Diagnosing prosthetic valve endocarditis with echocardiography

Prosthetic valve endocarditis (PVE) is a microbial infection of the valve. How do you diagnose PVE with ultrasound? Why do you need to differentiate between early and late PVE? When do patients need surgical treatment? Find out in this lesson presented by Samir Sulemane, a Senior Clinical Scientist and echocardiography expert at Royal Brompton and Harefield NHS Trust, UK.

Echocardiography of prosthetic heart valves is much more demanding, both to perform and to interpret, compared to the assessment of native heart valves. Learn how to use tools such as 2D, 3D, and transesophageal echocardiography in order to become a skilled decision-maker who can confidently talk to any cardiologist or cardiac surgeon about your patient’s prosthetic valve problem.

Is your patient’s prosthetic valve in tip-top shape? Master echo to thwart complications and confidently assess their valves.

Prosthetic valve endocarditis (or PVE) is a microbial infection of the valve. The lesions (called vegetations) consist of fibrin, platelets, and infectious microorganisms. In this Medmastery lesson, you'll learn how to interpret echocardiography findings to diagnose and treat PVE. PVE is classified as early or late, depending on when the infection occurs. Early PVE results from a bacterial infection acquired in the operating room and involves direct contamination of the valve or annulus. The mortality rate is very high, at around 70%.

But these infections should be prevented with stringent antiseptic techniques. Light PVE occurs when bacteria, fungi, or other germs from another part of your body, such as your mouth, spread through your bloodstream and attach to the prosthetic valve. This is observed in 25 to 80% of patients with PVE, with the most frequent causes being dental procedures, neurological infections, and urinary catheters. The cutoff point between early and late PVE is one year because of significant differences in the microbiology observed within the first year compared with after the first year. Prostheses made from metal or carbon prevent the appearance of microorganisms.

So infections in these valves generally originate from the sewing ring or thrombi located near the sewing ring. For bio-prosthetic valves, the infection is usually restricted to the leaflets. If the sewing ring is involved, the pathogenesis and clinical course are similar to PVE involving mechanical prosthesies. Staphylococci, streptococci, and enterococci are the main types of bacteria that cause PVE. The treatment of PVE depends on several aspects. If there are no contraindications, antibiotics are always the first treatment of choice.

Additionally, surgical removal and consequent re-replacement of the prosthetic valve is recommended if: the vegetation is larger than 10 millimeters, the vegetation is highly mobile, or the patient has sepsis persisting for more than 48 hours, despite effective antibiotic treatment guided by blood cultures.

Regarding treatment with antibiotics, PVE is typically associated with larger vegetations than those found in native valve endocarditis. So antibiotics must be given in high enough dosages to achieve maximum non-toxic serum concentrations that penetrate the vegetations. The duration of treatment is based on the vegetation size assessed by echocardiography and the minimal inhibitory concentrations (or MIC). This is the lowest concentration that will inhibit the visible growth of a microorganism.

For example, if the vegetation is less than 4 millimeters, the MIC should be between 2 and 0.1 microgram per millimeter. If the MIC was more than 4, antibiotic cure would be unlikely. And if the vegetation is more than 10 millimeters, the MIC has to be between 0.5 and 0.1 microgram per millimeter, or antibiotic cure would be unlikely. This 77-year-old gentleman underwent the Ross procedure to replace his diseased aortic valve with his own pulmonary valve. He was admitted to our center with positive blood cultures for a Staphylococcus epidermidis.

A large, highly mobile vegetation was present on the pulmonary valve. There were no contraindications for antibiotics, so the patient was given five weeks of antibiotic treatment, but they eventually had to be stopped due to signs of kidney damage. His mean pressure gradient was 27.53 millimeters of mercury, which suggested severe pulmonic stenosis secondary to endocarditis, and significant pulmonic regurgitation was also observed. Consequently, he was re-referred to the cardiac surgical team for a redo of the pulmonic valve. Diagnosing PVE with echocardiography requires examining the valve in different views, and clinical testing should be performed when a mobile vegetation is observed. The presence of stenosis or regurgitation is highly likely with PVE. So these should also be thoroughly assessed.