pg. E1 - E2
ABSTRACT: Infective endocarditis is one of the uncommon causes of complete atrioventricular (AV) block. Complications from aortic valve infection are more often associated with conduction abnormalities than with mitral valve endocarditis. In fact, complete AV block rarely occurs in mitral valve infections, with only a few cases having been reported. We report a case of mitral valve endocarditis in which the initial presentation was fever and newly developed, complete AV block. Patients with mitral valve endocarditis complicated by complete AV block are at high risk. Prompt investigation, administration of appropriate antibiotics and consideration of early surgical intervention are needed.
J INVASIVE CARDIOL 2010;22:E1–E2
Key words: AV block, Infective endocarditis
There are a number of etiologies responsible for newly diagnosed complete atrioventricular (AV) block. These include myocardial infarction, drug toxicity and myocarditis.1,2 Complication of infective endocarditis has been well described as one of the uncommon causes of this cardiac abnormality.1–3 Aortic valve endocarditis is more common, and is more often associated with conduction abnormality than is mitral valve endocarditis.1,2 In fact, high-grade conduction abnormality, especially complete AV block, is a rare presentation in patients with mitral valve infection.1,2,4 We report a case of mitral valve endocarditis in which the initial presentation was fever and complete AV block.
Case Report. A 78-year-old male presented to the emergency room with back pain and fever. His physical examination was remarkable for fever of 101 degrees Fahrenheit and tenderness in his back upon palpation at the vertebral level of T8–T10. He had no documented heart murmur or peripheral sign of infective endocarditis. His electrocardiogram (ECG) showed complete AV block, with a heart rate of 67 bpm (Figure 1). A blood culture was obtained, and the results showed methicillin-resistant Staphylococcus aureus (MRSA) in all samples. Urgent transesophageal echocardiography (TEE) revealed vegetations on the anterior mitral leaflet and partly in the intervalvular fibrosa area, as well as moderate mitral regurgitation (Figure 2). Magnetic resonance imaging (MRI) of his spine showed osteomyelitis of the thoracic spine at the level of T10–T12. He was treated with vancomycin and gentamicin for MRSA endocarditis and osteomyelitis. A surgical option was offered to the patient, but he refused it.
Discussion. Though disturbance of the cardiac conduction system is one of the possible complications of infective endocarditis, this conduction abnormality is rarely associated with infective endocarditis (1–15% of cases), at a rate which varies among studies.2,3,5 Moreover, it may represent the extension of an infection from the valve leaflets into the surrounding myocardium.1,6 These extravalvular extensions result from the development of aneurysms, intracardiac fistulas, valve dehiscence, and, most commonly, expansion of the infection to areas adjacent to the valve ring.1,2,7 Perivalvular extension is known to occur in 10–40% of all cases of native valve endocarditis and in 56–100% of prosthetic valve endocarditis cases.1–3 Perivascular extension and conduction abnormality occur more frequently in aortic valve endocarditis than in mitral valve endocarditis.1,2 This is inferred from the fact that, though the AV node lies adjacent to the mitral valve, the right and left bundle branches are anatomically more closely related to the aortic valve (Figure 3).1 The mechanisms that contribute to the development of this conduction abnormality are, indeed, anatomical destruction by the abscess, or the extension of inflammation and edema, which cause physiological interruption of the cardiac conduction system.2
Mitral valve endocarditis that expands to perivalvular tissue can cause supraventricular arrhythmias, as well as first-degree and second-degree AV block.1,2,4,8 Rarely, infection of the mitral valve is associated with nearly complete or complete AV block, with only a few cases reported.1,2,4 According to the literature, a new AV block has an overall positive predictive value of 66%, a specificity of 89%, and a sensitivity of 28% to 45% for identifying perivalvular extension in patients with infective endocarditis.2,6 Transthoracic echocardiography has a sensitivity of only 18–60%, while TEE is far more sensitive (76%) and specific (94%) for detecting perivalvular extension.1–3 As a result, TEE should be considered in all patients who have high-risk clinical features for developing this complication.2,3
Persistent conduction abnormality in native valve endocarditis, even after adequate antibiotic treatment, is a poor prognostic sign, and is often associated with invasive infection, hemodynamic deterioration due to valve dysfunction and a high mortality rate.1,2 The guidelines from the American Heart Association (AHA) and the American College of Cardiology (ACC) suggest that surgery for patients with endocarditis complicated by AV block is warranted and should be considered.9 It is worth mentioning that there is no prospective, randomized, controlled trial data on the subject of timing of surgery for patients with infective endocarditis; recommendations have been derived primarily from expert consensus.9,10
In conclusion, a physician whose patient has fever and newly developed AV block should be alert to the possibility of infective endocarditis with perivalvular extension. This mandates urgent evaluation with TEE, and investigation for perivalvular extension should not be limited only to the aortic valve area. Patients with mitral valve endocarditis and new onset of complete AV block are at high risk. Prompt administration of appropriate antibiotics and consideration of early surgical intervention are needed to decrease the morbidity and mortality associated with this condition.
From the Division of Cardiology and Department of Medicine, St. Vincent Hospital, Worcester, Massachusetts.
The authors report no conflicts of interest regarding the content herein.
Manuscript submitted June 9, 2009, provisional acceptance given August 4, 2009, final version accepted August 31, 2009.
Address for correspondence: Danai Kitkungvan, MD, Department of Medicine, St. Vincent Hospital, 123 Summer Street, Worcester, MA 01608. E-mail: kitkungvan@hotmail.com
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