Changes in epicardial and visceral adipose tissue depots following bariatric surgery and their effect on cardiac geometry

Abstract

Introduction: Obesity affects cardiac geometry, causing both eccentric (due to increased cardiac output) and concentric (due to insulin resistance) remodelling. Following bariatric surgery, reversal of both processes should occur. Furthermore, epicardial adipose tissue loss following bariatric surgery may reduce pericardial restraint, allowing further chamber expansion. We investigated these changes in a serial imaging study of adipose depots and cardiac geometry following bariatric surgery.

Methods: 62 patients underwent cardiac magnetic resonance (CMR) before and after bariatric surgery, including 36 with short-term (median 212 days), 37 medium-term (median 428 days) and 32 long-term (median 1030 days) follow-up. CMR was used to assess cardiac geometry (left atrial volume (LAV) and left ventricular end-diastolic volume (LVEDV)), LV mass (LVM) and LV eccentricity index (LVei - a marker of pericardial restraint). Abdominal visceral (VAT) and epicardial (EAT) adipose tissue were also measured.

Results: Patients on average had lost 21kg (38.9% excess weight loss, EWL) at 212 days and 36kg (64.7% EWL) at 1030 days following bariatric surgery. Most VAT and EAT loss (43% and 14%, p<0.0001) occurred within the first 212 days, with non-significant reductions thereafter. In the short-term LVM (7.4%), LVEDV (8.6%) and LAV (13%) all decreased (all p<0.0001), with change in cardiac output correlated with LVEDV (r=0.35,p=0.03) and LAV change (r=0.37,p=0.03). Whereas LVM continued to decrease with time (12% decrease relative to baseline at 1030 days, p<0.0001), both LAV and LVEDV had returned to baseline by 1030 days. LV mass:volume ratio (a marker of concentric hypertrophy) reached its nadir at the longest timepoint (p<0.001). At baseline, LVei correlated with baseline EAT (r=0.37,p=0.0040), and decreased significantly from 1.09 at baseline to a low of 1.04 at 428 days (p<0.0001). Furthermore, change in EAT following bariatric surgery correlated with change in LVei (r=0.43,p=0.0007).

Conclusions: Cardiac volumes show a biphasic response to weight loss, initially becoming smaller and then returning to pre-operative sizes by 1030 days. We propose this is due to an initial reversal of eccentric remodelling followed by reversal of concentric remodelling. Furthermore, we provide evidence for a role of EAT contributing to pericardial restraint, with EAT loss improving markers of pericardial restraint.

Trial registration: ClinicalTrials.gov NCT01284816.

Keywords: bariatric surgery; cardiac geometry; cardiac remodelling; epicardiac adipose tissue; obesity; weight loss.

Figure 1

CMR images. (A) – contouring of epicardial adipose tissue in the short axis view. (B) – 17 segment view overlayed on short axis images. Highlighting the septal segments (in orange) and the lateral segments (in green). (C) – Short axis view with measurements of the maximal anterior-posterior (AP) diameter parallel to the septum and maximal septal-lateral (SL) diameter orthogonal to the AP diameter, with left ventricular eccentricity index being calculated by diving AP/SL diameters.

Figure 2

Anthropomorphic changes following bariatric surgery. (A) – change in weight, (B) – percentage change in visceral adipose tissue, (C) – percentage change in epicardial adipose tissue, (D) – change in systolic blood pressure, (E) – change in HOMA-IR as a marker of insulin resistance, (F) – change in heart rate. HOMA-IR, homeostatic model assessment of insulin resistance. * < 0.05, ** < 0.01, ***<0.001, ****<0.0001, ns, Non significant.

Figure 3

Changes in cardiac geometry following bariatric surgery. (A) – percentage change in left ventricular mass, (B) – percentage change in left ventricular mass:volume ratio, (C) – percentage change in left ventricular end diastolic volume, (D) – percentage change in left atrial volume, (E) – percentage change in left ventricular stroke volume, (F) – percentage change in cardiac output. * < 0.05, ** < 0.01, ***<0.001, ****<0.0001, ns, Non significant.

Figure 4

The effect of epicardial adipose tissue on cardiac geometry following bariatric surgery. (A) – correlation between baseline lateral/septal wall thickness ratio and baseline epicardial adipose tissue, (B) – correlation between baseline lateral/septal wall thickness ratio and baseline visceral adipose tissue, (C) – change in left ventricular eccentricity index, (D) - correlation between left ventricular eccentricity index and baseline epicardial adipose tissue, (E) - correlation between change in left ventricular eccentricity index and change in epicardial adipose tissue, (F) – correlation between left ventricular eccentricity index and baseline visceral adipose tissue. *<0.05, *** < 0.001, **** < 0.0001 ns, Non significant.

Figure 5

(central figure) – following bariatric surgery the left ventricle undergoes a biphasic remodelling response. Initially there is a reversal of eccentric remodelling as total body tissue to perfuse falls, with reductions in left ventricular mass, end diastolic volume and epicardial adipose tissue. In the longer term there is a reversal of concentric remodelling as insulin resistance (HOMA-IR) decreases, with a further fall in left ventricular mass but an increase in end diastolic volume. LVEDV, left ventricular end diastolic volume; EAT, epicardial adipose tissue; LVM, left ventricular mass; HOMA-IR, homeostatic model assessment of insulin resistance. Created with BioRender.com.