Cardiac tamponade due to rupture of coronary artery fistula to the coronary sinus with giant aneurysm of coronary artery: usefulness of transthoracic echocardiography.

A 68-year-old woman was admitted to our hospital because of back pain and syncope. Transthoracic echocardiography revealed pericardial effusion, a collapsed right ventricle, a giant aneurysm connected to the coronary sinus, a dilated left main trunk coronary artery, and a dilated left circumflex artery (LCx). Furthermore, there was a coronary artery fistula arising from the LCx that drained into the coronary sinus. We diagnosed cardiac tamponade due to rupture of the coronary artery fistula or giant aneurysm, and successful emergency surgery was performed. Rupture of coronary artery aneurysm or coronary artery fistula is very rare. Transthoracic two-dimensional echocardiography was very useful in our case for the diagnosis of cardiac tamponade, giant coronary aneurysm, and coronary artery fistula.

Sirolimus-eluting stent versus balloon angioplasty for sirolimus-eluting stent restenosis: Insights from the j-Cypher Registry.

BACKGROUND: Optimal treatment strategies for restenosis of sirolimus-eluting stents (SES) have not been adequately addressed yet. METHODS AND RESULTS: During the 3-year follow-up of 12 824 patients enrolled in the j-Cypher registry, 1456 lesions in 1298 patients underwent target-lesion revascularization (TLR). Excluding 362 lesions undergoing TLR for stent thrombosis or TLR using treatment modalities other than SES or balloon angioplasty (BA), 1094 lesions with SES-associated restenosis in 990 patients treated with either SES (537 lesions) or BA (557 lesions) constituted the study population for the analysis of recurrent TLR and stent thrombosis after the first TLR. Excluding 24 patients with both SES- and BA-treated lesions, 966 patients constituted the analysis set for the mortality outcome. Cumulative incidence of recurrent TLR in the SES-treated restenosis lesions was significantly lower than that in the BA-treated restenosis lesions (23.8% versus 37.7% at 2 years after the first TLR; P<0.0001). Among 33 baseline variables evaluated, only hemodialysis was identified to be the independent risk factor for recurrent TLR by a multivariable logistic regression analysis. After adjusting for confounders, repeated SES implantation was associated with a strong treatment effect in preventing recurrent TLR over BA (odds ratio, 0.44; 95% confidence interval, 0.32 to 0.61; P<0.0001). The 2-year mortality and stent thrombosis rates between the SES- and the BA-treated groups were 10.4% versus 10.8% (P=0.4) and 0.6% versus 0.6%, respectively. CONCLUSIONS: Repeated implantation of SES for SES-associated restenosis is more effective in preventing recurrent TLR than treatment with BA, without evidence of safety concerns.

Effect of rivastigmine on plasma butyrylcholine esterase activity and plasma ghrelin levels in patients with dementia in Alzheimer's disease.

AIM: Alzheimer's disease causes loss of appetite, resulting in bodyweight reduction. This, in turn, causes progression of cognitive dysfunction and physical complications that hasten death. Earlier care for loss of appetite is essential in Alzheimer's disease management. Rivastigmine is a therapeutic agent for Alzheimer's disease that has dual inhibition effects on acetylcholine esterase and butyrylcholine esterase. Butyrylcholine esterase is known to degrade the gastric hormone, ghrelin, which regulates appetite; therefore, we considered that rivastigmine might have an effect on appetite. The present study aimed to evaluate the hypothesis that rivastigmine improves appetite in Alzheimer's disease patients. METHODS: Rivastigmine was given to mild-to-moderate Alzheimer's disease patients for 16 weeks. We evaluated the effects of rivastigmine on food intake, bodyweight, motivation (estimated by the vitality index), cognition function (estimated by the Hasegawa Dementia Scale-Revised), plasma butyrylcholine esterase activity, active ghrelin and inactive ghrelin. RESULTS: Plasma butyrylcholine esterase activity significantly decreased over time (percent change: -18.9 ± 27.0%, P < 0.05 at week 8; percent change: -33.4 ± 45.4%, P < 0.05 at week 16). Negative correlations were detected between percent changes in butyrylcholine esterase activity and active ghrelin (rs = -0.62, P = 0.033) or active/inactive ghrelin ratio (rs = -0.73, P = 0.007). Furthermore, motivation (including appetite) improved significantly (percent change: 17.9 ± 18.6%, P < 0.05 at week 16). CONCLUSIONS: The present study suggests that rivastigmine might improve appetite in mild-to-moderate Alzheimer's disease patients by suppressing degradation of plasma active ghrelin through the inhibition of plasma butyrylcholine esterase. Geriatr Gerontol Int 2018; 18: 886-891.

The Association of Bite Instability and Comorbidities in Elderly People.

