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168 J. A. Salotto
Antiplatelet agents
Purpose: prevent further platelet aggregation, thrombus propagation
and any further vessel occlusion.
Initiation of at least two antiplatelet agents is recommended in the
patient with suspected or confi rmed ACS.
Recommended agents: aspirin, thienopyridines, or glycoprotein IIb/
IIIa inhibitors.
Aspirin
Ö
— Non-enteric coated chewable aspirin should be given to all
patients with suspected ACS.
— Irreversibly inhibits platelet aggregation and causes vasodila-
tion by inhibiting thromboxane production.
— Dose: Aspirin 325 mg orally once, then 81 mg orally daily.
— Contraindications: active gastrointestinal bleed, aspirin hyper-
sensitivity, hepatic disease.
Thienopyridines: Clopidogrel (Plavix)
Ö
— Reduce platelet aggregation by blocking platelet adenosine
diphosphate receptors. Effects are additive with aspirin.
— Dose: Clopidogrel 300 mg PR once, then 75 mg PO daily.
— Hold for 5 days if planning CABG.
— Contraindicated in liver failure.
GPIIB/IIIA inhibitors: abciximab, eptifi batide, tirofi ban.
Ö
— Block IIB/IIIA receptor on platelets, and therefore inhibit fi -
brinogen-mediated platelet cross-linking.
— Used as an alternative to clopidogrel in high-risk patients,
those with ongoing ischemia, or as an adjunct to angioplasty
and PCI.
Anti-coagulants
Purpose: inhibit the clotting cascade, prevent further clot formation.
Ö
Evidence supports the use of unfractionated heparin, low-molecular
Ö
weight heparin, fondaparinux or bivalirudin in UA/NSTEMI.
In STEMI with revascularization planned, recommended agents
Ö
include unfractionated heparin and bivalirudin.
— Unfractionated heparin (UFH)
Acute Coronary Syndromes 169
9 Binds to antithrombin and inactivates thrombin and clot-
ting factors IXa and Xa, XIa, and XIIa.
9 Dose: bolus 60–70 units/kg, follow with infusion of 12–15
units/kg/hr with a goal activated partial thromboplastin
time at 1.5–2 times normal.
9 Must monitor for heparin-induced thrombocytopenia.
9 Consider bleeding risk before initiation.
— Low-molecular weight heparin (LMWH)
9 Recommended agent: enoxaparin (Lovenox).
9 Dose: enoxaparin IV bolus of 40 mg, follow with 1mg/kg
subcutaneously for 5 days.
9 In those treated invasively, LMWH has a higher bleeding
risk than unfractionated heparin.
— Fondaparinux (Arixtra).
9 A factor XA inhibitor.
9 Dose: fondaparinux 2.5 mg subcutaneously daily.
9 No risk of thrombocytopenia.
9 Preferred agent in patients treated conservatively with a
high bleeding risk.
9 Contraindicated in renal impairment and in patients who
weigh <50 kg.
— Bivalirudin
9 A direct thrombin inhibitor.
9 Acceptable for patients with heparin-induced thrombocyto-
penia, or for those treated with an invasive strategy and at
high risk for bleeding.
Treatment for complicated myocardial infarctions
For MI complicated with bradycardia or high-degree AV block:
Ö
— Temporary pacing
For MI complicated by cardiogenic shock:
Ö
— Vasopressors and inotropes: see Chapter 5-(v).
— Intra-aortic balloon pump is recommended to augment cardiac
output in patients who do not stabilize with maximal medical
therapy.
— Revascularization.
170 J. A. Salotto
For MI complicated by ventricular fi brillation:
Ö
— Cardiopulmonary resuscitation and early defi brillation.
— Medications according to the Advanced Cardiac Life Support
protocol.
Therapeutic hypothermia is now recommended for all resuscitated
Ö
patients with STEMI complicated by cardiac arrest.
Definitive therapy for ACS
• Treatment for UA/NSTEMI
Goal of immediate treatment is to provide relief of ischemia and to prevent
the recurrence of ischemic events.
In addition to anti-ischemic, antiplatelet, and anticoagulant therapy, two
treatment options exist for UA/NSTEMI:
Early conservative therapy
Maximal medical therapy, with invasive therapy only for refrac-
Ö
tory or recurrent ischemia. This is recommended for low-risk
patients without troponin elevation, hemodynamic instability,
prior CABG or PCI, or heart failure.
Early invasive strategy
Consists of catheterization followed by percutaneous coronary
Ö
intervention or coronary artery bypass grafting, depending on
anatomy (see below). Patients who benefi t most from this strategy include intermediate or high-risk patients (TIMI score >3),
known stenosis >70%, or those with hemodynamic instability,
prior CABG, PCI, or heart failure.
