This trial is active, not recruiting.

Conditions coronary heart disease, metabolic syndrome
Treatment omega 3 acid ethyl esters
Phase phase 3
Sponsor Beth Israel Deaconess Medical Center
Collaborator National Heart, Lung, and Blood Institute (NHLBI)
Start date June 2009
End date May 2016
Trial size 338 participants
Trial identifier NCT01624727, 2006P-000175, P50HL083813


The purpose of the study is to target inflammation to reduce progression of noncalcified plaque in the coronary arteries using an intensive lifestyle intervention with omega-3 fatty acid supplementation compared to standard of care.

United States No locations recruiting
Other Countries No locations recruiting

Study Design

Allocation randomized
Endpoint classification efficacy study
Intervention model parallel assignment
Masking open label
Primary purpose treatment
(No Intervention)
Those randomized to usual care will continue to follow the care provided by their cardiologist. They will have all the follow-up phone calls, visits and testing which the intervention group has.
(Active Comparator)
omega 3 acid ethyl esters
Lovaza 3.6 g daily

Primary Outcomes

The primary endpoint is change in coronary noncalcified plaque volume.
time frame: Baseline and 30 months

Secondary Outcomes

Coronary artery plaque assessment
time frame: Baseline and 30 months
Metabolic syndrome parameters
time frame: Baseline and 30 months
Inflammatory markers
time frame: Baseline and 30 months
Pericardial Fat
time frame: Baseline and 30 months
Insulin Resistance
time frame: Baseline and 30 months
Nonalcoholic steatohepatitis (NASH)
time frame: Baseline and 30 months
Improvement in Medications
time frame: Baseline and 30 months
New onset diabetes
time frame: Baseline and 30 months
Change in Metabolic Syndrome
time frame: Baseline and 30 months
Vitamin D and coronary plaque
time frame: Baseline and 30 months
Vitamin D levels and plaque progression
time frame: Baseline and 30 months
Cognitive function
time frame: Baseline, 1 year and 30-months
Exercise capacity and coronary plaque
time frame: Baseline
Urinary microalbumin and coronary plaque
time frame: Baseline and 30-months
Visceral Fat
time frame: Baseline and 30-months

Eligibility Criteria

Male or female participants from 21 years up to 80 years old.

Inclusion Criteria: 1. coronary artery disease 2. previous myocardial infarction 3. angioplasty (> 6 months ago) 4. previous coronary bypass surgery (> 12 months ago) 5. stable angina 6. non-calcified plaque on prior CT 7. abnormal exercise tolerance test 8. aged 21- 80 years 9. BMI ≥ 27 kg/m2 and ≤ 35 kg/m2 if female and ≤ 40 kg/m2 if male (a BMI > 24.5 for subjects from Asian origin) 10. stable dose of statin for 1 month at screening or unable to tolerate a statin 11. normal renal function - estimated creatinine clearance calculated using Cockcroft-Gault (CG) equation ≥60 at screening [eCrCLCG (ml/min) = [(140 - age) x weight (kg)]/[SCr(mg/dl) x 72] x [0.85 if female] or serum Cr < 1.3 12. ALT, AST) < 3 times upper limits of normal) 13. normal thyroid function or on stable dose replacement therapy 14. an ETT performed within 12 months prior Exclusion criteria 1. unstable angina (increase in frequency or severity of anginal episodes or development of chest pain at rest) 2. significant obstructive disease in left main coronary artery, ostial LAD or newly diagnosed three-vessel disease since prior cardiac catheterization by MDCTA 3. significant heart failure (NYHA class III and IV) 4. Current atrial fibrillation or Wolf-Parkinson-White (WPW) syndrome 5. allergy to beta-blocker in subjects with resting heart rate > 65 bpm 6. systolic blood pressure > 160 mm Hg 7. diastolic BP > 100 mm Hg 8. persons with allergies to iodinated contrast material or shellfish 9. allergy to nitroglycerin 10. history of asthma only if unable to tolerate beta-blockers 11. BMI > 35 kg/m2 if female and > 40 kg/m2 if male 12. body weight > 350 lbs 13. Use of drugs for weight loss [eg Xenical (orlistat), Meridia (sibutramine), Acutrim (phenylpropanolamine) or similar over-the-counter medications] within three months of screening 14. surgery within 30 days of screening 15. history of acquired immune deficiency syndrome or human immunodeficiency virus (HIV) 16. poor mental function or history of dementia/Alzheimer's Disease or on medications used for treatment of dementia [e.g. Tacrine (Cognex), Rivastigmine (Exelon), Galantamine (Razadyne, Reminyl), Donepezil (Aricept), Memantine (Namenda)] or any other reason to except patient difficulty in complying with the requirements of the study 17. medicine for erectile dysfunction within 72 hours prior to MDCTA 18. Prior stroke with residual cognitive deficit or functional deficit preventing any type of exercise 19. Current chemotherapy or radiation for malignancy 20. Current weekly alcohol consumption > 21 units/week (1 unit = 1 beer, 1 glass of wine, 1 mixed cocktail containing 1 ounce of alcohol) Exclusions based on nuclear imaging: 1. Transient cavity dilation 2. More than one vascular territory involved with reversible defect (multiple defects) 3. Reversible defects involving the anterior wall, septum or apex (LAD territory) Exclusions based on echocardiography imaging: 1. More than one vascular territory involved with inducible wall motion abnormalities (multiple defects) 2. Inducible wall motion abnormalities involving the anterior wall, septum or apex (LAD territory)

