Advances in ISSN: 2378-3168AOWMC

Obesity, Weight Management & Control
Research Article
Volume 4 Issue 2 - 2015
Cardiac Systolic and Diastolic Function can be Improved and Epicardial Fat be can Decreased Over a Very Short Period of Time in Obese Patients without Heart Disease by the Very Low Calorie Diet
Heidi Luotolahti1*, Jaakko Hartiala2, Ilkka Kantola1, Jorma Viikari3 and Matti Luotolahti2

1Department of Medicine, Turku University Hospital, Finland

2Department of Medicine and Clinical Physiology, University of Turku, Finland

3University of Turku, Finland

Received: October 6, 2015 | Published: February 11, 2016
*Corresponding author: Heidi Luotolahti, Satakunta Central Hospital, Clinical Teacher of Medicine, Department of Medicine, Turku University Hospital, Sairaalatie 3, 28500 Pori, Finland, Tel +358407453754; Fax +35826277999; Email:
Citation: Luotolahti H, Hartiala J, Kantola I, Viikari J, Luotolahti M (2016) Cardiac Systolic and Diastolic Function can be Improved and Epicardial Fat can be Decreased Over a Very Short Period of Time in Obese Patients without Heart Disease by the Very Low Calorie Diet. Adv Obes Weight Manag Control 4(2): 00082. DOI: 10.15406/aowmc.2016.04.00082


Objective: The objective of the study was to evaluate the effect of an eight week period of very low calorie diet (VLCD) on heart function and amount of epicardial adipose tissue in obese people without heart disease.

Methods: Fifty-two obese patients (38 women, 14 men, mean age 47.6 ± 12.3 years, mean BMI 46.2±7.0 kg/m2) were assigned to a VLCD enriched with vegetables for eight weeks. Transthoracic echocardiography was performed before and after the diet period. Left ventricular size, ejection fraction, diastolic function, left and right ventricular myocardial performance index (MPI) and thickness of epicardial adipose tissue were measured. Heart rate, blood pressure and plasma glucose and triglyceride concentration were also analysed.

Results: During the diet period the BMI decreased from 46.2±7.0 kg/m2 to 41.8± 6.1 kg/m2 (p<0.0001). The left ventricular MPI decreased from 0.42± 0.07 to 0.37± 0.07 (p<0.0001) and right ventricular MPI decreased from 0.30± 0.09 to 0.27± 0.09 (p=0.0256) showing significant systolic and diastolic improvement in the performance of both ventricles. The thickness of epicardial fat decreased from 4.4±1.5 mm to 3.4±1.4 mm (p<0.0001). The heart rate decreased from 75.8±9.7 beats/min to 67.0 ±10.3 beats/min (p<0.0001) and the systolic blood pressure decreased from 140±14.3 mmHg to 135.2±10.6 mmHg (p=0.0087). The plasma glucose concentration decreased from 6.71±1.96 mmol/l to 6.02±1.59 mmol/l (p<0.0001). The plasma triglyceride concentration decreased from 1.77±0.89 mmol/l to 1.36±0.68 mmol/l (p=0.0002).

Conclusion: VLCD caused during only eight weeks period significant reduction in BMI as well as in the amount of epicardial fat and significant improvement in the systolic and diastolic function of both ventricles in obese persons.

Keywords: Obesity; Cardiac performance; Myocardial performance index; Very low calorie diet; Epicardial fat; Pericardial fat; Weight reduction


NS: Not Significant; MPI: Myocardial Performance Index; ET: Ejection Time; IVCT: Isovolumic Contraction Time; IVRT: Isovolumic Relaxation Time; e’: Early Velocity of Mitral Annulus; a’: Late Velocity of Mitral Annulus; BMI: Body Mass Index; HDL: High Density Lipoprotein; P: Statistical Significance


Obesity is a major risk factor for cardiovascular diseases [1-3]. Obesity also represents an independent risk factor for congestive heart failure [4,5]. The haemodynamic hallmarks of obesity, increased heart rate and stroke volume, are thought to be a compensatory adaptation to increased adipose tissue mass at the expense of left ventricular remodelling, which can later progress to heart failure [6]. Increasing obesity is associated also with increasing severity of right ventricular dysfunction in overweight and obese subjects independent of sleep apnea [7]. Fatty heart (cor adiposum) often seen in obese persons has been known for more than 300 years [6]. Obesity has reached pandemic proportions [2,3,6]. Because of these well known facts it is of great importance to study obesity related cardiac functions. The objective of this study was to evaluate the effect of an eight week period of VLCD on heart function and the amount of epicardial adipose tissue in obese people without heart disease. Transthoracic echocardiography was used as a method for analysing cardiac function [8-12] and to measure the amount of epicardial fat [13].



