I. Problem/Condition.
Placement of prosthetic heart valves (PHV) may be done for various reasons. It is estimated that in the United States alone as many as 60,000 prosthetic heart valves are replaced. Effectively, a hospitalist is likely to come across a patient with an existing prosthetic heart valve. It is important to have a broad knowledge about the various types of prosthetic valves that are used and the complications that can be expected.
Simply speaking, the prosthetic valves can be classified as either mechanical or biological. Mechanical valves are the ones that are made out of synthetic material and frequently use tilting disks, ball mechanism or bileaflet components. In contrast, the biological prosthetic vales are made up of biological material that is harvested from animal (or human) source and is suitably treated. Some of the commons sources are bovine pericardium, porcine aortic valves and other human donors (autografts or homograft). SeeFigure 1Figure 2 andFigure 3 for types of valve.
Figure 1.
Starr-Edwards valve. Courtesy: Edwards Lifesciences LLC, Irvine, CA
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Figure 2.
Trifecta ™ pericardial tissue heart valve. Courtesy: St. Jude Medical, Inc., St. Paul, MN

Figure 3.
Regent™ aortic valve. Courtesy: St. Jude Medical, Inc., St. Paul, MN

Patients with the prosthetic heart valves can develop several complications and a hospitalist should be abreast with these – anticipating, diagnosing and managing these complications. Some of these complications include infection of a PHV, systemic embolization due to PHV, mechanical damage to red cells leading to hemolytic anemia, left ventricular dysfunction, bleeding, valvular obstruction, structural damage and complication related to anticoagulation.
II. Diagnostic Approach.
A. What are the differential diagnoses for this problem?
Patients with PHV are typically managed during the outpatient visits with the cardiologist and do get surveillance echocardiogram based on the nature of valves they have and clinical conditions.
PHV complications lend themselves to various differentials based on the nature of complication. Whether it is infectious, structural or functional complication, the clinician needs to entertain several differentials. Systemic embolization is an important differential in patients with PHV. Thrombi or vegetations may embolize. Clinical presentation may include asymptomatic events, TIA or stroke. The risk of systemic embolization is higher when anticoagulation is not adequate. Mechanical damage to red cells may lead to hemolytic anemias. Differentials in this regard should include the various causes of hemolytic anemias. Peripheral smear is often helpful in evaluating this complication.
Left ventricular dysfunction can ensue with or without congestive heart failure. Differentials to be considered in this category include other causes of cardiac congestion, medication effects, fluid overload and stenotic valves.
B. Describe a diagnostic approach/method to the patient with this problem.
The nature of the prosthetic heart valve may point one towards one complication more than the other. For instance, mechanical heart valves are more likely to have functional complications and anticoagulation related complications; while biological PHV lend themselves to more structural complications. Anticoagulations are rarely indicated for biological heart valves and hence a suitable history of medical compliance is more pertinent when a patient is on mechanical heart valve. The use of IV drugs, or a history of central line placement, means it is important to think on the lines of infective endocarditis.
1. Historical information important in the diagnosis of this problem.
The nature of prosthetic heart valve may point one towards one complication more than the other. For instance, mechanical heart valves are more likely to have functional complications and anticoagulation related complications; while biological PHV lend themselves to more structural complications. Anticoagulation is rarely indicated for biological heart valves and hence a suitable history of medical compliance is more pertinent when a patient is on mechanical heart valve. The use of IV drugs, history of central line placement, is both important to think on the lines of infective endocarditis.
2. Physical Examination maneuvers that are likely to be useful in diagnosing the cause of this problem.
A thorough physical examination is helpful to assess the patient in which complications of PHV are suspected. However, a detailed cardiac examination, skin exam and neurologic exam is essential. Functional heart murmurs can alert a clinician towards left ventricular dysfunction and valvular dysfunction.
Various clinical findings seen in patients with native valve endocarditis should be looked for; splinter hemorrhages, petechiae, Janeway lesions (erythematous lesions on palms and soles), Osler’s nodes (violaceous nodules on the finger pulps), Roth spot (retinal hemorrhagic lesions), are such corroborative findings. Neurologic examination may show evidence consistent with cerebrovascular events. Labored breathing, raised JVD may suggest heart failure in the setting of PHV obstruction.
3. Laboratory, radiographic and other tests that are likely to be useful in diagnosing the cause of this problem.
Blood tests, microbiology and imaging are very helpful in evaluating a patient suspected of having PHV complications. Hemogram may suggest presence of anemia and further evaluation for hemolytic anemia should be done. Peripheral smears may show fragmentation of red cells. Blood culture is very crucial in patients suspected to have developed infective endocarditis. Care should be taken in obtaining at least three set of cultures prior to initiating antibiotic treatment. Blood cultures from ports of central line, if present, should also be obtained. PT and INR are helpful in ascertaining anticoagulation compliance.
