US Pharm. 2014;39(2):HS13-HS16.
catheterization is a common procedure that is performed in hospitals
throughout the United States and worldwide. The procedure can be used
for diagnosis and treatment of cardiovascular disease. Pharmacists
should be aware of the benefits and risks involved in cardiac
catheterization and the associated drug therapy in order to help
determine appropriate treatment for patients.
Cardiac catheterization is a common procedure that is
performed in hospitals throughout the United States and worldwide.
Cardiac catheterization can be used for diagnosis and assessment of
cardiovascular disease. Additionally, it can be used therapeutically in
order to open an occluded blood vessel and has become an alternative to
surgery in some patients.1 Pharmacotherapy plays a large role
before, during, and after cardiac catheterization. The goal of this
article is to provide practicing pharmacists an overview of the most
common reasons for cardiac catheterization, describe the procedure and
its associated risks, and discuss the drugs that need be to administered
as part of the procedure.
Purpose of Cardiac Catheterization
Cardiac catheterization can be used for the diagnosis and
treatment of cardiovascular disease. Diagnostic cardiac catheterization
can be utilized to assess the presence and severity of cardiac disease
and may help in diagnosis in those patients who present with
inconclusive results with noninvasive testing.1 IV radiopaque
contrast dye can be administered just prior to the procedure in order
to visualize the coronary vessels and can help determine the severity of
coronary artery disease (CAD).2 During a right heart
catheterization, vascular resistance is measured by attaining pressures
in the heart, blood oxygen saturations, and the degree of
tricuspid/pulmonic stenosis. This can indicate the presence and severity
of pulmonary hypertension.1 During a left heart
catheterization, mitral and aortic valvular functions are assessed by
measuring the left ventricular pressure, left ventricular function,
vascular resistance, and coronary arterial anatomy.1
Therapeutic cardiac catheterization, such as percutaneous
coronary intervention (PCI) can be used in patients with occluded
arteries or blood vessels. Vascular access is obtained percutaneously
via the femoral, brachial, or radial vessels.3 A guidewire is
positioned past the stenosis through the lumen and a small angioplasty
balloon catheter is advanced over the guidewire. The balloon catheter is
then positioned into the artery across the stenotic area and inflated.
This inflation expands the stenotic area, thus restoring blood flow.3 The balloon is then deflated, withdrawn, and exchanged for a stent, which remains in place.3
According to the practice guidelines of the American Heart
Association (AHA), the American College of Cardiology Foundation
(ACCF), and the Society of Cardiovascular Angiography and Interventions
(SCAI), PCI is indicated for patients with any of the following cardiac
conditions: acute myocardial infarction; stable angina pectoris
unrelieved by medical therapy, unstable angina, or angina pectoris
following a coronary artery bypass graft (CABG); symptomatic restenosis
after previous PCI; and unsuitable or high-risk coronary anatomy that
could result in death.4 PCI is contraindicated in the
following patients: those with bleeding disorders, multiple PCI
restenosis, noncompliance with pre- and post-PCI instructions, and
inability to tolerate dual antiplatelet therapy following the procedure.3
Other types of therapeutic cardiac catheterization include
those for the treatment of congenital heart defects and for regaining
lost hemodialysis access. The use of cardiac catheterization in patients
with congenital heart defects may allow for the avoidance of surgery,
thus reducing recovery time and duration of hospitalization.5
Cardiac catheterization can also be used for patients with thrombosed
hemodialysis access. The use of this approach can prevent the use of
temporary hemodialysis catheters, thus allowing for the preservation of
venous segments for future access creation.3
Antithrombotic prophylaxis is an important aspect of
diagnostic cardiac catheterization and PCI. Current adjunctive
antithrombotic therapy prior to the procedure includes aspirin, a P2Y12
inhibitor (a chemoreceptor for adenosine diphosphate [ADP]), and
anticoagulant therapy in combination with a glycoprotein (GP) IIb/IIIa
receptor antagonist. Of note, patients undergoing cardiac
catheterization for diagnostic purposes with no intervention will
require only aspirin and an anticoagulant with GP IIb/IIIa
receptor–antagonist therapy. A P2Y12 inhibitor is administered if there is a high likelihood of stent placement during the diagnostic procedure.6 Aspirin produces its antiplatelet effects by inhibiting thromboxane A2 production via irreversible inhibition of cyclooxygenase in platelets.7
Patients already on aspirin therapy and undergoing catheterization
should take a total of 81 to 325 mg of aspirin before the procedure.
