In some instances, however, stable coronary artery
disease (CAD) may result in ACS in the absence of plaque rupture and
thrombosis, when physiologic stress (eg, trauma, blood loss, anemia,
infection, tachyarrhythmia) increases demands on the heart. The
diagnosis of acute myocardial infarction in this setting requires a
finding of the typical rise and fall of biochemical markers of
myocardial necrosis in addition to at least 1 of the following[1] (See Workup.):

  • Ischemic symptoms
  • Development of pathologic Q waves
  • Ischemic ST-segment changes on electrocardiogram (ECG) or in the setting of a coronary intervention
The
terms transmural and nontransmural (subendocardial) myocardial
infarction are no longer used because ECG findings in patients with this
condition are not closely correlated with pathologic changes in the
myocardium. Therefore, a transmural infarct may occur in the absence of Q
waves on ECGs, and many Q-wave myocardial infarctions may be
subendocardial, as noted on pathologic examination. Because elevation of
the ST segment during ACS is correlated with coronary occlusion and
because it affects the choice of therapy (urgent reperfusion therapy),
ACS-related myocardial infarction should be designated STEMI or NSTEMI.
(See Workup.) Attention to the underlying mechanisms of ischemia
is important when managing ACS. A simple predictor of demand is
rate-pressure product, which can be lowered by beta blockers (eg,
metoprolol or atenolol) and pain/stress relievers (eg, morphine), while
supply may be improved by oxygen, adequate hematocrit, blood thinners
(eg, heparin, IIb/IIIa agents such as abciximab, eptifibatide,
tirofiban, or thrombolytics), and/or vasodilators (eg, nitrates,
amlodipine). (See Medications.)In 2010, the American Heart Association (AHA) published new guideline recommendations for the diagnosis and treatment of ACS.

Etiology

Acute
coronary syndrome (ACS) is caused primarily by atherosclerosis. Most
cases of ACS occur from disruption of a previously nonsevere lesion (an
atherosclerotic lesion that was previously hemodynamically insignificant
yet vulnerable to rupture). The vulnerable plaque is typified by a
large lipid pool, numerous inflammatory cells, and a thin, fibrous cap. Elevated
demand can produce ACS in the presence of a high-grade fixed coronary
obstruction, due to increased myocardial oxygen and nutrition
requirements, such as those resulting from exertion, emotional stress,
or physiologic stress (eg, from dehydration, blood loss, hypotension,
infection, thyrotoxicosis, or surgery). ACS without elevation in demand requires a new impairment in supply, typically due to thrombosis and/or plaque hemorrhage.The
major trigger for coronary thrombosis is considered to be plaque
rupture caused by the dissolution of the fibrous cap, the dissolution
itself being the result of the release of metalloproteinases
(collagenases) from activated inflammatory cells. This event is followed
by platelet activation and aggregation, activation of the coagulation
pathway, and vasoconstriction. This process culminates in coronary
intraluminal thrombosis and variable degrees of vascular occlusion.
Distal embolization may occur. The severity and duration of coronary
arterial obstruction, the volume of myocardium affected, the level of
demand on the heart, and the ability of the rest of the heart to
compensate are major determinants of a patient's clinical presentation
and outcome. (Anemia and hypoxemia can precipitate myocardial ischemia
in the absence of severe reduction in coronary artery blood flow.) A
syndrome consisting of chest pain, ischemic ST-segment and T-wave
changes, elevated levels of biomarkers of myocyte injury, and transient
left ventricular apical ballooning (takotsubo syndrome) has been shown
to occur in the absence of clinical CAD, after emotional or physical
stress. The etiology of this syndrome is not well understood but is
thought to relate to a surge of catechol stress hormones and/or high
sensitivity to those hormones.

Prognosis

Six-month
mortality rates in the Global Registry of Acute Coronary Events (GRACE)
were 13% for patients with NSTEMI ACS and 8% for those with unstable
angina. An elevated level of troponin (a type of regulatory
protein found in skeletal and cardiac muscle) permits risk
stratification of patients with ACS and identifies patients at high risk
for adverse cardiac events (ie, myocardial infarction, death) up to 6
months after the index event.[3, 4] (See Workup.)The
PROVE IT-TIMI trial found that after ACS, a J-shaped or U-shaped curve
association is observed between BP and the risk of future cardiovascular
events.[5] LeLeiko
et al determined that serum choline and free F(2)-isoprostane are also
predictors of cardiac events in ACS. The authors evaluated the
prognostic value of vascular inflammation and oxidative stress
biomarkers in patients with ACS to determine their role in predicting
30-day clinical outcomes. Serum F(2)-isoprostane had an optimal cutoff
level of 124.5 pg/mL, and serum choline had a cutoff level of 30.5
µmol/L. Choline and F(2)-isoprostane had a positive predictive value of
44% and 57% and a negative predictive value of 89% and 90%,
respectively.[6] Testosterone
deficiency is common in patients with coronary disease and has a
significant negative impact on mortality. Further study is needed to
assess the effect of treatment on survival.[7] A
study by Sanchis et al suggests renal dysfunction, dementia, peripheral
artery disease, previous heart failure, and previous myocardial
infarction are the comorbid conditions that predict mortality in NSTEMI
ACS. In patients with comorbid conditions, the highest risk period was in the
first weeks after NSTEMI ACS. In-hospital management of patients with
comorbid conditions merits further investigation. In a study that
assessed the impact of prehospital time on STEMI outcome, Chughatai et
al suggest that “total time to treatment” should be used as a core
measure instead of “door-to-balloon time.” This
is because on-scene time was the biggest fraction of "pre-hospital
time.” The study compared groups with total time to treatment of more
than 120 minutes compared with 120 minutes or less and found mortalities
were 4 compared with 0 and transfers to a tertiary care facility were 3
compared with 1, respectively.

Patient Education

Patient
education of risk factors is important, but more attention is needed
regarding delays in door-to-balloon time, and one major barrier to
improving this delay is patient education regarding his or her symptoms.
Lack of recognition of symptoms may cause tremendous delays in seeking
medical attention. Educate patients about the dangers of
cigarette smoking, a major risk factor for coronary artery disease
(CAD). The risk of recurrent coronary events decreases 50% at 1 year
after smoking cessation. Provide all patients who smoke with guidance,
education, and support to avoid smoking. Smoking-cessation classes
should be offered to help patients avoid smoking after a myocardial
infarction. Bupropion increases the likelihood of successful smoking
cessation. Diet plays an important role in the development of
CAD. Therefore, prior to hospital discharge, a patient who has had a
myocardial infarction should be evaluated by a dietitian. Patients
should be informed about the benefits of a low-cholesterol, low-salt
diet. In addition, educate patients about AHA dietary guidelines
regarding a low-fat, low-cholesterol diet. A cardiac rehabilitation program after discharge may reinforce education and enhance compliance.The
following mnemonic may useful in educating patients with CAD regarding
treatments and lifestyle changes necessitated by their condition:

  • A = Aspirin and antianginals
  • B = Beta blockers and blood pressure (BP)
  • C = Cholesterol and cigarettes
  • D = Diet and diabetes
  • E = Exercise and education
For patients being discharged home, emphasize the following:

  • Timely follow-up with primary care provider
  • Compliance with discharge medications, specifically aspirin and other medications used to control symptoms
  • Need to return to the ED for any change in frequency or severity of symptoms
History

The severity and duration of coronary artery obstruction, the volume of
myocardium affected, the level of demand, and the ability of the rest of
the heart to compensate are major determinants of a patient's clinical
presentation and outcome. A patient may present to the ED because of a
change in pattern or severity of symptoms. Typically, angina is a
symptom of myocardial ischemia that appears in circumstances of
increased oxygen demand. It is usually described as a sensation of chest
pressure or heaviness that is reproduced by activities or conditions
that increase myocardial oxygen demand. A new case of angina is more
difficult to diagnose because symptoms are often vague and similar to
those caused by other conditions (eg, indigestion, anxiety). However,
not all patients experience chest pain. They may present with only
neck, jaw, ear, arm, or epigastric discomfort. Some patients, including
some who are elderly or who have diabetes, present with no pain,
complaining only of episodic shortness of breath, severe weakness,
light-headedness, diaphoresis, or nausea and vomiting. Elderly persons
may also present only with altered mental status. Those with preexisting
altered mental status or dementia may have no recollection of recent
symptoms and may have no complaints. In addition, evidence exists
that women more often have coronary events without typical symptoms,
which may explain the frequent failure of clinicians to initially
diagnose ACS in women. A summary of patient complaints is as follows:

  • Palpitations
  • Pain,
    which is usually described as pressure, squeezing, or a burning
    sensation across the precordium and may radiate to the neck, shoulder,
    jaw, back, upper abdomen, or either arm
  • Exertional dyspnea that resolves with pain or rest
  • Diaphoresis from sympathetic discharge
  • Nausea from vagal stimulation
  • Decreased exercise tolerance
Stable
angina involves episodic pain lasting 5-15 minutes, is provoked by
exertion, and is relieved by rest or nitroglycerin. In unstable angina,
patients have increased risk for adverse cardiac events, such as
myocardial infarction or death. New-onset exertional angina can occur at
rest and is of increasing frequency or duration or is refractory to
nitroglycerin. Variant angina (Prinzmetal angina) occurs primarily at
rest, is triggered by smoking, and is thought to be due to coronary
vasospasm.

Physical Examination

Physical

examination results are frequently normal. If chest pain is ongoing,
the patient will usually lie quietly in bed and may appear anxious,
diaphoretic, and pale. Physical findings can vary from normal to any of
the following:

  • Hypotension - Indicates ventricular dysfunction due to myocardial ischemia, infarction, or acute valvular dysfunction
  • Hypertension
    - May precipitate angina or reflect elevated catecholamine levels due
    to anxiety or to exogenous sympathomimetic stimulation
  • Diaphoresis
  • Pulmonary edema and other signs of left heart failure
  • Extracardiac vascular disease
  • Jugular venous distention
  • Cool, clammy skin and diaphoresis in patients with cardiogenic shock
In addition, a third heart sound (S3) may be present, and frequently, a fourth heart sound (S4)
exists. The latter is especially prevalent in patients with
inferior-wall ischemia and may be heard in patients with ischemia or
systolic murmur secondary to mitral regurgitation A systolic
murmur related to dynamic obstruction of the left ventricular (LV)
outflow tract may also occur. It is caused by hyperdynamic motion of the
basal left ventricular myocardium and may be heard in patients with an
apical infarct. A new murmur may reflect papillary muscle
dysfunction. Rales on pulmonary examination may suggest LV dysfunction
or mitral regurgitation.Patients who present to the ED with chest
pain who have a low short-term risk of a major adverse cardiac event
must be identified to facilitate early discharge in order to avoid
lengthy and costly hospital stays. The
ASPECT study tested a 2-hour, accelerated diagnostic protocol (ADP)
that included the use of a structured pretest probability scoring
method, electrocardiography, and a point-of-care biomarker panel that
included troponin, creatine kinase MB, and myoglobin levels. The study
suggests that ADP can identify patients at low risk for a short-term
major adverse cardiac event who may be suitable for early discharge;
such an approach could be used to decrease the overall observation
periods and admissions for chest pain and has the potential to affect
health-service delivery worldwide.