Objective The purpose was to evaluate the association between bite instability and comorbidities, comprehensive geriatric evaluations, or disabilities in elderly people. Methods A dentist examined the oral function, such as the bite stability, number of teeth, and the use of dentures, in 119 patients (93 women, mean age: 86.7±7.8) in 2 nursing homes for the elderly. The association between the oral function and the prevalence of diseases, including hypertension, diabetes mellitus, and dementia, was analyzed. Results The median number of teeth was 0 [0, 4]. The patients were divided into a bite-stable group (n=78, 66%) and bite-unstable group (n=41, 34%). The prevalence of hypertension was significantly higher in the bite-stable group than in the bite-unstable group (83% vs. 63%, respectively; p=0.0149), whereas the prevalence of diabetes mellitus was significantly lower in the bite-stable group than in the bite-unstable group (10% vs. 27%, respectively; p=0.0190). The prevalence of a cognitive function decline was significantly lower in the bite-stable group as well (59% vs. 83%, p=0.0082). According to the simplified comprehensive geriatric assessment 7, the bite-stable group scored significantly higher for instrumental activities of daily living (ADL) than the bite-unstable group (54% vs. 24%, respectively; p=0.0021). A multivariate logistic regression analysis demonstrated that bite instability was independently correlated with hypertension, diabetes mellitus, and instrumental activities of daily living. Conclusion Bite instability was independently associated with a decreased prevalence of hypertension or increased prevalence of diabetes mellitus and low levels of instrumental ADL in the elderly.

Relationship between vascular endothelial growth factor and left ventricular dimension in patients with acute myocardial infarction.

BACKGROUND: Although vascular endothelial growth factor (VEGF) is elevated in patients with acute myocardial infarction (AMI), the clinical significance of its elevation remains unclear. The present study was designed to determine the relationship between VEGF and left ventricular dimension in patients with AMI. METHODS AND RESULTS: Plasma VEGF levels were examined by enzyme-linked immunosorbent assay daily for one week and then weekly for four weeks in 38 patients with AMI (65.4 ± 1.7 years). Left ventriculography was performed at 14 days, 6 months, and 2 years after the onset of AMI. Plasma VEGF levels were significantly elevated and reached a peak on day 6. Peak plasma VEGF levels positively correlated with both end-diastolic and end-systolic volume indices at 14 days after the onset of AMI. When patients with AMI were divided into two groups according to plasma VEGF levels on admission, left ventricular volume indices were higher in the high VEGF group than in the low VEGF group at the subacute phase of AMI (14 days). These differences were no longer present in the chronic phase of AMI. CONCLUSION: Plasma VEGF levels were increased in patients with AMI, and peak levels were associated with left ventricular volume indices in the subacute phase, suggesting an important role of endogenous VEGF in the left ventricular dimension in patients with AMI.

Statins suppress interleukin-6-induced monocyte chemo-attractant protein-1 by inhibiting Janus kinase/signal transducers and activators of transcription pathways in human vascular endothelial cells.

BACKGROUND AND PURPOSE: The mechanisms of anti-inflammatory actions of statins, 3-hydroxy-3-methylglutaryl CoA (HMG-CoA) reductase inhibitors, remain unclear. We investigated the effects of statins on interleukin (IL)-6-induced monocyte chemo-attractant protein (MCP)-1 expression and monocyte chemotaxis. EXPERIMENTAL APPROACH: Cultures of human aortic endothelial cells (HAECs) were stimulated with IL-6 in the absence and presence of statins. Gene expression and protein secretion of MCP-1, phosphorylation of Janus kinase (JAK) and the signal transducers and activators of transcription (STAT) pathway, and human monocyte migration were examined. KEY RESULTS: IL-6 plus its soluble receptor sIL-6R (IL-6/sIL-6R) promoted THP-1 monocyte migration, and increased gene expression and protein secretion of MCP-1, more than IL-6 alone or sIL-6R alone. Various statins inhibited IL-6/sIL-6R-promoted monocyte migration and MCP-1 expression in HAECs. Co-incubation of mevalonate and geranylgeranyl pyrophosphate, but not farnesyl pyrophosphate, reversed the inhibitory effects of statins on MCP-1 expression. Geranylgeranyl transferase inhibitor, but not farnesyl transferase inhibitor, suppressed IL-6/sIL-6R-stimulated MCP-1 expression. IL-6/sIL-6R rapidly phosphorylated JAK1, JAK2, TYK2, STAT1 and STAT3, which were inhibited by statins. Transfection of STAT3 small interfering RNA (siRNA), but not STAT1 siRNA, attenuated the ability of IL-6/sIL-6R to enhance THP-1 monocyte migration. In addition, statins blocked IL-6/sIL-6R-induced translocation of STAT3 to the nucleus. CONCLUSIONS AND IMPLICATIONS: Statins suppressed IL-6/sIL-6R-induced monocyte chemotaxis and MCP-1 expression in HAECs by inhibiting JAK/STAT signalling cascades, explaining why statins have anti-inflammatory properties beyond cholesterol reduction.

Cardiotrophin-1 stimulates intercellular adhesion molecule-1 and monocyte chemoattractant protein-1 in human aortic endothelial cells.

