Rapid expansion of mycotic aneurysm of left coronary sinus of Valsalva causing myocardial ischemia: report of a case.

We described a 71-year-old female of aneurysm of the left sinus of Valsalva from mycotic origin. She underwent aortic valve replacement 11 years ago. Repeated CT scans showed rapidly growing aneurysm below the left coronary ostium. On sixth day after the admission, she suddenly developed myocardial ischemia complicated with ventricular fibrillation. The patient was treated with emergent aortic root replacement and she recovered. We recommend emergent surgical repair of mycotic saccular aneurysm of the left sinus of Valsalva because a delay of surgery could be fatal.

CD36/SR-B2-TLR2 Dependent Pathways Enhance Porphyromonas gingivalis Mediated Atherosclerosis in the Ldlr KO Mouse Model.

There is strong epidemiological association between periodontal disease and cardiovascular disease but underlying mechanisms remain ill-defined. Because the human periodontal disease pathogen, Porphyromonas gingivalis (Pg), interacts with innate immune receptors Toll-like Receptor (TLR) 2 and CD36/scavenger receptor-B2 (SR-B2), we studied how CD36/SR-B2 and TLR pathways promote Pg-mediated atherosclerosis. Western diet fed low density lipoprotein receptor knockout (Ldlr°) mice infected orally with Pg had a significant increase in lesion burden compared with uninfected controls.This increase was entirely CD36/SR-B2-dependent, as there was no significant change in lesion burden between infected and uninfected Cd36o/Ldlro mice [corrected]. Western diet feeding promoted enhanced CD36/SR-B2-dependent IL1ß generation and foam cell formation as a result of Pg lipopolysaccharide (PgLPS) exposure. CD36/SR-B2 and TLR2 were necessary for inflammasome activation and optimal IL1ß generation, but also resulted in LPS induced lethality (pyroptosis). Modified forms of LDL inhibited Pg-mediated IL1ß generation in a CD36/SR-B2-dependent manner and prevented pyroptosis, but promoted foam cell formation. Our data show that Pg infection in the oral cavity can lead to significant TLR2-CD36/SR-B2 dependent IL1ß release. In the vessel wall, macrophages encountering systemic release of IL1ß, PgLPS and modified LDL have increased lipid uptake, foam cell formation, and release of IL1ß, but because pyroptosis is inhibited, this enables macrophage survival and promotes increased plaque development. These studies may explain increased lesion burden as a result of periodontal disease, and suggest strategies for development of therapeutics.

Right-sided infective endocarditis with a ruptured sinus of Valsalva and multiple septic pulmonary emboli in a patient with atopic dermatitis.

We herein report the case of 34-year-old woman with acute tricuspid valve infective endocarditis (IE) associated with a ruptured sinus of Valsalva and multiple septic pulmonary emboli. She had no history of medical problems, except for atopic dermatitis (AD). Blood cultures identified methicillin-sensitive Staphylococcus aureus. Despite the administration of two months of antibiotic therapy, the patient experienced recurrent pulmonary emboli and developed heart failure due to a left-to-right shunt, whereas the area of vegetation did not change in size. She subsequently underwent surgery for shunt closure and tricuspid valve replacement. The AD was thought to be the cause of the patient's bacteremia, which consequently resulted in aggressive right-sided IE.

A single infection with Chlamydia pneumoniae is sufficient to exacerbate atherosclerosis in ApoE deficient mice.

Several studies have demonstrated a strong link between Chlamydia pneumoniae (Cp) infection and atherosclerosis progression/exacerbation. Here, we try to understand whether a single administration of Cp could exacerbate atherosclerosis. Apoe(-/-) mice were intranasally infected with Cp followed by a high fat diet. Mice were sacrificed at different time points after Cp infection to monitor the development of the atheroma. Cp infection increased lipid content in the aortic sinus of Apoe(-/-) mice starting from 8 weeks. This was associated with increased numbers of active myeloid dendritic cells and plasmacytoid DCs which were co-localized with T-cells in the atherosclerotic plaque. The serum levels of IFN-γ showed a Th1-like environment typical of atherosclerosis. In conclusion, we demonstrate that one dose of Cp could exacerbate atherosclerotic lesion development, triggering innate immune cell accumulation early on that allowed the involvement of Th1-like cells in the exacerbation of the atherosclerotic plaque at later time points.

