Pericardial Fat and the Risk of Heart Failure

2021 ◽  
Vol 77 (21) ◽  
pp. 2638-2652 ◽  
Author(s):  
Satish Kenchaiah ◽  
Jingzhong Ding ◽  
J. Jeffrey Carr ◽  
Matthew A. Allison ◽  
Matthew J. Budoff ◽  
...  
2021 ◽  
Vol 78 (15) ◽  
pp. e111
Author(s):  
Stefano Bonapace ◽  
Giulio Molon ◽  
Alessio Marinelli ◽  
Laura Lanzoni ◽  
Giovanni Targher

2016 ◽  
Vol 22 (9) ◽  
pp. S219
Author(s):  
Masaaki Konishi ◽  
Eiichi Akiyama ◽  
Noriaki Iwahashi ◽  
Toshiaki Ebina ◽  
Kazuo Kimura

Circulation ◽  
2017 ◽  
Vol 135 (suppl_1) ◽  
Author(s):  
J J Carr ◽  
Yaorong Ge ◽  
Edmond K Kabagambe ◽  
James G Terry ◽  
Donald Lloyd-Jones ◽  
...  

Background: Glagov identified cross-sectional enlargement and maintenance of the lumen of the coronary artery (CA) in post-mortem studies as an early feature of atherosclerotic coronary heart disease (CHD) that precedes the development of stenosis, coronary artery calcium (CAC) and plaque rupture. This structural change in the CA wall has been termed positive remodeling. We hypothesized that larger CA cross-sectional areas, consistent with positively remodeled CA, is associated with prevalent or soon-to-be incident coronary heart disease (CHD) and cardiovascular disease (CVD) events. Methods: In 2946 black and white male and female CARDIA participants aged 42-56 years, who had thin-slice (<1 mm), ECG gated, non-contrast coronary CT in 2010-2011, we measured CA cross-sectional area (CSA) in the proximal epicardial CA at 24 pre-specified locations. The mean of all measurements was calculated to provide a summary of all CA (CA CSA_all ). We performed logistic regression with medical-record adjudicated CVD prevalence (n=96) or incidence in the following 3 years (n=27) as the outcome, predicted from this estimate of positive remodeling adjusting for age, race, sex, presence of coronary artery calcium (CAC), and amount of pericardial fat as covariates. Results: CA CSA_all had a mean ± SD 21.2 ± 6.7 mm 2 . The adjusted odds ratio (OR) for having any CVD was 1.06 (95% CI 1.03-1.09, p<0.0001) per mm 2 (Table). ORs for CVD increased across quartiles of CA CSA_all . Corresponding OR for any coronary heart disease (n=66) was not significant, but was significant for stroke (n=42) and for heart failure (n=27). Further adjustment for traditional risk factors assessed in 2010-2011 did not alter these estimates substantially. Conclusion: Individuals with larger CA cross-sectional areas had increased odds of CVD, stroke, and heart failure, but not CHD, independent of CAC and pericardial fat. CA CSA_all may be an imaging biomarker of coronary positive remodeling and provide new insight into progression from subclinical to premature clinical CVD.


2015 ◽  
Vol 241 (2) ◽  
pp. 607-614 ◽  
Author(s):  
Cho-Kai Wu ◽  
Hao-Yuan Tsai ◽  
Mao-Yuan M. Su ◽  
Yi-Fan Wu ◽  
Juey-Jen Hwang ◽  
...  

Author(s):  
George Hug ◽  
William K. Schubert

A white boy six months of age was hospitalized with respiratory distress and congestive heart failure. Control of the heart failure was achieved but marked cardiomegaly, moderate hepatomegaly, and minimal muscular weakness persisted.At birth a chest x-ray had been taken because of rapid breathing and jaundice and showed the heart to be of normal size. Clinical studies included: EKG which showed biventricular hypertrophy, needle liver biopsy which showed toxic hepatitis, and cardiac catheterization which showed no obstruction to left ventricular outflow. Liver and muscle biopsies revealed no biochemical or histological evidence of type II glycogexiosis (Pompe's disease). At thoracotomy, 14 milligrams of left ventricular muscle were removed. Total phosphorylase activity in the biopsy specimen was normal by biochemical analysis as was the degree of phosphorylase activation. By light microscopy, vacuoles and fine granules were seen in practically all myocardial fibers. The fibers were not hypertrophic. The endocardium was not thickened excluding endocardial fibroelastosis. Based on these findings, the diagnosis of idiopathic non-obstructive cardiomyopathy was made.


Author(s):  
Chi-Ming Wei ◽  
Margarita Bracamonte ◽  
Shi-Wen Jiang ◽  
Richard C. Daly ◽  
Christopher G.A. McGregor ◽  
...  

Nitric oxide (NO) is a potent endothelium-derived relaxing factor which also may modulate cardiomyocyte inotropism and growth via increasing cGMP. While endothelial nitric oxide synthase (eNOS) isoforms have been detected in non-human mammalian tissues, expression and localization of eNOS in the normal and failing human myocardium are poorly defined. Therefore, the present study was designed to investigate eNOS in human cardiac tissues in the presence and absence of congestive heart failure (CHF).Normal and failing atrial tissue were obtained from six cardiac donors and six end-stage heart failure patients undergoing primary cardiac transplantation. ENOS protein expression and localization was investigated utilizing Western blot analysis and immunohistochemical staining with the polyclonal rabbit antibody to eNOS (Transduction Laboratories, Lexington, Kentucky).


2020 ◽  
Vol 134 (1) ◽  
pp. 71-72
Author(s):  
Naseer Ahmed ◽  
Masooma Naseem ◽  
Javeria Farooq

Abstract Recently, we have read with great interest the article published by Ibarrola et al. (Clin. Sci. (Lond.) (2018) 132, 1471–1485), which used proteomics and immunodetection methods to show that Galectin-3 (Gal-3) down-regulated the antioxidant peroxiredoxin-4 (Prx-4) in cardiac fibroblasts. Authors concluded that ‘antioxidant activity of Prx-4 had been identified as a protein down-regulated by Gal-3. Moreover, Gal-3 induced a decrease in total antioxidant capacity which resulted in a consequent increase in peroxide levels and oxidative stress markers in cardiac fibroblasts.’ We would like to point out some results stated in the article that need further investigation and more detailed discussion to clarify certain factors involved in the protective role of Prx-4 in heart failure.


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