Prosthetic Heart Valves Clinical Presentation

Updated: Jan 03, 2022
  • Author: Kirtivardhan Vashistha, MBBS; Chief Editor: Richard A Lange, MD, MBA  more...
  • Print


In patients with malfunctioning prosthetic heart 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.

Note the following:

  • 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 the patient's 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 sudden onset of dyspnea, syncope, or precordial pain.

  • Patients with acute aortic valve failure often experience sudden death. Survivors 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 the embolization. Stroke syndromes are the most common presentation, although patients may present with myocardial infarction, sudden death, or symptoms of visceral or peripheral embolization.

  • Symptoms due to anticoagulant-related hemorrhage are related to the site of the hemorrhage.

  • A history of fever should raise clinical suspicion of the possibility of prosthetic valve endocarditis: Be alert to fever, chills, fatigue, malaise, night sweats, signs and symptoms of heart failure, dyspnea, cough, pleuritic chest pain, new or changed heart murmur on auscultation, splenomegaly, septic shock or primary valvular failure, and/or septic emboli.

  • Hemolysis secondary to prosthetic valve: Note symptoms secondary to anemia and/or thrombocytopenia, such as pallor, dyspnea, bleeding and petechiae.

Physical Examination

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 may also 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 of tissue valves are similar to those of native valves. A low-frequency early opening sound may present in the mitral position.

Valve failure/thrombosis

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 because 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.

Acute valvular failure

Patients with acute valvular failure present with cardiogenic shock and severe hypotension. Note the following:

  • 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 the presence of an abnormal regurgitant murmur is an important clue to the presence of prosthetic valvular failure.

Subacute valvular failure

Patients with subacute valvular failure often present with signs of gradually worsening left-sided congestive heart failure, including the following:

  • Rales and jugular venous distention may be present.

  • Signs of right-sided failure, including hepatic congestion and lower extremity edema, may also 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.

Prosthetic valve endocarditis (PVE) manifestations

The clinical manifestations of PVE are often obscure. Note the following:

  • 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, are often absent in PVE.

  • Splenomegaly supports the diagnosis of PVE, but it 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 myocardial infarction, sudden death, or visceral or peripheral embolization. Systemic embolization should alert the clinician to suspect valve thrombosis or PVE.

Anticoagulant-related hemorrhage: Signs due to anticoagulant-related hemorrhage depend on the site of hemorrhage. [20, 21]