Fifty-two consecutive obese patients who could successfully complete eight weeks VLCD were enrolled in this study between the years 2005-2008. Their mean age was 47.6±12.3 years and mean BMI was 46.2±7.0 kg/m2. There were 38 women and 14 men. The exclusion criteria were cardiac disease, type 1 diabetes, kidney disease and serious mental problems. The demographics of the patients are seen in detail in Table 1.

Age (range)

47.6+12.3 (16-70) years

Sex: Female/male


BMI (range)

46.2+7.0 (33.1-65.0)

Weight (range)

134.0+24.7 (91-192) kg

Number of patients with hypertension

28/52 (54%)

Number of patients with type 2 diabetes

24/52 (46%)

Number of patients with impaired fasting glycaemia (IFG)

6/52 (12%)

Number of patients with medication

38/52 (73%)

ACE inhibitors or ARB:s

28/52 (54%)


18/52 (35%)


10/52 (19%)

Calcium channel blockers

6/52 (12%)

Other antihypertensive agents

3/52 (6%)

Lipid lowering agents

18/52 (35%)


4/52 (8%)

Oral glucose lowering agents

21/52 (40%)

Acetosalisylic acid

19/52 (37%)

Table 1: Baseline characteristics of the study participants (n = 52).


The subjects were assigned to a VLCD for eight weeks. The diet consisted of commercially available VLCD- products (Nutrilett®, Allevo®). All the VLCD formulas contained protein of soya. Other main ingredients in the formulas were fiber of soya, oil of soya, powder of milk, fiber of oats and oil of raps. The content of the VLCD formulas is seen in detail in Table 2.




Energy Kcal



Protein g



Carbohydrates g



Total fat g



Saturated fat g



Linoleic acid g



Linolenic acid g



Fiber g



Sodium g



Vitamin A µg



Vitamin D3 µg



Vitamin E µg



Vitamin K1 µg



Vitamin C µg



Thiamine mg



Riboflavin mg



Niacin mg



Vitamin B6 mg



Folic acid µg



Vitamin 12 µg



Biothine µg



Pantothenic acid mg



Calcium mg






Iron mg



Magnesium mg



Zinc mg



Copper mg



Iodine µg



Manganese mg



Chromium µg



Selene µg



Molybdene µg



Potassium g



Chloride g



Table 2: The daily content of energy and nutrients received from the VLCD formulas. Additional vegetables are not included in this table. Nutriton of women consisted of five units of VLCD formula and men had six units. There were some variations in the contents of the formulas.

In addition to the VLCD formulas the following vegetables were allowed freely during the diet: tomato, cucumber, lettuce, carrot, white cabbage, red cabbage, Brussels sprouts, leek, spinach, broccoli, parsley, sweet peppers, celery, cauliflower, radishes, Chinese cabbage and squash. Coffee, tea and light sodas were allowed. Alcohol was excluded. The estimated total amount of calories was 700-900 kcal/day.

No new medication was initiated at the beginning or during the VLCD. There were also no increased dosages of any medicine compared to the initial dosages. The amounts of the diuretics, glucose lowering agents and lipid lowering agents were reduced during the VLCD. The level of plasma glucose was followed carefully at regular intervals by the diabetic patients.

The eight week period of VLCD was chosen because it was a routine intervention in the treatment of severe obesity in the hospital. All VLCD formulas were bought by the patients themselves and they could choose between the two available products (Nutrilett® or Allevo® as they were sold in the year 2005). No contact was made to the manufacturers of these formulas. No financial support was thus received for anyone connected to this study. The compliance was based on the weekly visits to a nurse, where the patients were weighed and interviewed.


