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Results for “fat attenuation index”

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PubMed2026

Comprehensive assessment of vasospastic angina using coronary computed tomography angiography: synergistic value of the presence of myocardial bridge, perivascular inflammation, and myocardial extracellular volume fraction.

AIMS: Coronary computed tomography angiography (CCTA) has evolved beyond anatomical assessment to include sophisticated tissue characterization. While an elevated perivascular fat attenuation index around the right coronary artery (FAI-RCA) is known to reflect coronary inflammation in vasospastic angina (VSA), recurrent vasospasms may also induce chronic subclinical myocardial injury and subsequent remodelling, potentially associated with an increased myocardial extracellular volume fraction (ECV). However, the diagnostic integration of ECV and FAI-RCA for identifying VSA in patients with angina with non-obstructive coronary arteries (ANOCA) remains to be elucidated. METHODS AND RESULTS: This study included consecutive ANOCA patients who underwent CCTA with a dedicated ECV protocol, followed by an invasive spasm provocation test. Comprehensive CCTA analysis quantified both FAI-RCA and the transmural ECV gradient (the difference between endocardial and epicardial ECV: ECVEndo - ECVEpi). Of the 100 patients analysed (mean age: 65.3 ± 11.8 years; 55% male), 27 were diagnosed with VSA. Multivariable logistic regression analysis identified transmural ECV gradient [odds ratio (OR): 1.12, 95% confidence interval (CI): 1.01-1.25], presence of myocardial bridging (MB) (OR: 3.49, 95% CI: 1.25-9.74), and high FAI-RCA (> -70.95 Hounsfield units [HU]) (OR: 5.79, 95% CI: 2.06-16.30) as significant independent predictors of VSA (all P < 0.05). Notably, the integration of transmural ECV gradient provided incremental diagnostic value beyond FAI-RCA and MB, as assessed by the Net Reclassification Improvement and Integrated Discrimination Improvement. CONCLUSION: A multi-parametric CCTA approach potentially identifies patients at high risk for VSA. The significant association of the transmural ECV gradient with VSA suggests that myocardial remodelling imaging provides a novel diagnostic window into the cumulative myocardial impact of vasospasm, independent of active adipose tissue inflammation and the presence of MB.

Humans↗

PubMed1992

Diet and risk of clinical diabetes in women.

To determine the relations of diet with risk of clinical noninsulin-dependent diabetes, we analyzed data from a prospective cohort of 84360 US women. During 6 y of follow-up we identified 702 definite incident cases. Because body mass index (BMI) is a powerful risk factor for diabetes, we examined the relations of fat (including type), fiber, sucrose, and other components of diet to risk of diabetes, among women with BMIs (in kg/m2) less than 29 kg/m2. After controlling for body mass index, previous weight change, and alcohol intake, we observed no associations between intakes of energy, protein, sucrose, carbohydrate, or fiber and risk of diabetes. Compared with women in the lowest quintile of energy-adjusted intake, and relative risks (and tests for trend) for those in the highest quintile were 0.61 (P trend = 0.03) for vegetable fat, 0.62 (P trend = 0.008) for potassium, 0.70 (P trend = 0.005) for calcium, and 0.68 (P trend = 0.02) for magnesium. These inverse associations were attenuated among obese women (BMIs greater than or equal to 29).

Adult↗

PubMed1992

The roles of insulin, obesity, and fat distribution in the elevation of cardiovascular risk factors in impaired glucose tolerance. The San Luis Valley Diabetes Study.

The objective of this study was to determine whether a less favorable risk factor pattern for cardiovascular disease among persons with impaired glucose tolerance could be explained by fasting insulin, obesity, and/or a central distribution of body fat. Between 1984 and 1988, cardiovascular risk factors were examined cross-sectionally in Hispanic and non-Hispanic white participants in the San Luis Valley Diabetes Study who had either impaired (n = 173) or normal (n = 1,107) glucose tolerance. Sex-specific analysis of covariance models were constructed to adjust risk factor levels for age, age and insulin, and age, insulin, body mass index, and centrality index. Both males and females with impaired glucose tolerance had higher age-adjusted mean diastolic blood pressures, heart rates, uric acid levels, and triglyceride levels and lower levels of high density lipoprotein (HDL) cholesterol and HDL3 cholesterol than normal subjects; differences were significant for all risk factors except HDL cholesterol and HDL3 cholesterol in males. Differences in diastolic blood pressure in males, and differences in heart rate and triglyceride in both sexes, remained significant after adjustment for all covariates. However, differences in uric acid in males and differences in diastolic blood pressure and HDL3 cholesterol in females were attenuated to borderline significance levels. Differences in uric acid and HDL cholesterol in females were diminished to nonsignificant levels, especially after adjustment for obesity-related measures. With few exceptions, fasting insulin did not appear to play a major role in accounting for differences in these risk factors. With adjustment, ethnic differences (Hispanic vs. non-Hispanic white) were smaller and were statistically significant less often than differences observed between impaired and normal glucose tolerant groups. The authors concluded that hyperinsulinemia, obesity, and a central body fat distribution accounted for some, but usually not all, of the less favorable cardiovascular risk factor pattern found in subjects with impaired glucose tolerance.

Adult↗

PubMed1992

Weight loss normalizes the inhibitory effect of N6-(phenylisopropyl)adenosine on lipolysis in fat cells of massively obese human subjects.