Intercellular adhesion molecule-1 (ICAM-1) and monocyte chemoattractant protein-1 (MCP-1) play critical roles in mediating monocyte adhesion to the vascular endothelium and monocyte migration into the subendothelial regions of the vessels. Inasmuch as cardiotrophin-1 (CT-1), an IL-6-type cytokine, was expressed in human atherosclerotic plaque, we examined whether CT-1 induces monocyte adhesion and migration by stimulating gene and protein expressions of ICAM-1 and MCP-1 in human aortic endothelial cells (HAECs). Immunocytochemistry revealed that CT-1 increased intensity of ICAM-1 and MCP-1 immunoreactivity in HAECs. Adhesion assay and chemotaxis assay revealed that CT-1 increased human monocytic THP-1 cell adhesion to HAECs and promoted chemotaxis in THP-1 cells, which were attenuated by anti-ICAM-1 and anti-MCP-1 antibody, respectively. Western blot analysis showed that CT-1 increased phosphorylation of ERK1/2 MAP kinase, p38 MAP kinase, and Akt and that their inhibitors, PD-98059, SB-203580, and LY-294002, respectively, inhibited phosphorylation. RNase protection assay and ELISA demonstrated that CT-1 increased gene and protein expressions of ICAM-1 and MCP-1. EMSA revealed that CT-1 enhanced NF-kappaB DNA-binding activity. CT-1-mediated upregulation of ICAM-1 and MCP-1 was suppressed by PD-98059, SB-203580, LY-294002, and parthenolide. The present study demonstrates that CT-1 promotes monocyte adhesion and migration by stimulating ICAM-1 and MCP-1 through mechanisms that involve ERK1/2 MAP kinase, p38 MAP kinase, phosphatidylinositol 3-kinase, and NF-kappaB pathways and suggests that CT-1 plays an important role in the pathophysiology of vascular inflammation and atherosclerosis.

Plasma levels of soluble glycoprotein 130 in acute myocardial infarction.

OBJECTIVES: Soluble glycoprotein 130 (sgp130), a circulating form of receptor subunit for the interleukin (IL) -6 cytokine family, modulates the biological actions of its ligands as an inhibitory regulator. The role of sgpl30 in cardiovascular diseases such as acute coronary syndrome remains unknown. METHODS: Plasma levels of sgp130 were examined by enzyme-linked immunosorbent assay in 33 patients with acute myocardial infarction (AMI; mean age 67 +/- 2 years, 21 males and 12 females), who were admitted to our hospital within 24 hr of onset of AMI and survived for 4 weeks. RESULTS: Plasma sgp130 levels were significantly higher at admission (260.5 +/- 7.3 ng/ml), and were significantly lower from day 2 to day 5 (202.4 +/- 5.1 ng/ml at day 3) as compared with normal control subjects (n = 38, 227.1 +/- 5.6 ng/ml). The lowest sgp130 levels inversely correlated with white blood cell count at admission (r = -0.42, p < 0.05) and with peak C-reactive protein levels (r = -0.43, p < 0.05). Additional in vitro study revealed that incubation of AMI plasma with exogenous IL-6 plus soluble IL-6 receptor resulted in a decrease in plasma sgp130 levels, suggesting the possible reason for reduced plasma sgp130 levels in AMI. CONCLUSIONS: The present study indicates that plasma sgp130 levels were modulated during the time course of AMI and inversely associated with inflammation in AMI.

Dystrophin upregulation in pressure-overloaded cardiac hypertrophy in rats.

Dystrophin is a cytoskeletal protein localized to the sarcolemma of skeletal and cardiac muscle, and neurons. We have recently demonstrated that a significant cardiac damage including myocytes injury, inflammation, and fibrosis, was found in dystrophin-deficient myocardium during pressure overload [Kamogawa et al., 2001: Cardiovasc Res 50:509-515]. However, little is known about how the cardiac sarcolemmal cytoskeleton produces qualitative and quantitative changes in response to pressure overload. Accordingly, we investigated dystrophin gene expression and protein accumulation during cardiac hypertrophy. Cardiac hypertrophy was produced by banding of the abdominal aorta of rats. Total RNA from the left ventricle of the heart was used for a quantitative reverse transcription-polymerase chain reaction (RT-PCR). Dystrophin mRNA expression significantly increased by 33 +/- 18% at 1 day (P < 0.05) and 45 +/- 19% at 2 days (P < 0.01) after banding, while G3PDH mRNA showed no significant change. RT-PCR for dystrophin tissue-specific exon 1 revealed that only muscle type promoter, but not non-muscle type promoter (brain and Purkinje-cell type), was activated immediately after banding. Immunohistochemistry for dystrophin showed intense cellular membrane staining with an increase in the perimeter of the myocytes by 14% at 3 days (46.3 microm, P < 0.01) and 19% at 7 days (51.2 microm, P < 0.01) after banding. Western blotting also showed dystrophin protein increased by 14 +/- 6% at 2 days (P < 0.05) and by 32 +/- 10% at 3 days (P < 0.01) after aortic banding. In conclusion, upregulation of dystrophin mRNA expression and protein accumulation occurs in response to cardiac hypertrophy. These data and the vulnerability of dystrophin-deficient myocardium to pressure overload suggest that dystrophin could play an important role in maintaining the integrity of the sarcolemma.