Fibrinolysis should not be performed for NSTEMI.
Ö
• Treatment Options for STEMI
Reperfusion therapy should be performed in all eligible patients with per-
sistent ST-segment elevation or new left bundle branch block within 12
hours of symptom onset. Reperfusion therapy is also accepted for symptom onset 24 hours prior.
Options for reperfusion therapy include percutaneous coronary inter-
vention, fi brinolytic therapy, and coronary artery bypass surgery.
Acute Coronary Syndromes 171
Percutaneous coronary intervention (PCI):
Refers to angioplasty and/or stenting.
Indications:
First-line therapy for patients with one or two vessel coronary
Ö
artery disease in absence of left main disease.
STEMI and cardiogenic shock, irrespective of time delay.
Ö
Contraindications or failure of fi brinolysis.
Ö
For three vessel or left main disease if signifi cant delay to CABG
Ö
exists or if the patient is not a surgical candidate.
Benefi ts are time dependent and should be performed for STEMI
within 90–120 minutes of presentation.
PCI should be performed in STEMI patients with symptoms
Ö
<12 hours. It is acceptable for symptoms up to 24 hours.
PCI is not available at all hospitals, and transfer should be consid-
Ö
ered if transfer and PCI can be performed within 120 minutes of
diagnosis.
Advantages: decreased risk of vessel re-occlusion, bleeding, and
re-infarction, improved overall mortality when compared with
fi brinolysis.
Complications: embolization, acute stent thrombosis, arterial dissec-
tion and perforation, stroke, and femoral access site complications.
Adjuncts to PCI include:
Aspirin indefi nitely.
Ö
Thienopyridines for one year after bare metal stenting and beyond
Ö
one year for drug-eluting stents.
Unfractionated heparin or a GPIIb/IIIa inhibitor while inpatient.
Ö
Fibrinolytic therapy
An infusion of an agent which converts plasminogen to plasmin and
leads to clot lysis.
Agents include streptokinase, alteplase, reteplase, and tenecteplase.
Recommended for patients with STEMI with onset of symptoms less
than 12 hours and no access to PCI within 120 minutes of diagnosis,
in the absence of contraindications. Acceptable at up to 24 hours of
symptom onset.
Not indicated for STEMI and cardiogenic shock.
172 J. A. Salotto
Complications: intracerebral hemorrhage, bleeding requiring trans-
fusion, coronary vessel re-occlusion.
Contraindications to fi brinolytic therapy:
Any prior hemorrhagic stroke, head trauma, spinal trauma, or
Ö
ischemic stroke within three months, cerebral neoplasm or AV
malformation, active bleeding or clotting disorder, suspected aortic
dissection, or severe uncontrolled hypertension.
Relative contraindications to fi brinolytic therapy:
Prior ischemic stroke in over three months, oral anticoagulants,
Ö
pregnancy or within one week post-partum, refractory hypertension, advanced liver disease, active peptic ulcer, major surgery
within three weeks, gastrointestinal bleeding within one month,
dementia, non-compressible punctures (liver biopsy, lumbar
puncture), traumatic or prolonged CPR >10 min.
Adjuncts include:
Antiplatelet and anticoagulants.
Ö
Early routine catheterization.
Ö
Coronary artery bypass grafting (CABG)
First-line therapy for those patients with three or more vessel disease
and/or >50% left main coronary artery stenosis.
Revascularization (PCI vs. CABG) recommended for STEMI within
24 hours of symptom onset if features of severe heart failure, persistent
ischemia, or hemodynamic instability.
Emergent CABG is indicated in patients with an acute myocardial
infarction for patients with:
Refractory ischemia after successful or failed PCI.
Ö
Unfavorable coronary anatomy for PCI.
Ö
Cardiogenic shock or life-threatening ventricular arrhythmias in
Ö
the presence of left main stenosis >50% and/or 3-vessel disease.
Mechanical complications of MI including acute mitral regurgita-
Ö
tion, ventricular rupture or ventricular septal defect.
Mechanical complications after PCI including perforation, dissec-
Ö
tion, stent dislodgment or fractured guidewire.
Emergent CABG should not be performed after failed PCI in the
absence of ischemia.
Acute Coronary Syndromes 173
Sequelae of myocardial infarction
• Heart failure
Heart failure is associated with a poor short and long-term prognosis in
the acute phase of MI. Symptoms include rales, shortness of breath, sinus
tachycardia, and a third heart sound. Assess pulmonary congestion with
chest X-ray. An echocardiogram is the primary diagnostic tool. Treatment
includes oxygen, diuretics, inotropes as needed. Heart failure after MI is
an indication for angiography with intent for revascularization.
ACE inhibitors should be prescribed indicated in the absence of hypoten-
sion to prevent remodeling.
