Resolution of acromegalic cardiomyopathy in mild acromegalic physical abnormality after short-term octreotide therapy.

Congestive heart failure developed in a 42-year-old man who had very mild acromegalic features. Echocardiography showed a marked dilatation of the left ventricle and decreased systolic function. Laboratory examinations revealed the elevated levels of growth hormone and insulin-like growth factor-1 and pituitary microadenoma was demonstrated by magnetic resonance imaging. Although the extensive conventional medical treatment was ineffective, short-term addition of somatostatin analog, octreotide, rapidly improved his cardiac function. After discontinuation of octreotide, further improvement was observed with minimal residual diastolic dysfunction. All medical treatment could be stopped after successful trans-sphenoidal surgery. Early diagnosis and effective treatment is important to reverse the acromegalic cardiomyopathy.

Late thrombosis of a drug-eluting stent overlapped in the in-stent restenotic lesion of a bare metal stent.

Late stent thrombosis occurred in the lesion of a sirolimus-eluting stent implanted 6 months previously for an in-stent restenosis lesion in the distal right coronary artery. Seventeen days before admission due to acute myocardial infarction this time, aspirin was discontinued for colon polypectomy. Ticlopidine had been discontinued 3 months before the discontinuation of aspirin. In drug-eluting stent era, the interventional strategy and antiplatelet therapy require long term attention.

Oozing type of left ventricular rupture via subepicardial aneurysm diagnosed 5 months after myocardial infarction.

A 71-year-old man visited our hospital complaining of increasing fatigue and exertional dyspnea. He had had severe epigastric pain for the past 5 months. On admission, chest radiogram showed marked cardiac dilatation and echocardiogram massive pericardial effusion with a small subepicardial aneurysm at the posterior wall of the left ventricle. An urgent pericardiocentesis removed 1300 ml of bloody effusion. The red blood cell count of the pericardial effusion was similar to that of the peripheral blood, and there were no abnormal findings on cytologic and bacteriological examinations. Coronary angiography showed a blunt occlusion of the mid-portion of the circumflex artery. Left ventricular angiogram revealed aneurysmal deformity of the left ventricular posterior wall. These findings suggested that an oozing type of left ventricular rupture via a subepicardial aneurysm had occurred after the onset of myocardial infarction (MI), resulting in massive accumulation of pericardial effusion. The patient is presently doing well without any clinical symptoms 18 months after pericardiocentesis. This is the first case report in which a subepicardial aneurysm with massive pericardial effusion was detected in the chronic stage of MI and successfully managed without surgical repair.

Systolic anterior motion (SAM) of the posterior mitral leaflet: left ventricular outflow tract obstruction in a patient without left ventricular hypertrophy.

Systolic anterior motion (SAM) of the anterior mitral leaflet with mitral-septal contact was generally thought to be a major contributor to dynamic left ventricular outflow tract obstruction in patients with hypertrophic cardiomyopathy. We report an interesting case of SAM of the posterior mitral leaflet in a patient without left ventricular hypertrophy, which led to dynamic left ventricular obstruction.

Suppression of cytokines and nitric oxide production, and protection against lethal endotoxemia and viral myocarditis by a new NF-kappaB inhibitor.

BACKGROUND: Nuclear factor kappa B (NF-kappaB) is activated by several factors, which increase the inflammatory response, and this activation, in turn, leads to the expression of several genes such as cytokines, and may play an important role in cardiovascular diseases. AIMS: The aim of the study is to examine the effect of SUN C8079, a newly synthesized NF-kappaB inhibitor in vitro and in vivo. METHODS: We examined the effects of SUN C8079 on the transcriptional responses of NF-kappaB, on activation of NF-kappaB in electrophoretic mobility shift assay, and on the gene expressions of tumor necrosis factor (TNF)-alpha and iNOS. We also studied effects of SUN C8079 on lethal endotoxemia and viral myocarditis in mice. RESULTS: SUN C8079 inhibited the lipopolysaccharide (LPS)-induced expression of the genes of TNF-alpha and iNOS by inhibiting the activation of NF-kappaB in vitro. SUN C8079 inhibited the systemic release of TNF-alpha and improved mortality in LPS-treated mice. In addition to protecting mice against lethal endotoxemia, SUN C8079 prevented the development of myocarditis due to the encephalomyocarditis virus (EMCV), and inhibited the expressions of proinflammatory cytokines and the iNOS gene in cardiac tissues. CONCLUSION: These findings suggest that the activation of NF-kappaB plays an important role in the pathogenesis of endotoxemia and viral myocarditis, and that the NF-kappaB inhibitor, SUN C8079, may be therapeutic in these disorders.

Gene expression of cardiac mast cell chymase and tryptase in a murine model of heart failure caused by viral myocarditis.

This study examined the gene expression of mouse mast cell proteases to clarify their role in the pathophysiology of viral myocarditis. Male DBA/2 mice were inoculated intraperitoneally with the encephalomyocarditis virus and the gene expression of mast cell chymase, mouse mast cell protease (mMCP)-4 and -5, and tryptase, mMCP-6, matrix metalloproteinase (MMP)-9 and type-I procollagen was measured by real-time quantitative RT-PCR analysis. The gene expression of mMCP-4, -5 and -6 mRNA was increased at 5 days, and continued to increase to day 14, coinciding with a prominent inflammatory reaction and extensive myocardial necrosis and fibrosis. The gene expression of MMP-9 was also increased, and there was a significant correlation between upregulation of mast cell proteases and MMP-9. The gene expression of type-I procollagen was increased at 5 days and continued to increase to day 14, suggesting that a fibrotic process had already begun during the acute stage of viral myocarditis. These findings suggest that mast cell chymase and tryptase participate in the acute inflammation and remodeling process of viral myocarditis.