Complications

Complications
of ischemia include pulmonary edema, while those of myocardial
infarction include rupture of the papillary muscle, left ventricular
free wall, and ventricular septum.
Diagnostic Considerations

As many as half of all cases of ACS
are clinically silent in that they do not cause the classic symptoms of
this syndrome. Consequently, ACS goes unrecognized by the patient.
Maintain a high index of suspicion for ACS, especially when evaluating
women, patients with diabetes, older patients, patients with dementia,
and those with a history of heart failure. Although ST-segment
and T-wave changes are associated with CAD, alternative causes of these
findings are left ventricular aneurysm, pericarditis, Prinzmetal angina,
early repolarization, Wolff-Parkinson-White syndrome, and drug therapy
(eg, with tricyclic antidepressants, phenothiazines). Increasing
public awareness of the typical and atypical presentations of ACS is of
the utmost importance for optimal and timely treatment. Many patients do
not recognize that their symptoms are cardiac in origin and therefore
may delay seeking medical help. Guidelines from the European Society of
Cardiology (ESC)/American College of Cardiology (ACC)/American Heart
Association (AHA) recommend that patients with established CAD call
emergency medical services if they have chest pain that does not resolve
after they take a sublingual nitroglycerin tablet. Differentials

  • Anxiety
  • Aortic Stenosis
  • Asthma
  • Cardiomyopathy, Dilated
  • Esophagitis
  • Gastroenteritis
  • Hypertensive Emergencies in Emergency Medicine
  • Myocardial Infarction
  • Myocarditis
  • Pericarditis and Cardiac Tamponade


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PostSubject: Re: Acute Coronary Syndrome    Wed Jun 22, 2011 9:09 am

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Acute Coronary Syndrome Workup

Approach Considerations

As
previously mentioned, stable coronary artery disease (CAD) may result
in ACS in the absence of plaque rupture and thrombosis, when physiologic
stress (eg, trauma, blood loss, anemia, infection, tachyarrhythmias)
increases demands on the heart. In such cases, the diagnosis of acute
myocardial infarction can be made if workup reveals the typical rise and
fall of biochemical markers of myocardial necrosis along with either
the development of pathologic Q waves or the presence (on ECG or in the
setting of a coronary intervention) of ischemic ST-segment changes.
(However, the presence of ischemic symptoms can be substituted for the
Q-wave or ST-segment evidence.)[1] Non–ST-segment
elevation myocardial infarction (NSTEMI) is distinguished from unstable
angina by elevated levels of cardiac enzymes and biomarkers of myocyte
necrosis. Differentiation is generally based on 3 sets of biomarkers
measured at 6- to 8-hour intervals after the patient's presentation to
the ED. The current definition of NSTEMI requires a typical clinical
syndrome plus elevated troponin (or creatine kinase isoenzyme MB
[CK-MB]) levels to over 99% of the normal reference (with a coefficient
of variation of < 10% for the assay). Given this definition, nearly
25% of patients who were previously classified as having unstable angina
now fulfill the criteria for NSTEMI. Measure cardiac enzyme
levels at regular intervals, starting at admission and continuing until
the peak is reached or until 3 sets of results are negative. Biochemical
biomarkers (demonstrated in the image below) are useful for diagnosis
and prognostication.


This
plot shows changes in cardiac markers over time after the onset of
symptoms. Peak A is the early release of myoglobin or creatine kinase
isoenzyme MB (CK-MB) after acute myocardial infarction (AMI). Peak B is
the cardiac troponin level after infarction. Peak C is the CK-MB level
after infarction. Peak D is the cardiac troponin level after unstable
angina. Data are plotted on a relative scale, where 1.0 is set at the
myocardial-infarction cutoff concentration. Courtesy of Wu et al (1999).
ROC = receiver operating characteristic. Of note,
cardiac-specific troponins are not detectable in the blood of healthy
individuals; therefore, they provide high specificity for detecting
injury to cardiac myocytes. These molecules are also more sensitive than
CK-MB for myocardial necrosis and therefore improve early detection of
small myocardial infarctions. Although blood troponin levels increase
simultaneously with CK-MB levels (about 6 h after the onset of
infarction), they remain elevated for as long as 2 weeks. As a result,
troponin values cannot be used to diagnose reinfarction. New methods of
detecting troponins in the blood can measure levels as low as 0.1-0.2
ng/mL. Minor elevations in these molecules can be detected in the
blood of patients without ACS in the setting of myocarditis
(pericarditis), sepsis, renal failure, acute congestive heart failure
(CHF), acute pulmonary embolism, or prolonged tachyarrhythmias.

Electrocardiography





ECGs should be reviewed promptly. Involve a cardiologist when in doubt. Recording
an ECG during an episode of the presenting symptoms is valuable.
Transient ST-segment changes (>0.05 mV) that develop during a
symptomatic period and that resolve when the symptoms do are strongly
predictive of underlying CAD and have prognostic value. Comparison with
previous ECGs is often helpful. Alternative causes of ST-segment
and T-wave changes are left ventricular aneurysm, pericarditis,
Prinzmetal angina, early repolarization, Wolff-Parkinson-White syndrome,
and drug therapy (eg, with tricyclic antidepressants, phenothiazines). In
the emergency setting, ECG is the most important ED diagnostic test for
angina. It may show changes during symptoms and in response to
treatment, confirm a cardiac basis for symptoms. It also may demonstrate
preexisting structural or ischemic heart disease (left ventricular
hypertrophy, Q waves). A normal ECG or one that remains unchanged from
the baseline does not exclude the possibility that chest pain is
ischemic in origin. Changes that may be seen during anginal episodes
include the following:

  • Transient ST-segment elevations
  • Dynamic T-wave changes - Inversions, normalizations, or hyperacute changes
  • ST depressions - May be junctional, downsloping, or horizontal
In
patients with transient ST-segment elevations, consider LV aneurysm,
pericarditis, Prinzmetal angina, early repolarization, and
Wolff-Parkinson-White syndrome as possible diagnoses. Fixed changes
suggest acute myocardial infarction. When deep T-wave inversions
are present, consider the possibility of central nervous system (CNS)
events or drug therapy with tricyclic antidepressants or phenothiazines
as the cause. Diagnostic sensitivity may be increased by performing right-sided leads (V4 R), posterior leads (V8, V9), and serial recordings.ECGs from 2 patients are shown below.



A
50-year-old man with type 1 diabetes mellitus and hypertension presents
after experiencing 1 hour of midsternal chest pain that began after
eating a large meal. Pain is now present but is minimal. Aspirin is the
single drug that will have the greatest potential impact on subsequent
morbidity. In the setting of ongoing symptoms and electrocardiogram
(ECG) changes, nitrates titrated to 10% reduction in blood pressure and
symptoms, beta blockers, and heparin are all indicated. If the patient
continues to have persistent signs and/or symptoms of ischemia, addition
of a glycoprotein IIb/IIIa inhibitor should be

considered.



A
62-year-old woman with a history of chronic stable angina and a "valve
problem" presents with new chest pain. She is symptomatic on arrival,
complaining of shortness of breath and precordial chest tightness. Her
initial vital signs are blood pressure = 140/90 mm Hg and heart rate =
98. Her electrocardiogram (ECG) is as shown. She is given nitroglycerin
sublingually, and her pressure decreases to 80/palpation. Right
ventricular ischemia should be considered in this patient. In
difficult cases with nondiagnostic ECGs, such as those involving a left
bundle-branch block, early imaging is useful to assess wall-motion
abnormalities. An important use of noninvasive imaging is to classify a patient has having NSTEMI or true STEMI.The
Optimal Cardiovascular Diagnostic Evaluation Enabling Faster Treatment
of Myocardial Infarction (OCCULT-MI) trial compared the 80-lead (80L)
mapping system to standard 12-lead (12L) ECG. The study concluded that
the 80L body surface mapping technology detected more patients with MI
or ACS than the 12L ECG, while still maintaining a high degree of
specificity.[11]

Measurement of CK-MB Levels

CK-MB,
the isoenzyme specific to the heart muscle, was the principal biomarker
of cardiac injury until troponin supplemented it. In the setting
of myocardial infarction, plasma CK-MB concentrations typically rise
about 4-6 hours after the onset of chest pain. They peak within 12-24
hours and return to baseline levels within 24-48 hours. Serial
measurements obtained every 6-8 hours (at least 3 times) are warranted
until peak values are determined. The area under the
concentration-time curve for CK-MB created with serial measurements of
blood enzyme levels provides a reliable estimate of the size of the
infarct. Clinical settings other than ACS, such as trauma, heavy
exertion, and skeletal muscle disease (eg, rhabdomyolysis), may elevate
CK-MB values. Determination of subforms of CK-MB (CK-MB2 that is more specific to heart muscle) may improve the sensitivity of this test.

Measurement of Troponin levels

The
troponins are regulatory proteins found in skeletal and cardiac muscle.
The 3 subunits that have been identified include troponin I (TnI),
troponin T (TnT), and troponin C (TnC). The genes that code for the
skeletal and cardiac isoforms of TnC are identical; thus, no structural
difference exists between them. However, the skeletal and cardiac
subforms for TnI and TnT are distinct, and immunoassays have been
designed to differentiate between them. This explains the
cardiospecificity of the cardiac troponins. Skeletal TnI and TnT are
structurally different. No cross-reactivity occurs between skeletal and
cardiac TnI and TnT with the current assays. The cardiac
troponins are sensitive, cardiospecific, and provide prognostic
information for patients with ACS. They have become the cardiac markers
of choice for patients with ACS. Early studies on the release
kinetics of the cardiac troponins indicated that they were not early
markers of myocardial necrosis. The early generation troponin assays
yielded positive results within 4-8 hours after symptom onset, similar
in timing to the release of CK-MB; however, they remained elevated for
as long as 7-10 days post-myocardial infarction. Initial studies
on the cardiac troponins revealed a subset of patients with rest
unstable angina in whom CK-MB levels were normal but who had elevated
troponin levels. These patients had higher adverse cardiac event rates
(acute myocardial infarction, death) within the 30 days after the index
admission and a natural history that closely resembled patients with
NSTEMI. The table below outlines many of the initial studies on
troponins in ACS.


Use of cardiac markers in the ED. Studies on troponins in ACS. As
previously mentioned, an elevated troponin level also enables risk
stratification of patients with ACS and identifies patients at high risk
for adverse cardiac events (ie, myocardial infarction, death) up to 6
months after the index event.[3, 4] In
a study by Antman et al, the initial TnI level on admission in patients
with ACS correlated with mortality at 6 weeks. CK-MB levels, although
sensitive and specific for the diagnosis of acute myocardial infarction,
were not predictive of adverse cardiac events and had no prognostic
value.[3] The relationship between TnI levels and risk of cardiac events and mortality is demonstrated in the graphs below.


Use of cardiac markers in the ED. Troponin I levels and cardiac mortality in ACS.



