INTRODUCTION

Cardiac infections are classified by the affected site: endocardium, myocardium, or pericardium. Although the terms pericarditis, myocarditis, and endocarditis refer to inflammation in general, most cases are secondary to infectious disease.

EPIDEMIOLOGY AND PATHOPHYSIOLOGY

Infective endocarditis (IE) affects the endocardium, though inflammation may damage the cardiac valves themselves, as well as the underlying myocardium. IE more commonly affects the left side of the heart, more commonly affects males (2:1), and increases in incidence with age. The pathogenic agent is usually bacterial but may also be fungal, rickettsial, or protozoan, particularly in immunocompromised patients.

Infective endocarditis occurs when circulating pathogens adhere to the endocardium in areas of turbulent flow, particularly around cardiac valves. Host susceptibility is an integral part of the pathophysiology. Several decades ago, rheumatic fever was the most common cause of valvular lesions, and bacterial adherence to these damaged valves could occur in any age group. Now, congenital heart disease and degenerative valvular disease are the most common predisposing factors to IE, in children and the elderly, respectively. An increasing percentage of cases arise from prosthetic heart valves, which have enhanced susceptibility to infection.

When bacteremia is frequent, adherence to the endocardium may occur even in the absence of a valvular lesion, and intravenous drug users, immunocompromised patients, and those with indwelling vascular catheters or poor dental hygiene are at greater risk for IE.