Aortic stiffness and the amount of epicardial fat are both associated with cardiovascular risk. Cardiac Magnetic Resonance (CMR) can accurately determine epi- and paracardial fat volumes (EFV, ParaFV) and it can also assess aortic stiffness by measuring the aortic pulse wave velocity (PWV) ^1-3. We investigated PWV, EFV and ParaFV in hypertensive patients and healthy controls to evaluate if and resp. how they are correlated and how they correlate with the presence of diabetes mellitus (DM) and myocardial infarction (MI).

215 subjects (134 men; mean age 57.3±41.4year, mean BMI 27.9±5.3kg/m²) that consisted of 59 healthy controls and 156 hypertensive patients underwent comprehensive CMR exam (1.5 Tesla, Philips Healthcare).
Aortic PWV was assessed by a 2-dimensional (2D) velocity-encoded sequence perpendicular through the aorta ascendens (AA ) and descendens (AD) with retrospective ECG-gating during free breathing (number of heart phases = 130, maximum VE = 150cm/sec). PWV was calculated by dividing the distance between the section through the AA and through the proximal AD by the time between the arrival of the tangents of the velocity waveform at the section through AA and AD, respectively (figure 1) (Segment, version 1.9, R3918; http://segment.heiberg.se) ¹.
EFV & ParaFV were determined using a 3D transversal ECG-triggered and respiratory navigator gated mDixon-sequence ^2,4 (scan time: 7.5min; voxel size 1.5 x 1.5 x 3.0mm³; TR / TE1 / TE2 / α : 5.4ms / 1.8ms / 4.0ms / 20°; PI SENSE, acceleration factor 1.5 in both phase encoding directions; T2 prepulse 50ms; trigger delay: end-diastole; acquisition window: 100-156ms). In-phase, Opposed-phase, Water only (W), and Fat only (F) images were reconstructed online at the scanner ⁵. Fat-fraction maps were computed based on F- and W-images with an appropriate noise threshold and correction for relaxation effects to identify voxels containing ≥50% fat (figure 2).

Mean PWV was 8.8±2.8, mean EFV was 66.3±29.9ml/m² and mean ParaFV was 81.1±48.6ml/m².
PWV correlated with EFV (R= 0.436, P=<0.001 [Spearman-rho]). After adjustment for age, BMI and gender, epicardial fat volume was statistically significant associated with PWV (slope coefficient 1.737; P=0.017 with a confidence interval [CI] of 0.309-3.166). (figure 2). No association was found with ParaFV (P=0.091).
Healthy controls had lower PWV values and EFV&ParaFV than hypertensive patients. Hypertensive patients were divided into
(a) “group HTN” (N=156; patients without DM or MI),
(b) “group HTN+DM” (N=19; patients with DM but without MI), and
(c) “group MI” (N=53; patients with MI).
After adjustment for age, BMI and gender, “group HTN+DM” revealed higher values of PWV and EFV&ParaFV than “group HTN” (EFV P=0.012; ParaFV P=0.028; PWV P=0.028).
“Group MI” revealed higher values of PWV and EFV than “group HTN” (EFV P<0.004; PWV P<0.034; ParaFV P=0.249). No differences were observed between “group MI” and “group DM”.

A CMR-based quantification of cardiovascular risk parameters revealed a relationship of aortic stiffness and epicardial fat volumes with each other and with cardiovascular risk.
This may be explained by similar (pro-)inflammatory mechanisms, which act in epicardial fat and which also promote aortic atherosclerosis ^3,6.
Future studies should concentrate on the investigation of the relationships with regard to the prediction of cardiovascular events.

Aortic stiffness and epicardial fat volumes are related with each other and with CV risk, possibly influenced by similar (pro-)inflammatory mechanisms.