Use
of cardiac markers in the ED. Cardiac event rates in the platelet
receptor inhibition for ischemic syndrome (PRISM) study based on
troponin I results. Data from a meta-analysis indicated that
an elevated troponin level in patients without ST-segment elevation is
associated with a nearly 4-fold increase in cardiac mortality rate. For
the composite end point of acute myocardial infarction or death, an
elevated troponin level was associated with an odds ratio of 3.3.[12] The
TIMI IIIB, GUSTO IIa, GUSTO IV ACS, and Fragmin During Instability in
Coronary Artery Disease (FRISC) trial all demonstrated a direct
correlation between the level of TnI or TnT and the adverse cardiac
event rate and mortality rate in ACS.[3, 13, 14, 15, 16] These studies confirmed the use of the cardiac troponins TnI and TnT in risk stratification and therapeutic decision making. Studies
by Ohman et al and Stubbs et al revealed that an elevated troponin
level at baseline was an independent predictor of mortality even in
patients with chest pain and acute myocardial infarction with ST-segment
elevation who were eligible for reperfusion therapy.[13, 17] With
the introduction of increasingly sensitive and precise troponin assays,
up to 80% of patients with acute myocardial infarction will be found to
have an elevated troponin within 2-3 hours of ED arrival. With this
improved clinical performance in cardiac troponin assays, the so-called
rapidly rising cardiac biomarkers, such as myoglobin or CK-MB isoforms,
have little clinical utility.[18, 19, 20, 21] As a result, some authorities have called for a troponin standard alone and recommend eliminating CK-MB.[22] The
2007 American College of Cardiology (ACC) guidelines for NSTEMI
recommend that serial troponins be obtained for a definitive rule out at
baseline and 6-9 hours later. To establish the diagnosis of acute
myocardial infarction, only 1 elevated level above the established
cutoff is required. The demonstration of a rising or falling level is
needed to distinguish persistently elevated troponin levels (eg, in some
patients with renal failure) from those patients with acute myocardial
infarction.[23] If
myocardial injury is suspected despite negative cardiac-specific
troponin findings, additional, sensitive laboratory assays are
indicated.[24]

Measurement of Myoglobin Levels





Myoglobin
is not cardiac specific, but it may be detected as early as 2 hours
after myocardial necrosis starts. However, myoglobin results should be
supplemented with other, more specific cardiac biomarkers, such as CK-MB
or troponin. Myoglobin values have a high negative predictive value when blood is sampled in the first 4-8 hours after onset.

Complete Blood Count Determination

The
CBC count helps in ruling out anemia as a secondary cause of ACS.
Leukocytosis has prognostic value in the setting of acute myocardial
infarction.

Basic Metabolic Panel

Obtain
a basic metabolic profile, including a check of blood glucose level,
renal function, and electrolytes levels, for patients with new-onset
angina. Close monitoring of potassium and magnesium levels is important
in patients with ACS because low levels may predispose them to
ventricular arrhythmias. Routine measurement of serum potassium levels
and prompt correction are recommended. Creatinine levels must be
considered before using an angiotensin-converting enzyme (ACE) inhibitor
and particularly if cardiac catheterization is considered. Use of N -acetylcysteine and adequate hydration can help prevent contrast material–induced nephropathy.[25] Other useful metabolic profiles include amylase and lipase.

New Biomarkers

levels
of brain natriuretic peptide (BNP) and N-terminal pro-BNP (NT-pro-BNP)
are elevated in acute MI and provide predictive information for risk
stratification across the spectrum of ACS.[26, 27] However,
a single, low BNP level obtained within 4 hours of a patient presenting
to the ED does not identify the patient as low-risk for 30-day acute
myocardial infarction or death.[28] In
the future, a combination of levels of troponin (a biomarker for
myocardial necrosis), NT-pro-BNP (an indicator of elevated LV
end-diastolic pressure and wall stress), and C-reactive protein (CRP, an
estimate of the extent of systemic inflammation) may prove useful for
predicting the outcome of patients with ACS. Routine measurement of BNP and CRP levels in patients with ACS is not warranted at this time.Interleukin-6
is the major determinant of acute-phase reactant proteins in the liver,
and serum amyloid A is another acute-phase reactant. Elevations of
either of these can be predictive in determining increased risk of
adverse outcomes in patients with unstable angina. Several other
biomarkers with variable sensitivity and specificity have been
investigated, including sCD40 ligand, myeloperoxidase,
pregnancy-associated plasma protein-A, choline, placental growth factor,
cystatin C, fatty acid binding protein, ischemia modified albumin,
chemokines ligand-5 and -18 (mediators of monocyte recruitment induced
by ischemia), angiogenin, SCUBE1 (a novel platelet protein), and others.[29, 30] In
a study that included 107 patients presenting to an emergency
department with chest pain, ischemia modified albumin was not found to
have superior sensitivity and specificity over traditional biomarkers,
with a sensitivity of 0.86 and specificity of 0.49.[31]

Chest Radiography

Chest
radiography helps in assessing cardiomegaly and pulmonary edema, or it
may reveal complications of ischemia, such as pulmonary edema. It may
also provide clues to alternative causes of symptoms, such as thoracic
aneurysm or pneumonia (which can be a precipitating cause of ACS).

Echocardiography

Echocardiograms
may play an important role in the setting of ACS. Regional wall-motion
abnormalities can be identified with this modality, and echocardiograms
are especially helpful if the diagnosis is questionable. An
echocardiogram can also help in defining the extent of an infarction and
in assessing overall function of the left and right ventricles. In
addition, an echocardiogram can help to identify complications, such as
acute mitral regurgitation, LV rupture, and pericardial effusion. Absence
of segmental wall-motion abnormality on echocardiography during active
chest discomfort is a highly reliable indicator of a nonischemic origin
of symptoms, although echocardiography is of limited value in patients
whose symptoms have resolved or who have pre-existing wall-motion
abnormalities.

Myocardial Perfusion Imaging





Radionuclide
myocardial perfusion imaging has been shown to have favorable
diagnostic and prognostic value in the emergent setting, with an
excellent early sensitivity in the detection of acute myocardial
infarction not found in other testing modalities. A normal
resting perfusion imaging study has been shown to have a negative
predictive value of more than 99% in excluding myocardial infarction.
Observational and randomized trials of rest and stress imaging in the ED
evaluation of patients with chest pain have demonstrated reductions in
unnecessary hospitalizations and cost savings compared with routine
care. Perfusion imaging has also been used in risk stratification
after myocardial infarction and for measurement of infarct size to
evaluate reperfusion therapies. Novel "hot spot" imaging
radiopharmaceuticals that visualize infarction or ischemia are currently
undergoing evaluation and hold promise for future imaging of ACS.

Cardiac Angiography

Cardiac catheterization helps in defining coronary anatomy and the extent of a patient’s disease. Patients
with cardiogenic shock, intractable angina (despite medication), severe
pulmonary congestion, or right ventricular (RV) infarction should
immediately undergo cardiac catheterization. (Cardiogenic shock is
defined as a systolic BP of less than 90 mm Hg in the presence of organ
hypoperfusion.) For high-risk patients with ACS without
persistent ST elevation, angiography with glycoprotein IIb/IIIa
inhibition has been recommended. The earlier that coronary angiography
is performed, the lower the risk of recurrent ischaemia.[32] This also shortens the hospital stay for those patients. Most
patients benefit from angiography when they have a TIMI (Thrombolysis
in Myocardial Infarction) risk score of less than 3 points (see the
Table below). Table. TIMI Risk Score for Unstable Angina and NSTEMI[33] (Open Table in a new window)
Characteristic Risk Score
History
Age ≥65 years1
At least 3 risk factors for coronary heart disease1
Previous coronary stenosis ≥50%1
Use of aspirin in previous 7 days1
Presentation
At least 2 anginal episodes in the previous 24 hours1
ST-segment elevation on admission ECG1
Elevated levels of serum biomarkers1
Total Score0-7
Note:
Event rates significantly increased as the TIMI risk score increased in
the test cohort in the TIMI IIB study. Rates were 4.7% for a score of
0/1, 8.3% for 2, 13.2% for 3, 19.9% for 4, 26.2% for 5, and 40.9% for
6/7 (P < .001, χ2 test for the trend). The
pattern of increasing event rates with increasing TIMI risk score was
confirmed in all 3 validation groups (P < .001).


Computed Tomography Coronary Angiography and CT Coronary Artery Calcium Scoring

Dual-source
64-slice CT scanners can do a full scan in 10 seconds and produce
high-resolution images that allow fine details of the patient's coronary
arteries to be seen. This technology allows for noninvasive and early
diagnosis of CAD and thus earlier treatment before the coronary arteries
become more or completely occluded. It permits direct visualization of
not only the lumen of the coronary arteries but also plaque within the
artery. Dual-source 64-slice CT scanning is being used with intravenous
(IV) contrast to determine if a stent or graft is open or closed. CT
coronary artery scoring is emerging as an attractive risk
stratification tool in patients who are low risk for ACS. This imaging
modality exposes the patient to very little radiation (1-2 msV). No
contrast is needed, and the study does not have a requirement for heart
rate.[34] The
CAPTURE study, a randomized diagnostic trial, compared the efficacy a
comprehensive cardiothoracic CT examination in the evaluation of
patients presenting to the emergency department with undifferentiated
acute chest discomfort or dyspnea.[35] Comprehensive
cardiothoracic CT scanning was reasonable, with a similar diagnostic
yield to dedicated protocols, but it did not reduce the length of stay,
rate of subsequent testing, or costs. The “triple rule out” protocol
might be helpful in the evaluation of select patients, but these
findings suggest that it should not be routinely used with the
expectation that it will improve efficiency or reduce resource use.

Other Techniques

Optical
coherence tomography (OCT), palpography, and virtual histology are
being studied for use in identifying vulnerable plaques.Noninvasive
whole-blood test prior to coronary angioplasty may be useful for
assessing obstructive CAD in patients without diabetes.[36] Stress
cardiac magnetic resonance imaging (MRI) in an observation unit setting
has shown to reduce the medical costs, compared with inpatient care,
for patients who present with emergent, non-low-risk chest pain, without
missing acute coronary syndrome.[37] The
CAPTURE study, a randomized diagnostic trial, compared the efficacy a
comprehensive cardiothoracic CT examination in the evaluation of
patients presenting to the emergency department with undifferentiated
acute chest discomfort or dyspnea.[38] Comprehensive
cardiothoracic CT scanning was reasonable, with a similar diagnostic
yield to dedicated protocols, but it did not reduce the length of stay,
rate of subsequent testing, or costs. The “triple rule out” protocol
might be helpful in the evaluation of select patients, but these
findings suggest that it should not be routinely used with the
expectation that it will improve efficiency or reduce resource use.