A two-dimensional Doppler echocardiographic examination was performed before and after the diet period. Parasternal long-axis views were used for measuring left ventricular cavity size and ejection fraction and left atrial diameter. Pulsed wave (H4.0 MHz) Doppler transmitral and transtricuspid flow images were acquired from the apical four-chamber view at the mitral and tricuspid leaflet tips. Left ventricular ejection time was obtained by pulsed wave Doppler in the left ventricular outflow tract of the apical long axis view. Right ventricular ejection time was interrogated by pulsed wave Doppler in the right ventricular outflow tract of parasternal short-axis view. Pulsed Doppler recordings were made at a sweep speed of 100 mm/s. The images were recorded digitally (Syngo Dynamics, Siemens Medical System, U.S.A.) for later analysis.

The MPI (Tei index) was calculated as the sum of isovolumic contraction and relaxation times divided by ejection time. For left ventricular MPI Doppler measurements were averaged over five cycles and for right ventricular MPI over three cycles.

Left ventricular annular velocities were recorded from the apical 4-chamber view with pulsed wave Doppler tissue imaging (DTI) with the 5.0 mm Doppler sample imaging at the septal and lateral mitral annulus of the left ventricle to obtain early and late mitral annular velocities (e’ and a’) Both annular velocity values were averaged over three cardiac cycles. The velocity ratio e’/a’ recorded from septal annulus was calculated and used for evaluation of left ventricular diastolic function [12]. If recording of velocities from the septal annulus were inadequate the recordings from lateral annulus were used.

Epicardial fat thickness was measured in end diastole on the free wall of the right ventricle from the parasternal long-axis view (2-dimensional) as previously described [13]. Three measurements were averaged for the final result.

All the echocardiograms were obtained by the same physician (ML) with echocardiographic accreditation of European Society of Cardiology. He knew whether the patient was in the beginning of the diet or at the end of the diet. All the echocardiograms were performed by using an ACUSON SEQUOIA C 256 system (Acuson, Mountain View, CA, U.S.A.), using a H 4.0 MHz transducer recorded with a simultaneous electrocardiogram.

Haemodynamic measurements

Blood pressure at rest was measured before and after the diet. The heart rate at rest was registered before and after the diet period during the echocardiographic examination.

Laboratory analysis

The fasting plasma glucose level, total cholesterol, high density lipoprotein (HDL) and triglyceride concentration were measured before and after the diet.

Statistical analysis

To compare differences before and after the diet student t tests for paired data were performed. Statistical significance was determined at a p value of <0.05. The study protocol was approved by the Ethics Committee of the Hospital District of Southwest Finland.


BMI decreased from 46.± 7.0 kg/m2 to 41.8 ±6.1 kg/m2 (p < 0.0001) during the diet period.


All the patients were in sinus rhythm during echocardiographic recordings. There were no significant changes in the diameter or ejection fraction of left ventricle or in the diameter of left atrium. The left ventricular MPI decreased in 48/52 (92%) patients, remained as the same in 3/52 (6%) and increased in 1/52 (2%) patient. The mean change in the MPI was from 0.42±0.07 to 0.37±0.07 indicating significant systolic and diastolic improvement of left ventricular performance. There was a significant improvement in both components of the left ventricular MPI. The ejection time of the left ventricle increased from 300±19 msec to 321±22 msec (p<0.0001). The sum of the isovolumic contraction time and isovolumic relaxation time decreased from 125±22 msec to 117±23 msec (p<0.0001) Table 3.


Before Diet

After Diet

Change in %


Left ventricular MPI




< 0.0001

Left ventricular ET (msec)


321+ 22



Left ventricular IVCT+IVRT (msec)





Right ventricular MPI





Left ventricular e'/a'

1.03+ 0.29

1.12+ 0.03



Epicardial fat (mm)




< 0.0001

Pericardial fat




< 0.0001

Epicardial fat + pericardial fat




< 0.0001

Left ventricular diastolic diameter (mm)





Left ventricular ejection fraction (%)





Left atrial diameter (mm)





Table 3: Results of echocardiographic measurements.

