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360 Anticoagulation Therapy
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prolonged therapy for patients who are at high risk of
stroke based on CHADS
Continuous ECG monitoring to screen for asymptomatic
of CHA2DS2-VASc).
2
AF should be considered prior to discontinuing system
atic anticoagulation.
REFERENCES AND KEY ARTICLES*
*1. January CT, Wann LS, Alpert JS, et al. 2014 AHA/ACC/HRS guideline for the
management of patients with atrial fibrillation: executive summary: a report of the
American College of Cardiology/American Heart Association Task Force on practice
guidelines and the Heart Rhythm Society. Circulation. 2014;130:2071-2104.
*2. You JJ, Singer DE, Howard PA, et al. Antithrombotic therapy for atrial fibrillation:
Antithrombotic Therapy and Prevention of Thrombosis. 9th ed. American College of
Chest Physicians Evidence-based Clinical Practice Guidelines. Chest. 2012;141:e531S575S.
3. Lopes RD, Crowley MJ, Shah BR, et al. Stroke Prevention in Atrial Fibrillation.
Rockville, MD: Agency for Healthcare Research and Quality; 2013.
4. Van Gelder IC, Hagens VE, Bosker HA, et al. A comparison of rate control and rhythm
control in patients with recurrent persistent atrial fibrillation. New Engl J Med.
2002;347:1834-1840.
5.
Wyse DG, Waldo AL, DiMarco JP, et al. A comparison of rate control and rhythm control
in patients with atrial fibrillation. New Engl J Med. 2002;347:1825-1833.
6. Connolly SJ, Eikelboom J, Joyner C, et al. Apixaban in patients with atrial fibrillation.
New Engl J Med. 2011;364:806-817.
7. Whitlock RP, Sun JC, Fremes SE, et al., American College of Chest Physicians.
Antithrombotic and thrombolytic therapy for valvular disease: Antithrombotic Therapy
and Prevention of Thrombosis. 9th ed. American College of Chest Physicians Evidencebased Clinical Practice Guidelines. Chest. 2012;141:e576S-600S.
Gage BF, Waterman AD, Shannon W, et al. Validation of clinical classification schemes
8.
for predicting stroke: results from the National Registry of Atrial Fibrillation. JAMA.
2001;285:2864-2870.
9. Lip GY. The balance between stroke prevention and bleeding risk in atrial fibrillation: a
delicate balance revisited. Stroke. 2008;39:1406-1408.
10. Holbrook A, Schulman S, Witt DM, et al. Evidence-based management of
anticoagulant therapy: Antithrombotic Therapy and Prevention of Thrombosis. 9th
ed. American College of Chest Physicians Evidence-based Clinical Practice Guidelines.
Chest. 2012;141:e152S-184S.
11. Witt DM, Delate T, Hylek EM, et al. Effect of warfarin on intracranial hemorrhage
incidence and fatal outcomes. Thromb Res. 2013;132:770-775.
12. Hylek EM, Go AS, Chang Y, et al. Effect of intensity of oral anticoagulation on stroke
severity and mortality in atrial fibrillation. New Engl J Med. 2003;349:1019-1026.
13. King SB, III, Smith SC, Jr., Hirshfeld JW, Jr., et al. 2007 Focused Update of the ACC/
AHA/SCAI 2005 Guideline Update for Percutaneous Coronary Intervention: a report of
the American College of Cardiology/American Heart Association Task Force on Practice
-
ATRIAL FIBRILLATION 361
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Guidelines: 2007 Writing Group to Review New Evidence and Update the ACC/AHA/
SCAI 2005 Guideline Update for Percutaneous Coronary Intervention, Writing on Behalf
of the 2005 Writing Committee. Circulation. 2008;117:261-295.
Kim TH, Kim JY, Mun HS, et al. Heparin bridging in warfarin anticoagulation
14.
therapy initiation could increase bleeding in non-valvular atrial fibrillation patients: a
multicenter propensity-matched analysis. J Thromb Haemost. 2015;13:182-190.