• Cardiogenic shock
A state of systemic hypoperfusion characterized by a systolic pressure
<90 mm Hg or a cardiac index <1.8 L/min/m2 caused by loss of viable
myocardium. Most cases occur within 24 hours of infarct. Diagnosis of
cardiogenic shock is commonly made with the use of ECHO or a pulmonary artery catheter. See Chapter 5-(ii) for more details.
Treatment: fl uids and inotropes to target a wedge pressure >15 mmHg
and a cardiac index >2 L/kg/min. Agents include dobutamine, milrinone,
and dopamine as needed [See Chapter 5-(v)]. IABP can be used when
needed as a bridge to defi nitive therapy. Emergent PCI or CABG is indicated for patients with shock due to cardiac failure after STEMI regardless
of time delay.
• Right ventricular (RV) infarction
This manifests with a clinical triad of hypotension, clear lung fi elds, and
elevated jugular venous pressure. Treatment recommendations include
maintaining RV preload and reducing afterload. Milrinone is a commonly
used inotrope. Defi nitive treatment is reperfusion.
• Mitral regurgitation (MR)
Mitral regurgitation commonly develops within 2–7 days of MI due to
mitral annulus dilation due to post-infarction LV remodeling or secondary
to papillary muscle dysfunction or rupture after inferior MI.
Exam reveals a new-onset systolic murmur. Diagnosis is with ECHO.
Patients with acute MR should undergo mitral valve replacement prompt-
ly, as they may deteriorate suddenly. IABP is used as a bridge to defi nitive
care.
174 J. A. Salotto
• Cardiac rupture
Free wall rupture
An acute free wall rupture presents with recurrent chest pain, ST and
T-wave changes on EKG, with fast progression to hypotension, cardiovascular collapse and death. In a minority of cases, presentation is
subacute, and with accurate diagnosis there is time to intervene.
Risk factors include: fi rst MI, anterior infarction, older age, and female
sex.
Physical exam demonstrates signs of tamponade: hypotension, jugu-
lar venous distention, and muffl ed heart sounds. Rupture is confi rmed
with ECHO.
Those who survive require emergent surgery, with operative mortality
greater than 50%.
Ventricular septal rupture
Most commonly manifests in fi rst 24 hours after fi brinolysis for STE-
MI with sudden severe clinical deterioration accompanied by a loud
systolic murmur and cardiogenic shock.
ECHO will show the location and size of the defect.
Treatment includes vasodilators ( nitroglycerine), and IABP if in shock
in preparation for surgery. Emergent surgery is always indicated as
defect may expand abruptly.
• Left ventricular aneurysm
Ventricular aneurysms usually form after a large, transmural myocardial
infarct.
True aneurysms form when blood fl ow stretches and thins necrotic mus-
cle, which fi broses and forms an aneurysm. These rarely rupture, but contain thrombus and may lead to embolic events. Surgery is indicated for
heart failure, refractory arrhythmias or recurrent thromboembolism.
False aneurysms result from a small free wall rupture contained by peri-
cardium. They require urgent surgical intervention due to rupture risk.
• Pericardial effusion
Effusions are common after myocardial infarction, and often asymptomatic.
Must exclude free-wall rupture, especially if effusion is more than 1 cm
wide.
Hold anticoagulation if effusion >1cm or enlarging.
Acute Coronary Syndromes 175
• Pericarditis
Infl ammation and fi brosis are usually localized to the area of infarction.
Include in differential for recurrent chest pain after myocardial infarction.
Symptoms include sharp chest pain which is pleuritic in nature and
positional. Clinical fi ndings include a new pericardial rub, an elevated
neutrophil count, and fever.
Treat: NSAIDS or aspirin.
• Arrhythmias [Chapter 5-(vi)]
Arrhythmias following myocardial infarction are very common. They may
be atrial, ventricular, or secondary to conduction system disturbances.
The most common supraventricular arrhythmia is atrial fi brillation.
Sinus bradycardia is common after STEMI. It is generally asymptomatic
and needs no intervention other than to hold beta-blockers. For symptomatic or hemodynamically signifi cant bradycardia treat with atropine and
temporary pacing if unresponsive to medical therapy.
Ventricular tachyarrhythmias are a major source of sudden death after MI.
They are most commonly noted within 12 hours after a myocardial infarction. Treatment is immediate defi brillation for ventricular fi bril lation and
ventricular tachycardia with appropriate antiarrhythmic pharmacotherapy.
Use of prophylactic beta-blockers in the setting of STEMI reduces the
incidence of VF. Correction of magnesium and potassium defi cits also
helps to minimize risk.
Prophylactic use of antiarrhythmics is not recommended after NSTEMI.
