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A 58-year-old homeless male with a history of hypertension and dyslipidemia presented with complaints of 4-weeks of worsening substernal chest pain, dyspnea, fevers and night sweats. Initial electrocardiogram showed 2 mm of ST-segment elevation in leads V2-V4 consistent with an anterior ST elevation myocardial infarction (STEMI).Emergent coronary angiography showed a filling defect within the mid left anterior descending artery (LAD) with 80% stenosis and TIMI grade 3 flow. Manual aspiration thrombectomy did not retrieve any debris. Subsequent angiography showed no change to the appearance of the stenosis. Percutaneous coronary intervention (PCI) was performed with placement of a drug eluting stent. Hemodynamics revealed a mean aortic valve (AV) gradient of 32 mmHg. Transthoracic echocardiography showed severely thickened AV leaflets with mobile elements consistent with vegetation, moderate AV stenosis and mild to moderate AV regurgitation. Transesophageal echocardiography showed multiple bulky mobile calcific densities on the AV. Serial blood cultures were repeatedly negative. Further evaluation for culture-negative endocarditis revealed a Bartonella henselae IgG Titer 1:512 and a positive Bartonella quintana DNA PCR. An MRI of the brain showed numerous foci of acute and subacute emboli. The patient received combination antibiotic therapy and subsequently underwent surgical bioprosthetic aortic valve replacement with single vessel coronary artery bypass grafting to the LAD.We report a unique case of anterior STEMI as the presenting manifestation of culture negative infectious endocarditis. To our knowledge, this is the first reported case of Bartonella endocarditis resulting in septic coronary embolism. Best practices in the management of septic coronary embolism are not well defined, with overall low success rates of thrombolytic therapy and primary PCI and a high overall 30-day mortality. At the time of presentation, coronary angiography showed TIMI grade 3 flow, and a conservative approach may have been indicated given the angiographic appearance of the lesion. A focus on organism identification and antibiotic therapy with early surgical management may have been a more optimal approach given the mechanism of myocardial injury.

Introduction:There is significant evidence suggesting the predictive value of worsening carotid artery stenosis. We examined the impact of disease progression in patients with asymptomatic carotid artery stenosis on the incidence of ischemic stroke.Hypothesis:We believe carotid artery disease progression is a risk factor for ischemic stroke.Methods:We retrospectively evaluated 499 carotid artery doppler ultrasounds (CDU) without severe ICA stenosis at baseline performed at a single academic medical center between 2008 and 2011. The studies analyzed all had at least one subsequent CDU 11 months later for evaluation of disease progression. Symptomatic patients (stroke or TIA within 6 months) and carotid arteries with prior intervention were excluded. Baseline demographic and clinical data were recorded. Progression on CDU was defined as progression of disease to a higher category of stenosis that was at least 50% (moderate [50-79%], severe [80-99%], or occluded [100%]). The primary outcome assessed was the incidence of ipsilateral ischemic stroke as diagnosed with radiography (CT or MRI). Univariate logistic regression analysis was performed to evaluate for differences in the incidence of stroke between those CDU with and without evidence of disease progression.Results:Of the 499 CDU evaluated, 408 were negative for progression, while 91 showed evidence of disease progression. Those with disease progression did not have a significant increase in the incidence of stroke as compared to those without progression (1.1% vs 3.69%, P = 0.206).Conclusions:Carotid artery stenosis progression does not appear to have a significant role in the incidence of ipsilateral ischemic stroke. Thus, our study suggests the importance of investigating other factors that may better predict the risk for stroke in patients with asymptomatic carotid artery stenosis at baseline.