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1.  Cilostazol Add-On Therapy in Patients with Mild Dementia Receiving Donepezil: A Retrospective Study 
PLoS ONE  2014;9(2):e89516.
Goal
Combinatorial therapy directed at both vascular and neurodegenerative aspects of dementia may offer a promising strategy for treatment of dementia, which often has a multifactorial basis in the elderly. We investigated whether the phosphodiesterase III inhibitor cilostazol, which is often used in the prevention of stroke and peripheral artery disease, may delay cognitive decline in the elderly receiving donepezil.
Methods
Medical records were retrospectively surveyed to identify patients who had received donepezil for more than one year and had undergone Mini-Mental State Examination (MMSE) at least at two time points. Those with an initial MMSE score of less than 27 points were subjected to analysis (n = 156), with a cut-point of 21/22 applied to assign them to mild (n = 70) and moderate/severe (n = 86) dementia. The change of total MMSE score per year was compared between patients who had received donepezil and those given both donepezil and cilostazol.
Findings
In patients with mild dementia who had received donepezil and cilostazol (n = 34; 77.2±6.8 years old), the annual change in MMSE score was −0.5±1.6 during an observational period of 28.6±11.7 months, with those receiving donepezil only (n = 36; 78.4±6.5 years old) scoring less (−2.2±4.1) during 30.4±12.8 months with a statistical intergroup difference (p = 0.022). Multivariate analysis showed that absence of cilostazol treatment was the only significant predictor of MMSE decline. A positive effect of cilostazol was found in three subscale scores of MMSE, orientation for time or place and delayed recall. By clear contrast, in patients with moderate/severe dementia, there were no intergroup differences in decrease of total or subscale MMSE scores between the two groups.
Conclusions
These results suggest potential for cilostazol treatment in the suppression of cognitive decline in patients receiving donepezil with mild dementia but not in those with moderate/severe dementia.
doi:10.1371/journal.pone.0089516
PMCID: PMC3935872  PMID: 24586841
2.  Miglitol improves postprandial endothelial dysfunction in patients with acute coronary syndrome and new-onset postprandial hyperglycemia 
Background
Hyperglycemia, a risk factor for development of cardiovascular disease, causes endothelial dysfunction. Alpha-glucosidase inhibitors (α-GIs) improve postprandial hyperglycemia (PPHG) and may have favorable effects on associated cardiovascular disease. Effects of α-GIs in patients with acute coronary syndrome (ACS) and PPHG remain unclear; thus, we assessed the effect of α-GI miglitol on endothelial function in such patients by digital reactive hyperemia peripheral arterial tonometry (RH-PAT).
Methods
Fifty-four patients with ACS who underwent primary percutaneous coronary intervention were enrolled in the study: 36 with new-onset PPHG and 18 with normal glucose tolerance. Eighteen PPHG patients were given 50 mg of miglitol with each meal for 1 week. Endothelial function was assessed on the basis of the RH-PAT index (RHI) before and after the 1-week miglitol treatment. The other 18 PPHG patients and the 18 NGT patients were not given any anti-diabetic agent for 1 week, and endothelial function was assessed.
Results
Postprandial RHI decreased significantly in patients with PPHG. Miglitol improved PPHG significantly; postprandial RHI also improved (p = 0.007). Significant inverse correlation was found between the postprandial change in RHI and postprandial fasting-to-60-minutes surge in glucose (r = -0.382, p = 0.009). Moreover, the improvement in endothelial function correlated with the reduced postprandial glucose surge achieved with miglitol (r = -0.462, p = 0.001).
Conclusions
Postprandial changes in glucose are related to endothelial dysfunction in ACS. Miglitol-based improvement in PPHG appears to improve endothelial function. The effect of miglitol on glucose-dependent endothelial function might improve outcomes of ACS.
doi:10.1186/1475-2840-12-92
PMCID: PMC3691582  PMID: 23777506
Postprandial hyperglycemia; Endothelial function; Reactive hyperemia peripheral arterial tonometry; Acute coronary syndrome; Alpha-glucosidase inhibitor; Miglitol
3.  Mitral valve repair in patient with absent right superior vena cava in visceroatrial situs solitus 
We report on a 74-year-old woman with an absence of right superior vena cava in visceroatrial situs solitus who underwent mitral valve plasty for severe mitral regurgitation. Preoperative three-dimensional computed tomography revealed an absent right and persistent left superior vena cava that drained into the right atrium by way of the coronary sinus. Perioperaively, placement of pulmonary artery catheter, site of venous cannulation, and management of associated rhythm abnormalities were great concern. Obtaining the information about this central venous malformation preoperatively, we performed mitral valve plasty without any difficulties related to this anomaly.
doi:10.1186/1749-8090-8-9
PMCID: PMC3560078  PMID: 23317475
Absent right superior vena cava; Persistent left superior vena cava; Visceroatrial situs solitus; Mitral valve plasty
4.  High HbA1c levels correlate with reduced plaque regression during statin treatment in patients with stable coronary artery disease: Results of the coronary atherosclerosis study measuring effects of rosuvastatin using intravascular ultrasound in Japanese subjects (COSMOS) 
Background
The incidence of cardiac events is higher in patients with diabetes than in people without diabetes. The Coronary Atherosclerosis Study Measuring Effects of Rosuvastatin Using Intravascular Ultrasound in Japanese Subjects (COSMOS) demonstrated significant plaque regression in Japanese patients with chronic coronary disease after 76 weeks of rosuvastatin (2.5 mg once daily, up-titrated to a maximum of 20 mg/day to achieve LDL cholesterol <80 mg/dl).
