Sulfated polysaccharide fucoidan ameliorates experimental autoimmune myocarditis in rats.

Homing of cardiac myosin-specific CD4-positive T cells into the myocardium is the initial pathologic event of experimental autoimmune myocarditis (EAM). Subsequently, various bystander inflammatory cells are recruited into the myocardium crossing vascular endothelial cell walls. Sulfated polysaccharide fucoidan binds selectin nonselectively and blocks its function. Therefore, this study was designed to evaluate whether in vivo fucoidan treatment can improve EAM. A 21-day infusion of physiological saline or fucoidan was administrated intraperitoneally to the rats with sham operation (sham-saline, n = 5; sham-fucoidan, n = 6) or those with cardiac myosin injection (EAM-saline, n = 10; EAM-fucoidan, n = 10). After 3 weeks, fucoidan treatment improved left ventricular ejection fraction (79.04 ± 2.81 vs 65.94% ± 3.22%; P < .01 vs EAM-saline) with a reduced ratio of heart weight to body weight (4.016 ± 0.239 vs 4.975 ± 0.252 mg/g; P < .05 vs EAM-saline) in EAM. Furthermore, fucoidan treatment decreased serum levels of BNP (292.0 ± 53.4 vs 507.4 ± 89.2 ng/mL; P < .05 vs EAM-saline) and the myocarditis area (31.66 ± 1.53 vs 42.51% ± 3.24%; P < .01 vs EAM-saline) in EAM. These beneficial effects of fucoidan were accompanied by inhibition of both macrophage and CD4-positive T-cell infiltration into the myocardium. Fucoidan, a nonselective selectin blocker, attenuates the progression of EAM. This observation may be explained, at least in part, by blocking the extravasation of inflammatory cells into the myocardium.

Transient left ventricular dysfunction associated with severe Legionella infection.

Legionella infection, although commonly seen as pneumonia, can also manifest systemic involvement. Here, we describe a case of sporadic Legionella infection coinciding with pneumonia, rhabdomyolysis, renal failure, and severe left ventricular dysfunction, which subsequently developed refractory septic shock. An endomyocardial biopsy revealed no findings of interstitial inflammatory infiltrates. After 3 days of intensive care, including percutaneous cardiopulmonary support, intraaortic balloon pumping, and continuous hemodialysis with endotoxin adsorption therapy, left ventricular wall motion improved spontaneously in accordance with a decrease in the concentration of inflammatory cytokines. Cardiac complications are rare but Legionella infection should be considered as a possible etiology of left ventricular dysfunction in patients with sepsis.

Takotsubo cardiomyopathy after delivery in an oestrogen-deficient patient.

Takotsubo cardiomyopathy is characterised by a reversible left ventricular wall motion abnormality that is observed as apical ballooning without significant coronary arterial stenosis; it occurs predominantly in postmenopausal women. Here, we report a case of Takotsubo cardiomyopathy after delivery in a patient with oestrogen deficiency due to Turner's syndrome. This case shows the pathogenic role of an inadequate oestrogen level in Takotsubo cardiomyopathy.

Inverted Takotsubo contractile pattern caused by pheochromocytoma with tall upright T-waves, but not typical deep T-wave inversion.

We describe a 36-year-old woman with inverted Takotsubo cardiomyopathy caused by pheochromocytoma crisis. In the acute phase, her electrocardiogram showed ST segment depression in lead II, III, aVF and V2 through V5. On day 14, tall upright T-waves were observed in leads V2 through V5 despite heart failure and basal to midventricular ballooning improved on day 4, and all electrocardiographic abnormalities finally normalized after surgical removal of the pheochromocytomas. This is the first report of electrocardiographic course of inverted Takotsubo cardiomyopathy, and these findings seem as if the inverted electrocardiographic findings are contrary to those of apical ballooning.

Long-term carperitide treatment attenuates left ventricular remodeling in rats with heart failure after autoimmune myocarditis.

The effect of carperitide, recombinant human atrial natriuretic peptide, on chronic heart failure (HF) has not been clarified. We investigated the beneficial effects of chronic carperitide treatment in rats with HF after experimental autoimmune myocarditis. A 28-day infusion of carperitide (n = 14) or vehicle (n = 14) was administrated to the rats 4 weeks after experimental autoimmune myocarditis induction. After 4 weeks, the myocardial levels of cyclic guanosine monophosphate (cGMP), left ventricular function, myocyte hypertrophy, interstitial fibrosis, myocardial capillary vessel density, and activity of one prominent substrate of cGMP, vasodilator-stimulated phosphoprotein (VASP) that may enhance angiogenesis, were measured. Carperitide treatment increased the myocardial levels of cGMP and attenuated the functional severity along with a decreased myocyte cross-sectional area, interstitial fibrosis, and an increased capillary to myocyte ratio. Furthermore, carperitide treatment enhanced the phosphorylation of VASP at Ser239, which was preferentially phosphorylated by cGMP-dependent protein kinase but not Ser157, which was preferentially phosphorylated by cyclic adenosine monophosphate-dependent protein kinase. Long-term carperitide treatment attenuates ventricular remodeling and ameliorates the progression of chronic HF. The effects of carperitide treatment are associated with increased neovascularization among the residual myocytes and an increase of VASP activation.

Irreversible dilated cardiomyopathy after surgical resection of pheochromocytomas associated with von Hippel-Lindau disease.

