Prosthetic Heart Valves Clinical Presentation

In patients with malfunctioning prosthetic valves, symptoms are dependent on the type of valve, its location, and the nature of the complication. With valvular breakage or dehiscence, failure often occurs acutely with rapid hemodynamic deterioration. Failure occurs more gradually with valve thrombosis, calcification, or degeneration.

• Information about the type of valve is important; the potential for complications depends on valve type and position. Sources include a wallet-sized identification card (typically given to the patient at the time of surgery) and/or a review of medical records.
• Review of the operative report may be useful. If the native valve annulus is described as being heavily calcified or infected, the chance of a perivalvular leak is greater.
• Patients with acute prosthetic valve failure often present in extremis with the sudden onset of dyspnea, syncope, or precordial pain.
• Patients with acute aortic valve failure often experience sudden death. Those surviving have acute severe dyspnea, sometimes accompanied by precordial pain, or syncope.
• Patients with subacute valvular failure present with symptoms of gradually worsening congestive heart failure. This includes increasing dyspnea with exertion, orthopnea, paroxysmal nocturnal dyspnea, and fatigue. They also may present with unstable angina or, at times, be entirely asymptomatic.
• Patients with embolic complications have symptoms related to the site of embolization. Stroke syndromes are the most common presentation, although patients may present with myocardial infarction (MI), sudden death, or symptoms of visceral or peripheral embolization.
• Symptoms due to anticoagulant-related hemorrhage are related to the site of hemorrhage.
• A history of fever should alert the physician's suspicion to the possibility of PVE.

• Normal prosthetic heart valve sounds

  • Mechanical valves: Tilting disc and bileaflet valves have a loud, high-frequency, metallic closing sound. This frequently can be heard without a stethoscope. Absence of this distinct closing sound is abnormal and implies valve dysfunction. These valves also may have a soft opening sound. Caged ball valves (Starr-Edwards) have low-frequency opening and closing sounds of nearly equal intensity.
  • Tissue valves: Closing sounds are similar to those of native valves. A low-frequency early opening sound may present in the mitral position.
  • Muffled or absent normal prosthetic heart sounds may be a clue to valve failure or thrombosis.
• Prosthetic heart valve murmurs

  • Aortic prosthetic valves: Because of their smaller orifice size, all aortic valves often produce some degree of outflow obstruction with a resultant systolic ejection murmur. Caged ball and small porcine valves produce the loudest murmurs. The intensity of the murmur increases with rising cardiac output. Tilting disc valves and bileaflet valves do not occlude their outflow tract completely when closed, allowing some back flow. This causes a low-intensity diastolic murmur. Suspect prosthetic aortic valve failure in a patient with a greater than 2/6 diastolic murmur. Caged ball and tissue valves cause no diastolic murmur since they completely occlude their outflow tract in the closed position. Consider any degree of diastolic murmur in these patients pathologic until proven otherwise.
  • Mitral prosthetic valves: Caged ball valves may cause a low-grade systolic murmur due to the turbulent flow caused by the cage projecting into the left ventricle. Consider any holosystolic murmur greater than 2/6 pathologic in a patient with an artificial mitral valve. Short diastolic murmurs may be heard with bioprostheses and, occasionally, with the St. Jude bileaflet valve. These are best heard at the apex with the patient in the left lateral decubitus position.
• Patients with acute valvular failure present with cardiogenic shock and severe hypotension.

  • Evidence of poor tissue perfusion is present, including diminished peripheral pulses, cool or mottled extremities, confusion or unresponsiveness, and decreased urine output.
  • A hyperdynamic precordium and right ventricular impulse is present in 50% of patients with acute valvular failure.
  • Absence of a normal valve closure sound or presence of an abnormal regurgitant murmur is an important clue to the presence of prosthetic valvular failure.
• Patients with subacute valvular failure often present with signs of gradually worsening left-sided congestive heart failure.

  • Rales and jugular venous distention may be present.
  • Patients with subacute valvular failure may present with a new regurgitant murmur or absence of normal closing sounds.
  • A new or worsening hemolytic anemia may be the only presenting abnormality in patients with subacute valvular failure.
• The clinical manifestations of PVE are often obscure.

  • Fever occurs in 97% of patients with PVE.
  • A new or changing murmur is present in 56% of patients. Absence of a murmur does not exclude the diagnosis. Valvular dehiscence, stenosis, or perforation causes the murmur. They may not occur early in the course of the illness.
  • Signs considered classic for native valve endocarditis, including petechiae, Roth spots, Osler nodes, and Janeway lesions, often are absent in PVE.
  • Splenomegaly supports the diagnosis but is present in only 26% of early PVE cases and in 44% of late PVE cases.
  • PVE may present as congestive heart failure, septic shock, or primary valvular failure.
  • Systemic emboli may be the presenting symptom in 7-33% of cases of PVE. This is more common with fungal etiologies.
• Thromboembolic complications: Patients with complications related to embolization present with signs related to the site of embolization. Stroke syndromes are the most common; however, patients may present with MI, sudden death, or visceral or peripheral embolization. Systemic embolization should alert the physician to suspect valve thrombosis or PVE.
• Anticoagulant-related hemorrhage: Signs due to anticoagulant-related hemorrhage depend on the site of hemorrhage.^{[3, 4]}

• Prosthetic valve endocarditis (PVE) has been divided into 2 subcategories. These reflect differences in clinical features, microbial patterns, and mortality. Early PVE occurs within 60 days of valve insertion, whereas late PVE occurs after 60 days.

  • Early PVE is usually the result of perioperative contamination. Causative organisms include Staphylococcus epidermidis (25-30%), Staphylococcus aureus (15-20%), gram-negative aerobes (20%), fungi (10-12%), streptococci (5-10%), and diphtheroids (8-10%).
  • Late PVE is usually the result of transient bacteremia from dental or genitourinary sources, GI manipulation, or intravenous drug abuse. The causative organisms are similar to those causing native valve endocarditis. These include Streptococcus viridans (25-30%), S epidermidis (23-38%), S aureus (10-12%), gram-negative bacilli (10-12%), group D streptococci (10-12%), fungi (5-8%), and diphtheroids (4-5%).
• Multiple negative blood culture results are unusual with common pathogens but often are seen more commonly with infections by the Haemophilus aphrophilus, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and Kingella kingae (HACEK) group; Serratia and Rickettsia species; as well as Aspergillus, Histoplasma, and Candida species.
• Rarely, Brucella can cause PVE.^[5]