Myocardial Tissue Remodeling in Adolescent Obesity

Author:

Shah Ravi V.12,Abbasi Siddique A.1,Neilan Tomas G.12,Hulten Edward1,Coelho‐Filho Otavio3,Hoppin Alison4,Levitsky Lynne5,de Ferranti Sarah6,Rhodes Erinn T.7,Traum Avram8,Goodman Elizabeth9,Feng Henry1,Heydari Bobak1,Harris William S.10,Hoefner Daniel M.10,McConnell Joseph P.10,Seethamraju Ravi11,Rickers Carsten12,Kwong Raymond Y.1,Jerosch‐Herold Michael1

Affiliation:

1. Noninvasive Cardiovascular Imaging Section, Cardiovascular Division, Department of Medicine and Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA

2. Division of Cardiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA

3. Cardiology Division, State University of Campinas (UNICAMP), Campinas, Sao Paulo, Brazil

4. Division of Gastroenterology, MassGeneral Hospital for Children, Boston, MA

5. Division of Endocrinology, MassGeneral Hospital for Children, Boston, MA

6. Preventative Cardiology, Boston Children's Hospital, Boston, MA

7. Division of Endocrinology, Boston Children's Hospital, Boston, MA

8. Division of Nephrology, MassGeneral Hospital for Children, Boston, MA

9. Center for Child & Adolescent Health Research and Policy, MassGeneral Hospital for Children, Boston, MA

10. Health Diagnostics Laboratory, Richmond, VA

11. Siemens Healthcare, Erlangen, Germany

12. Department of Pediatric Cardiology, University Hospital of Schleswig‐Holstein, Germany

Abstract

Background Childhood obesity is a significant risk factor for cardiovascular disease in adulthood. Although ventricular remodeling has been reported in obese youth, early tissue‐level markers within the myocardium that precede organ‐level alterations have not been described. Methods and Results We studied 21 obese adolescents (mean age, 17.7±2.6 years; mean body mass index [ BMI ], 41.9±9.5 kg/m 2 , including 11 patients with type 2 diabetes [T2D]) and 12 healthy volunteers (age, 15.1±4.5 years; BMI , 20.1±3.5 kg/m 2 ) using biomarkers of cardiometabolic risk and cardiac magnetic resonance imaging ( CMR ) to phenotype cardiac structure, function, and interstitial matrix remodeling by standard techniques. Although left ventricular ejection fraction and left atrial volumes were similar in healthy volunteers and obese patients (and within normal body size‐adjusted limits), interstitial matrix expansion by CMR extracellular volume fraction ( ECV ) was significantly different between healthy volunteers (median, 0.264; interquartile range [IQR], 0.253 to 0.271), obese adolescents without T2D (median, 0.328; IQR, 0.278 to 0.345), and obese adolescents with T2D (median, 0.376; IQR, 0.336 to 0.407; P =0.0001). ECV was associated with BMI for the entire population ( r =0.58, P <0.001) and with high‐sensitivity C‐reactive protein ( r =0.47, P <0.05), serum triglycerides ( r =0.51, P <0.05), and hemoglobin A1c ( r =0.76, P <0.0001) in the obese stratum. Conclusions Obese adolescents (particularly those with T2D) have subclinical alterations in myocardial tissue architecture associated with inflammation and insulin resistance. These alterations precede significant left ventricular hypertrophy or decreased cardiac function.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Cardiology and Cardiovascular Medicine

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