Pheochromocytoma occasionally can lead to left ventricular dysfunction, which is known to be transient. Here, we described a patient showing irreversible dilated cardiomyopathy after surgical resection of pheochromocytomas associated with von Hippel-Lindau disease.

A pilot-controlled study of myeloperoxidase-specific anti-neutrophil cytoplasmic autoantibody (MPO-ANCA) in the coronary circulation.

Hereby we report our observations derived from a pilot-study of 39 subjects (30 patients with coronary artery disease [CAD] and 9 non-CAD controls). In this work, we aimed to evaluate MPO-ANCA titer in the human coronary circulation for the first time; and examine its possible association with CAD and some cytokines/inflammatory markers. We found higher mean coronary MPO-ANCA titer in CAD subjects than in non-CAD controls; beside significant positive correlations between MPO-ANCA titers and both C-reactive protein and interleukin-6 levels. Thus, we might suggest the possible involvement of MPO-ANCA in coronary atherogenesis indirectly through modulating some pro-inflammatory cytokines/markers; that a large-scale study of MPO-ANCA in CAD patients may be warranted in the future.

Angiopoietin-1, angiopoietin-2 and tie-2 in the coronary circulation of patients with and without coronary collateral vessels.

BACKGROUND: The role of the angiopoietin (Ang)/Tie-2 system in coronary collateral growth is not well understood, so the purpose of this study was to investigate and elucidate the relationship of this system to coronary collateral formation in patients with coronary artery disease (CAD). METHODS AND RESULTS: Fifty-nine patients with CAD were recruited. Blood samples from the left ventricle (LV) and coronary sinus (CS) were obtained during cardiac catheterization, and serum concentrations of Ang-1, Ang-2, and Tie-2 were measured by enzyme-linked immunosorbent assay. Patients were then classified as mild CAD (n=30), defined as

Impact of percutaneous coronary intervention on the levels of interleukin-6 and C-reactive protein in the coronary circulation of subjects with coronary artery disease.

Many clinical studies have evaluated the inflammatory response (mainly interleukin [IL]-6 and C-reactive protein [CRP]) after percutaneous coronary intervention (PCI) in patients with coronary artery disease (CAD). The aim of this study was to verify the source of possible elevation of IL-6 and CRP after PCI using coronary sinus sampling. We studied 87 subjects who underwent coronary angiography for diagnostic, therapeutic, or follow-up purposes. Blood samples were taken by the PCI team during the catheterization study from the coronary sinus. We measured coronary IL-6 levels by sandwich enzyme-linked immunosorbent assay, and high-sensitivity CRP levels were measured by latex immunonephelometry. The subjects were then classified according to their coronary angiographic findings into non-CAD (no evidence of significant organic CAD), mild CAD (1 vessel narrowed), and severe CAD (>or=2 vessels narrowed) groups. PCI (including stent deployment) was performed in 16 patients with CAD. The mean coronary IL-6 value was higher in the severe than in the mild CAD group (3.67 +/- 2.48 vs 2.3 +/- 1.15 pg/ml, p = 0.027). The mean coronary IL-6 value was higher in the subjects who underwent PCI than in those who did not (2.9 +/- 1.23 vs 1.87 +/- 0.9 pg/ml, p = 0.037), and the same was found regarding CRP (1.244 +/- 0.72 vs 0.498 +/- 0.51 mg/L, p = 0.032). The coronary IL-6 values correlated positively with the coronary CRP values (r = 0.374, p = 0.017). In conclusion, the increase in coronary IL-6 and CRP levels after PCI in patients with CAD might be attributed to their release from the coronary atheroma secondary to the direct mechanical effect applied on the atheroma itself by balloon inflation and stent deployment.

Cardioprotective effects of recombinant human erythropoietin in rats with experimental autoimmune myocarditis.

Erythropoietin (EPO) has been known to have cytoprotective effects on several types of tissues, presumably through modulation of apoptosis and inflammation. The effect of EPO on myocardial inflammation, however, has not yet been clarified. We investigated the cardioprotective effects of EPO in rats with experimental autoimmune myocarditis (EAM). Seven-week-old Lewis rats immunized with cardiac myosin were treated either with EPO or vehicle and were examined on day 22. EPO attenuated the functional and histological severity of EAM along with suppression of mRNAs of tumor necrosis factor (TNF)-alpha and interleukin (IL)-6 in the hearts as well as a reduction of apoptotic cardiomyocytes. The EPO receptor (EPO-R) was upregulated in the myocardium of EAM compared with that of healthy rats. These results may suggest that EPO ameliorated the progression of EAM by modulating myocardial inflammation and apoptosis.

Pericardial abscess detected by Gallium-67 scintigraphy 40 years after cardiac surgery.

A 45-year-old female who had cardiac surgery 40 years earlier was transferred to our hospital because of refractory fever. Echocardiography showed an intrapericardial mass. Gallium-67 (67Ga) scintigraphy revealed abnormal accumulation at the same site of the intrapericardial mass and thoracoscopy revealed that the mass was a pericardial abscess (PA). After surgical resection, drainage and antibiotic therapy, her fever subsided and the abnormal accumulation of 67Ga disappeared. This case showed a very rare clinical course of PA and the importance of 67Ga scintigraphy for its diagnosis.