Huei Fong Hung

The diagnostic accuracy of 256-row computed tomographic angiography compared with invasive coronary angiography in patients with suspected coronary artery disease

AIMS To assess the diagnostic accuracy of 256-row computed tomographic angiography (CTA) in patients with suspected coronary artery disease (CAD). Non-invasive imaging of the coronary artery by CTA has increasingly been used in recent years. The accuracy of 256-row CTA has not yet been studied. We sought to assess the accuracy of 256-row CTA compared with invasive coronary angiography (ICA) in the diagnosis and assessment of CAD. METHODS AND RESULTS We prospectively evaluated 104 consecutive individuals who accepted CTA and then underwent ICA. The presence of stenosis > or =50% was considered obstructive. The diagnostic accuracy of CTA for detecting obstructive stenosis was compared with that of ICA. The area under the receiver-operating-characteristic curve (AUC) was used to evaluate the diagnostic accuracy of CTA relative to ICA. A total of 86 patients had obstructive CAD. The patient-based analysis of CTA for detecting stenosis > or =50% according to ICA revealed an AUC of 0.744 [95% confidence interval (CI), 0.572-0.916], with a sensitivity of 98.8%, a specificity of 50%, a positive predictive value (PPV) of 92.4%, and a negative predictive value (NPV) of 87.5%. The segment-based analysis revealed an AUC of 0.915 (95% CI, 0.847-0.982), with a sensitivity of 93.5%, a specificity of 95%, a PPV of 77.6%, and an NPV of 98.7%. The vessel-based analysis revealed an AUC of 0.887 (95% CI, 0.808-0.966), with a sensitivity of 94.3%, a specificity of 87.3%, a PPV of 82.7%, and an NPV of 95.9%. CONCLUSION 256-Row CTA is a highly sensitive test of CAD and has a high predictive value. 256-Row CTA may be a potential alternative to detect coronary artery stenosis and rule out CAD in suspected patients.

The molecular regulation of resistin expression in cultured vascular smooth muscle cells under hypoxia

Objectives Resistin has a potential role in atherosclerosis because resistin produces proinflammatory effects in the vascular wall. However, the molecular mechanism of resistin increase in atherosclerosis remains unclear. Hypoxia plays an important role in vascular remodeling and directly affects vascular smooth muscle cells functions. We sought to investigate the molecular regulation of resistin expression under hypoxia in cultured vascular smooth muscle cells. Methods Vascular smooth muscle cells from thoracic aorta of adult Wistar rats were cultured and subjected to hypoxia at 2.5% oxygen in a hypoxic chamber. Western blot, real-time PCR, reactive oxygen species assay, and promoter activity were measured. Results Hypoxia significantly increased the resistin protein (3.5-fold, P < 0.001) and mRNA (4.8-fold, P < 0.001) expression as compared with the control cells. The specific extracellular signal-regulated kinase (ERK) inhibitor PD98059, antioxidant N-acetylcysteine, and ERK siRNA attenuated the induction of resistin protein by hypoxia. It increased the phosphorylated ERK protein expression (3.2-fold, P < 0.001), whereas pretreatment with PD98059 and N-acetylcysteine significantly blocked the increase of phosphorylated ERK by hypoxia. It also increased the reactive oxygen species production (9.3-fold, P < 0.001), and pretreatment with N-acetylcysteine significantly blocked the induction of reactive oxygen species by hypoxia. Hypoxia increased resistin promoter activity (5.1-fold, P < 0.001), and the activity was abolished when nuclear factor of activating T cells in the promoter area was mutated. Pretreatment with PD98059 and N-acetylcysteine significantly attenuated the resistin promoter activity induced by hypoxia. Conclusion Hypoxia increases the resistin expression in cultured rat vascular smooth muscle cells under hypoxia. The hypoxia-induced resistin is mediated through reactive oxygen species, ERK mitogen-activated protein (MAP) kinase and nuclear factor of activating T cells pathway.

Human mesenchymal stem cells improve myocardial performance in a splenectomized rat model of chronic myocardial infarction

BACKGROUND/PURPOSE Cellular therapy has been applied to animal studies and clinical trials for acute or subacute myocardial infarction. Little is known about the effect of cell therapy on chronic myocardial infarction. The goal of this study was to investigate myocardial performance after human bone marrow-derived mesenchymal stem cell (hMSCs) transplantation in rats with chronic myocardial infarction. METHODS The hMSCs were obtained from adult human bone marrow and expanded in vitro. The purity and characteristics of hMSCs were identified by flow cytometry and immunophenotyping. Splenectomy in male rats was performed to prevent immune reaction. One week after splenectomy, ligation of the left anterior descending coronary artery was performed to induce myocardial infarction. Four weeks after ligation of the coronary artery, culture-expanded hMSCs were injected intramyocardially at the left anterior free wall. Left ventricular function measured by echocardiography, infarct size and immunohistochemical stain were performed to evaluate the effect of the therapy. RESULTS The engrafted hMSCs were positive for the cardiac marker troponin T. Infarct size (35.4 +/- 3.4% vs. 53.3 +/- 3.0%, p < 0.001) and fibrotic area (2.6 +/- 0.1% vs. 5.9 +/- 0.2%, p < 0.001) were significantly smaller in the hMSC-treated group than in the control group at 28 days after therapy. hMSC transplantation resulted in smaller left ventricular end-diastolic dimension (6.5 +/- 0.1 mm vs. 7.9 +/- 0.7 mm, p < 0.001) and better left ventricular ejection fraction (88.7 +/- 1.2% vs. 65.8 +/- 2.5%, p < 0.001) than in the control group. Capillary density was markedly increased after hMSC transplantation compared with the control group. CONCLUSION This study demonstrates that intramyocardial transplantation of hMSCs improves cardiac function after chronic myocardial infarction through enhancement of angiogenesis and myogenesis in the ischemic myocardium. Transplantation of hMSCs for myocardial regeneration may become the future therapy for chronic myocardial infarction.

