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Introduction: Accumulation of excess intra-peritoneal fat is associated with left ventricular (LV) dysfunction in those not receiving treatment for cancer. We sought to determine if increases in intra-peritoneal fat were associated with declines in LV ejection fraction (LVEF) after receipt of potentially cardio-toxic chemotherapy. Methods: In 61 patients (32 lymphoma, 23 breast cancer, 6 sarcoma) we obtained magnetic resonance imaging (MRI) assessments of abdominal fat (intra-peritoneal [IP], retroperitoneal [RP] and subcutaneous [SQ]) at the level of the L2 vertebra, as well as LVEF prior to and 24 months after initiating cardio-toxic chemotherapy (70% doxorubicin, 1% trastuzumab, 5% taxol, 26% docetaxel, and 67% cyclophosphamide). Correlations between 24-month change in LVEF and baseline measures of body mass index (BMI), IP, RP & SQ fat were identified after accounting for baseline LVEF, height, gender, anthracycline use, and time. Results: A total of 61 participants (age 53 ± 15 yrs; 32% men, 78% Caucasian) exhibited an average baseline BMI of 30 ± 6 kg/m2, height of 170 ± 11cm, and a baseline LVEF of 62 ± 8%. After accounting for height, baseline LVEF, anthracycline use, gender and time between visits, baseline IP fat volume was associated with a LVEF decline (r=-0.27, p=0.047) while BMI, RP and SC fat were not (p= 0.09 to 0.41 for all). Those older than median age of 52 yrs. with high IP fat trended toward greater declines in LVEF (r=0.31, p=0.082) when compared to younger individuals (<52 yrs.) (r=0.24, p=0.346). Within the entire cohort, those with high IP/low SQ fat experienced marked declines in LVEF (p= 0.026). Conclusions: Pre-chemotherapy intra-peritoneal fat (not necessarily reflected in an assessment of BMI) is associated with declines in LVEF 2 years after receipt of cardio-toxic chemotherapy. These findings suggest those with larger amounts of intra-peritoneal fat are at higher risk for developing left ventricular dysfunction upon receipt of cardio-toxic chemotherapy. [ABSTRACT FROM AUTHOR]

Background and aims To determine whether epicardial (EAT) and paracardial adipose tissue (PAT) volume and attenuation are associated with high-risk coronary plaque features. Methods In subjects with suspected acute coronary syndrome (ACS) enrolled in the ROMICAT II trial, EAT and PAT volumes indexed to body surface area (BSA) and attenuation were measured on non-contrast coronary artery calcium score (CACS) CT. High-risk plaque features (napkin-ring sign, positive remodeling, low density plaque, spotty calcium) and stenosis were assessed on coronary CT angiography (CTA). The association of EAT and PAT volume and attenuation with high-risk plaque and whether this was independent of clinical risk assessment, CACS and significant coronary artery disease (CAD) was determined. Results Of 467 (mean 54 ± 8 yrs, 53% male) with CACS and CTA, 167 (36%) had high-risk plaque features. Those with high-risk plaque had significantly higher indexed EAT (median 59 (Q1-Q3:45–75) cc/m 2 vs. 49 (35–65) cc/m 2 , p < 0.001) and PAT volume (median:51 (36–73) cc/m 2 vs. 33 (22–52) cc/m 2 , p < 0.001). Higher indexed EAT volume was associated with high-risk plaque [univariate OR 1.02 (95%-CI:1.01–1.03) per cc/m 2 of EAT, p < 0.001], which remained significant [univariate OR 1.04 (95%-CI:1.00–1.08) per cc/m 2 of EAT, p = 0.040] after adjustment for risk factors, CACS, and stenosis ≥50%. Higher indexed PAT volume was associated with high-risk plaque in univariate analysis [OR 1.02 (1.01–1.03) per cc/m 2 of PAT, p < 0.001], though this was not significant in multivariate analysis. At a threshold of >62.3 cc/m 2 , EAT volume was associated with high-risk plaque [univariate OR 2.50 (95%-CI:1.69–3.72), p < 0.001)], which remained significant [OR 1.83 (95%-CI:1.10–3.05), p = 0.020] after adjustment. Subjects with high-risk plaque had lower mean attenuation EAT (−88.1 vs. −86.9 HU, p = 0.008) and PAT (−106 vs. −103 HU, p < 0.001), though this was not significant in multivariable analysis. Conclusions Greater volumes of EAT are associated with high-risk plaque independent of risk factors, CACS and obstructive CAD. This observation supports possible local influence of EAT on development of high-risk coronary plaque. [ABSTRACT FROM AUTHOR]

Background and aims Total coronary artery calcium (CAC) burden is associated with an increased cardiovascular risk, while local CAC may represent stable plaques. We determined differences in relationship of total CAC with acute coronary syndrome (ACS) and local CAC with culprit lesions in patients with suspected ACS. Methods We performed computed tomography (CT) for CAC and CT angiography to assess the presence of significant stenosis and high-risk plaque (positive remodeling, low CT attenuation, napkin-ring sign, spotty calcium) in 37 patients with ACS and 223 controls. Total and segmental Agatston scores were measured. Culprit lesions were assessed in subjects with ACS. Results Patients (n = 260) with vs. without ACS had higher total CAC score (median 229, 25 th -75 th percentile 75–517 vs. 27, 25 th -75 th percentile 0–99, p <0.001), higher prevalence of significant stenosis (78% vs. 7%, p <0.001) and high-risk plaque (95% vs. 59%, p <0.001). In those with ACS, culprit (n = 41) vs. non-culprit (n = 200) lesions, had similar segmental CAC score (median 22, 25 th -75 th percentile 4–71 vs. 14, 25 th -75 th percentile 0–51; p = 0.37 ), but higher prevalence of significant stenosis (81% vs. 11%, p <0.001) and high-risk plaque (76% vs. 51%, p =0.005). Significant stenosis (odds ratio 40.2, 95%CI 15.6–103.9, p <0.001) and high-risk plaque (odds ratio 3.4, 95%CI 1.3–9.1, p =0.02), but not segmental CAC score (odds ratio 1.0, 95%CI 1.0–1.0, p =0.47), were associated with culprit lesions of ACS. Conclusions Total CAC burden was associated with ACS but segmental CAC was not associated with culprit lesions. Our findings suggest that total but not local CAC is a marker of ACS risk and support the hypothesis that extensive local CAC is a marker of plaque stability. [ABSTRACT FROM AUTHOR]