Hemostasis as soon as possible? The role of the time to angioembolization in the management of pelvic fracture.

Introduction: While transcatheter arterial embolization (TAE) is an effective way to control arterial bleeding associated with pelvic fracture, delayed TAE may increase mortality risk. The purpose of the current study was to determine how time to TAE affects outcomes in patients with pelvic fracture in the emergency department. Methods: From January 2014 to December 2016, the trauma registry and medical records of patients with pelvic fracture who underwent TAE were retrospectively reviewed. The relationship between the time to TAE and patient outcomes was evaluated. The characteristics of surviving and deceased patients were also compared to search for prognostic factors affecting survival. Results: Eighty-four patients were enrolled in the current study. Among patients with pelvic fracture who underwent TAE, the overall mortality rate was 16.7%. There were positive relationships between the time to TAE and the requirement for blood transfusion and between the time to TAE and intensive care unit (ICU) length of stay (LOS). Nonsurviving patients were significantly older (57.4 ± 23.3 vs. 42.7 ± 19.3 years old, p = 0.014) and had higher injury severity scores (ISSs) (36.4 ± 11.9 vs. 23.9 ± 10.9, p < 0.001) than were observed in surviving patients. There was no significant difference in the time to TAE between nonsurviving and surviving patients (76.9 ± 47.9 vs. 59.0 ± 29.3 min, p = 0.068). The multivariate logistic regression analysis showed that ISS and age served as independent risk factors for mortality. Every one unit increase in ISS or age resulted in a 1.154- or 1.140-fold increase in mortality, respectively (p = 0.033 and 0.005, respectively). However, the time to TAE serves as an independent factor for ICU LOS (p = 0.015). Conclusion: In pelvic fracture patients who require TAE for hemostasis, longer time to TAE may cause harm. An early hemorrhage control is suggested.

Effects of chronic hepatitis C infection on arterial stiffness.

Nonalcoholic fatty liver disease (NAFLD) is associated with increased arterial stiffness. Although chronic hepatitis C virus (HCV) infection was shown to be associated with metabolic disorder and chronic inflammation, the effects of chronic HCV infection on arterial stiffness remain unclear. This study recruited 221 patients including 32 normal controls, 72 NAFLD patients, and 117 subjects with HCV infection. Arterial stiffness was assessed by peripheral arterial stiffness index, Compliance Index (CI), and central arterial stiffness index, Stiffness Index derived from digital volume pulse by photoplethysmography. Levels of oxidative stress marker and inflammatory markers were also measured. The HCV group had significantly lower CI (4.8 ± 3.1 units vs. 3.9 ± 2.1 units vs. 3.0 ± 1.7 units; P for trend <.001) and higher Stiffness Index (7.0 ± 1.6 m/s vs. 8.3 ± 2.3 m/s vs. 8.4 ± 2.3 m/s; P for trend = .001) compared with the normal controls and NAFLD groups. Multivariate linear regression analysis showed that CI was independently correlated with systolic blood pressure (beta = -0.202, P = .013) and HCV infection (beta = -0.216, P = .036). Chronic HCV infection was independently associated with peripheral arterial stiffness. Peripheral arterial stiffness in chronic HCV infection was not associated with a marker of general inflammation (high-sensitivity C-reactive protein); however, a role for more specific markers of inflammation cannot be ruled out.

Complex IV subunit 1 defect predicts postoperative survival in hepatocellular carcinoma.

Mitochondrial oxidative phosphorylation (OXPHOS) is responsible for adenosine triphosphate synthesis and OXPHOS deficiency plays a significant role in tumorigenesis. The defects of mitochondrial-encoded OXPHOS subunits have been found in normal and cirrhotic liver, however their contributions in hepatocellular carcinoma (HCC) are not clear. The present study aimed to examine these defects in resected HCC tissues. In total, 102 human HCC tissues were collected from patients undergoing curative resection, and immunohistochemical staining was performed to assess tissue expression of complex I subunit 6, complex III subunit 3, complex IV subunit 1 (CIV-1) and complex V subunit 6. Cox proportional hazard model analysis was performed, including all clinicopathological factors, to postoperatively estimate the overall survival rate. The results showed that the majority of HCC tissues contained various degrees of expression defects for OXPHOS subunits. Among these, the major CIV-1 defect (expression defect area of >25% of the examined area) (P<0.001) and early distant metastasis (P<0.001) were independently associated with the overall survival rate. Kaplan-Meier analysis also demonstrated that the major CIV-1 defect was significantly associated with a poor overall survival rate (log-rank, P=0.002). The findings in the present study clearly indicate that the major CIV-1 expression defect may serve as an independent negative prognostic factor in HCC patients following curative resection.

