Obesity-related hepatic steatosis is a major risk factor for metabolic and cardiovascular disease. Fat reduced hypocaloric diets are able to relieve the liver from ectopically stored lipids. We hypothesized that the widely used low carbohydrate hypocaloric diets are similarly effective in this regard. A total of 170 overweight and obese, otherwise healthy subjects were randomized to either reduced carbohydrate (n 5 84) or reduced fat (n 5 86), total energy restricted diet (230% of energy intake before diet) for 6 months. Body composition was estimated by bioimpedance analyses and abdominal fat distribution by magnetic resonance tomography. Subjects were also submitted to fat spectroscopy of liver and oral glucose tolerance testing. In all, 102 subjects completed the diet intervention with measurements of intrahepatic lipid content. Both hypocaloric diets decreased body weight, total body fat, visceral fat, and intrahepatic lipid content. Subjects with high baseline intrahepatic lipids (>5.56%) lost %7-fold more intrahepatic lipids compared with those with low baseline values (<5.56%) irrespective of diet composition. In contrast, changes in visceral fat mass and insulin sensitivity were similar between subgroups, with low and high baseline intrahepatic lipids. Conclusion: A prolonged hypocaloric diet low in carbohydrates and high in fat has the same beneficial effects on intrahepatic lipid accumulation as the traditional low-fat hypocaloric diet. The decrease in intrahepatic lipids appears to be independent of visceral fat loss and is not tightly coupled with changes in whole body insulin sensitivity during 6 months of an energy restricted diet. (HEPATOLOGY 2011;53:1504-1514
A comprehensive CMR approach is a useful tool to monitor the reversible and irreversible myocardial tissue injuries over the course of myocarditis and to differentiate acute from healed myocarditis in patients with still-preserved ejection fraction.
BackgroundThe aim of the study was to test the reproducibility and variability of myocardial T2 mapping in relation to sequence type and spatial orientation in a large group of healthy volunteers. For control T2 mapping was also applied in patients with true edema. Cardiovascular magnetic resonance (CMR) T2-mapping has potential for the detection and quantification of myocardial edema. Clinical experience is limited so far. The variability and potential pitfalls in broad application are unknown.MethodsHealthy volunteers (n = 73, 35 ± 13 years) and patients with edema (n = 28, 55 ± 17 years) underwent CMR at 1.5 T. Steady state free precession (SSFP) cine loops and T2-weighted spin echo images were obtained. In patients, additionally late gadolinium enhancement images were acquired. We obtained T2 maps in midventricular short axis (SAX) and four-chamber view (4CV) based on images with T2 preparation times of 0, 24, 55 ms and compared fast low angle shot (FLASH) and SSFP readout. 10 volunteers were scanned twice on separate days. Two observers analysed segmental and global T2 per slice.ResultsIn volunteers global myocardial T2 systematically differed depending on image orientation and sequence (FLASH 52 ± 5 vs. SSFP 55 ± 5 ms in SAX and 57 ± 6 vs. 59 ± 6 ms in 4CV; p < 0.0001 for both). Anteroseptal and apical segments had higher T2 than inferior and basal segments (SAX: 59 ± 6 vs. 48 ± 5 ms for FLASH and 59 ± 7 vs. 52 ± 4 ms for SSFP; p < 0.0001 for both). 14 volunteers had segments with T2 ≥ 70 ms. Mean intraobserver variability was 1.07 ± 1.03 ms (r = 0.94); interobserver variability was 1.6 ± 1.5 ms (r = 0.87). The coefficient of variation for repeated scans was 7.6% for SAX and 6.6% for 4CV. Mapping revealed focally increased T2 (73 ± 9 vs. 51 ± 3 ms in remote myocardium; p < 0.0001) in all patients with edema.ConclusionsMyocardial T2 mapping is technically feasible and highly reproducible. It can detect focal edema und differentiate it from normal myocardium. Increased T2 was found in some volunteers most likely due to partial volume and residual motion.
Purpose:To determine the regime of linear contrast enhancement in human first-pass perfusion cardiovascular magnetic resonance (CMR) imaging to improve accuracy in myocardial perfusion quantification. Materials and Methods:A total of 10 healthy subjects were studied on a clinical 1.5T MR scanner. Seven doses of Gd-DTPA ranging from 0.00125 to 0.1 mmol/kg of body weight (b.w.) were administered as equal volumes by rapid bolus injection (6 mL/second). Resting periods of 15 minutes were introduced after delivery of Gd doses Ͼ0.01 mmol/kg b.w. For each subject, two series of rest perfusion scans were performed using two different multislice saturation-recovery perfusion sequences. Maximum contrast enhancement and maximum upslope were obtained in the blood pool of the left ventricular (LV) cavity and in the myocardium. The range of linear contrast-dose relation was determined by linear regression analysis.Results: MR signal intensity increased linearly for contrast agent concentrations up to 0.01 mmol/kg b.w. in the LV blood pool and up to 0.05 mmol/kg b.w. in the myocardium. For Gd concentrations exceeding these thresholds the signal intensity response was not linear with respect to the contrast agent dose. Conclusion:Quantitative evaluation of cardiac MR perfusion data needs to account for signal saturation in both the LV blood pool and the myocardium.