Pseudoaneurysm of the sinus of Valsalva with coronary artery compression as the primary manifestation of infective endocarditis: a case report.

A pseudoaneurysm of the native sinus of Valsalva compressing a coronary artery is extremely rare. Herein, the case is reported of infective endocarditis with a pseudoaneurysm of the sinus of Valsalva compressing the right coronary artery as the primary diagnostic finding, and its successful treatment. It is suggested that patients with suspected pseudoaneurysms of the sinus of Valsalva should undergo cardiac computed tomographic angiography for diagnosis of this condition.

Endocarditis with ruptured sinus of Valsalva aneurysm caused by nonvaccine Streptococcus pneumoniae serotype 21.

Sinus of Valsalva aneurysm is a rare, catastrophic complication of endocarditis. We report an unusual case of ruptured sinus of Valsalva aneurysm associated with endocarditis that was caused by Streptococcus pneumoniae serotype 21. The patient, a 12-year-old girl, underwent surgical repair of the aneurysm and was given intravenous antibiotics for 6 weeks. She was doing well at the 6-week follow-up visit. This case is unusual because of the patient's young age at presentation, the absence of predisposing factors, and the isolation of a nonvaccine serotype 21, which revealed the epidemiologic changes of invasive pneumococcal disease. To our knowledge, this is the first reported case of endocarditis caused by this S. pneumoniae serotype.

Rupture of non-coronary sinus of valsalva with infective endocarditis of naive tricuspid valve presenting with recurrent ill-sustained ventricular tachycardia.

Infective endocarditis affecting the tricupid valve due to rupture of non-coronary sinus of Valsalva is distinctly rare. We are reporting such a rare case, presenting with recurrent ill sustained ventricular tachycardia.

Surgically treated infective endocarditis involving the aortic bicuspid valve and ventricular septum revealing aortic regurgitation and a Gerbode defect.

A 41-year-old man who had been previously diagnosed with bicuspid aortic valve presented to our hospital with repeating episodes of fever. Echocardiography revealed vegetation in the bicuspid valve as well as left-to-right shunt, making one suspicious of rupture of the sinus of Valsalva. Under the diagnosis of infective endocarditis of the aortic valve and rupture of the sinus of Valsalva, the patient underwent a surgical operation. Operative findings showed normal sinus of Valsalva; but a communication between the left ventricle and right atrium was present, suggesting a Gerbode defect. The patient was treated by autologous pericardial patch closure and aortic valve replacement and was dismissed from the hospital without major complications.

Aortocavitary fistula without aneurysm and transient incomplete atrioventricular block due to infective endocarditis.

A 67-year-old man with persistent fever and moderate aortic valve regurgitation was transferred. He suffered from incomplete atrioventricular block (AVB), and temporary pacing was needed. Left-to-right shunt flow from the aorta to the right atrium was found without an aneurysm. Operative findings indicated that the aortic valve was highly calcified. The orifice of an aortocavitary fistula (ACF) was detected in the sinus of Valsalva and the right atrium. Patch repair of the aortic annulus with complete débridement of the abscess cavity was performed, a procedure that consisted of aortic valve replacement directly to the Gore-Tex patch and aortic root replacement. His postoperative course was uneventful, but a pacemaker was implanted owing to complete AVB. To our knowledge, this is a rare case in which infective endocarditis was complicated by ACF without an aneurysm of the sinus of valsalva (SV) on the noncoronary cusp to the right atrium and transient incomplete AVB (Mobitz type II) occurring simultaneously.

Chlamydia pneumoniae infections augment atherosclerotic lesion formation: a role for serum amyloid P.