Increased aortic stiffness and attenuated lysyl oxidase activity in obesity.

OBJECTIVE: One potential mechanism through which obesity exerts adverse effects on the vascular system is by increasing aortic stiffness, a change known to be predictive of increased cardiovascular mortality. The aim of this study was to investigate the pathophysiology that links obesity to aortic stiffening. APPROACH AND RESULTS: Obese (ob/ob) mice were used to examine physical, morphological, and molecular changes in the aorta in response to obesity. ob/ob mice had increased aortic pulse wave velocity and tissue rigidity. ob/ob aorta exhibited decreases of lysyl oxidase (LOX) activity and cross-linked elastin, and increases of elastin fragmentation and elastolytic activity. The aortas of ob/ob mice were surrounded by a significant amount of proinflammatory and pro-oxidative perivascular adipose tissue. In vitro studies revealed that the conditioned medium from differentiated adipocytes or the perivascular adipose tissue of ob/ob mice attenuated LOX activity. Furthermore, inhibition of LOX in wild-type lean mice caused elastin fragmentation and induced a significant increase in pulse wave velocity. Finally, we found that obese humans had stiffer arteries and lower serum LOX levels than do normal-weight humans. CONCLUSIONS: Our results demonstrated that obesity resulted in aortic stiffening in both humans and mice, and established a causal relationship between LOX downregulation and aortic stiffening in obesity.

Effects of deranged glucose homeostasis on peripheral arterial stiffness index in patients with pre-diabetes mellitus.

Premature arteriosclerosis may be one of the mechanisms linking pre-diabetes mellitus (pre-DM) and cardiovascular disease. We sought to characterize premature arteriosclerosis in pre-DM using different arterial stiffness indices and to find the independent contributors of this process. We recruited 33 patients without DM, 53 patients with pre-DM, and 34 subjects with DM. Both the compliance index (CI) and stiffness index (SI) were measured. Patients with pre-DM and DM had lower CI (3.8 ± 2.1 versus 5.2 ± 3.0 units; P < 0.05 and 3.6 ± 1.8 versus 5.2 ± 3.0 units; P < 0.05, respectively) and higher SI (8.0 ± 2.0 versus 6.7 ± 1.6 m/s; P < 0.01 and 9.4 ± 2.3 versus 6.7 ± 1.6 m/s; P < 0.001, respectively) than patients without DM. Using multivariate linear regression analysis, age, heart rate, and HOMA index were independent determinants for SI (whole model: R(2) = 0.47, P < 0.001), whereas male gender, hsCRP, and HOMA index were independent determinants for CI (whole model: R(2) = 0.34, P < 0.01). The HOMA index was an independent determinant for arterial stiffness. Increased insulin resistance may associate with increased arterial stiffness at peripheral arteries in pre-DM patients.

Effects of increased systemic inflammation and central obesity on arterial stiffness in patients with nonalcoholic fatty liver disease.