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Acute Coronary Syndrome Treatment & Management

Approach Considerations

Initial
therapy for acute coronary syndrome should focus on stabilizing the
patient's condition, relieving ischemic pain, and providing
antithrombotic therapy to reduce myocardial damage and prevent further
ischemia. Morphine (or fentanyl) for pain control, oxygen, sublingual
and/or IV nitroglycerin, soluble aspirin 162-325 mg, and clopidogrel
with a 300- to 600-mg loading dose are given as initial treatment. In
complete vessel occlusion without collateralization of the
infarct-related vessel, there is little utility in “pushing nitrates.” High-risk
patients with non-ST-segment elevation myocardial infarction (NSTEMI
ACS) should receive aggressive care, including aspirin, clopidogrel,
unfractionated heparin or low–molecular weight heparin (LMWH),
intravenous platelet glycoprotein IIb/IIIa complex blockers (eg,
tirofiban, eptifibatide), and a beta blocker. The goal is early
revascularization. Intermediate-risk patients with NSTEMI ACS
should rapidly undergo diagnostic evaluation and further assessment to
determine their appropriate risk category. Low-risk patients with
NSTEMI ACS should undergo further follow-up with biomarkers and
clinical assessment. Optimal medical therapies include use of standard
medical therapies, including beta blockers, aspirin, and unfractionated
heparin or LMWH. The Clopidogrel in Unstable Angina to Prevent Recurrent
Events (CURE) study showed that clopidogrel would be beneficial even in
low-risk patients.[39] If no further pain occurs, and follow-up studies are negative, a stress study should drive further management. Monitor
and immediately treat arrhythmias in the first 48 hours. Pay attention
to exacerbating factors, such as disturbances in electrolytes
(especially potassium and magnesium), hypoxemia, drugs, or acidosis.
Correct these factors accordingly. Humidified oxygen may reduce
the risk of nosebleeds in patients with ACS who are receiving
antiplatelet and antithrombin therapy.Do not administer nitrates
if the patient is hypotensive (systolic BP < 90 mm Hg); if RV
infarction, large pericardial effusion, or severe aortic stenosis is
suspected; or if the patient recently received phosphodiesterase-5
inhibitors (eg, sildenafil). Patients with known hypersensitivity
to antiplatelet agents, active internal bleeding, and bleeding
disorders should not receive antiplatelet or antithrombotic therapy. Some
patients with intractable chest pain or severe hypotension may require
the insertion of an intra-aortic balloon pump. The EuroHeart survey
showed a nearly 40% reduction in the risk of death in patients with ACS
who received support with an intra-aortic balloon pump. This benefit was
independent of the status of the ST segment. Congestive heart
failure (CHF) can be due to systolic dysfunction or diastolic
dysfunction in the setting of myocardial infarction. Aggressive
treatment is indicated to prevent worsening of the situation. Patients
presenting with cardiogenic shock should undergo percutaneous coronary
intervention (PCI) as soon as possible. Cardiogenic shock is associated
with a high mortality rate. Pressor agents, such as dopamine, and
inotropic agents, such as dobutamine, may be needed. In a prospective,
natural-history study of coronary atherosclerosis, patients underwent
3-vessel coronary angiography and gray-scale and radiofrequency
intravascular ultrasonographic imaging after PCI.[40] Recurrent
ischemia may be due to incomplete reperfusion. In the setting of PCI,
consider stent thrombosis as a possible cause. Whether drug-eluting
stents have an increased rate of thrombosis compared with bare metal
stents is unclear.Drug-eluting stents are linked with fewer
periprocedural risks but tend to have high incidence of postprocedural
complications including myocardial infarction, repeat procedures, and
12-month major adverse cardiac and brain complications, compared with
coronary bypass surgery.[41] One
study by Ribichini et al suggests that prednisone treatment after bare
metal stents or drug-eluting stent implantation results in a better
event-free survival at 1 year.[42] In
a study of 3031 patients, Mehta et al found that early intervention
(coronary angiography < or = 24 h after randomization) in patients
with ACS did not differ greatly from delayed intervention (coronary
angiography > or = 36 h randomization) in the prevention of primary
outcomes (ie, composite of death, myocardial infarction, or stroke at 6
mo). Early intervention did reduce the rate of secondary outcomes (ie,
death, myocardial infarction, or refractory ischemia at 6 mo) and
improved primary outcomes in patients who were at highest risk (ie,
GRACE risk score >140).[43] In
a Swedish registry of patients with STEMI from 1996-2007, reported an
increase in the prevalence of evidence-based treatments.[44] The
use of aspirin, clopidogrel, beta blockers, statins, and ACE inhibitors
all increased. Clopidogrel increased from 0% to 82%, statins increased
from 23% to 83%, and various ACE inhibitors increased by a large margin.
A decrease was reported in 30-day and 1-year mortality that was
sustained during long-term follow-up. By following the proper
guidelines, patients who have experienced STEMI have higher survival
rates.

Pharmacologic Anti-ischemic Therapy





Nitrates

Nitrates do not improve mortality.[45] However,
they provide symptomatic relief by means of several mechanisms,
including coronary vasodilation, improved collateral blood flow,
decrease in preload (venodilation and reduced venous return), and
decrease in afterload (arterial vasodilation). Care should be taken to
avoid hypotension, because this can potentially reduce coronary
perfusion pressure (diastolic BP - LV diastolic pressure). Beta-blockers

Beta-blockers are indicated in all patients unless they have the following contraindications:

  • Systolic blood pressure less than 90 mm Hg
  • Cardiogenic shock
  • Severe bradycardia
  • Second- or third-degree heart block
  • Asthma or emphysema that is sensitive to beta agonists
  • Peripheral vascular disease
  • Uncompensated CHF
Beta
blockers reduce oxygen demand and ventricular wall tension. They also
decrease mortality and adverse cardiovascular events. These drugs may
prevent mechanical complications of myocardial infarction, including
rupture of the papillary muscle, left ventricular free wall, and
ventricular septum. Beta blockers meliorate dynamic obstruction of the
left ventricular outflow tract in patients with apical infarct and
hyperdynamic basal segments. The most frequently used regimen is
IV metoprolol 2-5 mg given every 5 minutes (up to 15 mg total) followed
by 25-100 mg given orally twice a day. Beta-blockers should not be used acutely in patients with cardiogenic shock or signs of heart failure on presentation.

Pharmacologic Antithrombotic Therapy

Aspirin

Aspirin
permanently impairs the cyclooxygenase pathway of thromboxane A2
production in platelets, in this way inhibiting platelet function.
Aspirin reduces morbidity and mortality and is continued indefinitely.[46] Clopidogrel

Clopidogrel
(thienopyridine) inhibits adenosine 5'-diphosphate (ADP)–dependent
activation of the glycoprotein IIb/IIIa complex, a necessary step for
platelet aggregation. This process results in intense inhibition of
platelet function, particularly in combination with aspirin. In the CURE
trial, thienopyridine reduced the rate of myocardial infarction by 20%.[39] Clopidogrel
is a class I recommendation for patients when an early
noninterventional approach is planned in therapy for at least 1 month
and ideally up to 1 year.[47] When
percutaneous coronary intervention (PCI) is planned, clopidogrel
300-600 mg should be given as early as possible before or at the time of
PCI.[47] Clopidogrel,
75 mg daily, is continued for at least 12 months after PCI, if the
patient is not at high risk for bleeding, according to 2011 ACCF/AHA
guidelines (class I recommendation).[47] Early discontinuation should be considered if the risk of bleeding-related morbidity outweighs the anticipated benefits. The
optimal loading dose for clopidogrel is still being evaluated. Reports
show that a loading dose of 600 mg might be more beneficial than 300 mg.
Withhold clopidogrel for at least 5 days before elective coronary
artery bypass grafting (CABG). Since 12% of patients with non-ST
elevation ACS have coronary anatomy that favors CABG, the use of
clopidogrel is withheld until coronary angiography at some institutions.
Clopidogrel can be considered an alternative to aspirin in patients with aspirin intolerance or who are allergic to aspirin.Patients with chronic kidney disease who have low platelet response to clopidogrel tend to have worse outcomes after PCI.[48] A
consensus statement issued by the American College of Cardiology,
American College of Gastroenterology, and American Heart Association in
November 2010 addresses the issue of concomitant use of proton pump
inhibitors (PPIs) and thienopyridine antiplatelet drugs.[49] The group’s findings and recommendations are listed below.

  • Clopidogrel reduces major CV events compared with placebo or aspirin.
  • Dual
    antiplatelet therapy with clopidogrel and aspirin, compared with
    aspirin alone, reduces major CV events in patients with established
    ischemic heart disease, and it reduces coronary stent thrombosis but is
    not routinely recommended for patients with prior ischemic stroke
    because of the risk of bleeding.[50]
  • Clopidogrel alone, aspirin alone, and their combination are all associated with increased risk of GI bleeding.
  • Clopidogrel
    requires metabolic activation by cytochrome P450 2C19 (CYP2C19). PPIs
    that inhibit CYP2C19 are commonly coadministered with clopidogrel to
    reduce the risk of GI bleeding. A study by Simon et al showed that PPI
    use is not associated with an increased risk of cardiovascular events or
    mortality in patients who have been treated with clopidogrel for a
    recent MI, regardless of CYP2C19 genotype.[51]
  • Patients
    with prior GI bleeding are at highest risk for recurrent bleeding on
    antiplatelet therapy; other risk factors include advanced age,
    concurrent use of anticoagulants, steroids, or NSAIDs including aspirin,
    and Helicobacter pylori infection; risk increases as the number of risk factors increases.
  • Use
    of PPIs or histamine H2 receptor antagonists (H2RAs) reduces the risk
    of upper GI bleeding compared with no therapy; PPIs reduce upper GI
    bleeding to a greater degree than do H2Ras.
  • PPIs
    are recommended to reduce GI bleeding among patients with a history of
    upper GI bleeding; PPIs are appropriate in patients with multiple risk
    factors for GI bleeding who require antiplatelet therapy.
  • Routine
    use of either a PPI or an H2RA is not recommended for patients at lower
    risk of upper GI bleeding, who have much less potential to benefit from
    prophylactic therapy.
  • Clinical
    decisions regarding concomitant use of PPIs and thienopyridines must
    balance overall risks and benefits, considering both CV and GI
    complications.
  • Pharmacokinetic and
    pharmacodynamic studies, using platelet assays as surrogate endpoints,
    suggest that concomitant use of clopidogrel and a PPI reduces the
    antiplatelet effects of clopidogrel; the strongest evidence for an
    interaction is between omeprazole and clopidogrel; it is not established
    that changes in these surrogate endpoints translate into clinically
    meaningful differences.
  • Observational
    studies and a single randomized clinical trial have shown inconsistent
    effects on CV outcomes of concomitant use of thienopyridines and PPIs; a
    clinically important interaction cannot be excluded, particularly in
    certain subgroups, such as poor metabolizers of clopidogrel.
  • The
    role of either pharmacogenomic testing or platelet function testing in
    managing therapy with thienopyridines and PPIs has not yet been
    established.
Prasugrel

Like clopidogrel,
prasugrel is a thienopyridine ADP receptor inhibitor that inhibits
platelet aggregation. It has been approved in the United States and has
been shown to reduce new and recurrent myocardial infarctions.[52] The
loading dose is 60 mg PO once and maintenance is 10 mg PO qd (given
with aspirin 75-325 mg/d). Prasugrel is indicated for the reduction of
thrombotic cardiovascular events (including stent thrombosis) with ACS
that is managed with PCI.The 2011 ACF/AHA guidelines advise that a
loading dose of prasugrel be given as soon as possible, once coronary
anatomy is defined and a decision is made to proceed with PCI. Prasugrel
should be administered no later than 1 hour after PCI. Maintenance
therapy with prasugrel is continued for at least 1 year after PCI.[47] Early discontinuation should be considered if the risk of bleeding-related morbidity outweighs the anticipated benefits. One
study, however, found that significant, sometimes fatal, bleeding
occurred more frequently with prasugrel than with clopidogrel, although
the overall mortality rate did not differ significantly between a
treatment group receiving prasugrel and another receiving clopidogrel.[53, 52] Ticagrelor

Ticagrelor
is the first reversible oral P2Y receptor antagonist. It provides
faster, greater, and more consistent ADP-receptor inhibition than does
clopidogrel.[54] Abciximab, eptifibatide, and tirofiban

Glycoprotein IIb/IIIa receptor antagonists include abciximab[55, 56] , eptifibatide[57] , and tirofiban[58] .
These drugs inhibit the glycoprotein IIb/IIIa receptor, which is
involved in the final common pathway for platelet adhesion and
aggregation. (See the image below.)