Multiple reports have demonstrated an association between Chlamydia pneumoniae (Cpn) and cardiovascular disease. In this study we evaluated the effect of Cpn infections on early lesion progression in C57BL/6J mice. Since plaque formation in these mice does not develop past the initial stage, we thought these mice might be a better model for unravelling the effect of Cpn infection on early lesion type progression. C57BL/6J mice were fed an atherogenic diet and injected 10 times with 5 x 10(7) IFU Cpn or mock. At sacrifice, lesion number, size and type were analysed. To study the role of Cpn in inflammation, serum amyloid P (SAP) in plasma was determined as well as T-cells, macrophages and SAP in the lesions. In the aortic sinus of both groups, type 2 lesions were found. Cpn infection resulted in a 2.2-fold increase in total lesion size (Cpn: 10821+/-2429 microm(2)vs mock: 5022+/-1348 microm(2); p=0.04). No difference in lesion number was observed. Also, Cpn infection increased SAP in the lesions from 1.10(-4)+/-0.1.10(-4) SAP-positive cells/lesion area to 10.10(-4)+/-1.10(-4) SAP-positive cells/lesion area (p=0.05). The influx of T-lymphocytes and macrophages in the lesions as well as SAP plasma levels were not different between groups. Multiple Cpn infections resulted in a significant increase in total lesion size of C57BL/6J mice. Increase in total SAP-positive area in infected mice suggests a role for this acute-phase protein in lesion enlargement.

Experimental infective endocarditis induced by human supragingival dental plaque in rats.

Human dental plaque is thought to contribute to disease, not only in the oral cavity but also at other body sites. To investigate the pathogenicity of dental plaque in tissues remote from the mouth, we examined the ability of human supragingival dental plaque to induce infective endocarditis (IE) in rats. In total, 15 out of 27 catheterized rats survived after intravenous injections with human supragingival dental plaque suspensions containing 3 x 10(6) colony-forming units (CFU) of bacterial cells. In surviving rats, infected vegetations were formed in all except one rat. The microbial composition of the infected vegetations was different from that of the respective dental plaque inocula, with Streptococcus oralis comprising the majority of the isolates. In rats affected with endocarditis, the aortic sinus was filled with fibrinous vegetation containing bacteria. Inflammatory cells infiltrated the aortic valve, the aorta adjacent to the valve, and the cardiac muscles. The inoculation of catheterized rats with a cell suspension of S. oralis isolate (5 x 10(6) CFU) was not lethal but capable of inducing endocarditis in all animals. The results suggest that if dental plaque were introduced into the bloodstream, it could serve as a potent source of bacteria causing IE in humans.

Infective endocarditis resulting in rupture of sinus of Valsalva with a rupture site communicating with both the right atrium and right ventricle.

This report describes a patient with a rupture of the noncoronary sinus of Valsalva caused by erosion of its wall by a large right atrial vegetation not attached to the tricuspid valve without aortic valve involvement. The rupture site was located right posterior to the tricuspid septal leaflet and communicated both with the right atrium and the right ventricular inflow tract, resulting in a significant left-to-right shunt leading to severe right heart failure and shock. The diagnosis was made by transthoracic and transesophageal echocardiography. To our knowledge no similar case has been reported in the literature.

Echocardiographic features of an unruptured mycotic aneurysm of the right aortic sinus of Valsalva.

This report describes a 25-year-old man with a pierced tongue in whom Streptococcus constellatus endocarditis of the aortic valve developed. Bacterial endocarditis in this patient was complicated by the development of a mycotic aneurysm of the right aortic sinus of Valsalva. Transthoracic and transesophageal echocardiographic studies were useful for the diagnosis of this rare lesion. Findings were confirmed at operation.

Rupture of a sinus of Valsalva aneurysm due to Aspergillus endocarditis.

We report a case of rupture of an acquired sinus of Valsalva aneurysm secondary to Aspergillus endocarditis in a patient with chronic lymphocytic leukaemia and idiopathic thrombocytopaenia purpura. Despite adequate repair and haemodynamic correction, with an apparent excellent initial result, the patient died of overwhelming sepsis at twelve days postoperatively. This case demonstrates an unusual cause of rupture of a sinus of Valsalva aneurysm and the morbidity associated with immunological dysfunction in the post-operative period.

An unusual case of Q fever endocarditis.

We describe a patient with unusual features of Q fever endocarditis. The unusual features of this case were the presence of an abscess surrounding the involved aortic valve and the appearance of circulating anticoagulants in the patient's serum.