Patients not on aspirin therapy should receive 325 mg of
nonenteric-coated aspirin. In all patients, aspirin 81 mg should be
P2Y12 Inhibitors: The P2Y12 inhibitors, also known as the thienopyridines, produce their effect by blocking the ADP-P2Y12 receptors on platelets to inhibit platelet aggregation.7
Several new drugs in this class have been introduced to the market in
recent years, including prasugrel and ticagrelor. These agents have been
incorporated into the most recent guidelines from the ACCF/AHA/SCAI.4
A loading dose of clopidogrel 600 mg, prasugrel 60 mg, or ticagrelor
180 mg is administered to the patient prior to PCI. Patients with
bare-metal or drug-eluting stent placement should continue P2Y12 inhibitor therapy for 1 year with clopidogrel 75 mg daily, prasugrel 10 mg daily, or ticagrelor 90 mg twice daily (TABLE 1).4
Of note, prasugrel should be avoided in patients with history of stroke
or transient ischemic attack (TIA) because of the increased risk of
bleeding. Patients with a drug-eluting stent and low bleeding risk may
be advised to continue therapy up to 15 months. Patients undergoing PCI
without stent placement should continue P2Y12 therapy for 14 to 28 days. The combination of aspirin plus a P2Y12 inhibitor is known as dual-antiplatelet therapy (DAPT) and is recommended for all patients to prevent premature thrombosis with both types of stent placement.4
Heparins and Bivalirudin: Anticoagulation, generally with unfractionated heparin (UFH), is also recommended (TABLES 2 and 3).4,7
Additionally, a GP IIb/IIIa receptor antagonist should be
coadministered with UFH to reduce the risk of thrombus formation at the
puncture site, on the coronary guidewire, and in indwelling cardiac
catheters.4 UFH binds to antithrombin and inhibits multiple factors in the blood-clotting cascade.8
UFH should be started preprocedure with a bolus dose of 50 to 70 U/kg
followed by a continuous infusion to achieve and maintain therapeutic
activated clotting time (ACT) between 200 and 250 seconds, per
ACCF/AHA/SCAI guidelines.8,9 When UFH is given without a GP
IIb/IIIa receptor antagonist, the bolus dose should be increased to 70
to 100 U/kg followed by continuous infusion to achieve and maintain
therapeutic ACT between 250 and 350 seconds.4 UFH should be discontinued immediately after catheterization is complete.7
In some cases, patients are already receiving anticoagulation with
enoxaparin, and this medication can be continued in place of UFH, along
with a GP IIb/IIIa receptor antagonist.
Editor's Note 3/21/14: Bolus dose for Argatroban corrected to 350 mcg/kg (not mg/kg).
If UFH or enoxaparin is contraindicated, as in
heparin-induced thrombocytopenia, bivalirudin alone or argatroban along
with a GP IIb/IIIa receptor antagonist can be substituted.4
Bivalirudin, a direct thrombin inhibitor, should always be administered
alone due to increased risk of bleeding events associated with use in
combination with a GP IIb/IIIa receptor antagonist. Bivalirudin alone is
also recommended in place of UFH in patients at risk for bleeding
events. It is initiated with an IV bolus of 0.75 mg/kg followed by 1.75
mg/kg/h continuous infusion. An additional bolus of 0.3 mg/kg can be
administered if needed. Bivalirudin should be discontinued immediately
after PCI completion.4,7 Of note, if fondaparinux is chosen
as the anticoagulant prior to PCI, it should not be the only
anticoagulant administered. An additional anticoagulant with anti-IIa
activity will need to be administered in combination.4
GP IIb/IIIa Receptor Antagonists: A
GP IIb/IIIa receptor antagonist should also be started prior to PCI.
These drugs block platelet aggregation by inhibiting the cross-linking
of platelets at the IIb and IIIa receptor sites.7 There are
several options within this class. Recommended GP IIb/IIIa receptor
antagonists include abciximab, tirofiban, and eptifibatide (TABLE 3).7
Hospitals generally will not carry all of the GP IIb/IIIa receptor
antagonists on formulary due to cost. Efficacy between the individual
drugs in the class is comparable.
Abciximab is started at a bolus dose of 0.25 mg/kg
followed by 0.125 mcg/kg/min continuous infusion. Tirofiban can also be
used in place of abciximab, with a bolus dose of 25 mcg/kg followed by
0.15 mcg/kg/min continuous infusion. Eptifibatide is another option and
should be initiated with a bolus of 180 mcg/kg, followed by 2 mcg/kg per
minute continuous infusion. A second bolus of 180 mcg/kg is
administered 10 minutes after the first bolus. Both tirofiban and
eptifibatide require dosage reduction in patients with renal disease.4,10
Abciximab should be continued for 12 hours postprocedure, while
eptifibatide or tirofiban should be continued for 12 to 18 hours.7
Other supportive therapies that may be used during catheterization and
PCI include IV fluids for hydration and blood pressure stabilization,
antihypertensives, vasodilators, and sedatives/anxiolytics.6
As technology and experience with cardiac catheterization
has evolved, the risk of complications associated with the procedure has
decreased. The complication rate varies based on diagnostic versus
interventional use of catheterization (TABLE 4).3
Complications can range from minor issues with no long-term effects to
major complications that require emergency care or surgical intervention
and can lead to irreversible damage or death. However, the risk of
major complications is under 1%.3 Major complications may
include myocardial infarction, cerebrovascular events/stroke, cardiac
perforation, and cardiac arrhythmias. Patients with comorbid conditions
such as left ventricular dysfunction, valvular heart disease, a prior
CABG, congestive heart failure, and renal insufficiency are at higher
risk of complications.
