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The incidence of heart valve hemangioma is very low and is mostly observed in the mitral and tricuspid valve. In 2006, two cases of aortic valve hemangioma were reported for the first time, including one with calcifying aortic valve stenosis. We now present a case of aortic valve hemangioma in a patient suffering from aortic valve insufficiency combined with atherosclerotic thickening. [ABSTRACT FROM AUTHOR]

Eur J Clin Invest 2010; 40 (1): 4–10 Background Recent studies indicate a role for complement in the pathogenesis of aortic valve disease. However, the role of naturally occurring anti-complement mediators in this context is unknown. In this study, we have analysed this in three different pathological conditions of the aortic valve: degeneration, atherosclerosis and bacterial endocarditis. Materials and methods Human aortic valves were obtained at autopsy ( n = 30): 5 control valves, 10 aortic valves with atherosclerotic changes, 10 aortic valves with degenerative changes and 5 degenerative changed aortic valves with bacterial infection. These valves were analysed immunohistochemically for the presence of activated complement (C3d and C5b9) and the complement inhibitors C1-inh and clusterin. Areas of positivity were then quantified. Results C3d, C5b9 and the complement inhibitors C1-inh and clusterin depositions were mainly found in the endothelium and extracellular matrix in aortic valves. All these mediators were already present in control valves, but the area of positivity increased significantly in response to the different diseases, with the highest increase in response to bacterial endocarditis. Interestingly, in all three aortic diseases, the depositions of complement were significantly more widespread than that of their inhibitors. Conclusions Our study indicates that anti-complement mediators (C1-inh and clusterin) are deposited in diseased aortic valves together with activated complement, indicating an existing counter response against complement locally in the valve. However, deposition of activated complement is significantly more widespread than that of its inhibitors, which could explain ongoing inflammation in those diseased aortic valves. [ABSTRACT FROM AUTHOR]

Background Several studies have suggested an association between Chlamydophila pneumoniae ( Cp) infection and atherosclerosis. A recent study detected Cp DNA in the saphenous vein of 12% of all patients before bypass grafting and in 38% of failed grafts. We used a system in which human veins were perfused with autologous blood under arterial pressure. Materials and methods Veins were surplus segments of saphenous veins of coronary artery bypass grafting (CABG) patients. Vein grafts were perfused with the blood of the same patient after CABG procedures. Veins were analysed for Cp-specific membrane protein using immunohistochemical and PCR analysis. Veins were analysed before and after perfusion (up to 4 h). The number of Cp positive cells was then quantified in the vein layers. Results Cp protein was detected within macrophages only. In non-perfused veins, Cp was present in the adventitia in 91% of all patients, in the circular (64%) and longitudinal (23%) layer of the media. No positivity was found in the intima. Perfusion subsequently resulted in a significant increase of Cp positive cells within the circular layer of the media that, however, differed strongly between different patients. Cp DNA was not detected by PCR in those specimens. Conclusion Cp protein was present in 91% of veins, but the number of positive cells differed remarkably between patients. Perfusion of veins resulted in increased infiltration of Cp into the circular layer. These results may point to a putative discriminating role of Cp with respect to graft failure between different patients. [ABSTRACT FROM AUTHOR]

Background Secretory type-II phospholipase A2 (sPLA2-II) is a cardiovascular risk marker since higher levels of this acute phase protein imply an increased risk for coronary artery disease. Moreover, it is hypothesized that local activity of sPLA2-II in the atherosclerotic plaque facilitates an inflammatory response to induce plaque instability or rupture. We have studied the presence of sPLA2-II in culprit lesions in the coronary arteries of patients with acute myocardial infarction (AMI) or angina pectoris. Materials and methods We performed a histological examination of culprit lesions in 41 patients with stable (SAP) or unstable angina pectoris (UAP), or AMI using directed coronary atherectomy (DCA). Frozen slides were analysed immuno-histochemically for the presence of sPLA2-II, macrophages and smooth muscle cells. Immunopositive areas were calculated as a percentage of the total tissue area using image analysis software. Results Intracellular sPLA2-II was found in atherosclerotic lesions in the macrophages of the intima as well as in vascular smooth muscle cells. Next to this, extracellular sPLA2-II depositions were also found. These depositions were significantly more extensive in patients with AMI, i.e. 26%median[6%25th(percentile)–44%75th(percentile)] of the intima area, than in patients with SAP 0%median (0%25th–10%75th; P = 0·013) or UAP 0%median (0%25th–0%75th; P = 0·04). Conclusions Extracellular sPLA2-II is more abundantly present in atherosclerotic culprit lesions that have led to myocardial infarction. This suggests a role for extracellular sPLA2-II in the development of complications of atherosclerotic lesions in coronary arteries. [ABSTRACT FROM AUTHOR]

Impaired perfusion of the heart induces a local inflammatory response, which involves deposition of C-reactive protein and complement activation products C3d and C5b-9. We investigated whether reperfusion or reinfarction enhances these phenomena in humans.Depositions of C-reactive protein and complement were quantified in tissue samples of infarcted myocardium from 76 patients who had died after acute myocardial infarction. The extent of depositions in patients treated with reperfusion or suffering from reinfarction was compared with that in patients who had no reperfusion or reinfarction.Patients with reinfarction had significantly more extensive depositions of C-reactive protein and complement (C3d and C5b-9) in the infarcted myocardium than patients without reinfarction. Similarly, patients who received reperfusion therapy had more extensive depositions also than those who had not received this therapy.Both reinfarction and reperfusion therapy significantly increase the extent of C-reactive protein and complement depositions in human myocardial infarcts.Eur J Clin Invest 2004; 34 (12): 803 –810See Commentary on page 800. [ABSTRACT FROM AUTHOR]