Infective endocarditis

Introduction

The investigation and management of infective endocarditis in the developed world have changed radically over the past 30 years.1 Non-invasive imaging, molecular science, diagnostic protocols, and curative surgery have all become commonplace, yet the incidence remains unchanged and annual mortality approaches 40%.2

The lack of impact of modern medicine reflects important changes in the causes of the disease. In Western populations in particular, chronic rheumatic heart disease is now an uncommon antecedent, whereas degenerative valve disease in elderly people, intravenous drug misuse, preceding valve replacement, or vascular instrumentation have become increasingly frequent, coinciding with an increase in staphylococcal infections and those due to fastidious organisms. Furthermore, previously undetected pathogens are now being identified with the disease, and multidrug resistant bacteria challenge conventional treatment regimens. Meanwhile, rheumatic valve disease remains endemic in the developing world, where modern investigations and management are the privilege of the well off few who live in large urban areas.3 ^{w1 w2} In this review, we outline the modern understanding, investigation, and management of this perplexing and enigmatic condition.

Who gets infective endocarditis?

The incidence of infective endocarditis is approximately 1.7-6.2 cases per 100 000 patient years,6 although rates are higher in at risk cohorts such as intravenous drug users.^w3 Men are more often affected than women (in a ratio of 2:1), and the incidence progressively increases with age. Underlying degenerative aortic and mitral valve disease now predominate over rheumatic disease,^w4 although in one recent French study 47% of patients with infective endocarditis presented without previous knowledge of an underlying cardiac disorder.7 The relation to dental surgery has been overemphasised in the past, and infective endocarditis is now more likely in the context of previous valve surgery or as a consequence of iatrogenic or nosocomial infection.8

What is the underlying pathophysiology?

Ulceration on the valvular endothelial surface promotes …