Nonalcoholic fatty liver disease (NAFLD) is associated with increasing arterial stiffness. We studied the effects of inflammation on different measurements of arterial stiffness in NAFLD. We recruited 80 patients with NAFLD and 40 control subjects. Both compliance index (CI) and stiffness index (SI) were measured. Patients with NAFLD had significantly lower CI (3.8 ± 2.1 vs 4.9 ± 2.9 units; P < .05) and higher SI (8.5 ± 2.4 vs 7.1 ± 1.5 m/s; P < .05) than the controls. Patients with NAFLD were further divided into 2 groups according to the median level of high-sensitivity C-reactive protein (hs-CRP). The CI was significantly lower in patients with NAFLD with high hs-CRP than in those with low hs-CRP (3.2 ± 1.7 vs 4.4 ± 2.5 units; P < .05); however, SI was not statistically different. We further found that waist circumference (odds ratio, 1.06; 95% confidence interval, 1.01-1.13; P < .05) was the only independent factor that predicted low CI (

Increased C-reactive protein is associated with future development of diabetes mellitus in essential hypertensive patients.

Coexistence of hypertension and diabetes mellitus (DM) increases the risk of cardiovascular disease. However, factors associated with future development of DM have not been well elucidated in patients already having essential hypertension. This study prospectively included 168 patients (mean age 41 +/- 7 years, 112 men) with essential hypertension. All patients did not have DM and vascular or renal complications initially. Baseline demographic data, blood pressure, body mass index, and antihypertensive agents were carefully evaluated and serum high-sensitivity C-reactive protein (hsCRP) was measured at the beginning of the study. All of the patients were followed for at least 6 months. The study endpoint was occurrence of new DM. After a mean follow-up period of 32 +/- 10 months, 22 subjects (13.1%) developed new DM. Patients with new DM had higher baseline glucose (105.2 +/- 11.8 vs 94.2 +/- 8.0 mg/dl, P < 0.001), triglyceride level (213.7 +/- 112.4 vs 155.6 +/- 83.2 mg/dl, P = 0.04), log hsCRP (0.31 +/- 0.44 vs 0.19 +/- 0.25 mg/dl, P = 0.016), and lower high-density lipoprotein (40.2 +/- 7.8 vs 46.6 +/- 14.4 mg/dl, P = 0.045). Total cholesterol, low-density lipoprotein, homeostasis model assessment index, and adiponectin were not different in patients with or without new DM. Among antihypertensive agents, only use of beta-blocker was significantly associated with new DM (P = 0.008). Multivariate Cox regression analysis showed log hsCRP (hazard ratio [HR] 9.77, 95% confidence interval [CI] 2.97-32.10, P < 0.001), age (HR 1.21, 95% CI 1.06-1.38, P = 0.004), and baseline glucose level (HR 1.11, 95% CI 1.06-1.15, P < 0.001) to be independent predictors for occurrence of new DM. High-sensitivity CRP was an independent factor for future development of DM in essential hypertensive patients. Increased inflammation might have a key role in the pathogenesis of DM in hypertension.

Association of central aortic pressures indexes with development of diabetes mellitus in essential hypertension.

BACKGROUND: Diabetes mellitus (DM) and hypertension (HT) frequently coexist. Increased central aortic pressures indexes are associated with HT; however, possible associations of these indexes with future development of DM have never been studied in HT. METHODS: We recruited 178 patients with uncomplicated nondiabetic HT in this study. Baseline glucose, insulin, lipid profiles, and central aortic pressure indexes obtained using applanation tonometry were measured at the beginning of the study. Patients were followed for new-onset DM. RESULTS: After a mean follow-up period of 31 ± 12 months, 22 patients (12.4%) developed new-onset DM. In multivariate regression analyses adjusted for age, sex, and mean blood pressure (BP) in model 1, we found that central systolic BP (CSBP; hazard ratio 1.24, 95% CI 1.10-1.41, P < 0.001), and augmentation index (AIx) corrected at heart rate 75/min (AIx(75); hazard ratio 1.58, 95% CI 1.11-1.58, P < 0.05) were independent predictors for new-onset DM. After adjustment for age, sex, mean BP, glucose concentration, and ß-blocker use in model 2, we found that CSBP (hazard ratio 1.36, 95% CI 1.19-1.55, P < 0.001) and AIx(75) (hazard ratio 1.71, 95% CI 1.16-2.52, P < 0.01) were independent predictors for new-onset DM. CONCLUSIONS: CSBP and AIx(75) were independent factors for future DM in essential hypertensive patients. Increased central pressure indexes were associated with risk of DM in essential hypertension.