NS: Not Significant; MPI: Myocardial Performance Index; ET: Ejection Time; IVCT: Isovolumic Contraction Time; IVRT: Isovolumic Relaxation Time; e': Early Velocity of Mitral Annulus; a': Late Velocity of Mitral Annulus

The corresponding change in the mean values of the right ventricular MPI were from 0.30± 0.09 to 0.27±0.09 (p=0.0256). The e’/a’ velocity ratio in the left ventricle increased from 1.0± 0.29 to 1.12 ±0.30 (p=0.0025) indicating significant improvement in the diastolic function of the left ventricle. The thickness of the epicardial adipose tissue on the right ventricle was 4.4 ±1.5 mm before and 3.4 ±1.5 mm after the diet (p<0.0001).

Haemodynamic changes

Significant decrease in heart rate was seen during the diet period from 75.8± 9.7 beats/min to 67.0± 10.3 beats/min (p<0.0001). Systolic blood pressure decreased from 140.0±14.3 mmHg to 135.2 ±10.6 mmHg (p=0.0087) and diastolic from 84.1± 9.0 mmHg to 81.5±8.1 mmHg (p<0.0436). The heart rate x systolic blood pressure product decreased from 10605± 1718 to 9075±1686 (p<0.0001) Table 4.


Before Diet

After Diet

Change in %


BMI (kg/m2)




< 0.0001

Heart rate (beats/min)




< 0.0001

Systolic blood pressure (mmHg)





Diastolic blood pressure (mmHg)





Heart rate (beats/min) x systolic blood pressure (mmHg)




< 0.0001

Trigly (mmol/l)





Gluc (mmol/l)




< 0.0001

Glycocylated haemoglobin (%)




< 0.0001

Total cholesterol (mmol/l)





HDL/total cholesterol (%)





Low density lipoprotein





Table 4: Results of metabolic and hemodynamic findings.

BMI: Body Mass Index; HDL: High Density Lipoprotein; P: Statistical Significance

Laboratory analysis

The fasting plasma glucose decreased from 6.71± 1.96 mmol/l to 6.02±1.59 mmol/l (p<0.0001) and triglyceride decreased from 1.77± 0.89 mmol/l to 1.36±0.68 (p=0.0002).


We used eight weeks VLCD enriched with vegetables as an intervention method to receive these changes. No patients had diagnosed heart disease but persons with type 2 diabetes and hypertension were included in the study group. The changes of the diet in our study were clear caloric restriction, decrease in the amount of fat and carbohydrates, increase in the amount of soyaprotein and guaranteed amounts of daily allowances of micronutrients and increase in percentage of the daily calories received from the vegetables.

This study showed significant improvement in both systolic and diastolic cardiac functions of both ventricles in obese persons after eight weeks of VLDC. These persons had no heart disease and had normal ejection fractions at rest. It also shows clear decrease of epicardial fat at the same time and also this change occurred rapidly than previously reported. To our knowledge this is the first study that simultaneously shows these changes in that period of time after the change of diet.

At the same time significant beneficial haemodynamic changes, decrease in heart frequency and blood pressure, happened and the improvement of rate-pressure product suggested decreased cardiac workload. Also BMI reduction of 9.5% occurred in these patients and the blood fasting glucose and triglyceride levels decreased significantly.

Morbid obesity is a high-output state [6] which includes also hyperkinetic systole [14,15] with high ejection fraction of left ventricle at rest [16]. Therefore, the use of mere ejection fraction and its equivalents as a measure of change in left ventricular systolic function is controversial in persons without heart disease and therefore we used echocardiographic determination of MPI, as an indicator of change in cardiac function. MPI combines both systolic and diastolic functions and is a measure of effectiveness of cardiac cycle [17] and offers an accurate method to study early changes in cardiac performance [18].

Few clinical studies have shown a relationship between changes in cardiac function and dietary changes in obese persons [19]. Weight loss can be associated with improved left ventricular diastolic function [19-27] but improvement in left ventricular systolic function at rest has before our study been confined to those with depressed systolic function at baseline [19,22,27]. Even after bariatric surgery which often causes substantial weight loss, improvement of systolic function has been limited to those with depressed left ventricular systolic function before surgery [19,28,29].