Use
of cardiac markers in the ED. Effect of time to treatment in patients
with acute coronary syndrome (ACS) who are treated with the GIIb/IIIa
inhibitor eptifibatide. Use eptifibatide or tirofiban in patients with high-risk features in whom invasive treatment is not planned.The
use of eptifibatide 12 hours or more before angiography was not
superior to the provisional use of eptifibatide after angiography,
according to results from the EARLY ACS trial. The study compared a
strategy of early, routine administration of eptifibatide with delayed,
provisional administration in patients who had ACS without ST-segment
elevation and who were assigned to an invasive strategy. The study also
found that early use of eptifibatide was associated with an increased
risk of non–life-threatening bleeding and the need for transfusion.[59] Two
trials with tirofiban and 1 trial with eptifibatide documented their
efficacy in unstable angina/NSTEMI patients, only some of whom underwent
interventions. These antagonists are a class I recommendation in
patients in whom catheterization and PCI are planned. Intermediate- and
high-risk patients appear to respond favorably to glycoprotein IIb/IIIa
inhibitors.[60] They include patients with ST-segment depression, elevated risk scores, elevated serum troponin levels[61] , and/or diabetes mellitus. Currently,
IIb/IIIb antagonists in combination with aspirin are considered
standard antiplatelet therapy for patients at high risk for unstable
angina.

Pharmacologic Anticoagulation Therapy

Unfractionated heparin

A
study by Oler et al found that unfractionated heparin was associated
with a 33% reduction in the risk of myocardial infarction or death in
patients with unstable angina who were treated with aspirin plus
heparin, compared with patients who were treated with aspirin alone.[62] The
FUTURA/OASIS-8 randomized trial found that low-dose unfractionated
heparin, 50 U/kg (regardless of use of glycoprotein IIb/IIIa
inhibitors), compared with standard-dose unfractionated heparin, 85 U/kg
(60 U/kg with Gp IIb/IIIa inhibitors), did not reduce major peri-PCI
bleeding and vascular access-site complications.[63] Low–molecular-weight heparin

LMWHs
might be superior to unfractionated heparin in reducing cardiovascular
outcomes, with a safety profile similar to that of heparin in patients
receiving medical care. Conflicting results emerged from 9
randomized trials directly comparing LMWH with unfractionated heparin.
Two trials evaluated dalteparin, another evaluated nadroparin, and 6
evaluated enoxaparin.[64, 65] Trials
with dalteparin and nadroparin reported similar rates of nonfatal
myocardial infarction or death compared with heparin, whereas 5 of 6
trials of enoxaparin found point estimates for death or nonfatal
myocardial infarction that favored enoxaparin over heparin. The benefit
of enoxaparin appeared to be driven largely by a reduction in nonfatal
myocardial infarction, especially in the cohort of patients who had not
received any open-label anticoagulant therapy before randomization. In
addition, a systematic review comparing LMWH with unfractionated
heparin found no significant difference in benefits between the 2 drugs.
Aside from the possible medical benefits of using LMWH in place
of unfractionated heparin, advantages of LMWH include ease of
administration, absence of need for anticoagulation monitoring, and
potential for overall cost savings. Although 3 LMWHs are approved for
use in the United States, only enoxaparin is currently approved for use
in unstable angina. Lev et al found that the combination of eptifibatide
with enoxaparin appears to have a more potent antithrombotic effect
than that of eptifibatide and unfractionated heparin.[66] The
role of LMWHs in patients for whom PCI is scheduled is relatively ill
defined. However, it is likely to be at least equivalent to that of
heparin. It appears reasonable to minimize the risk of excessive
anticoagulation during PCI by avoiding crossover of anticoagulants (ie,
maintain consistent anticoagulant therapy from the pre-PCI phase
throughout the procedure itself). Additional experience with regard to
the safety and efficacy of the concomitant administration of LMWHs with
Gp IIb/IIIa antagonists and fibrinolytic agents is currently being
acquired.

Thrombolysis

Prehospital
thrombolysis allows eligible patients to receive thrombolysis 30-60
minutes sooner than if treatment were given in the ED; however,
prehospital thrombolysis is still under investigation and has not become
a trend, as a result of unproven benefit and an increase in the
availability of PCI in many medical centers as an alternative to
thrombolysis for STEMI.The Remodeling With Erythropoietin After
Large Myocardial Infarction (REVEAL) trial evaluated the safety and
efficacy of a single intravenous bolus of epoetin alfa in patients with
STEMI who had successful reperfusion with primary or rescue PCI.[67] A
single intravenous bolus of epoetin alfa within 4 hours of PCI did not
reduce infarct size and was associated with higher rates of adverse
cardiovascular events.Although PCI is the preferred treatment for
STEMI, the distance to primary PCI centers and the inherent time delay
in delivering primary PCI limits widespread use of this treatment.
Prehospital electrocardiographic (ECG) diagnosis and direct referral for
primary PCI enables patients with STEMI living far from a PCI center to
achieve a system delay comparable to patients who are closer to a PCI
center.[68]

Coronary Interventions

An
early invasive strategy (ie, diagnostic angiography with intent to
perform revascularization) is indicated in unstable angina/NSTEMI
patients who have refractory angina or hemodynamic or electrical
instability without serious comorbidities or contraindications to such
procedures.[22] An
early invasive strategy is also indicated in initially stabilized
unstable angina/NSTEMI patients who do not have serious comorbidities or
contraindications to such procedures and who have an elevated risk for
clinical events. According to the 2011 American College of
Cardiology Foundation/American Heart Association (ACCF/AHA) guidelines,
an early invasive strategy (ie, within 12-24 hours of admission) is a
reasonable choice for initially stabilized high-risk patients with
unstable angina/NSTEMI; for patients not at high risk , a delayed invasive approach is also reasonable (class IIa recommendation).[47] In
NSTEMI ACS, early revascularization reduces myocardial infarction and
death rates compared with a more selective strategy, particularly in
high-risk patients. Use of Gp IIb/IIIa blockers followed by early
invasive catheterization is the most logical approach. An early invasive
strategy should be considered in patients with large myocardial
infarction, hypotension, shock, RV infarction, and refractory chest
pain. In the Invasive Versus Conservative Treatment in Unstable
Coronary Syndromes (ICTUS) trial, an early invasive strategy had no
apparent long-term benefit in reducing death or myocardial infarction.
After stratification for risk, analysis of 5-year clinical outcomes in
patients presenting with non-ST-segment elevation ACS and elevated
troponin T (TnT) level showed that cumulative myocardial infarction or
death rates were 22.3% in the early invasive group versus 18.1% in the
selective invasive group. No difference was observed in mortality or
myocardial infarction.[69]

Concomitant Therapy

Current
guidelines for patients with moderate- or high-risk ACS recommend an
early invasive approach with concomitant antithrombotic therapy,
including aspirin, clopidogrel, and unfractionated or LMWH. The Acute
Catheterization and Urgent Intervention Triage Strategy (ACUITY) trial
evaluated the role of thrombin-specific anticoagulation with bivalirudin
in this patient population. In patients with moderate- or high-risk ACS
who were undergoing invasive treatment with glycoprotein IIb/IIIa
inhibitors, bivalirudin was associated with rates of ischemia and
bleeding that were similar to those with heparin. Bivalirudin alone was
associated with similar rates of ischemia and significantly lower rates
of bleeding.[70] Further,
glycoprotein IIb/IIIa inhibitors can be initiated at the time of
angiography; routine administration 12-24 hours before the procedure
carries an increased risk of bleeding and no improvement in outcome.


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Acute Coronary Syndrome Medication

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Medication Summary

The goals of treatment are to preserve patency of the coronary artery,
augment blood flow through stenotic lesions, and reduce myocardial
oxygen demand. All patients should receive antiplatelet agents, and
patients with evidence of ongoing ischemia should receive aggressive
medical intervention until signs of ischemia, as determined by symptoms
and ECG, resolve.

Antiplatelet agents

Class Summary

Antiplatelets inhibit the cyclooxygenase system, decreasing the level of thromboxane A2,
which is a potent platelet activator. Antiplatelet therapy reduces
mortality by reducing the risk of fatal strokes and fatal myocardial
infarctions.

Aspirin (Anacin, Ascriptin, Bayer Aspirin)

Adult Dosing & Uses

Dosing Forms & Strengths

tablet

  • 81mg
  • 300mg
  • 325mg
  • 500mg
  • 650mg
tablet, quick-release

  • 325mg
  • 500mg
tablet, chewable

  • 81mg
tablet, enteric coated

  • 975mg



tablet, continual release

  • 800mg




Analgesic/Antipyretic



325-650 mg PO/PR q4-6hr PRN
Controlled/extended/delayed-released products: 650-1300 mg enteric coated PO q8hr; no more than 3.9 g/day

Acute Myocardial Infarction

160-325 mg as soon as possible (within minutes of symptoms)

Myocardial Infarction Prophylaxis

75 to 325 mg PO qDay
Ischemic Stroke & Transient Ischemic Attack

160-325 mg PO qDay

Osteoarthritis

Up to 3 g/day PO in divided doses

Percutaneous Transluminal Coronary Angioplasty

325 mg PO 2 hours presurgery
160-325 mg PO qDay maintenance

Rheumatoid Arthritis

3 g/day PO in divided doses
Increase as needed for anti-inflammatory efficacy with target plasma salicylate levels of 150 to 300 mcg/mL

Spondyloarthropathies

Up to 4 g/day PO in divided doses

Unstable Angina Pectoris

75-325 mg PO qDay

See Also Combos

with oxycodone
with acetaminophen
Butalbital, Codeine, Propoxyphene, Other

Other Indications & Uses

Pain, fever, inflammatory conditions, dyspepsia, platelet aggregation prophylaxis, thromboembolism, transient ischemic attack
Primary prevention of MI
Pediatric Dosing & Uses

