After an initial attack and the generation of immunologic memory, patients are increasingly vulnerable to disease reactivation with any subsequent streptococcal infections. Carditis is likely to worsen with each recurrence, and the damage is cumulative. However, chronic rheumatic carditis usually is not clinically evident until years or even decades after the initial episode of rheumatic fever. At that time, the signs and symptoms of valvular disease depend on which cardiac valve(s) is involved. In addition to various cardiac murmurs, cardiac hypertrophy and dilation, and CHF, patients with chronic rheumatic heart disease often have arrhythmias (particularly atrial fibrillation in the setting of mitral stenosis), and thromboembolic complications due to atrial mural thrombi. In addition, scarred and deformed valves are more susceptible to infective endocarditis. The long-term prognosis is highly variable. In some cases, a relentless cycle of valvular deformity ensues, yielding hemodynamic abnormality, which begets further deforming fibrosis. Surgical repair or replacement of diseased valves—mitral valvuloplasty—has greatly improved the outlook for patients with rheumatic heart disease.
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Infective endocarditis (IE) is a microbial infection of the heart valves or the mural endocardium that leads to the formation of vegetations composed of thrombotic debris and organisms, often associated with destruction of the underlying cardiac tissues. The aorta, aneurysmal sacs, other blood vessels, and prosthetic devices also may become infected. Although fungi, rickettsiae (agents of Q fever), and chlamydial species can cause endocarditis, the vast majority of cases are caused by extracellular bacteria.
Infective endocarditis is classified into acute and subacute forms based on the tempo and severity of the clinical course; the distinctions are related to the virulence of the responsible microbe and whether underlying cardiac disease is present. Of note, a clear delineation between acute and subacute endocarditis is not always possible, and many cases fall somewhere along the spectrum between the two forms.
Acute endocarditis refers to tumultuous, destructive infections, frequently involving a highly virulent organism attacking a previously normal valve. It is associated with of substantial morbidity and mortality, even with appropriate antibiotic therapy and/or surgery.
Subacute endocarditis refers to infections by organisms of low virulence affecting a previously abnormal heart, especially scarred or deformed valves. The disease typically appears insidiously and—even if untreated— follows a protracted course of weeks to months; most patients recover after appropriate antibiotic therapy.
Infective endocarditis can develop on previously normal valves, but cardiac abnormalities predispose to such infections; rheumatic heart disease, mitral valve prolapse, bicuspid aortic valves, and calcific valvular stenosis are all common substrates. Prosthetic heart valves (discussed later) now account for 10% to 20% of all cases of IE. Sterile platelet-fibrin deposits at sites of pacemaker lines, indwelling vascular catheters, or endocardium damage by flow “jets” stemming from preexisting cardiac disease all can be foci for bacterial seeding and development of endocarditis. Host factors such as neutropenia, immunodeficiency, malignancy, diabetes mellitus, and alcohol or intravenous drug abuse also increase the risk for IE and adversely affect outcomes.