Echocardiogram is helpful in assessing cardiac function, heart valve structure and functionality and also looks at vegetations. Often times, transthoracic echo may not provide adequate information and transesophageal echo may be required. Acoustic shadow casted by the prosthetic valve may not allow adequate visualization of abscesses, vegetations, thrombi and pannus and this warrants Trans Esophageal Echocardiogram (TEE). For paravalvular leaks as well, TEE is a superior diagnostic modality. In essence, if a complications of PHV is suspected, there is a high likelihood TEE will be required.
SeeFigure 4 andFigure 5
Figure 4.
Echocardiogram showing a working St Jude¹s Valve in MitralPosition, Normal (Courtesy: Daniel G. Blanchard, MD, FACC)

Figure 5.
Echocardiogram showing a St Jude¹s Valve in Mitral Position, with thrombosis(Courtesy: Daniel G. Blanchard, MD, FACC)

C. Criteria for Diagnosing Each Diagnosis in the Method Above.
Infective endocarditis: Many diagnostic criteria exist for diagnosis of Infective endocarditis, of which the Duke criteria is most commonly used. The detailed criteria are discussed in the chapter on infective endocarditis. Set of three blood cultures should be obtained and an echocardiogram should be performed to look for vegetations. TEE is superior to trans thoracic echocardiogram to identify valvular vegetations. Acoustic shadow due to prosthetic material may not allow adequate visualization on trans thoracic echo. TEE also is superior in identifying abscesses. Transthoracic echocardiogram is helpful in evaluating patients with PHV endocarditis but a TEE may still be required eventually.
There are not distinct criteria set aside to establish diagnosis of systemic embolization and several other complications related to PHV. However, both transthoracic and trans esophageal echo is helpful in making several diagnoses. Left ventricular function, valvular structure, any related obstruction, vegetations and stenosis may be visualized and quantified from echo findings.
D. Over-utilized or “wasted” diagnostic tests associated with the evaluation of this problem.
N/A
III. Management while the Diagnostic Process is Proceeding.
A. Management of Clinical Problem Prosthetic Heart Valves.
Infective endocarditis is not an uncommon complication of PHV. Bacteremia, sepsis, presence of central venous catheters is common in clinical settings where the suspicion of development of infective endocarditis should be high. Isolation of offending organism is critical in managing IE appropriately. Common agents causing PHV endocarditis includeStaphylococcus aureus, Streptococci, culture negative and fungal sources. The antibiotic treatment should be targeted towards these agents.
Empiric treatment for fungal causes is not routinely done, unless the suspicion is very high. Empirically, pending microbiologic data, the treatment should be initiated with vancomycin, gentamicin and either a carbapenam or cefepime. The antibiotics regimen should be subsequently tailored based on susceptibility data. Unlike native valve endocarditis, staphylococcal infection is more common in patients with prosthetic valve endocarditis.
Streptococcal endocarditis should be treated with a combination of beta lactam antibiotic and an aminoglycoside. One such commonly used regimen consists of penicillin and gentamicin, of which gentamicin is used for 2 weeks, and the gentamicin course can be extended if there is relative resistance to penicillins. In patients with penicillin allergy other considerations include ceftriaxone, cefotaxime and vancomycin.
Antibiotic treatment alone may not be sufficient to treat prosthetic valve endocarditis. Consideration should be given to valvular replacement, especially if a spread from the valve to adjacent cardiac tissue is noted. A cardiothoracic surgery evaluation should be made in these patients. See the chapter prosthetic valve endocarditis for other details of management..
Systemic embolization is more often seen in the patients with mechanical valve prosthesis. Such patients should already be on anticoagulants. Resuming anticoagulation and if anticoagulation is inadequate, optimizing it is necessary. Biological PHV may also be implicated in systemic embolization. The management centers around addressing the sequelae of such systemic emboli. If the reason is suboptimal function or poor valve design, PHV replacement may be necessary. Statistically, mitral PHV tend to have much higher systemic embolization rates as compared to aortic PHV. Type of PHV also has a bearing on systemic embolization. For instance, Starr Edwards valve, a ball type valve, has been associated with higher incidences of systemic embolization.