Dosing Forms & Strengths

tablet

  • 81mg
  • 300mg
  • 325mg
  • 500mg
  • 650mg
tablet, quick-release

  • 325mg
  • 500mg
tablet, chewable

  • 81mg
tablet, enteric coated

  • 975mg
tablet, continual release

  • 800mg
Not indicated with viral illness (risk of Reye's syndrome)
Analgesic/Antipyretic

<12 years old: 10-15 mg/kg/dose PO q4hr, up to 60-80 mg/kg/day
12 years or older: As in adults


Juvenile Rheumatoid Arthritis



<25 kg: 60-100 mg/kg/day PO divided q6-8hr (maintain serum salicylate 150-300 mcg/mL)
25 kg or heavier: 2.4-3.6 g/day

Kawasaki Disease

Febrile phase: 80-100 mg/kg/day PO divided q6hr
After defervesces: 3-6 mg/kg PO qDay

Other Information

Toxic dose: 200 mg/kg
Early
administration of aspirin (eg, Anacin, Ascriptin, Bayer Aspirin) in
patients with acute myocardial infarction may reduce cardiac mortality
in the first month. The adult dose is 160-324 mg PO or chewed. It can be
administered as a suppository if the patient is unable to take PO
medications. Aspirin reduces morbidity and mortality and is continued
indefinitely. Nitrates

Class Summary

Nitrates oppose coronary artery spasm and reduce myocardial oxygen demand by reducing preload and afterload.Nitroglycerin (Nitro-Bid)


Nitroglycerin
(Nitro-Bid) causes relaxation of the vascular smooth muscle via
stimulation of intracellular cyclic guanosine monophosphate production,
causing a decrease in blood pressure. Nitrates do not improve mortality.[45] However,
they provide symptomatic relief by means of several mechanisms,
including coronary vasodilation, improved collateral blood flow,
decrease in preload (venodilation and reduced venous return), and
decrease in afterload (arterial vasodilation). Care should be taken to
avoid hypotension, because this can potentially reduce coronary
perfusion pressure (diastolic BP - LV diastolic pressure).

Analgesics

Class Summary

These agents reduce pain which decreases sympathetic stress, in addition to providing some preload reduction.
Morphine sulfate (Duramorph, Astramorph, MS Contin)

Adult Dosing & Uses

Dosing Forms & Strengths

tablet/capsule, extended release: Schedule II

  • 10mg
  • 15mg
  • 20mg
  • 30mg
  • 45mg
  • 50mg
  • 60mg
  • 75mg, 90mg, 100mg, 120mg, 200mg
injectable solution: Schedule II

  • 0.5mg/mL
  • 1mg/mL
  • 2mg/mL
  • 4mg/mL
  • 5mg/mL
  • 8mg/mL
  • 10mg/mL
  • 15mg/mL, 25mg/mL, 50mg/mL



injectable solution, liposomal: Schedule II

  • 10mg/mL
tablet: Schedule II

  • 15mg
  • 30mg
suppository: Schedule II

  • 5mg
  • 10mg
  • 20mg
  • 30mg

oral solution: Schedule II

  • 10mg/5mL
  • 20mg/5mL
  • 100mg/5mL
Pain

Oral

  • Immediate-release: 10-30 mg q4hr
  • Oral solution: 10-20 mg q4hr
  • Controlled-release: 15-30 mg SR q8-12hr
  • Avinza (extended-release capsule): total daily morphine dose qDay, no more than 1600 mg/day
  • Kadian (extended-release capsule): Administer half of total daily morphine dose q12hr or total dose q24hr
SC/IM: 5-20 mg/70kg q4hr
IV: 2.5-15 mg/70 kg infused over 3-5 minutes q4hr
Rectal: 10-20 mg q4hr
Epidural: 5-10 mg qDay
Intrathecal: 0.2-1 mg qDay + available infusion of naloxone

Liposomal

  • C-section: 10 mg lumbar epidural prior to surgery
  • Other surgery: 10-15 mg
Other Indications & Uses

Acute and chronic pain, post-op pain, anesthesia supplement, labor
Dyspnea due to acute LV failure and pulmonary edema
Pediatric Dosing & Uses

Dosing Forms & Strengths

tablet/capsule, extended release: Schedule II

  • 10mg
  • 15mg
  • 20mg
  • 30mg
  • 45mg
  • 50mg
  • 60mg
  • 75mg, 90mg, 100mg, 120mg, 200mg
injectable solution: Schedule II

  • 0.5mg/mL
  • 1mg/mL
  • 2mg/mL
  • 4mg/mL
  • 5mg/mL
  • 8mg/mL
  • 10mg/mL
  • 15mg/mL, 25mg/mL, 50mg/mL
injectable solution, liposomal: Schedule II

  • 10mg/mL
tablet: Schedule II

  • 15mg
  • 30mg



suppository: Schedule II

  • 5mg
  • 10mg
  • 20mg
  • 30mg



oral solution: Schedule II

  • 10mg/5mL
  • 20mg/5mL
  • 100mg/5mL


Analgesia/Tetralogy (Cyanotic) Spells



Neonates (<28 days old): 0.3-1.2 mg/kg/day divided q4hr IM/SC/slow IV
Immediate release: 0.2-0.5 mg/kg/dose PO q4-6hr PRN
Controlled release: 0.6-1.2 mg/kg/day divided q12hr PRN PO
0.1-0.2 mg/kg/dose IV/IM/SC q2-4hr PRN

Continuous IV Infusion

Neonates (<28 days old): 0.01-0.02 mg/kg/hr IV infusion
Postop pain: 0.01-0.04 mg/kg/hr IV infusion
Sickle cell and cancer: 0.04-0.07 mg/kg/hr IV infusion

Continuous: 0.025-2.6 mg/kg/hr IV/SC (average: 0.06 mg/kg/hr)
Morphine
sulfate (Duramorph, Astramorph, MS Contin) is the drug of choice for
narcotic analgesia because of its reliable and predictable effects,
safety profile, and ease of reversibility with naloxone. Morphine
sulfate administered intravenously may be dosed in a number of ways and
commonly titrated until the desired effect is obtained. Beta-adrenergic blockers

Class Summary

Beta
blockers have antiarrhythmic and antihypertensive properties, as well
as the ability to reduce ischemia. They minimize the imbalance between
myocardial supply and demand by reducing afterload and wall stress. In
patients with acute MI, they decrease infarct size as well as short- and
long-term mortality, which is a function of their anti-ischemic and
antiarrhythmic properties. These drugs may prevent mechanical
complications of myocardial infarction, including rupture of the
papillary muscle, left ventricular free wall, and ventricular septum.
Beta blockers ameliorate dynamic obstruction of the left ventricular
outflow tract in patients with apical infarct and hyperdynamic basal
segments. They should not be used acutely in patients with cardiogenic
shock or signs of heart failure on presentation.
Metoprolol (Lopressor)

Adult Dosing & Uses

Dosing Forms & Strengths

injectable solution

  • 1mg/mL
tablet, including extended release

  • 25mg
  • 50mg
  • 100mg
  • 200mg

Acute Myocardial Infarction, Early Treatment (Metoprolol Tartrate)

2.5-5 mg rapid IV q2-5min, up to 15 mg over 10-15 minutes, THEN 15 minutes after last IV & receiving 15 mg IV
50 mg PO q6hr x48 hours, THEN
50-100 mg PO BID
If full IV dose not tolerated: 25-50 mg PO q6hr after last IV


Congestive Heart Failure

Toprol XL only (metoprolol succinate)

  • Initial: 25mg PO qDay
  • Increase dose q2Weeks PRN
  • No more than 200 mg/day
  • NYHA class II or > reduce dose 12.5 mg PO qDay
  • 50-100 mg PO qDay initial, titrate to no more than 400 mg/day PO
Hypertension

Lopressor (metoprolol tartrate)

  • Initial: 100 mg/day PO qDay or divided BID PO
  • May be increased at weekly or longer intervals
  • Effective dosage range 100-450 mg/day divided BID PO
  • Take with or immediately following meals
  • No more than 400 mg/day
Toprol XL (metoprolol succinate)

  • 25-100 mg PO qDay
  • May be increased at weekly or longer intervals, usual range 50-100 mg/day
  • Tablet should not be chewed or crushed
  • No more than 400 mg/day
Angina

Lopressor (metoprolol tartrate)

  • Initial: 100 mg/day divided BID PO
  • May be increased at weekly or longer intervals
  • Effective dosage range 100-400 mg/day divided BID PO
  • Take with or immediately following meals
  • No more than 400mg/day
Toprol XL (metoprolol succinate)

  • 100 mg PO qDay
  • May be increased at weekly or longer intervals
  • Tablet should not be chewed or crushed
  • No more than 400mg/day
Administration

When switching from immediate release to extended release, the same total daily dose of metoprolol should be used
When switching between oral and IV dosage forms, equivalent beta-blocking effect achieved in a 2.5:1 (oral:IV) ratio

Additional Information

Less effective than thiazide diuretics in black and geriatric patients

Shown to decrease mortality in hypertension and post-myocardial infarction

Other Indications & Uses

Acute Tachyarrhythmias (ACLS): 5 mg IV over 1-2 minutes q5-15min; maximum 15 mg
VTach (Off-label): Initial 100 mg/day PO qDay or divided BID/TID, may increase qWeek PRN up to 450 mg/day
Aggressive Behavior (Off-label): Lopressor 200-300 mg/day PO
Migraine, prophylaxis (Off-label): Lopressor 50-100 mg PO BID
Hyperthyroidism (Off-label): 50-100 mg PO qDay
Post-MI, CHF (Toprol XL only)-wait until patient stable for 2-4 weeks
Off-label: Atrial fibrillation/atrial flutterPediatric Dosing & Uses

Dosing Forms & Strengths

injectable solution

  • 1mg/mL
tablet, including extended release

  • 25mg
  • 50mg
  • 100mg
  • 200mg
VTach (Off-label)

1-5 mg/kg/day divided BID PO

Other Indications & Uses

Not FDA-approved

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Metoprolol (Lopressor) is a selective beta1-adrenergic receptor blocker
that decreases the automaticity of contractions. During IV
administration, blood pressure, heart rate, and ECG should be carefully
monitored. The goal of treatment is to reduce the patient's heart rate
to 60-90 beats/min.
Esmolol (Brevibloc)


Adult Dosing & Uses



Dosing Forms & Strengths




infusion bags

  • 2g/100mL
  • 2.5g/250mL



injectable solution

  • 10mg/mL

Intraoperative Tachycardia/Hypertension


Immediate control

  • Initial bolus: 80 mg (~1 mg/kg) IVP over 30 sec, THEN
  • 0.15-0.3 mg/kg/min IV infusion PRN
Postoperative/gradual control

  • Load 0.5 mg/kg over 1 min, THEN
  • 0.05 mg/kg/min IV x4 min
  • If inadequate response in 5 min
  • 2nd loading dose of 0.5 mg/kg/min x1 min, THEN
  • 0.1 mg/kg/min
Supraventricular Tachycardia