Methods
In this subanalysis of COSMOS, we examined the association between HbA1c and plaque regression in 40 patients with HbA1c ≥6.5% (high group) and 86 patients with HbA1c <6.5% (low group).
Results
In multivariate analyses, HbA1c and plaque volume at baseline were major determinants of plaque regression. LDL cholesterol decreased by 37% and 39% in the high and low groups, respectively, while HDL cholesterol increased by 16% and 22%, respectively. The reduction in plaque volume was significantly (p = 0.04) greater in the low group (from 71.0 ± 39.9 to 64.7 ± 34.7 mm3) than in the high group (from 74.3 ± 34.2 to 71.4 ± 32.3 mm3). Vessel volume increased in the high group but not in the low group (change from baseline: +4.2% vs −0.8%, p = 0.02). Change in plaque volume was significantly correlated with baseline HbA1c.
Conclusions
Despite similar improvements in lipid levels, plaque regression was less pronounced in patients with high HbA1c levels compared with those with low levels. Tight glucose control during statin therapy may enhance plaque regression in patients with stable coronary disease.
Trial registration
ClinicalTrials.gov, Identifier NCT00329160
doi:10.1186/1475-2840-11-87
PMCID: PMC3444370  PMID: 22831708
Atherosclerosis; Coronary artery disease; Intravascular ultrasound; HbA1c; Rosuvastatin
5.  Hepatitis C virus enhances incidence of idiopathic pulmonary fibrosis 
AIM: To investigate the cumulative development incidence and predictive factors for idiopathic pulmonary fibrosis in hepatitis C virus (HCV) positive patients.
METHODS: We studied 6150 HCV infected patients who were between 40-70 years old (HCV-group). Another 2050 patients with hepatitis B virus (HBV) were selected as control (HBV-group). The mean observation period was 8.0 ± 5.9 years in HCV-group and 6.3 ± 5.5 years in HBV-group. The primary goal is the development of idiopathic pulmonary fibrosis (IPF) in both groups. The cumulative appearance rate of IPF and independent factors associated with the incidence rate of IPF were calculated using the Kaplan-Meier method and the Cox proportional hazard model. All of the studies were performed retrospectively by collecting and analyzing data from the patient records in our hospital.
RESULTS: Fifteen patients in HCV-group developed IPF. On the other hand, none of the patients developed IPF in HBV-group. In HCV-group, the cumulative rates of IPF development were 0.3% at 10th year and 0.9% at 20th year. The IPF development rate in HCV-group was higher than that in HBV-group (P = 0.021). The IPF development rate in patients with HCV or HBV was high with statistical significance in the following cases: (1) patients ≥ 55 years (P < 0.001); (2) patients who had smoking index (package per day × year) of ≥ 20 (P = 0.002); (3) patients with liver cirrhosis (P = 0.042).
CONCLUSION: Our results indicate that age, smoking and liver cirrhosis enhance the development of IPF in HCV positive patients.
doi:10.3748/wjg.14.5880
PMCID: PMC2751899  PMID: 18855988
Hepatitis B virus; Hepatitis C virus; Idiopathic pulmonary fibrosis; A retrospective cohort study
6.  Psychological and weight-related characteristics of patients with anorexia nervosa-restricting type who later develop bulimia nervosa 
Background
Patients with anorexia nervosa-restricting type (AN-R) sometimes develop accompanying bulimic symptoms or the full syndrome of bulimia nervosa (BN). If clinicians could predict who might change into the bulimic sub-type or BN, preventative steps could be taken. Therefore, we investigated anthropometric and psychological factors possibly associated with such changes.
Method
All participants were from a study by the Japanese Genetic Research Group for Eating Disorders. Of 80 patients initially diagnosed with AN-R, 22 changed to the AN-Binge Eating/Purging Type (AN-BP) and 14 to BN for some period of time. The remaining 44 patients remained AN-R only from the onset to the investigation period. Variables compared by ANOVA included anthropometric measures, personality traits such as Multiple Perfectionism Scale scores and Temperament and Character Inventory scores, and Beck Depression Inventory-II scores.
Results
In comparison with AN-R only patients, those who developed BN had significantly higher current BMI (p < 0.05) and maximum BMI in the past (p < 0.05). They also scored significantly higher for the psychological characteristic of parental criticism (p < 0.05) and lower in self-directedness (p < 0.05), which confirms previous reports, but these differences disappeared when the depression score was used as a co-variant. No significant differences were obtained for personality traits or depression among the AN-R only patients irrespective of their duration of illness.