Additional Information

Official title Slowing HEART diSease With Lifestyle and Omega-3 Fatty Acids (HEARTS)
Principal investigator Francine K Welty, MD, PhD
Description Study Design: This is a randomized, parallel study design with a usual care control group. 278 subjects with coronary heart disease (CHD) are being randomized to intensive lifestyle intervention (exercise and nutrition counselling geared toward weight loss with omega-3 supplementation) or standard of care (139 in each arm). Multidetector computed tomographic angiography (MDCTA) is performed at baseline to quantitate the amount of noncalcified and calcified coronary plaque and again at 30 month follow-up to determine if there has been a change in the volume of noncalcified or total plaque. The primary endpoint is change in coronary noncalcified plaque volume during the 30 months of intervention between active and standard of care. Hypothesis: Percent change in progression of coronary plaque volume will be less for the active lifestyle intervention compared to standard of care. Secondary endpoints include plasma levels of inflammatory markers, lipids and measures of insulin sensitivity. Secondary outcomes include testing the hypothesis that targeting inflammation with lifestyle will be associated with: 1. Change in total plaque volume per patient. 2. Improvement in the metabolic syndrome assessed by measures of waist/hip ratio, systolic and diastolic blood pressure, lipid profiles (total cholesterol, triglycerides, HDL and LDL), and abdominal adiposity quantitated by computerized tomography. 3. Reduction of mediators of inflammation in the circulation including CRP, PAI-1, serum amyloid A, MMP-9 and fibrinogen, pro-inflammatory cytokines including IL-6, TNF-a and IL-1b, the adhesion molecules VCAM-1 and ICAM-1, increase in adiponectin and reduction in serum nitrotyrosine as a marker of oxidative stress. 4. Reduction of insulin resistance assessed by fasting insulin and homeostasis model assessment of insulin resistance (HOMA-IR). 5. Reduction of inflammation in the liver associated with nonalcoholic steatohepatitis (NASH), a newly recognized component of the metabolic syndrome, and reduction of fatty liver quantitated by computerized tomography and levels of AST and ALT as markers of liver inflammation related to NASH. 6. Comparison of rates of addition of anti-hypertensive, diabetic, or lipid lowering medication. 7. Comparison of numbers of persons with metabolic syndrome who progress to diabetes between groups. 8. Comparison of numbers of persons who regress from ATPIII metabolic syndrome criteria. 9. Investigation of the relationship between vitamin D status and coronary calcification, as well as with insulin resistance (HOMA-IR), beta-cell function (HOMA-%beta), and serum levels of inflammatory cytokines and adhesion molecules, known to be related to CVD risk. 10. Determination of whether baseline vitamin D levels predict clinical response to the lifestyle intervention, and whether hypovitaminosis D is associated with plaque progression.
Trial information was received from ClinicalTrials.gov and was last updated in November 2015.
Information provided to ClinicalTrials.gov by Beth Israel Deaconess Medical Center.