CMR-Flow
Khaoula Bouazizi, PhD
Research Engineer
Laboratoire d'Imagerie Biomédicale, France
Khaoula Bouazizi, PhD
Research Engineer
Laboratoire d'Imagerie Biomédicale, France
Mohamed Zarai, MSc
Study Engineer
IHU ICAN, France
Abdallah Noufaily, MD
Dr
University Hospital Pitie-Salpetriere, France
Mikaël Prigent, MRT
MR Technician
IHU ICAN, France
Thomas Dietenbeck, PhD
Associate professor
Laboratoire d'Imagerie Biomédicale, Ile-de-France, France
Emilie Bollache, PhD
Researcher
Laboratoire d'Imagerie Biomédicale, France
Toan Nguyen, MD
Dr
Trousseau Hospital, France
Valeria Della Valle, MD
Dr
University Hospital Pitie-Salpetriere, France
Eléonore Blondiaux, MD, PhD
Professor
Trousseau Hospital, France
Karine Clément, MD, PhD
Professor
University Hospital Pitie-Salpetriere, Ile-de-France, France
Judith Aron-Wisnewsky, MD, PhD
Professor
University Hospital Pitie-Salpetriere, France
Fabrizio Andreelli, MD, PhD
Professor
University Hospital Pitie-Salpetriere, France
Alban Redheuil, MD, PhD
Professor
Pitié-Salpêtrière Hospital - Sorbonne University, France
Nadjia Kachenoura, PhD
Research Director
Laboratoire d'Imagerie Biomédicale, France
Type-2 diabetes mellitus (T2D) is a prevalent disease associated with cardiovascular risk. Increased aortic stiffness is a major vascular consequence of T2D. Excessive accumulation of epicardial adipose tissue (EAT) is related to cardio-metabolic complications. Since EAT is metabolically active, it could affect arterial hemodynamics through EAT-mediated metabolic pathways. Accordingly, our aims were to evaluate whether aortic flow parameters differed in T2D patients as compared to controls and to evaluate their associations with EAT, as an index of cardiometabolic severity.
Methods:
We studied 65 individuals from the METACARDIS-MRI subgroup of the METACARDIS study (NCT02059538), including 36 T2D patients (20 females, age: 55±10 years) and 29 healthy controls (11 females, age: 52±11 years). MRI data were obtained using a 1.5 T scanner (Siemens, Germany). A cine SSFP sequence was used to extract left ventricular (LV) mass (LVM) and volumes, as well as EAT volume (Medis, The Netherlands), which was defined as the adipose tissue between the epicardium and the outer pericardium (Figure 1).
Aortic imaging included cine SSFP and 2D phase-contrast (PC) sequences acquired transverse to the aorta at the level of the pulmonary artery bifurcation with simultaneous central blood pressure measurements.
The ArtFun software (LIB, Sorbonne Université, France) was used to automatically measure: 1) the ascending (AA) aorta cross-sectional areas and 2) AA global (GF), forward (FF) and backward (BF) flow volumes and peaks. BF was then expressed in percentage of FF. Aortic distensibility was deduced from aortic cine images.
Results:
EAT indexed by BSA was significantly higher in T2D patients than in controls (Figure 2), by almost 2 folds on average. Such difference remained significant after adjustment for age, central pulse pressure and BMI. There was no effect of treatment (insulin and/or metformin) on EAT volume in patients. EAT measurement was reproducible (intra- and inter-operator coefficients of variations: 4 and 6%, respectively).
AA was significantly larger and stiffer in T2D, as revealed by lower distensibility (p≤0.01) and higher arch PWV (p=0.01) than in controls. There was significantly higher proportion of BF in T2D patients as compared to controls (Table 1).
Significant negative correlations were observed between EAT and AA (r=-0.30, p=0.02) distensibility. EAT was positively and significantly correlated to the BF to FF volume ratio (Figure 3) in AA. Such associations remained significant after adjustment for age, sex, central pulse pressure and BMI.
Conclusion:
We found a significant relationship between functional aortic alterations, particularly increased aortic stiffness and flow disturbances with the higher metabolic risk profile defined by increased EAT volume in T2D patients. These findings suggest that increased EAT could participate to the pathophysiology of aortic degeneration through direct or indirect pathways including chronic inflammation.