ArticleCureus2022
Infective Endocarditis in Hypertrophic Obstructive Cardiomyopathy After Etonogestrel Implant Removal.
Article in Cureus, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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3 authors at 2 institutions in 1 country.
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Abstract
The modified Duke criterion "predisposing heart condition" is poorly defined, and is based on outdated studies of the epidemiology of infective endocarditis (IE). Hypertrophic obstructive cardiomyopathy (HOCM) is not classified as a modified Duke criterion for the diagnosis of IE but is associated with a higher incidence of IE nonetheless. The presence of a cardiovascular implantable electronic device (CIED) is independently associated with an increased risk of IE. Patients with HOCM may be candidates for the implantation of an automated internal cardiac defibrillator (AICD) for the prevention of sudden cardiac death. Previous studies of the risk of IE in patients with HOCM did not make a distinction for patients with CIEDs. We present a case of a 25-year-old female with HOCM and an AICD for primary prevention, who presented with sudden right-sided hemiplegia, aphasia, dysarthria, and a low-grade fever. CT angiography demonstrated large vessel occlusion of the terminal left internal carotid artery and proximal middle cerebral artery (MCA), prompting emergent treatment with mechanical thrombectomy, which achieved full recanalization and full reperfusion. Cardioembolic stroke was suspected. She had no arrhythmias, a transthoracic echocardiogram showed new mitral valve vegetation. The etiology of the stroke was determined to be septic emboli from mitral valve subacute bacterial endocarditis and two blood cultures grew staph epidermidis. Ten days prior to presentation, she had undergone removal of an etonogestrel implant in her arm, and this was the suspected source of initial bacteremia and valvular seeding. She was treated with a six-week course of vancomycin with improvement and maintained on daily minocycline as long as the AICD were to remain in place. Our patient started developing symptoms of endocarditis after the removal of her etonogestrel implant, had no other recent procedures, and had good dentition. Hence, we maintain that this was the likely source of her initial bacteremia that led to valvular seeding and resultant IE. This is the first reported case of etonogestrel implant removal-related endocarditis. Further studies of the association between etonogestrel implant removal, transient bacteremia, and valvular seeding leading to IE are warranted. Clinicians should be reminded of the increased risk of IE in patients with HOCM. Identifying HOCM patients at higher risk for IE, i.e. dilated left atrium and/or CIEDs is easier to accomplish with current cardiac imaging techniques.
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