Both epicardial and peri-aortic adipose tissue blunt heart rate recovery beyond body fat mass.

Background: Epicardial adipose tissue (EAT) as a marker of metabolic disorders has been shown to be closely associated with a variety of unfavorable cardiovascular events and cardiac arrhythmias. Data on regional-specific visceral adiposity outside the heart and its modulation on autonomic dysfunction, particularly heart rate recovery after exercise, remain obscure. Methods: We studied 156 consecutive subjects (mean age: 49.3 ± 8.0 years) who underwent annual health surveys and completed treadmill tests. Multi-detector computed tomography-based visceral adiposity, including EAT and peri-aortic fat (PAF) tissue, was quantified using dedicated software (Aquarius 3D Workstation, TeraRecon, San Mateo, CA, USA). We further correlated EAT and PAF with blood pressure and heart rate (HR) recovery information from an exercise treadmill test. Metabolic abnormalities were scored by anthropometrics in combination with biochemical data. Results: Increased EAT and PAF were both associated with a smaller reduction in systolic blood pressure during the hyperventilation stage before exercise compared to supine status (ß-coefficient (coef.): -0.19 and -0.23, respectively, both p < 0.05). Both visceral adipose tissue mediated an inverted relationship with heart rate recovery at 3 (EAT: ß-coef.: -0.3; PAF: ß-coef.: -0.36) and 6 min (EAT: ß-coef.: -0.32; PAF: ß-coef.: -0.34) after peak exercise, even after adjusting for baseline clinical variables and body fat composition (all p < 0.05). Conclusion: Excessive visceral adiposity, whether proximal or distal to the heart, may modulate the autonomic response by lowering the rate of HR recovery from exercise after accounting for clinical metabolic index. Cardiac autonomic dysfunction may partly explain the increase in cardiovascular morbidity and mortality related to both visceral fats.

Beyond malignancy: the role of carbohydrate antigen 125 in heart failure.

Carbohydrate antigen 125 (CA-125), traditionally a tumor marker for screening, diagnosis, and monitoring in ovarian malignancy, had recently been shown increasing evidence and more extensively recognized/explored as a novel surrogate of heart failure (HF). The exact mechanisms underlying the pathophysiologic link between elevated serum CA-125 concentration and HF may be multi-factorial, with both mechanical and inflammatory process including numerous potential cytokines involved. Accumulating data had consistently indicated its diagnostic and prognostic role in HF patients in various clinical settings, however, there is limited clinical information regarding the incremental value or head-to-head comparison of such marker to other well-established HF markers. In this brief review, we aimed to discuss the biosynthesis, and potential insights of underlying pathophysiologies associated with CA-125 secretion in the scenarios of cardiac structural/functional alterations and HF, and further explored its current usage and roles in several recent reports.

Cardiac Systolic Mechanics in Heart Failure with Preserved Ejection Fraction: New Insights and Controversies.

UNLABELLED: Heart failure with preserved ejection fraction (HFpEF) is a cardinal and complex syndrome tightly linked to several co-morbidities, and is currently emerging as a new public health problem in the elderly population. However, despite aggressive intervention, patients with HFpEF typically have a poor prognosis. Part of the reason underlying this phenomenon can be attributed to the insufficiently understood pathophysiology behind this syndrome. Traditional echocardiography-derived parameters such as left ventricular (LV) ejection fraction (LVEF) may not be useful in characterizing such a clinical disorder, or in further identifying the subjects at risk, owing in part to its lack of power to disclose subclinical systolic dysfunction in such a clinical scenario. Herein, we briefly reviewed the clinical manifestations and risk factors of HFpEF, and further provided insights into the understanding of the ventricular architecture and cardiac mechanics underlying HFpEF by utilizing advanced cardiovascular imaging modalities, with a special focus on myocardial deformation. KEY WORDS: Heart failure; Speckle tracking imaging; Strain.