Theoretical plausible mechanisms may explain this rapid change in cardiac function seen in our study. It has been discussed whether the caloric restriction or weight loss itself plays the key role in the improvement of diastolic function [30,31]. Riordan et al. [31] have shown that a yearlong caloric restriction or increase of exercise leading to weight loss can improve left ventricular diastolic function in healthy non-obese persons. Meyer et al. [30] have shown that long-term caloric restriction ameliorates the age-associated decline in diastolic function in healthy, non-obese individuals. Hammer et al. [24] have shown improved diastolic function after a 16-week caloric restriction in obese patients with diabetes mellitus type 2. The weight loss in these patients was over 20% during the diet (VLCD).

In general, caloric restriction with adequate nutrition intake can cause metabolic adaptations including decreased metabolic, hormonal and inflammatory risk factors for diabetes and cardiovascular disease [32-34]. Caloric restriction has been proposed [35] to increase bioavailability of NO and inhibit inflammatory pathways thus suppressing initiation or progression of vascular disease.

Fatty infiltration of cardiomyocytes has been reported in obese patients with heart failure [6,36] and the amount of myocardial fat has been shown to correlate with the amount of epicardial fat [37]. In obese diabetics [24] myocardial triglyceride content decreased and diastolic function improved after weight loss over 20%. In the study of Viljanen et al. [38] caloric restriction with VLCD for six weeks decreased myocardial triglyceride content by 31%. Fatty heart can be prevented by lifestyle modification and interventions, so it is important to recognize its existence as early as possible [6].

The anatomical close connection between excess epicardial fat and myocardium might increase the weight of the ventricles thus increasing the effort involved in pumping and also allow the local paracrine hormonal interaction between epicardial adipose tissue and myocardium [39,40].

The epicardial fat is metabolically active visceral fat [13] and a source for inflammatory mediators [41]. It could be speculated that the amount of metabolically active fat that is abolished adjacent to the cardiac muscle could cause the positive change. Some harmful metabolites could disappear from the area very near the cardiac muscle.

In our study the improvement in the cardiac systolic and diastolic function occurred rapidly, much more rapidly than one could expect based on traditional concept of the functions of the heart. In our study the relative improvement in heart function and relative decrease in epicardial fat were bigger than the relative decrease of BMI thus together with rapid change suggesting again that metabolic changes might play bigger role than the weight loss itself. Most patients remained very obese also afterwards suggesting that the weight loss itself cannot alone explain this success.

The method to receive this improvement is physiological, low-cost and can be achieved with little medical supervision and without any exercise plan. The change in the composition of the diet was drastic. Obviously drastic changes in the diet can cause drastic changes in cardiac function even in the short term.


Caloric restriction with VLCD caused after only eight weeks of diet a significant improvement in the cardiac systolic and diastolic performance and a reduction of epicardial fat in obese persons. At the same time beneficial haemodynamic changes occurred as well as a significant reduction in BMI. It is unclear how generalizable these results are. Further study is needed. These fast results might offer new motivations to weight loss efforts and approaches into the prevention of the heart failure in obese persons.


We are grateful to Tuulikki Koistinen, Kirsi-Marja Osmonsalo, Pirjo Ojanen and Riitta Seppälä for the great work process done together during this study. There was no outside funding/support for this research.