Conclusion
The present findings suggest a tendency toward obesity among patients who cross over from AN-R to BN. Low self-directedness and high parental criticism may be associated with the development of BN by patients with AN-R, although the differences may also be associated with depression.
doi:10.1186/1751-0759-2-5
PMCID: PMC2275291  PMID: 18267038
7.  Hyperglycemia alters PI3k and Akt signaling and leads to endothelial cell proliferative dysfunction 
Diabetes mellitus is a major risk factor for the development of vascular complications. We hypothesized that hyperglycemia decreases endothelial cell (EC) proliferation and survival via phosphatidylinositol 3-kinase (PI3k) and Akt signaling pathways. We cultured human umbilical vein ECs (HUVEC) in 5, 20, or 40 mM d-glucose. Cells grown in 5, 20, and 40 mM mannitol served as a control for osmotic effects. We measured EC proliferation for up to 15 days. We assessed apoptosis by annexin V and propidium iodide staining and flow cytometry, analyzed cell lysates obtained on culture day 8 for total and phosphorylated PI3k and Akt by Western blot analysis, and measured Akt kinase activity using a GSK fusion protein. HUVEC proliferation was also tested in the presence of pharmacological inhibitors of PI3k-Akt (wortmannin and LY294002) and after transfection with a constitutively active Akt mutant. ECs in media containing 5 mM d-glucose (control) exhibited log-phase growth on days 7–10. d-Glucose at 20 and 40 mM significantly decreased proliferation versus control (P < 0.05 for both), whereas mannitol did not impair EC proliferation. Apoptosis increased significantly in HUVEC exposed to 40 mM d-glucose. dGlucose at 40 mM significantly decreased tyrosine-phosphorylated PI3k, threonine 308-phosphorylated-Akt, and Akt activity relative to control 5 mM d-glucose. Pharmacological inhibition of PI3k-Akt resulted in a dose-dependent decrease in EC proliferation. Transfection with a constitutively active Akt mutant protected ECs by enhancing proliferation when grown in 20 and 40 mM d-glucose. We conclude that d-glucose regulates Akt signaling through threonine phosphorylation of Akt and that hyperglycemia-impaired PI3k-Akt signaling may promote EC proliferative dysfunction in diabetes.
doi:10.1152/ajpheart.01088.2004
PMCID: PMC1618822  PMID: 15964918
endothelial cell proliferation; diabetes mellitus; phosphatidylinositol 3-kinase; protein kinase B; Akt; endothelial cell apoptosis
8.  Mid-Ventricular Obstructive Hypertrophic Cardiomyopathy Associated with an Apical Aneurysm: Evaluation of Possible Causes of Aneurysm Formation 
Yonsei Medical Journal  2007;48(5):879-882.
Mid-ventricular obstructive hypertrophic cardiomyopathy (MVOHCM) is a rare type of cardiomyopathy, associated with apical aneurysm formation in some cases. We report a patient presenting with ventricular fibrillation, an ECG with an above normal ST segment, and elevated levels of cardiac enzymes but normal coronary arteries. Left ventriculography revealed a left ventricular obstruction without apical aneurysm. There was a significant pressure gradient between the apical and basal sites of the left ventricle. Cine magnetic resonance imaging (MRI), performed on the 10th hospital day, showed asymmetric septal hypertrophy, mid-ventricular obstruction, and an apical aneurysm with a thrombus. The first evaluation by contrast-enhanced imaging showed a subendocardial perfusion defect and delayed enhancement. It was speculated that the intraventricular pressure gradient, due to mid-ventricular obstruction, triggered myocardial infarction, which subsequently resulted in apical aneurysm formation.
doi:10.3349/ymj.2007.48.5.879
PMCID: PMC2628158  PMID: 17963350
Mid-ventricular obstructive hypertrophic cardiomyopathy; magnetic resonance imaging
9.  Mid-Ventricular Hypertrophic Obstructive Cardiomyopathy Presenting with Acute Myocardial Infarction 
Texas Heart Institute Journal  2007;34(4):475-478.
Mid-ventricular hypertrophic obstructive cardiomyopathy is a rare type of cardiomyopathy that can be accompanied by apical aneurysm. We report the case of a patient who presented with ventricular fibrillation, ST-segment elevation on electrocardiography, and cardiac-enzyme elevation, in the presence of normal coronary arteries. Echocardiography and magnetic resonance imaging showed an hourglass appearance of the left ventricle with an aneurysm in the apex. Left-heart catheterization and continuous-wave Doppler echocardiography revealed a pressure gradient between the apical and basal chambers of the left ventricle. Impaired coronary artery circulation might play a role in the development of mid-ventricular obstruction in patients with mid-ventricular hypertrophic obstructive cardiomyopathy.
PMCID: PMC2170479  PMID: 18172535
Cardiomyopathy, hypertrophic/complications/physiopathology; heart aneurysm/etiology; magnetic resonance imaging; myocardial infarction; thallium radioisotopes/diagnostic use; tomography, emission computed, single-photon; ventricular outflow obstruction/diagnosis

Results 1-10 (10)