Haemophilus Parainfluenzae mural endocarditis with large atrial septal defect and peripheral embolization.

Mural endocarditis is a rare subclass of infective endocarditis (IE) associated with intra-cardiac tumors, prosthesis, valvular vegetation's, or structural abnormalities such as ventricular septal defects. Bacteria classified as HACEK (Haemophilus species, Aggregatibacter actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and Kingella kingae) are rare causes of IE found in only 1.3% to 10% of cases. We describe the second reported case of mural endocarditis involving the left ventricle (LV) caused by a Haemophilus species. A young male with no prior intravenous drug use, valvular heart disease, or recent dental work presented with splenic infarcts. H. para-influenza was identified on blood cultures. Cardiac imaging revealed a 1.5 cm LV mass underneath the posterior leaflet of the mitral valve and a large Atrial Septal Defect (ASD). Awaiting surgery, the patient sustained embolic and hemorrhagic cerebral events. The patient underwent debulking of LV mass, ASD closure, and mitral valve repair complicated by post-pericardiotomy syndrome, and he completed six weeks of ceftriaxone therapy. The patient met modified Duke Criteria, but the diagnosis was challenging due to absence of risk factors, sub-acute symptom onset, delayed blood culture growth, and ambiguous characterization of the mass on imaging. .

Cellularity and structure of fresh human coronary thrombectomy specimens; presence of cells with markers of progenitor cells.

Acute coronary syndromes and acute myocardial infarctions are often related to plaque rupture and the formation of thrombi at the site of the rupture. We examined fresh coronary thrombectomy specimens from patients with acute coronary syndromes and assessed their structure and cellularity. The thrombectomy specimens consisted of platelets, erythrocytes and inflammatory cells. Several specimens contained multiple cholesterol crystals. Culture of thrombectomy specimens yielded cells growing in various patterns depending on the culture medium used. Culture in serum-free stem cell enrichment medium yielded cells with features of endothelial progenitor cells which survived in culture for a year. Immunohistochemical analysis of the thrombi revealed cells positive for CD34, cells positive for CD15 and cells positive for desmin in situ, whereas cultured cell from thrombi was desmin positive but pancytokeratin negative. Cells cultured in endothelial cell medium were von Willebrand factor positive. The content of coronary thrombectomy specimens is heterogeneous and consists of blood cells but also possibly cells from the vascular wall and cholesterol crystals. The culture of cells contained in the specimens yielded multiplying cells, some of which demonstrated features of haematopoietic progenitor cells and which differentiated into various cell-types.

An inflammatory pathway of IFN-gamma production in coronary atherosclerosis.

Inflammation is associated with the pathogenesis of coronary atherosclerosis, although the mechanisms remain unclear. We investigated whether cytokine secretion by innate immune responses could contribute to the production of proarteriosclerotic Th1-type cytokines in human coronary atherosclerosis. Cytokines were measured by ELISA in the plasma of patients with coronary atherosclerosis undergoing cardiac catheterization. IL-18 was detected in all subjects, whereas a subset of patients demonstrated a coordinated induction of other IFN-gamma-related cytokines. Specifically, elevated plasma levels of IL-12 correlated with that of IFN-gamma and IFN-gamma-inducible chemokines, defining an IFN-gamma axis that was activated independently of IL-6 or C-reactive protein. Systemic inflammation triggered by cardiopulmonary bypass increased plasma levels of the IFN-gamma axis, but not that of IL-18. Activation of the IFN-gamma axis was not associated with acute coronary syndromes, but portended increased morbidity and mortality after 1-year follow-up. IL-12 and IL-18, but not other monokines, elicited secretion of IFN-gamma and IFN-gamma-inducible chemokines in human atherosclerotic coronary arteries maintained in organ culture. T cells were the principal source of IFN-gamma in response to IL-12/IL-18 within the arterial wall. This inflammatory response did not require, but was synergistic with and primed for TCR signals. IL-12/IL-18-stimulated T cells displayed a cytokine-producing, nonproliferating, and noncytolytic phenotype, consistent with previous descriptions of lymphocytes in stable plaques. In contrast to cognate stimuli, IL-12/IL-18-dependent IFN-gamma secretion was prevented by a p38 MAPK inhibitor and not by cyclosporine. In conclusion, circulating IL-12 may provide a mechanistic link between inflammation and Th1-type cytokine production in coronary atherosclerosis.

Atrial Fibrillation in the Elderly: Who is at Risk?

Atrial fibrillation is recognized by all clinicians as an important arrhythmia. Its importance relates to the increased risk for cardioembolic stroke. The elderly are the most commonly affected. They have the highest incidence of atrial fibrillation and are the patients most vulnerable to the risk of stroke. It has been stated that the incidence of atrial fibrillation is only 0.2 per 1000 in patients aged 30-39. This figure increases to 39.0 per 1000 in patients 80-89 years old. Among patients seeking medical attention the prevalence can be even greater (Fig. 1). Atrial fibrillation's contribution to the risk of stroke increases with age. In patients 50-59 years of age it is estimated that 6.7% of strokes are associated with atrial fibrillation. In patients aged 80-89 this figure increases to 36.2%.1 This review will explore common etiologies leading to atrial fibrillation in the elderly. Important reversible causes will be emphasized. Some of the reasons this common arrhythmia is an especially important risk factor for cardioembolic stroke in this group will be illustrated.