Hyperbaric oxygen induces placental growth factor expression in bone marrow-derived mesenchymal stem cells

The bone marrow is home to mesenchymal stem cells (MSCs) that are able to differentiate into many different cell types. The effect of hyperbaric oxygen (HBO) on MSCs is poorly understood. Placental growth factor (PlGF) is an attractive therapeutic agent for stimulating revascularization of ischemic tissue. HBO has been shown to improve diabetic wound healing by increase circulating stem cells. We hypothesized that HBO induces PlGF expression in bone marrow-derived MSCs. The MSCs were obtained from adult human bone marrow and expanded in vitro. The purity and characteristics of MSCs were identified by flow cytometry and immunophenotyping. HBO at 2.5 ATA (atmosphere absolute) significantly increased PlGF protein and mRNA expression. The induction of PlGF protein by HBO was significantly blocked by the addition of N-acetylcysteine, while wortmannin, PD98059, SP600125 and SB203580 had no effect on PlGF protein expression. However, the specific inhibitor of nitric oxide synthase, L-NAME did not alter the PlGF protein expression induced by HBO. HBO significantly increased the reactive oxygen species production and pretreatment with N-acetylcysteine significantly blocked the induction of reactive oxygen species by HBO. HBO significantly increased the migration and tube formation of MSCs and pretreatment with N-acetylcysteine and PlGF siRNA significantly blocked the induction of migration and tube formation by HBO. In conclusion, HBO induced the expression of PlGF in human bone marrow-derived MSCs at least through the oxidative stress-related pathways, which may play an important role in HBO-induced vasculogenesis.

Admission hyperglycemia predicts poorer short‐ and long‐term outcomes after primary percutaneous coronary intervention for ST‐elevation myocardial infarction

Admission hyperglycemia is associated with poor outcome in patients with myocardial infarction. The present study evaluated the relationship between admission glucose level and other clinical variables in patients with ST‐elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI).

Significance of left circumflex artery-related acute myocardial infarction without ST-T changes

INTRODUCTION Left circumflex (LC)-related acute myocardial infarction (AMI) presenting without ST-T changes has been underdiagnosed in the emergency department. There is little information on its clinical features and significance. AIMS The aims of the study were to investigate the clinical characteristics and outcomes of LC-related AMI without ST-T changes. POPULATION AND METHODS Ninety-six patients were admitted for LC-related AMI. Comparisons between those with and without ST-T changes were analyzed. RESULTS Twenty-two patients (23%) did not have ST-T changes, whereas 74 patients (77%) had them. Patients without ST-T changes had younger age (55.6 + or - 16.8 vs 62.6 + or - 12.0 years, P = .03), fewer presented as Killip III/IV (4.5% vs 27.4%, P = .02) and with lower creatine kinase (1647.3 + or - 1602.2 vs 2778.2 + or - 2343.3 IU/L, P = .037) and creatine kinase-MB (136.8 + or - 130.3 vs 247.7 + or - 200.0 IU/L, P = .017), and more were with concurrent culprit lesion in the middle or distal LC and right- or balanced-dominant coronary circulation (86.4% vs 44.6%, P < .001). During follow-up, the need for repeat percutaneous coronary intervention (48.6% vs 45.5%, P = .40) and recurrent infarction (13.5% vs 13.6%, P = .62) were similar between the 2 groups. The 30-day mortality (0% vs 5.4%, P = .35) and overall mortality rate (4.5% vs 12.2%, P = .28) between them were not different statistically. CONCLUSION The relatively lower prevalence of LC-related AMI without ST-T changes in the study might be underestimated. These patients have smaller infarct size than patients with ST-T changes without differences in the short- and long-term outcomes between them.

Renal dysfunction and the risk of postoperative atrial fibrillation after cardiac surgery: role beyond the CHA2DS2-VASc score.

AIMS To investigate whether renal dysfunction is a useful predictor of postoperative atrial fibrillation (POAF) after cardiac surgery. We also aimed to determine whether the addition of renal dysfunction into the scoring system could improve diagnostic accuracy of the CHA2DS2-VASc score to predict POAF. METHODS AND RESULTS The study prospectively enrolled 350 consecutive patients who underwent cardiac surgery. Echocardiography was performed before cardiac surgery. Renal dysfunction was defined as estimated glomerular filtration rate < 60 mL min(-1) 1.73 m(-2). All patients were monitored with continuous electrocardiographic telemetry for the occurrence of POAF until the day of hospital dismissal. Postoperative atrial fibrillation occurred in 103 of 350 patients (29%). Patients with POAF was associated with longer intensive care unit stay compared with those without POAF (3.7 ± 2.2 vs. 3.1 ± 1.4 days, P = 0.002). Both the CHA2DS2-VASc score and renal dysfunction were independent predictors of POAF in multivariate analysis. Renal dysfunction can further stratify patients with a CHA2DS2-VASc score of 0 or 1 into two groups with different POAF rates (3.1% vs. 68.8%, P < 0.001). A new scoring system (R-CHA2DS2-VASc score) derived by assigning an additional point representing renal dysfunction to the CHA2DS2-VASc score could improve its predictive accuracy. The area under the receiver operating characteristic curve increased from 0.68 to 0.71 (P < 0.001). Furthermore, the rate of left ventricular diastolic dysfunction also increased with increasing renal dysfunction. CONCLUSION Renal dysfunction, associated with left ventricular diastolic dysfunction, was a significant risk factor for POAF after cardiac surgery and may improve the diagnostic accuracy of the CHA2DS2-VASc score.