1. Fat cells were isolated from massively obese patients at or before gastric bypass, from other patients after normalization of body weight after gastric bypass or gastroplasty (post-bypass patients) and from control subjects of a stable normal body weight. 2. The inhibition of isoprenaline-stimulated lipolysis by N6-(phenylisopropyl)adenosine in the presence of adenosine deaminase was much attenuated in cells from the massively obese patients as compared with those from normal-weight control subjects, but was normal in cells from post-bypass patients. 3. Isolated fat cells of the massively obese patients were larger (913 +/- 197 pl, mean +/- SEM) than those of the normal-weight group (437 +/- 95 pl). The volume of cells from the post-bypass patients was only 125 +/- 49 pl, although the body mass index of this group was almost exactly the same as that of the normal-weight control subjects. 4. Although epidemiological studies have suggested that genetic factors are important in the development and maintenance of obesity, these results demonstrate that the changes observed in the inhibitory regulation of lipolysis in obesity are secondary.

Adenosine Deaminase↗

PubMed2026

Genetically Predicted Muscle Mass and Function in Relation to Deep Vein Thrombosis: A Two-step Mendelian Randomization Study Highlighting the Mediating Role of BMI.

BackgroundSarcopenia is observationally linked to venous thromboembolism, but the causal architecture and underlying biological pathways remain largely unclear. This study investigated the causal effects of sarcopenia-related traits on lower extremity deep vein thrombosis (DVT) and quantified potential mediating mechanisms.MethodsWe performed two-sample bidirectional Mendelian randomization (MR) and two-step mediation MR using large-scale GWAS data from UK Biobank, EMBL-EBI, and FinnGen. Exposures included appendicular lean mass (ALM), leg fat-free mass (LFM), hand grip strength, and walking pace. Eighteen candidate mediators were screened for indirect pathways.ResultsGenetically predicted higher ALM was significantly associated with increased DVT risk (FinnGen: OR = 1.288, 95% CI: 1.215-1.365, P < 0.001). Similar positive associations were observed for LFM (OR = 1.920-1.954, P < 0.001). By contrast, muscle functional traits - grip strength and walking pace - demonstrated no consistent causal effects. Reverse MR confirmed a unidirectional relationship. Body mass index (BMI) emerged as a pivotal mediator, accounting for 7.58% - 10.50% of the ALM-DVT effect and 52.74% - 62.73% of the LFM-DVT effect. Notably, the independent effect of ALM was largely attenuated after adjusting for metabolic confounders in multivariable MR.ConclusionGenetic predisposition to high muscle mass, rather than functional strength, increases DVT risk. This relationship appears to be significantly driven by metabolic adiposity, suggesting that the "muscle-vascular-coagulation" interaction is partly explained by body-size-related metabolic burden. Risk stratification should integrate muscle mass evaluation with comprehensive metabolic health assessments.

Humans↗

PubMed1992

Estimation of changes in genetic parameters in selected lines of mice using REML with an animal model. 2. Body weight, body composition and litter size.

Restricted Maximum Likelihood (REML) with an animal model was used to estimate genetic parameters of body weight, body consumption and litter size of lines of mice selected for 20 generations on an index of lean mass at 10 weeks in males, highly correlated with body weight, and for a further 18 generations on body weight at 10 weeks in males and females. Univariate and multivariate estimates of heritability were about 0.5 and those of common environment correlations were about 0.25 for both body weight and composition. Body weight and fat pad weight had genetic and phenotypic correlations of about 0.5. The heritability estimate of litter size was about 0.15 from univariate analysis, rather lower from multivariate, and the estimate of its genetic correlation with body weight was about 0.25. There were reductions in heritability of both body weight and litter size in later generations, even though full pedigrees were fitted and inferences made to the base population, but a plateau in response to selection for increased body weight could not be explained by a complete attenuation of genetic variance.

Animals↗

PubMed1992

Hemodynamics of the male fat distribution pattern.

A male fat distribution pattern with abdominal obesity increases the risk for hypertension and cardiovascular disease, and is closely linked to a number of metabolic aberrations including insulin resistance. Recent observations suggest that changes in the peripheral vasculature may be of pathophysiological importance for the development of hypertension and its associated metabolic disturbances. We therefore investigated the hemodynamic correlates of abdominal obesity. A central fat distribution was found to be associated with a specific hemodynamic profile, characterized by elevated total peripheral resistance and lower cardiac output. In response to sympathoadrenal activation during mental stress, the normal cardiac output-dependent pressor response was reversed into a systemic vasoconstrictor response. There was a direct relationship between degree of abdominal obesity (expressed as waist-hip ratio) and fasting serum insulin. Furthermore, the stress-induced increase in total peripheral resistance correlated positively with fasting serum insulin concentration, whereas there was an inverse relation between serum insulin and cardiac output and heart rate. In a second study, the circulatory responses to stress during physiological hyperinsulinemia were investigated. During hyperglycemic hyperinsulinemia the central hemodynamic response to stress was changed into a systemic vasoconstrictor response. In the forearm the physiological vasodilation during stress was markedly attenuated, suggesting that insulin may have peripheral vascular effects. In conclusion, central obesity is associated with a specific hemodynamic pattern characterized by higher total peripheral resistance and lower cardiac output, and a vasoconstrictor response to psychosocial stress. This hemodynamic response pattern may be related to insulin metabolism.

Adolescent↗