Lu Y, Won KA, Nelson BJ, et al. Characteristics of the amiodarone-warfarin interaction
15.
during long-term follow-up. Am J Health-Syst Pharm. 2008;65:947-952.
16. Reddy VY, Sievert H, Halperin J, et al. Percutaneous left atrial appendage closure vs
warfarin for atrial fibrillation: a randomized clinical trial. JAMA. 2014;312:1988-1998.
17. Varosy PD. Lariat-Small Step or Giant Leap? JAMA Intern Med. 2015;175(7):1110-
1111.
*18. Calkins H, Kuck KH, Cappato R, et al. 2012 HRS/EHRA/ECAS expert consensus
statement on catheter and surgical ablation of atrial fibrillation: recommendations
for patient selection, procedural techniques, patient management and follow-up,
definitions, endpoints, and research trial design. J Interv Card Electrophysiol.
2012;33:171-257.
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15
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Chapter
ACUTE CORONARY SYNDROMES
Sarah A. Spinler
EPIDEMIOLOGY OF ACS
It is estimated that more than 1.1 million patients experience an acute coronary
syndrome (ACS) each year, with 813,000 diagnosed with myocardial infarction (MI).1
Of patients presenting with suspected ACS, international registry data indicate
that approximately 31% have ST segment elevation (STE) MI, 32% non-ST segment
elevation (NSTE) MI, 26% unstable angina, 8% another cardiac diagnosis, and 4%
noncardiac final diagnosis (see Table 15-1).
2
TABLE 15-1: In-Hospital Outcomes of ACS with MI
Estimated In-Hospital Outcomes STEMI NSTEMI Unstable Angina
Death (%) 6.2 2.9 1.7
Reinfarction (%) 12 10 1.2
Heart failure (%) 15 10 6
Stroke (%) 1 0.5 0.2
Major bleeding (%) 1.4 1.2 0.5
2
PATHOPHYSIOLOGY AND EPIDEMIOLOGY OF
ACS
ACSs, (MI, or myocardial ischemia) are caused by partial or complete thrombotic
occlusion of a coronary artery due to plaque rupture, erosion, fissuring, or dissection (Figure 15-1).
SIGNS AND SYMPTOMS OF ACS
Signs
•
Electrocardiogram (ECG) changes: ST-segment elevation, ST-segment depression,
T-wave inversion, new left bundle branch block, Q waves (Figures 15-2A and B).
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Myocardial infarction:
Cross Section of a Coronary Artery
partial occlusion
B
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Arterial wall
Arterial blood
Clot
complete occlusion
FIGURE 15-1. Pathophysiology of ACS
Unstable angina:
A
FIGURE 15-2. Electrocardiographic Findings in ACS
A. ST-segment elevation; B. ST-segment depression.
ACUTE CORONARY SYNDROMES 365
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•
Elevated biochemical markers: elevated troponin T or I,* elevated creatine
kinase MB.
•
Acute heart failure or cardiogenic shock: rales, S3, hypoxia, hypotension, pulmonary edema on chest x-ray.
•
Ventricular arrhythmias.
*Negative biomarkers measured within 6 hours of symptom onset should be
remeasured 8–12 hours after symptom onset; positive biomarkers may be
remeasured at 6–8-hour intervals until a peak is observed.
Symptoms
•
Anterior medial chest pain, pressure, tightness, or squeezing occurring at rest.
•
Radiation of chest discomfort to left arm, shoulder, back, or jaw.
•
Increasing frequency, severity, or duration of angina.
•
Nausea, vomiting.
DIAGNOSTIC CRITERIA FOR ACS
Universal Criteria for Acute Myocardial Infarction
3
Diagnosis of MI is made by any one of the following criteria:
•
Detection of a rise or fall in biochemical markers (troponin preferred) with at least
one value above the 99th percentile of a normal reference population (upper
reference limit) together with at least one of the following:
Symptoms of ischemia
New or presumed new electrocardiography (ECG) changes
(ST-segment, T-wave changes, or new left bundle branch block)
Development of pathological Q waves on the ECG
Imaging evidence of new loss of viable myocardium or new regional
wall motion abnormality (akinesis, dyskinesis) on echocardiogram
Identification of intracoronary thrombus by angiography or on
autopsy
•
Sudden, unexplained cardiac death involving cardiac arrest with symptoms
suggestive of ischemia.
