Prosthetic valves are implanted in approximately 40,000 patients
per year in the U.S.23 There are >80 types of artificial
valves, each with advantages and disadvantages. Patients who receive
prosthetic valves are instructed to carry a descriptive card in
their wallet. Prosthetic valves can be divided into two basic groups:
mechanical and bioprostheses. Mechanical valves are more durable
with lower failure rates, but have a higher risk for thromboembolic
complications. Bioprostheses, from porcine, bovine, or human sources,
are less thrombogenic, but are more likely to fail and require repeat
surgery. Complications of prosthetic valves are more common in patients
who have advanced heart disease, including cardiac dilatation, LVH,
congestive heart failure, dysrhythmias, or coronary artery disease.
Bleeding complications are more common in patients with mechanical
valves due to long-term anticoagulation with warfarin.2,24,25
Bleeding and systemic thromboembolism are common complications
of prosthetic heart valves. Even with anticoagulation, the rate
of thromboembolism is 1% to 2% per year.2 Embolic
risk is increased during the first 3 postoperative months and is
more common in mitral than aortic valve replacement. Antiplatelet
therapy is recommended for all patients with prosthetic valves.
Lifelong anticoagulation with warfarin is required for all patients
with mechanical valves to reduce the risk of thromboembolism. The
rate of bleeding complications is dependent upon the type and intensity
of anticoagulation. Major bleeding complications from warfarin occur
in approximately 1.4% of prosthetic valve patients per year.26
Thrombus formation on prosthetic valves can also interfere with
valve function. If the clot becomes large enough, it may obstruct
flow through the valve or prevent closure, resulting in regurgitation.
Dysfunction from thrombi may present acutely with sudden severe
symptoms or cause slow, progressive deterioration. Mechanical valves
may also suddenly fracture or fail. These failures usually cause
acute onset of symptoms and may be fatal before corrective surgery
can be accomplished. Bioprostheses gradually degenerate from thinning,
stiffening, or tearing, resulting in valvular incompetence. Paravalvular
regurgitation is a rare complication of prosthetic valves, typically
caused by dehiscence of sutures securing the prosthetic valve. Patients
with prosthetic valves are also vulnerable to hemodynamic compromise
from new-onset arrhythmias, such as atrial fibrillation.
Patients with artificial valves develop endocarditis at a rate
of 0.1% to 2.3% per year.27 Infections
occur most frequently during the first 2 months after surgery. The
most common organism during the initial postoperative period is S.
epidermidis followed by S. aureus. Gram-negative
organisms and fungi are also frequent causes of early endocarditis. Late
cases of endocarditis (after the initial 2-month postoperative period)
are similar to those affecting native valves. The most frequent
organism is Streptococcus viridans, but Serratia and Pseudomonas are
also implicated. Patients with prosthetic valve endocarditis may
develop a valve ring abscess, fistula, or paravalvular leak, which
requires valve replacement. Mechanical prostheses often cause intravascular
hemolysis, which is rarely clinically significant.
Although valve replacement relieves valvular obstruction and
regurgitation, it does not reverse the remodeling of the heart that
occurs in patients with chronic valvular disease. Thus, many patients
have persistent cardiac symptoms after valve replacement. Long-standing
volume or pressure overload leads to ventricular dysfunction, and
many patients continue to have dyspnea and symptoms of heart failure.
Patients are also likely to have concomitant coronary artery disease,
systemic hypertension, or atrial fibrillation.
Symptoms of prosthetic valve dysfunction depend on the type of
valve and its location. Signs and symptoms of mitral or aortic stenosis
and regurgitation are described in the preceding sections on native
valves. However, patients with prosthetic valves experience some
symptoms specific to the presence of the artificial valve.
Valve thrombosis commonly causes minor embolic episodes, such
as transient neurologic symptoms, amaurosis fugax, or self-limited
ischemic episodes in the extremities or organs. Major embolic events
include stroke, mesenteric infarction, or sudden death. Anticoagulant
therapy may cause major bleeding, with hemorrhagic stroke the most
common lethal bleeding complication.