Expression of matrix metalloproteinases-13 in the damage process of rat articular chondrocyte induced by fluoride and aluminium / 中国地方病学杂志

Objective To observe the influence of fluoride and aluminum on the expression of matrix metalloproteinase-13(MMP-13) in rat articular chondrocytes. Methods Original generation chondrocytes of rats was cultured and divided into fluoride group, aluminum group, fluoride plus aluminum group and control group. NaF and A1C13 at concentrations of 1 mmol/L and 2 mmol/L were administered to intoxicate the cells for 24, 48, 72 h respectively. Cells were extracted to undergo reverse transcription the polymerase chain reaction(RT-PCR) at different times to observe mRNA expression of MMP-13, and protein expression was detected by Western-blot. Results In 24 h, the content of MMP-13 mRNA in fluoride group(0.830±0.043), aluminum group(1.279±0.060) and fluoride plus aluminum group(0.983±0.028) was higher than that in the control group(0.707±0.026, P<0.05), and relative expression of MMP-13 mRNA in aluminum group was the highest. In 48 h, the content of MMP-13 mRNA in fluoride group (0.964±0.180), aluminum group (1.333±0.105) and fluoride plus aluminum group (0.915±0.137) was higher than that in the control group(0.660±0.055, P<0.05), and the relative expression in aluminum group was the highest. In 72 h, the content of MMP-13 mRNA in fluoride group(0.866±0.115), aluminum group(0.846±0.089) and fluoride plus aluminum group(0.967±0.196) had no statistical significance(P>0.05) compared with the control group(0.809±0.179). In 24 h, the content of MMP-13 protein in fluoride group(1.050±0.084), aluminum group(1.010±0.113) and fluoride plus aluminum group(0.977±0.202) had no statistical significance(P>0.05) compared with the control group(0.860±0.038). In 48 h, the content of MMP-13 protein in fluoride group(0.671±0.020), aluminum group(1.134±0.094) and fluoride plus aluminum group (0.923±0.087) was higher than that in the control group (0.647±0.025, P<0.05), but no significant difference being observed between groups (P>0.05). In 72 h, the content of MMP-13 protein in fluoride group(0.672±0.022), aluminum group(1.088±0.072) and fluoride plus aluminum group(0.772±0.030) was higher than that in the control group(0.577±0.026, P<0.05). It was the highest in the aluminum group, the intra-group difference had statistical significance(P<0.05). Conclusions Fluoride and aluminum damage chondrocytes to some extent, toxicity of aluminum itself is greater than fluoride and fluoride plus aluminum. Abnormal expression of MMP-13 can be observed in the chondrocyte damage process induced by fluoride and aluminum.

Mitochondrial DNA alterations in blood of the humans exposed to N,N-dimethylformamide.

N,N-Dimethylformamide (DMF) has been widely used in industries because of its extensive miscibility with water and solvents. Its health effects include hepatotoxicity and male reproductoxicity, possibly linked with mitochondrial DNA (mtDNA) alterations including mtDNA common deletion (DeltamtDNA(4977)) and mtDNA copy number. The relationship between DMF exposure and mtDNA alterations, however, has not been postulated yet. The purposes of this study were to investigate whether the DMF exposure is associated with DeltamtDNA(4977) and mtDNA copy number and to evaluate the DMF-derived mtDNA alterations are more associated with exposure to the airborne DMF concentrations or to the levels of two urinary DMF biomarkers of N-methylformamide (NMF) and N-acetyl-S-(N-methylcarbamoryl) cysteine(AMCC). Thirteen DMF-exposed workers and 13 age and seniority-matched control workers in a synthetic leather factory were monitored on their airborne DMF, NMF and AMCC in the urine as well as DeltamtDNA(4977) and mtDNA copy number in blood cells. We found that the frequencies of relative DeltamtDNA(4977) in DMF-exposed group were significantly higher than those in the control group. Moreover, elevation in the proportion of DeltamtDNA(4977) of individuals with high urine AMCC (U-AMCC) and airborne DMF levels were significantly higher than those without. We conclude that long-term exposure to DMF is highly associated with the alterations of mtDNA in urine and blood cells. The DeltamtDNA(4977) was more significantly related to repeated exposure to DMF and mtDNA copy number was more closely related to short-term DMF exposure. We also confirmed that U-AMCC is more appropriate to serve as a toxicity biomarker for DMF exposure than U-NMF. Further study with a larger number of subjects is warranted.