No treatment is required for ventricular ectopic beats or nonsustained ven-
tricular tachycardia.
Implantable cardioverter-defi brillators are recommended prior to dis-
charge for those patients with sustained VT/VF > 48 hours after STEMI to
prevent sudden cardiac death.
Post-myocardial infarction hospital care
• Ambulate 12–24 hours after MI when possible.
• Blood pressure control, with beta-blockade, target: 140/90 mmHg.
• Blood glucose control in diabetics, target 100–180 mg/dL, avoid hypogly-
cemia.
• Continue antiplatelet agents:
Aspirin daily.
176 J. A. Salotto
Clopidogrel for at least one year for all patients with bare metal or drug-
eluting stents.
• Statin therapy for lipid management and plaque stabilization.
• PPI if need for dual antiplatelet therapy, especially if high-risk for gastroin-
testinal bleed.
• DVT/PE prophylaxis.
• Angiotensin-converting enzyme inhibitors (ACE-Is)
Vasodilatory effects which reduce myocardial oxygen demand.
Inhibits post-myocardial infarction remodeling.
Start in fi rst 24 hours after myocardial infarction if no contraindication.
Avoid in hypotension, renal failure, or hyperkalemia.
• Angiotensin-receptor blockers are acceptable alternatives for those who
cannot tolerate ACE-Is.
• Consider a repeat ECHO to assess cardiac function and rule out intra-
ventricular thrombus.
• Discuss goals for exercise, dietary counseling, lipid management, and smok-
ing cessation.
Practical Algorithm(s)/Diagrams
Cardiac chest pain or
suspicion for ACS
Perform EKG
Serial Troponin Assay
Risk Stratification
Troponins Positive
EKG shows no
ST-segment changes
or EKG equivocal
Fig. 1. Diagnostic algorithm for suspected ACS.
Troponins Positive
EKG shows STEMI
Troponins Positive
EKG shows NSTEMI
Consider
ECHO
Search for nonACS source for
elevated troponins
(+)
(–)
Urgent/Emergent
Revascularization
Low risk
Medium or high risk
features
Angiography and
PCI vs. CABG
New wall motion
abnormality
or newly depressed
cardiac function
Angiography
Maximal
Medical
therapy
Persistent or
recurrent ischemia
Acute Coronary Syndromes 177
Review of Current Literature with References
• A prospective trial by Devereaux et al. looked at over 8,300 patients enrolled
in a randomized prospective trail of beta-blocker therapy before and after
non-cardiac surgery. They found the rate of postoperative myocardial infarction to be 5%, and of those with infarction, 74% had clinical evidence of
infarct within 48 hours of operation. A majority (65%) of myocardial infarctions were asymptomatic with a diagnosis made based upon elevated cardiac
enzymes. Most postoperative myocardial infarctions demonstrated ST-wave
depression or T-wave inversion. The authors recommend cardiac biomarker
monitoring in the early postoperative period. In this study, risk factors for MI
included older age, vascular surgery, urgent or emergent surgery, postoperative bleeding, creatinine >2 mg/dl, and sustained increases in heart rate of
more than 10 beats per minute (Ann Int Med 2011; 154: 523–528).
• Another study examined a cohort of 377 randomized patients after elective
vascular surgery and found the rate of perioperative MI in this group to be
around 26.5%. This was not influenced by pre-operative coronary revascularization or extent of coronary artery disease. Predictors of MI included
abdominal aortic surgery, diabetes, and baseline ST-T wave abnormalities.
Patients were not randomized to therapy with beta-blockade (Eur Heart J
2008; 29: 294–401).
• A prospective trial by Keller et al. examined the sensitivity of various cardiac
biomarkers in the detection of ACS. In 1,800 patients with suspected ACS,
a 3-hour troponin assay had a sensitivity of 98%, a negative predictive value
of 99.4% and a positive predictive value of 96% in the presence of a serial
change from baseline (JAMA 2011; 306(24): 2684–2693).
• The Vascular Events in Non-cardiac Surgery Patients Cohort Evaluation
(VISION) study was an international prospective study including over 15,000
surgical patients. They showed a strong association between peak troponin
levels in the first three days after surgery and 30-day mortality. Time to death
after peak troponin values varied between one and two weeks. They suggest
the use of routine post-operative troponin monitoring to improve risk stratification and increase the opportunity for early intervention [JAMA 2012;
307(21): 2295–2304].
• The use of oxygen is a therapy for ACS has been debated in the literature.
One study by Mc Nulty et al. looked at the effect of 100% oxygen in
18 patients with stable coronary heart disease undergoing elective cardiac
catheterization. They found an increase in coronary resistance of 40%, decreased
coronary blood flow of 30%, and a blunted response to acetylcholine (an arterial