Load: 0.5mg/kg IV over 1 min, THEN
Maint: start 0.05 mg/kg/min IV x4 min, may incr by 0.05 mg/kg up to 0.2 mg/kg/min
If HR/BP not controlled after 5 min, repeat bolus (ie, 500 mcg/kg/min x1 min), then initiate infusion of 100 mcg/kg/min IV
May administer a 3rd bolus if needed, then a maintenance infusion of 150 mcg/kg/min IV
Higher maintenance doses may be required, up to 250-300 mcg/kg/min


Hypertensive Emergency

Load 0.25-0.5 mg/kg IVP over 1 min, THEN
0.05-0.1 mg/kg/min IV x4 min
May repeat loading dose or incr infusion up to 0.3 mg/kg/min if necessary

Additional Information

Less effective than thiazide diuretics in black and geriatric patients


Shown to decrease mortality in hypertension and post-myocardial infarction

Other Indications & Uses

Paroxysmal Atrial Tachycardia, PSVT, ST
Off-label: Acute MI, angina, NSTEMI
Pediatric Dosing & Uses


Dosing Forms & Strengths

infusion bags

  • 2g/100mL
  • 2.5g/250mL

injectable solution

  • 10mg/mL

Supraventricular Tachycardia (Off-label), Postoperative Hypertension (Off-label)


Load with 500-600 mcg/kg IV over 2 min, THEN 200 mcg/kg/min IV infusion (range 50-250 mcg/kg/min)Glycoprotein IIB/IIIA inhibitors

Class Summary

Glycoprotein IIb/IIIa receptor antagonists include abciximab[55, 56] , eptifibatide[57] , and tirofiban[58] .
Glycoprotein IIb/IIIa antagonists prevent the binding of fibrinogen,
thereby blocking platelet aggregation. These drugs inhibit the
glycoprotein IIb/IIIa receptor, which is involved in the final common
pathway for platelet adhesion and aggregation. Currently, GP IIb/IIIb
receptor antagonists in combination with aspirin are considered standard
antiplatelet therapy for patients at high risk for unstable angina.
Abciximab (ReoPro)


Adult Dosing & Uses

Dosing Forms & Strengths

injectable solution

  • 2mg/mL
Ajunct to PCI

Prevention of cardiac ischemic complications in patients undergoing PCI
0.25 mg/kg IV bolus over at least 1 min, 10-60 min before start of PCI, THEN
0.125 mcg/kg/min (not to exceed 10 mcg/min) cont IV infusion x12 hr


Unstable Angina

Indicated for prevention of cardiac complications in patients with unstable angina with PCI planned within 24 hr
0.25 mg/kg IV bolus over at least 1 minute, THEN
0.125 mcg/kg/min (not to exceed 10 mcg/min ) IV infusion x18-24 hours concluding 1 hour post-PCI
Stop continuous infusion of abciximab in patients with failed PCIs


Other Indications & Uses

Prevention of cardiac ischemic complications in

  • Patients undergoing Percutaneous Coronary Intervention (PCI)
  • Patients with unstable angina and NSTEMI not responding to conventional treatment with PCI planned within 24 hours
Off-label: Adjunctive therapy during thrombolysisPediatric Dosing & Uses

Safety and efficacy not established

Abciximab (ReoPro) is a chimeric human-murine monoclonal antibody. It
binds to receptors with high affinity and reduces platelet aggregation
by 80%. Inhibition of platelet aggregation persists for up to 48 hours
after the end of infusion. Abciximab has been approved for use in
elective/urgent/emergent percutaneous coronary intervention
Eptifibatide (Integrilin)


Adult Dosing & Uses



Dosing Forms & Strengths




injection solution

  • 2mg/mL
  • 75mg
  • 100mL

Acute Coronary Syndromes (ACS)

180 mcg/kg IV bolus, THEN
2 mcg/kg/min IV for up to 72 hours


Percutaneous Coronary Intervention (PCI)

180 mcg/kg IV, THEN
Continuous infusion 2 mcg/kg/min with another 180 mcg/kg IV bolus 10 minutes after 1st one
Continue infusion for at least 12 hours


Renal Impairment



(CrCl <50 mL/min)
ACS: 180 mcg/kg IV, THEN continuous infusion 1 mcg/kg/min
PCI: 180 mcg/kg IV, THEN continuous infusion 1 mcg/kg/min with another 180 mcg/kg IV bolus 10 minutes after 1st one
Hemodialysis: Safety and using during hemodialysis not established


Geriatric Dosing



In clinical trials, incidence of bleeding complications was
higher in the elderly in both placebo and eptifibatide groups, and the
incremental risk of eptifibatide-associated bleeding was greater in the
older patientsPediatric Dosing & Uses



Not recommendedEptifibatide (Integrilin) is an antagonist of the platelet GP IIb/IIIa
receptor; it reversibly prevents von Willebrand factor, fibrinogen, and
other adhesion ligands from binding to the GP IIb/IIIa receptor. The end
effect is the inhibition of platelet aggregation. The effects persist
over the duration of maintenance infusion and are reversed when infusion
ends. Use eptifibatide (or tirofiban, see below) in patients with
high-risk features in whom invasive treatment is not planned.

Tirofiban (Aggrastat)

Tirofiban (Aggrastat) is a nonpeptide antagonist of the GP IIb/IIIa
receptor. It is a reversible antagonist of fibrinogen binding. When
administered intravenously, more than 90% of platelet aggregation is
inhibited. Tirofiban has been approved for use in combination with
heparin for patients with unstable angina who are being treated
medically and for patients undergoing percutaneous coronary
intervention.

Adult Dosing & Uses

Dosing Forms & Strengths

injectable solution, concentrate

  • 250mcg/mL

infusion solution

  • 2.5mg/250mL
  • 5mg/100mL
Acute Coronary Syndromes (ACS)

0.4 mcg/kg/min IV for 30 minutes, THEN
0.1 mcg/kg/min IV for 48-108 hours


Percutaneous Cardiovascular Intervention (PCI)



Continue 0.1 mcg/kg/min IV through procedure & for 12-24 hours after


Renal Impairment



ClCr <30 mL/min: reduce dose to 50% of normal rate


Other Indications & Uses



Not FDA-approved for PCI without ACS
Anticoagulants

Class Summary

Anticoagulants are used to prevent recurrence of clot after a spontaneous fibrinolysis.
Heparin


Heparin augments the activity of antithrombin III and prevents the
conversion of fibrinogen to fibrin. It does not actively lyse but is
able to inhibit further thrombogenesis. This agent prevents recurrence
of a clot after spontaneous fibrinolysis.

Adult Dosing & Uses

Dosing Forms & Strengths

injectable solution

  • 1000 units/mL
  • 5000 units/mL
  • 10,000 units/mL

General Dosing Guidelines


Please see your institutional protocol for recommended dosage & desired aPTT values

Weight Based

  • Load: 50-150 units/kg IV bolus
  • Maint: 15-25 units/kg/hr IV infusion



Nonweight Based

  • Load: 5000 unit IV bolus
  • SC: range from 2500-10,000 units at varying intervals

Prevent Postop Thromboemboli

SQ: 5,000 unit SQ 2hr prior to surgery, then q8-12 hr x7d or patient is ambulatory

Intermittent IV
Initial: 10,000 units, then 50-70 units/kg q4-6hr
IV
Infusion: weight based dosing per institution

Clot Prevention in CV Surgery

Initial: 150 units/kg IV or SQ for total body perfusion for open-heart surgery

300 units/kg for procedures <60 min

400 units/kg for procedures >60 minutes

Deep Vein Thrombosis

IV: 80 units/kg or 5000 unit IV push, then 18 units/kg/hr (continuous infusion)

SQ (monitored): 250 units/kg, then 250 units/kg q12h


Other Information

Adjust heparin dose based on desired aPTT (us. 1.5-2.5x normal)

Other Indications & Uses


Prophylaxis & treatment of venous thrombosis, PE, A-fib with embolization, DIC, cerebral thrombosis in evolving stroke
Adjunct in treatment of coronary occlusion in acute MIPediatric Dosing & Uses

Dosing Forms & Strengths

injectable solution

  • 1000 units/mL
  • 5000 units/mL
  • 10,000 units/mL

Systemic Heparinization

Please see your institutional protocol for recommended dosage & desired aPTT values

< 1 year old

  • IV Infusion: initial load dose: 75 units/kg over 10 min, then initial maint dose: 28 units/kg/hr
  • Adjust heparin dose based on desired aPTT


Related Topics
ECG VIDEOS PACKAGE the Best untill Now
The ESC Textbook of Cardiovascular Imaging
ECG-SAP III: Electrocardiography Self-Assessment Program
Echo Made Easy
How to record ECG
Basic and Bedside Electrocardiography 2011
ECGs for Nurses (Essential Clinical Skills for Nurses)


.


> 1 year old

  • Intermittent IV: Initial 50-100 units/kg, then 50-100 units/kg q4h
    IV
  • Infusion: initial load dose; 75 units/kg over 10 min, then initial maint dose 20 units/kg/hr
  • Adjust heparin dose based on desired aPTT


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Low molecular weight heparins

Class Summary

LMWH
is indicated for treatment of ST-segment elevation myocardial
infarction (STEMI) managed medically or with subsequent PCI. It is also
indicated as prophylaxis for ischemic complications caused by unstable
angina and non–Q-wave myocardial infarction. Aside from the
possible medical benefits of using LMWH in place of unfractionated
heparin, advantages of LMWH include ease of administration, absence of
need for anticoagulation monitoring, and potential for overall cost
savings. Although 3 LMWHs are approved for use in the United States,
only enoxaparin is currently approved for use in unstable angina.
Enoxaparin (Lovenox)


Low-molecular-weight heparin (enoxaparin; Lovenox), which is produced by
partial chemical or enzymatic depolymerization of unfractionated
heparin, binds to antithrombin III, enhancing its therapeutic effect.
The heparin–antithrombin III complex binds to and inactivates activated
factor X (Xa) and factor II (thrombin). LMWH differs from unfractionated
heparin by having a higher ratio of antifactor Xa to antifactor IIa
than does unfractionated heparin. Maximum antifactor Xa and antithrombin
activities occur 3-5 hours after administration.