Mechanical damage to red cells can lead to hemolytic anemia. Variable pressure gradients, prosthetic valve regurgitation, paravalvular leak and mechanical shearing of the red cells, can all lead to hemolysis. Treatment modalities in these scenarios include iron supplementation to promote erythropoiesis, blood transfusion and occasionally addition of erythropoietin to promote erythropoiesis along with iron supplementation. It is not common, but may be necessary to have replacement or exchanging one valve for the other if anemia cannot be acceptably corrected.
Left ventricular dysfunction may ensue in patients with PHV. This may be with or without heart failure. Treatment in such a scenario is similar to that of left ventricular dysfunction in native valve patients. Heart failure and its management are discussed elsewhere. Occasionally however, when the cause is attributed to valve malfunctioning or failure or paravalvular leak a replacement of such a valve may be necessary.
Development of pannus, thrombus or vegetation may lead tovalvular obstruction, which is manifest by clinical symptoms of shortness of breath and other findings consistent with congestive heart failure. An echocardiographic demonstration of significantly raised pressure gradient across PHV is suggestive of such a development of PHV obstruction. Surgical correction may be required to correct such an obstruction.
When the obstruction is due to development of thrombosis, it is usually in the setting of inadequate anticoagulation. Given the high risk nature of valvular replacement/surgical correction, thrombolysis with streptokinase, urokinase and alteplase is also an alternative, and quite often preferred over surgery. Aggressive anticoagulation should be instituted following successful outcome of either of these interventions. Unfractionated heparin IV and warfarin should be used to bridge, and after attaining adequate anticoagulation for 1-2 days, heparin may be discontinued. The INR goal ranges for mitral and aortic prosthetic valve are 3.5 to 4.5 and 3.0 to 4.0 respectively, along with aspirin.
Pannus formation in contrast is not amenable to fibrinolytics treatment. If pannus formation is critical, re-operation is the only realistic option. Vegetations if infectious need appropriate antimicrobial treatment and refractory vegetations leading to valvular obstruction may require surgery.
Structural damages frequently require re-operation.Complications related to anticoagulationare more commonly seen in the patients with mechanical PHV. Patients with mechanical valve are usually on chronic anticoagulation and are prone to develop bleeding. This scenario can be precipitated due to compliance issues, initiation of antibiotic treatments and dietary changes. Optimization of anticoagulation may be required. Biological PHV don’t typically require anticoagulation, unless there is another indication for anticoagulation.
B. Common Pitfalls and Side-Effects of Management of this Clinical Problem.
N/A
IV. What's the evidence?
Huang, G, Rahimtoola, SH.. “Prosthetic heart valve”. Circulation. vol. 7123. 2011. pp. 2602-5. Review. No abstract available.PUBMED:
Bonow, RO, Carabello, BA, Chatterjee, K, de Leon, AC, Faxon, DP, Freed, MD. “Writing Committee Members; American College of Cardiology/American Heart Association Task Force. 2008 Focused update incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease): endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons”. Circulation. vol. 118. 2006. pp. e523-661.
Alpert, JS. “The thrombosed prosthetic valve current recommendations based on evidence from the literature”. J Am Coll Cardiol. vol. 41. 2003. pp. 659-60.
Olmos, L, Salazar, G, Barbetseas, J, Quiñones, MA, Zoghbi, WA.. “Usefulness of transthoracic echocardiography in detecting significant prosthetic mitral valve regurgitation”. Am J Cardiol. vol. 15;83. 1999. pp. 199-205.
Rahimtoola, SH. “Choice of prosthetic heart valve in adults, an update”. J Am Coll Cardiol. vol. 1;55. 2010. pp. 2413-26.
Cannegieter, SC, Rosendaal, FR, Briët, E. ” Thromboembolic and bleeding complications in patients with mechanical heart valve prostheses”. Circulation. vol. 89. 1994. pp. 635-41.
Chan, WS, Anand, S, Ginsberg, JS. “Anticoagulation of pregnant women with mechanical heart valves: a systematic review of the literature”. Arch Intern Med. vol. 24;160. 2000. pp. 191-6..
Daniel, WG, Mügge, A, Grote, J, Hausmann, D, Nikutta, P, Laas, J, Lichtlen, PR, Martin, RP. “Comparison of transthoracic and transesophageal echocardiography for detection of abnormalities of prosthetic and bioprosthetic valves in the mitral and aortic positions”. Am J Cardiol. vol. 15;71. 1993. pp. 210-5.
Daniel, WG, Mügge, A, Martin, RP, Lindert, O, Hausmann, D, Nonnast-Daniel, B, Laas, J, Lichtlen, PR. ” Improvement in the diagnosis of abscesses associated with endocarditis by transesophageal echocardiography”. N Engl J Med. vol. 21;324. 1991. pp. 795-800.
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