  1. Ogden CL, Carroll MD, Curtin LR, McDowell MA, Tabak CJ, et al. (2006) Prevalence of overweight and obesity in the United States, 1999-2004. JAMA 295(13): 1549-1555.
  2. Poirier P, Giles TD, Bray GA, Hong Y, Stern JS, et al. (2006) Obesity and cardiovascular disease: Pathophysiology, evaluation, and effect of weight loss. An update of the 1997 American heart association scientific statement on obesity and heart disease from the obesity committee of the council on nutrition, physical activity, and metabolism. Circulation 113(6): 898-918.
  3. Lavie CJ, Milani RV, Ventura HO (2009) Obesity and cardiovascular disease. Risk factor, paradox, and impact of weight loss. J Am Coll Cardiol 53(21): 1925-1932.
  4. Kasper EK, Hruban RH, Baughman KL (1992) Cardiomyopathy of obesity: a clinicopathologic evaluation of 43 obese patients with heart failure. Am J Cardiol 70(9): 921-924.
  5. Kenchaiah S, Evans JC, Levy D, Wilson PW, Benjamin EJ, et al. (2002) Obesity and the risk of heart failure. N Engl J Med 347(5): 305-313.
  6. Szczepaniak LS, Victor RG, Orci L, Unger RH (2007) Forgotten but not gone: The rediscovery of fatty heart, the most common unrecognized disease in America. Circ Res 101(8): 759-767.
  7. Wong CY, O'Moore-Sullivan T, Leano R, Hukins C, Jenkins C, et al. (2006) Association of subclinical right ventricular dysfunction with obesity. J Am Coll Cardiol 47(3): 611-616.
  8. Cheitlin MD, Alpert JS, Armstrong WF, Aurigemma GP, Beller GA, et al. (1997) ACC/AHA guidelines for the clinical application of echocardiography; a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Clinical Application of Echocardiography). Developed in collaboration with the American Society of Echocardiography. Circulation 95(6): 1686-1744.
  9. Tei C (1995) New noninvasive index for combined systolic and diastolic function. J Cardiol 26(2): 135-136.
  10. Tei C, Ling LH, Hodge DO, Bailey KR, Oh JK, et al. (1995) New index of combined systolic and diastolic myocardial performance: A simple and reproducible measure of cardiac function – A study in normals and dilated cardiomyopathy. J Cardiol 26(6): 357-366.
  11. Feigenbaum H, Armstrong WF, Ryan T (2005) Feigenbaum's Echocardiography. (6th edn), Lippincott, Williams & Wilkins, USA.
  12. Nagueh SF, Appleton CP, Gillebert TC, Marino PN, Oh JK, et al. (2009) Recommendations for the evaluation of left ventricular diastolic function by echocardiography. J Am Soc Echo 22(2): 107-133.
  13. Iacobellis G, Assael F, Ribaudo MC, Zappaterreno A, Alessi G, et al. (2003) Epicardial fat from echocardiography: A new method for visceral adipose tissue prediction. Obesity Research 11(2): 304-310.
  14. Iacobellis G, Ribaudo MC, Leto G, Zappaterreno A, Vecci E, et al. (2002) Influence of excess fat on cardiac morphology and function: study in uncomplicated obesity. Obes Res 10(8): 767-773.
  15. Pascual M, Pascual DA, Soria F, Vicente T, Hernandez AM, et al. (2003) Effects of isolated obesity on systolic and diastolic left ventricular function. Heart 89(10): 1152-1156.
  16. Iacobellis G, Ribaudo MC, Zappaterreno A, Iannucci CV, DiMario U, et al. (2004) Adapted changes in left ventricular structure and function in severe uncomplicated obesity. Obes Res 12(10): 1616-1621.
  17. Kapetanikis S, Bhan A, Monaghan MJ (2008) Echo determinants of dyssynchrony (atrioventricular and inter- and intraventricular) are predictors of response to cardiac resynchronization therapy. Echocardiography 25(9): 1020-1029.
  18. Palloshi A, Fragasso G, Silipigni C, Locatelli M, Cristell N, et al. (2004) Early detection by the Tei index of carvedilol-induced improved left ventricular function in patients with heart failure. Am J Cardiol 94(11): 1456-1459.
  19. Wong C, Marwick TH (2007) Obesity cardiomyopathy: diagnosis and therapeutic implications. Nat Clin Pract Cardiovasc Med 4(9): 480-490.
  20. Mac Mahon SW, Wilcken DE, Macdonald GJ (1986) The effect of weight reduction on left ventricular mass: a randomized controlled trial in young, overweight hypertensive patients. N Engl J Med 314(6): 334-339.
  21. Corrao S, Arnone S, Scaglione R, Amato V, Amico G, et al. (2000) Effects of a short-term hypoenergetic diet on morphofunctional left ventricular parameters in centrally obese subjects: an echocardiographic study. Panminerva Med 42(2): 123-129.