Acute onset of respiratory distress, pulmonary edema, and
cardiogenic shock may be associated with mechanical valve failure,
tearing of a bioprosthesis, or a large clot obstructing the valve
or preventing closure. These failures often result in sudden
death before corrective surgery can be done. A paravalvular leak
also presents with congestive heart failure. The severity of symptoms
is dependent on leak size and how rapidly the leak develops. Slowly
progressive development of heart failure may occur with gradual
accumulation of a prosthetic valve thrombus.
Cardiac auscultation of patients with prosthetic valves can suggest
valve dysfunction. Mechanical valves normally have a loud, clicking,
metallic sound associated with valve closure. Therefore, valve dysfunction
should be suspected in any patient with a quiet mechanical valve.
Systolic murmurs of prosthetic aortic valves are common, particularly
in mechanical models, but loud diastolic murmurs should be considered
pathologic. A loud holosystolic murmur indicates valve dysfunction
in patients with mitral valve prostheses. Patients with bioprostheses
usually have a normal S1 and S2, with no abnormal
opening sounds. Aortic bioprostheses are usually associated with
a short mid-systolic murmur. The mitral bioprostheses may be associated
with a short diastolic rumble.
Prosthetic Valve Dysfunction or Complications
Evaluation for prosthetic valve dysfunction is required in any
patient with a valve replacement and new or progressive dyspnea,
congestive heart failure, decreased exercise tolerance, or chest
pain. Thromboembolism, septic embolism, or intracranial hemorrhage
should be suspected in any patient with a prosthetic valve and new
focal neurologic deficit. Finally, endocarditis must be considered
in patients with persistent fever.
Patients with suspected prosthetic valve dysfunction, thromboembolism,
or endocarditis should receive emergent echocardiography. Transesophageal
echocardiography is more sensitive than transthoracic in evaluation
of prosthetic valves. Chest radiography lacks sensitivity and specificity
but may show a change in valve position or signs of heart failure.
A head CT should be obtained in patients with focal neurologic deficits
to evaluate for hemorrhage or embolic stroke. Patients on warfarin
may require a complete blood count and coagulation studies. Blood cultures
should be obtained on patients with suspected endocarditis.
Patients with suspected acute prosthetic valve dysfunction should
be evaluated by a cardiothoracic surgeon for possible emergency
surgery. Acute prosthetic valvular dysfunction due to thrombotic
obstruction may be treated with thrombolytic therapy28 but
requires consultation with a cardiologist. Lesser degrees of obstruction
should be treated by optimizing anticoagulation. Consultation with
a cardiologist should be considered before discharging a patient
with suspected prosthetic valve dysfunction.
Anticoagulation with Prosthetic Valves
Management of patients with prosthetic valves in the ED requires knowledge
of the recommendations on anticoagulation and reversal of excessive
anticoagulation. Mechanical valves require anticoagulation with
warfarin, but the intensity varies, depending on the location and type
of valve. Mechanical mitral valves require an INR of 2.5 to 3.5, whereas
bileaflet mechanical valves in the aortic position require an INR of
2.0 to 3.0.2,7 Aspirin is recommended for all patients
with prosthetic valves—mechanical or bioprosthetic.2
Excessive anticoagulation creates a dilemma because although
an INR >5 poses significant risk for hemorrhage, a rapid decrease
in the INR may lead to thromboembolism. Patients with an INR of
5 to 10 without bleeding may be treated by withholding warfarin
or administering 1.0 to 2.5 milligrams of oral vitamin K. Patients
with severe bleeding complications are best treated with fresh frozen
plasma. Universal donor fresh frozen plasma (AB+) can be
given without the need for type and cross-match of blood. Parenteral,
high-dose vitamin K should be avoided, as it often leads to overcorrection.2