Local vascular complications are the most common type of
complication associated with cardiac catheterization. They are also the
single greatest source of morbidity. Some of these complications include
vessel thrombosis, distal embolization, and bleeding. Vessel thrombosis
and embolization usually occur when a piece of plaque or a clot
imperceptibly breaks free after contact with the catheter. Poorly
controlled bleeding at the entry site is associated with a poorly placed
puncture, vessel lacerations, excess anticoagulant use, and unskillful
technique with a closure device. This can lead to hemorrhage and
hematoma formation, usually within 12 hours of the procedure, and may
require surgical interventions and blood transfusions. Patients may also
experience false aneurysms or arteriovenous fistulas that can appear
days to weeks after the procedure and require surgical interventions.10
While an important and required part of cardiac
catheterization, the use of contrast can also lead to complications such
as allergic or anaphylactic reactions and nephropathy in some patient
populations. Those with penicillin, seafood, or atopic allergies or past
reactions to contrast are at a higher risk for complications.
Premedicating these patients with glucocorticoids, H1 antihistamines, and H2
antihistamines can decrease the risk of such complications.
Additionally, ionic contrast should be avoided and replaced with low- or
iso-osmolar nonionic contrast.
Certain patient populations may also experience
contrast-related nephropathy, including those with a history of
diabetes, renal failure, and volume depletion. Patients who receive
larger volumes of contrast are also at increased risk for
nephrotoxicity. These patients should receive IV hydration pre- and
postprocedure, and the amount of contrast used during the procedure
should be minimized. Serum creatinine should be monitored in these
patients for 3 to 5 days after catheterization.
can also be administered pre- and postprocedure as a protective
strategy; however, clinical studies show questionable value.6,10
Cardiac catheterization is a common procedure that is
generally well tolerated. Pharmacists should be aware of the benefits
and risks associated with the procedure and associated drug therapy.
Pharmacists in the community setting are in a position to answer
patients’ questions regarding the cardiac catheterization procedure and
the need for adherence with DAPT following hospital discharge.
Pharmacists in hospital settings can play a role in guiding drug choices
and developing a drug formulary of antiplatelets and anticoagulants for
the procedure. These pharmacists can also ensure that patients are
discharged on appropriate antiplatelet therapy to prevent future
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2. Scanlon P, Faxon D, Smith S Jr, et al. ACC/AHA
guidelines for coronary angiography: executive summary and
recommendations. A report of the American College of Cardiology/American
Heart Association Task Force on Practice Guidelines (Committee on
Coronary Angiography) developed in collaboration with the Society for
Cardiac Angiography and Interventions. Circulation. 1999;99:2345-2357.
3. Kern MJ. Interventional Cardiac Catheterization Handbook. 3rd ed. Philadelphia, PA: Elsevier Saunders; 2013.
4. Levine GN, Bates ER, Blankenship JC, et al. 2011
ACCF/AHA/SCAI guideline for percutaneous coronary intervention: a report
of the American College of Cardiology Foundation/American Heart
Association Task Force on Practice Guidelines and the Society for
Cardiovascular Angiography and Interventions. Circulation. 2011;124:e574-e651.
5. Krasemann T, Qureshi S. Treatment of congenital heart defects using interventional catheterization. Cardiology. 2007;26:97-106.
6. Bashore TM, Balter S, Barac A, et al. 2012 American
College of Cardiology Foundation/Society for Cardiovascular Angiography
and Interventions expert consensus document on cardiac catheterization
laboratory standards update. J Am Coll Cardiol. 2012;59:2221-2305.
7. Spinler SA, De Denus S. Chapter 24. Acute coronary syndromes. In: Wells BG, ed. Pharmacotherapy: A Pathophysiologic Approach. 8th ed. New York, NY: McGraw-Hill; 2011.
8. Zehnder JL. Chapter 34. Drugs used in disorders of coagulation. In: Katzung BG, Masters SB, Trevor AJ, eds. Basic & Clinical Pharmacology. 12th ed. New York, NY: McGraw-Hill; 2012.
9. O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA
guideline for the management of ST-elevation myocardial infarction: a
report of the American College of Cardiology Foundation/American Heart
Association Task Force on Practice Guidelines. Circulation. 2013;127:e362-e425.
10. Baim DS, Simon DI. Chapter 3. Complications and the optimal use of adjunctive pharmacotherapy. In: Baim DS, ed. Grossman’s Cardiac Catheterization, Angiography, and Intervention. 7th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2006.
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