  22. Marfella R, Esposito K, Siniscalchi M, Cacciapuoti F, Giugliano F, et al. (2004) Effect of weight loss on cardiac syncronization and proinflammatory cytokines in premenopausal obese women. Diabetes Care 27(1): 47-52.
  23. Wong CY, Byrne NM, O'Moore-Sullivan T, Hills AP, Prins JB, et al. (2006) Effect of weight loss due to lifestyle intervention on subclinical cardiovascular dysfunction in obesity (body mass index >30 kg/m2). Am J Cardiol 98(12): 1593-1598.
  24. Hammer S, Snel M, Lamb HJ, Jazet IM, van der Meer RW, et al. (2008) Prolonged caloric restriction in obese patients with type 2 diabetes mellitus decreases myocardial triglyceride content and improves myocardial function. J Am Coll Cardiol 52(12): 1006-1012.
  25. Iacobellis G, Singh N, Wharton S, Sharma AM (2008) Substantial changes in epicardial fat thickness after weight loss in severely obese subjects. Obesity 16(7): 1693-1697.
  26. Rider OJ, Francis JM, Ali MK, Petersen SE, Robinson M, et al. (2009) Beneficial cardiovascular effects of bariatric surgical and dietary weight loss in obesity. J Am Coll Cardiol 54(8): 718-726.
  27. de las Fuentes L, Waggoner AD, Mohammed BS, Stein RI, Miller BV, et al. (2009) Effect of moderate diet-induced weight loss and weight regain on cardiovascular structure and function. J Am Coll Cardiol 54(25): 2376-2381.
  28. Alaud-din A, Meterissian S, Lisbona R, MacLean LD, Forse RA (1990) Assessment of cardiac function in patients who were morbidly obese. Surgery 108(4): 809-818.
  29. Alpert MA, Terry BE, Lambert CR, Kelly DL, Panayiotou H, et al. (1993) Factors influencing left ventricular systolic function in nonhypertensive morbidly obese patients, and effect of weight loss induced by gastroplasty. Am J Cardiol 71(8): 733-737.
  30. Meyer TE, Kovacs SJ, Ehsani AA, Klein S, Holloszy JO, et al. (2006) Long-term caloric restriction ameliorates the decline in diastolic function in humans. J Am Coll Cardiol 47(2): 398-402.
  31. Riordan MM, Weiss EP, Meyer TE, Ehsani AA, Racette SB, et al. (2008) The effects of caloric restriction- and exercise-induced weight loss on left ventricular diastolic function. Am J Physiol Heart Circ Physiol 294(3): H1174-H1182.  
  32. Heilbronn LK, de Jonge L, Frisard MI, DeLany JP, Larson-Meyer DE, et al. (2006) Effect of 6-month calorie restriction on biomarkers of longevity, metabolic adaptation, and oxidative stress in overweight individuals. JAMA 295(13): 1539-1548.
  33. Fontana L (2006) Excessive adiposity, calorie restriction, and aging. JAMA 295(13): 1577-1578.
  34. Fontana L, Klein S (2007) Aging, adiposity, and calorie restriction. JAMA 297(9): 986-994.
  35. Ungvari Z, Parrado-Fernandez C, Csiszar A, de Cabo R (2008) Mechanisms underlying caloric restriction and lifespan regulations. Implications for vascular aging. Circ Res 102(5): 519-529.
  36. Sharma S, Adrogue JV, Golfman L, Uray I, Lemm J, et al. (2004) Intramyocardial lipid accumulation in the failing human heart resembles the lipotoxic rat heart. FASEB J 18(14): 1692-1700.
  37. Kankaanpää M, Lehto H-R, Pärkkä JP, Komu M, Viljanen A, et al. (2006) Myocardial triglyceride content and epicardial fat mass in human obesity: relationship to left ventricular function and serum free fatty acid levels. J Clin End & Metab 91(11): 4689-4695.
  38. Viljanen APM, Karmi A, Borra R, Pärkkä JP, Lepomäki V, et al. (2009) Effect of caloric restriction on myocardial fatty acid uptake, left ventricular mass, and cardiac work in obese adults. Am J Cardiol 103(12): 1721-1726.
  39. Iacobellis G, Ribaudo MC, Zappaterreno A, Iannucci CV, Leonetti F (2004) Relation between epicardial adipose tissue anf left ventricular mass. Am J Cardiol 94(8): 1084-1087.
  40. Iacobellis G, Corradi D, Sharma AM (2005) Epicardial adipose tissue: anatomic, biomolecular and clinical relationships with the heart. Nat Clin Pract Cardiovasc Med 2(10): 536-543.
  41. Mazurek T, Zhang LF, Zalewski A, Mannion JD, Diehl JT, et al. (2003) Human epicardial adipose tissue is a source of inflammatory mediators. Circulation 108(20): 2460-2466.
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