Antithrombotic Therapy for Cerebrovascular Disorders: Infective (Bacterial) Endocarditis

Antithrombotic Therapy for Cerebrovascular Disorders: Infective (Bacterial) EndocarditisInfective (Bacterial) Endocarditis
The prevalence of embolic stroke in patients with infective endocarditis is about 20% in recent series, surprisingly similar to older reports despite important changes in the clinical spectrum of endocarditis. In 1 recent large series, the majority of emboli occurred during uncontrolled infection (at presentation or within 48 h of admission), with a stroke risk of only 2-6% during the remainder of the acute course. No strokes occurred in 38 patients with prosthetic valve endocarditis once infection was controlled (usually within 48 h of admission). Recurrent stroke after initial event occurred at a rate of 0.5%/day in native valve endocarditis, with recurrence often heralding relapse/uncontrolled infection. Strokes were usually small to moderate in size and tended to be single, unifocal in nonvirulent infections, and multiple, multifocal in Staphylococcus aureus endocarditis. Embolism risk was not related to valve site in native mitral and aortic endocarditis but was higher in patients withStaph aureus endocarditis and in patients with mechanical prosthetic valves (Table 6). The stroke risk with Staph aureus endocarditis of native mitral and/ or aortic valves appears to be lower in addicts (16%) than in nonaddicts (33%). While previous studies have linked the presence of valvular vegetations detected echocardiographically to an increased risk of emboli, 2 recent studies failed to confirm this association. When only late emboli (48 h or more after admission) were considered, 15% of patients with vegetations experienced embolism compared with 7% of those without vegetations. Careful review of recent data suggests that control of infection causes a dramatic decrease in the risk of embolism in infective endocarditis. There appears to be little role for anticoagulation in patients with native valve endocarditis. there
Mycotic aneurysm rupture complications occur during the acute course of infective endocarditis in fewer than 2% of patients. The most frequent mechanism of brain hemorrhage is pyogenic erosion of an arterial wall in patients with Staph aureus endocarditis, occurring in about 20% of these patients during uncontrolled infection.
Table 6—Prevalence of Embolism and CNS Hemorrhage in Infective Endocarditis

N % Stroke % Non-CNS Emboli % Brain Hemorrhage
Native mitral 59 19 10 3
Native aortic 61 16 11 8
Native mitral and aortic 13 31 15 15
All mitral and/or aortic 133 19 11 7
Staphylococcus aureus 36 28 8 17
Nonvirulent Streptococcus 69 13 13 3
Tricuspid 33 6 0 0
Bioprosthetic valve 17 12 6 12
Mechanical prosthetic valve 21 29 14 10