OBJECTIVEWeight loss reduces abdominal and intrahepatic fat, thereby improving metabolic and cardiovascular risk. Yet, many patients regain weight after successful diet-induced weight loss. Long-term changes in abdominal and liver fat, along with liver test results and insulin resistance, are not known.RESEARCH DESIGN AND METHODSWe analyzed 50 overweight to obese subjects (46 ± 9 years of age; BMI, 32.5 ± 3.3 kg/m2; women, 77%) who had participated in a 6-month hypocaloric diet and were randomized to either reduced carbohydrates or reduced fat content. Before, directly after diet, and at an average of 24 (range, 17–36) months follow-up, we assessed body fat distribution by magnetic resonance imaging and markers of liver function and insulin resistance.RESULTSBody weight decreased with diet but had increased again at follow-up. Subjects also partially regained abdominal subcutaneous and visceral adipose tissue. In contrast, intrahepatic fat decreased with diet and remained reduced at follow-up (7.8 ± 9.8% [baseline], 4.5 ± 5.9% [6 months], and 4.7 ± 5.9% [follow-up]). Similar patterns were observed for markers of liver function, whole-body insulin sensitivity, and hepatic insulin resistance. Changes in intrahepatic fat und intrahepatic function were independent of macronutrient composition during intervention and were most effective in subjects with nonalcoholic fatty liver disease at baseline.CONCLUSIONSA 6-month hypocaloric diet induced improvements in hepatic fat, liver test results, and insulin resistance despite regaining of weight up to 2 years after the active intervention. Body weight and adiposity measurements may underestimate beneficial long-term effects of dietary interventions.
ClinicalTrials.gov NCT00956566.
Abstract-In animals, carbohydrate and fat composition during dietary interventions influenced cardiac metabolism, structure, and function. Because reduced-carbohydrate and reduced-fat hypocaloric diets are commonly used in the treatment of obesity, we investigated whether these interventions differentially affect left ventricular mass, cardiac function, and blood pressure. We randomized 170 overweight and obese subjects (body mass index, 32.9Ϯ4.4; range, 26.5-45.4 kg/m 2 ) to 6-month hypocaloric diets with either reduced carbohydrate intake or reduced fat intake. We obtained cardiac MRI and ambulatory blood pressure recordings over 24 hours before and after 6 months. Ninety subjects completing the intervention period had a full cardiac MRI data set. Subjects lost 7.3Ϯ4.0 kg (7.9Ϯ3.8%) with reduced-carbohydrate diet and 6.2Ϯ4.2 kg (6.7Ϯ4.4%) with reduced-fat diet (PϽ0.001 within each group; Pϭnot significant between interventions). Caloric restriction led to similar significant decreases in left ventricular mass with low-carbohydrate diets (5.4Ϯ5.4 g) or low-fat diets (5.2Ϯ4.8 g; PϽ0.001 within each group; Pϭnot significant between interventions). Systolic and diastolic left ventricular function did not change with either diet. The 24-hour systolic blood pressure decreased similarly with both interventions. Body weight change (ϭ0.33; Pϭ0.02) and percentage of ingested n-3 polyunsaturated fatty acids (ϭϪ0.27; Pϭ0.03) predicted changes in left ventricular mass. In conclusion, weight loss induced by reduced-fat diets or reduced-carbohydrate diets similarly improved left ventricular mass in overweight and obese subjects over a 6-month period. However, n-3 polyunsaturated fatty acid ingestion may have an independent beneficial effect on left ventricular mass. O besity is associated with increased left ventricular (LV) mass, 1,2 a potential contributor to heart failure, cardiovascular events, and mortality. 3,4 Energy-restricted diets decrease LV mass in conjunction with body weight loss. [5][6][7] In addition to caloric intake, dietary macronutrient composition appears to influence cardiac metabolism, structure, and function, 8 as well as vascular compliance. 9 In animals, high-fat feeding attenuated cardiac hypertrophy and remodeling, 10,11 whereas high-carbohydrate feeding accelerated the process. 12 Excessive simple sugars and saturated fatty acid ingestion worsened cardiac structure and function. 13,14 In contrast, n-3 polyunsaturated fatty acid supplementation attenuated cardiac hypertrophy and fibrosis in rats. 15,16 Therefore, in addition to caloric intake, macronutrient content and composition could affect LV mass and ventricular function during energy restricted diets. Carbohydrate-restricted and fat-restricted diets are commonly prescribed. 17 Whether macronutrient content, without changing physical activity, affects hypocaloric diet-induced changes in LV mass and function has not been investigated in humans. The issue is important given the independent prognostic role of LV mass on cardiovascular events. ...
In this study, we provide direct functional evidence for the stimulation of coronary arteriogenesis via ECP in patients with stable coronary artery disease. These data might open a novel noninvasive and preventive treatment avenue for patients with non-acute vascular stenotic disease.
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