•
For patients undergoing percutaneous coronary intervention (PCI):
If preprocedure troponin negative—elevated troponin level >5 x
above the 99th percentile of the upper reference limit.
If preprocedure positive—elevated troponin level that rises >20%.
With symptoms suggestive of myocardial ischemic, new ischemic
ECG changes, or angiographic evidence consistent with a proce
dural complication or imaging suggestive of new loss of viable
myocardial or a new regional wall motion abnormality.
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Myocardial infarction is classified as:
•
Type 1: Spontaneous MI related to atherosclerotic plaque rupture, fissuring,
erosion, or dissection with resulting thrombus leading to decreased myocardial
blood flow and necrosis.
•
Type 2: Demand ischemia with an imbalance between myocardial oxygen supply
and demand.
•
Type 3: Cardiac death with symptoms suggestive of myocardial ischemia and
presumed new ECG changes, but death occurred before biomarkers could be
obtained.
•
Type 4a: MI related to PCI.
•
Type 4b: MI related to stent thrombosis.
RISK STRATIFICATION FOR NSTE ACS
An early invasive approach with coronary angiography and revascularization
with either PCI or coronary artery bypass graft (CABG) is recommended for
high-risk patients with NSTE ACS defined as either TIMI risk score of ≥5
(Table 15-2) or GRACE risk score >140 (Figure 15-3).
On-line risk calculators:
On-line risk calculators are available for
NSTE ACS.
4-8
TIMI Risk Score5: http://www.mdcalc.com/
timi-risk-score-for-uanstemi/
Grace Risk Score8: http://gracescore.org/
WebSite/default.aspx?ReturnUrl=%2f
ANTICOAGULATION CONSIDERATIONS IN
PATIENTS WITH ACS
Bleeding Definitions
Bleeding in ACS clinical trials is typically classified using either the TIMI,
GUSTO, or BARC bleeding definitions (see Table 15-3).
9
Relationship Between aPTT and anti-Factor Xa for
Unfractionated Heparin and Outcomes
•
Recent clinical trials have targeted a therapeutic range of 50–70 seconds without
calibration to anti-factor Xa activity to account for reagent variability.
•
Data evaluating bleeding and thrombotic risk with unfractionated heparin (UFH)
in ACS are sparse and consist of post-hoc analysis of large, randomized trials.
ACUTE CORONARY SYNDROMES 367
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TABLE 15-2: TIMI Risk Score for NSTE ACS
4,5
One point is assigned for each of the seven medical history and clinical presentation findings.
The point total is calculated, and the patient is assigned a risk for experiencing the composite
endpoint of death, myocardial infarction, or urgent need for revascularization as follows:
• Age ≥65 years
• Three or more CHD risk factors: smoking, hypercholesterolemia, hypertension, diabetes
mellitus, family history of premature CHD death/events
• Known CAD (≥50% stenosis of at least one major coronary artery on coronary angiogram)
• Aspirin use within the past 7 days
• Two or more episodes of chest discomfort within the past 24 hr
• ST-segment depression ≥0.5 mm
•
Positive biochemical marker for infarction
High Risk Medium Risk Low Risk
TIMI risk score TIMI risk score TIMI risk score
5–7 points 3–4 points 0–2 points
TIMI Risk Score Mortality, MI, or Severe Recurrent Ischemic Requiring Urgent Target
Vessel Revascularization
0/1 4.7%
2 8.3%
3 13.2%
4 19.9%
5 26.2%
6/7 40.9%
•
Data supporting the therapeutic range of 50–70 seconds are strongest from
early fibrinolytic trials.