Adult Dosing & Uses



Dosing Forms & Strengths




multidose vial

  • 300mg/3mL



prefilled syringe

  • 30mg/0.3mL
  • 40mg/0.4mL
  • 60mg/0.6mL
  • 80mg/0.8mL
  • 100mg/mL
  • 120mg/0.8mL
  • 150mg/mL




Knee/Hip Replacement Surgery



30 mg SC BID (start post-op)
Renal Impairment (<30 mL/min): 30 mg SC qDay


General Surgery, Alternative Hip Replacement



40 mg SC qDay, begin pre-op
Renal Impairment (<30 mL/min): 30 mg SC qDay


DVT With or Without PE, Treatment; Unstable Angina, Non-Q-Wave MI



1 mg/kg SC BID OR (inpatient only) 1.5 mg/kg SC qDay
Renal Impairment (<30 mL/min): 1 mg/kg SC qDay


STEMI




<75 years old: 30 mg IV bolus x1 + 1 mg/kg SC x1, THEN 1 mg/kg SC q12hr

  • Renal Impairment (<30 mL/min): 30 mg IV bolus x1 + 1 mg/kg SC x1, THEN 1 mg/kg SC qDay
  • PCI patients: Additional 0.3 mg/kg IV bolus if last SC given >8 hours before balloon inflation


>75 years old: 0.75 mg/kg SC q12hr (No IV Bolus!)
Renal Impairment (<30 mL/min): 1 mg/kg SC qDay


Abdominal Surgery; Illness with Restricted Mobility



40 mg SC qDay


Administration



Administer deep SC alternating right & left anterior &
posterior abdominal walls into skin fold held between thumb &
forefinger


Other Information



Low Body Weight (<45 kg): Reduce dosage


Other Indications & Uses



Prophylaxis of DVT in patients undergoing abdominal surgery who
are at risk for thromboembolic complications, in patients undergoing hip
replacement surgery, during & following hospitalization, in
patients undergoing knee replacement surgery, & in patients at risk
for thromboembolic complications due to severely restricted mobility
during acute illness
Prophylaxis of ischemic complications of unstable angina and non-Q-wave MI, when concurrently administered with aspirin
Inpatient treatment of acute DVT with or without PE, when administered in conjunction with warfarin
Outpatient treatment of acute DVT without PE when administered in conjunction with warfarin
Pediatric Dosing & Uses



Dosing Forms & Strengths




multidose vial

  • 300mg/3mL



prefilled syringe

  • 30mg/0.3mL
  • 40mg/0.4mL
  • 60mg/0.6mL
  • 80mg/0.8mL
  • 100mg/mL
  • 120mg/0.8mL
  • 150mg/mL




Safety & efficacy not established
DVT, Prophylaxis (Off-label)



<2 months old: 0.75 mg/kg SC q12hr
2 months old - 18 years old: 0.5 mg/kg SC q12hr


DVT, Treatment (Off-label)



<2 months old: 1.5 mg/kg SC q12hr
>2 months old: 1 mg/kg SC q12hr
Direct thrombin inhibitors

Class Summary

Direct
thrombin inhibitors bind directly to the anion binding site and the
catalytic sites of thrombin to produce potent and predictable
anticoagulation.
Hirudin (Lepirudin, Refludan)

Hirudin (Lepirudin, Refludan) is the prototype of direct thrombin
inhibitors. Hirudin binds directly to the anion binding site and the
catalytic sites of thrombin to produce potent and predictable
anticoagulation. Currently, hirudin is indicated only in patients who
are unable to receive heparin because of heparin-induced
thrombocytopenia.
Adult Dosing & Uses



Dosing Forms & Strengths




powder for injection

  • 50mg/vial




Heparin-induced Thrombocytopenia



0.4 mg/kg (not to exceed 44 mg) IV over 15-20 sec initially, THEN
0.15 mg/kg/hr (not to exceed 16.5 mg/hr) IV for 2-10 day


Dose adjustment



Maintain aPTT ratio 1.5-2.5; monitor 4 hr after initial dose, then qD
If aPTT high: Stop infusion for 2 hr, then restart infusion at 50% dose (no bolus)
If aPTT low: Increase dose in steps of 20%


Renal Impairment (CrCl <60 mL/min)



Initial 0.2 mg/kg (no more than 22 mg) IV over 15-20 sec, THEN
CrCl 45-60 mL/min: 0.075 mg/kg/hr
CrCl 30-44 mL/min: 0.045 mg/kg/hr
CrCl 15-29 mL/min: 0.0225 mg/kg/hr
CrCl <15 mL/min: contraindicated


Other Indications & Uses



Heparin-induced thrombocytopenia & associated thromboembolic diseasePediatric Dosing & Uses



Dosing Forms & Strengths




powder for injection

  • 50mg/vial




Safety & efficacy not establishedBivalirudin (Angiomax)

Bivalirudin (Angiomax) is a synthetic analogue of recombinant hirudin.
It inhibits thrombin and is used for anticoagulation in unstable angina
in patients undergoing PTCA. Potential advantages over conventional
heparin therapy include more predictable and precise levels of
anticoagulation, activity against clot-bound thrombin, absence of
natural inhibitors (eg, platelet factor 4, heparinase), and continued
efficacy following clearance from plasma (because of binding to
thrombin).
Adult Dosing & Uses



Dosing Forms & Strengths




powder for injection

  • 250mg




Anticoagulant in Patients Undergoing PTCA/PCI or PCI with HITS/HITTS



Intended for use with aspirin (300 to 325 mg daily)
0.75 mg/kg IV bolus, initially, followed by continuous infusion at rate of 1.75 mg/kg/hr for duration of procedure
Perform activated clotting time (ACT) 5 minutes after bolus dose
May administer additional 0.3 mg/kg bolus if necessary
May continue infusion following PCI beyond 4 hours (optional post
PCI, at discretion of treating health care provider) initiated at rate
of 0.2 mg/kg/hr for up to 20 hours PRN


Other Indications & Uses



USA patients or patients with hepatin-induced thrombocytopenia undergoing PCI
Off-label: STEMIPediatric Dosing & Uses



Not recommendedAdenosine diphosphate receptor antagonists

Class Summary

Two
thienopyridine, clopidogrel and ticlopidine, are adenosine
5'-diphosphate (ADP) antagonists that are approved for antiplatelet
activity. Both have irreversible antiplatelet activity but take several
days to manifest. A potential additive benefit exists when ADP
antagonists are used in conjunction with aspirin. These drugs may be
considered alternatives to aspirin in patients with aspirin intolerance
or who are allergic to aspirin.


Related Topics
ECG VIDEOS PACKAGE the Best untill Now
The ESC Textbook of Cardiovascular Imaging
ECG-SAP III: Electrocardiography Self-Assessment Program
Echo Made Easy
How to record ECG
Basic and Bedside Electrocardiography 2011
ECGs for Nurses (Essential Clinical Skills for Nurses)


.

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Clopidogrel (Plavix)


Clopidogrel (Plavix) inhibits ADP-dependent
activation of the glycoprotein IIb/IIIa complex, a necessary step for
platelet aggregation. This process results in intense inhibition of
platelet function, particularly in combination with aspirin. Clopidogrel
can be considered an alternative to aspirin in patients with aspirin
intolerance or who are allergic to aspirin. The CURRENT-OASIS 7 trial
suggests that a 7-day double-dose clopidogrel regimen can be considered
for patients with acute coronary syndromes, as the efficacy and safety
did not differ from that of a high- and low-dose aspirin regimen.
However, there is no benefit in the double-dose treatment for patients
who are undergoing an early invasive strategy.[71] Clopidogrel is a class I recommendation for patients when an early noninterventional approach is planned in therapy.[72] When
percutaneous coronary intervention (PCI) is planned, clopidogrel is
started and continued for at least 1 month and for up to 9 months, if
the patient is not at high risk for bleeding. Clopidogrel is
generally preferred over ticlopidine (Ticlid), because it more rapidly
inhibits platelets and appears to have a more favorable safety profile. Clopidogrel
has been suggested to be less effective in reducing the rate of
cardiovascular events in individuals who carry the loss-of-function CYP2C19 alleles. However, a 2010 study concluded that patients with ACS or atrial fibrillation respond well to clopidogrel, regardless of CYP2C19 loss-of-function carrier status.[73]
Adult Dosing & Uses



Dosing Forms & Strengths




tablet

  • 75mg
  • 300mg




Acute Coronary Syndrome



Unstable angina, non-ST-segment elevation myocardial infarction:
300 mg initial loading dose, follow by 75 mg PO qDay in combination with
aspirin 75-325 mg PO qDay
ST-segment elevation myocardial infarction: 75 mg PO qDay in combination with aspirin 75-162 mg/day


Recent MI, Stroke, or Established Peripheral Arterial Disease



75 mg PO qDay


Other Information




CYP2C19 Poor Metabolizers

  • CYP2C19 poor metabolizers associated with diminished antiplatelet response to clopidogrel
  • Although a higher dose regimen (600 mg loading dose followed by
    150 mg once daily) in poor metabolizers increases antiplatelet
    response; an appropriate dose regimen for poor metabolizers has not been
    established in a clinical outcome trial




Other Indications & Uses



Reduce risk of recurrence in patients with recent ischemic stroke
Reduction of ischemic events/reinfarcation/death in ACS (unstable angina/NSTEMI/STEMI)Pediatric Dosing & Uses



Not recommended
Ticlopidine (Ticlid)

Beneficial effects were noted in patients with UA after 2 wk of use in
one randomized trial. When compared to controls, ticlopidine use
decreased vascular deaths and nonfatal MIs.
Adult Dosing & Uses



Dosing Forms & Strengths




tablet

  • 250mg




Discontinued in United States
Stroke



250 mg PO BID with food


Coronary Artery Stent Thrombosis, Prevention



250 mg PO BID with aspirin x 30 days OR
(ACCP): Load 500 mg, THEN 250 mg BID for at least 10-14 days following successful stent placement


Other Information



Monitor: CBC, LFT's prior to starting & q2Weeks for 1st 3 months


Other Indications & Uses



Reduce risk of thrombotic stroke: only in patients allergic to
ASA or who failed ASA; prevention of coronary artery stent thrombosis
Off-label: CABG, chronic arterial occlusion, glomerulonephritis,
intermittent claudication, open heart surgery, sickle cell disease,
unstable anginaPediatric Dosing & Uses



<18 years old: safety & efficacy not established
Prasugrel (Effient)


Thienopyridine drug that inhibits platelet activation and aggregation
through the irreversible binding of its active metabolite to ADP
platelet receptors (specifically the P2Y12 receptor). Platelet
inhibition is the result of this action.Indicated to reduce
thrombotic cardiovascular (CV) events (including stent thrombosis) with
acute coronary syndrome (ACS) that is managed with percutaneous coronary
intervention (PCI). Specifically for unstable angina or non –
ST-elevation myocardial infarction (NSTEMI) or with ST-elevation
myocardial infarction (STEMI) when managed with primary or delayed PCI.Reduces rate of combined endpoint of CV death, nonfatal MI, or nonfatal stroke compared with clopidogrel.
Adult Dosing & Uses



Acute Coronary Syndrome



Loading dose: 60 mg PO once
Maintenance dose: 10 mg PO qDay with aspirin 75–325 mg/day;
bleeding risk may increase if weight <60 kg, consider 5 mg PO qDay
(efficacy/safety not established)


Other Indications & Uses




Indicated to reduce
thrombotic cardiovascular events (including stent thrombosis) with ACS
that is managed with percutaneous coronary intervention (PCI) with
either of the following:

  • unstable angina or non-ST-elevation myocardial infarction (NSTEMI)
  • ST-elevation myocardial infarction (STEMI) when managed with primary or delayed PCI




Geriatric Dosing



In patients ≥ 75 years of age, prasugrel is generally not
recommended because of increased risk of fatal and intracranial bleeding
and uncertain benefit, except in high-risk patients (diabetes or prior
MI), where its effect appears to be greater and its use may be
considered.Pediatric Dosing & Uses



Not recommended

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