GUSTO-1 trial of patients with STEMI treated with fibrinolytics,
No evidence of increased thrombotic risk with aPTTs <50 seconds.
Increased mortality and reinfarction risk, as well as bleeding, was
In GUSTO-IIb, another STEMI fibrinolytic trial, weight was the
10–13
an aPTT of 50–70 seconds was associated with the lowest rates of
30-day mortality, stroke, and bleeding.
found in patients with aPTTs >70 seconds.
10
10
10
strongest predictor of a therapeutic aPTT and a simulated bolus
dose of 60 units/kg and initial infusion of 12 units/kg/hr resulted in
the highest proportion of therapeutic aPTTs. An aPTT of approxi
mately 70 seconds and an initial infusion dose of 12 units/kg/hr
were associated with the lowest mortality rate.
11
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FIGURE 15-3. GRACE Risk Score
Source: Reprinted with permission from Pieper KS, Gore JM, FitzGerald G, et al. Validity
of a risk-prediction tool for hospital mortality: the Global Registry of Acute Coronary
Events. Am Heart J. 2009;157:1097-1105; copyright © 2009 with permission from
Elsevier.
aPTT target range of 50–70 seconds using weight-based heparin
Patients with STEMI treated with reteplase and heparin with or
Higher aPTTs >70 seconds were associated with bleeding, but there
Lower aPTTs <50 seconds were also associated with worse
dosing nomograms was tested prospectively in the GUSTO-V trial.
without abciximab.
was no association between peak aPTT and mortality.
outcomes.
12
12
12
12
ACUTE CORONARY SYNDROMES 369
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TABLE 15-3: Bleeding Definitions
TIMI Non-CABG–Related Bleeding
Major Any intracranial bleeding (excluding microhemorrhages <10 mm evident
Minor Clinically overt (including imaging), resulting in hemoglobin drop of 3 to
Requiring medical
attention
Minimal Any overt bleeding event that does not meet the criteria above
GUSTO Bleeding
Severe or lifethreatening
Moderate Requiring blood transfusion but not resulting in hemodynamic
only on gradient-echo MRI)
Clinically overt signs of hemorrhage associated with a drop in hemoglobin
of ≥5 g/dL
Fatal bleeding (bleeding that directly results in death within 7 days)
<5 g/dL
Any overt sign of hemorrhage that meets one of the following criteria and
does not meet criteria for a major or minor bleeding event, as defined
above
Requiring intervention (medical practitioner-guided medical or surgical
treatment to stop or treat bleeding, including temporarily or permanently
discontinuing or changing the dose of a medication or study drug)
Leading to or prolonging hospitalization
Prompting evaluation (leading to an unscheduled visit to a healthcare
professional and diagnostic testing, either laboratory or imaging)
Intracerebral hemorrhage
Resulting in substantial hemodynamic compromise requiring treatment
compromise
9
Mild Bleeding that does not meet above criteria
Bleeding Academic Research Consortium (BARC) Bleeding
Type 0 No bleeding
Type 1 Bleeding that is not actionable and does not cause the patient to seek
Type 2 Any clinically overt sign of hemorrhage that “is actionable” and
Type 3 a.
Type 4 CABG-related bleeding within 48 hr
Type 5 a. Probable fatal bleeding
consultation or treatment
requires diagnostic studies, treatment by a healthcare professional, or
hospitalization and does not fit the criteria for Type 3, 4, or 5 bleeding
Overt bleeding plus hemoglobin drop of 3 to <5 g/dL (provided
hemoglobin drop is related to bleed); transfusion with overt bleeding
b. Overt bleeding plus hemoglobin drop <5 g/dL (provided
hemoglobin drop is related to bleed); cardiac tamponade; bleeding
requiring surgical intervention for control; bleeding requiring IV
vasoactive agents
c. Intracranial hemorrhage confirmed by autopsy, imaging, or lumbar
puncture; intraocular bleed compromising vision
b. Definite fatal bleeding (overt or autopsy or imaging confirmation)
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