4. Discussion:
Patients with CAD had higher values of EAT. EAT-T by echocardiography
correlated with EAT-V by CTA and was an independent predictor of CAD.
Individuals with an EAT-T (PLAX) ≥3.9 mm and EAT-T (PSAX) ≥3.8 mm had
Odd’s ratio of 2.8 and 2.6 respectively of having CAD. The sensitivity
of these parameters to detect CAD was over 80% with specificity in the
range of 50%. The marker was an independent risk factor after adjusting
for clinical risk score of QRISK 3 which includes traditional risk
factors.
Previous studies have shown positive correlation of EAT with indices of
obesity like BMI (8). So, to nullify the effect of
obesity on EAT and for better refinement of data, its indexed value was
also evaluated in our study. Odds ratio of having CAD was higher for
indexed EAT-T values as compared to absolute values in our study, which
further signified the importance of neutralizing the effect of obesity
on EAT measurement by indexing it to body surface area.
Epicardial adipose tissue surrounding the heart has been postulated in
contributing to the development of coronary atherosclerosis by various
mechanisms (3). One such mechanism is EAT acting as
inflammatory organ leading to local secretion of various adipo-cytokines
and inflammatory mediators like tumour necrosis factor, interleukin-6
and free fatty acids from epicardial adipocytes which may adversely
affect coronary arteries (9, 10). Recent studies have
also found that EAT was associated with the presence of high-risk
vulnerable plaques (11).
EAT-V measured by CTA in multiple studies has been associated with CAD.
Iwasaki et al (12) measured EAT-V in patients who
underwent CTA and found that patients with significant coronary artery
stenosis had higher EAT-V. K Yamashita et al (13)showed that EAT-V was associated with total coronary plaque burden and
vulnerable lipid rich necrotic plaques, and Ueno et al(14) showed independent association of chronic total
occlusions with EAT-V. A recent study by Wenji Yu et al in Chinese
population also revealed association of EAT volume to obstructive CAD(15). Thus EAT-V has emerged as a reliable risk
predictor of CAD, plaque burden and vulnerable plaques, and EAT-T by
echocardiography in our study showed good correlation with it.
On the other hand, echocardiographic EAT-T has not been widely studied
due to the proposed limitations of measurement in linear dimensions,
inter-observer variation and lack of good acoustic windows(16, 17). There are only few studies of EAT-T by
echocardiography and have shown its association with CAD severity
(assessed by various scores like Gensini score, SYNTAX score, and number
of epicardial vessels involved), and with the presence of CAD (cut off
being taken from 50% to 70% diameter stenosis) (18,
19). Verma B. et al showed that EAT-T has positive correlation with
waist circumference, LDL-C level, Gensini score, and SYNTAX score, and
also showed that EAT-T is independent predictor of CAD after adjusting
for all conventional risk factors (20). All these
studies have adjusted for conventional risk factors in a multivariate
model for showing EAT-T as independent predictor of CAD. However, in our
study we included QRISK3 score in multivariate model. Since calculation
of QRISK3 score require all conventional risk factors and is a better
predictor of CAD and future CV events than individual conventional risk
factor, therefore putting it in a multivariate model enhanced the
independent predictive value of EAT-T.
Erkan et al observed mean EAT values of 4.3±0.9 mm, 5.2±1.5 mm, and
7.5±1.9 mm in patients with normal coronary arteries, minimal CAD, and
significant CAD, respectively. In that study, a EAT cut-off value of 5.8
mm predicted significant CAD (AUC: 0.875; P < 0.001, 95% CI:
0.825–0.926) in that study (21). While various other
studies found a threshold of 6-7 mm as elevated EAT-T(22, 23). In our study, optimum EAT cut-off value to
predict CAD was identified as ≥3.9 mm on PLAX view (AUC: 0.68, 95% CI:
0.58-0.79) with a sensitivity of 84 % and a specificity of 55 %,
respectively. These variations in EAT cut-offs in different studies may
be explained by ethnic differences in the threshold for association with
CAD as described by Moharram et al (24).
Our study had the following limitations. This was a single centre study
with moderate number of patients. The above findings and cut-offs need
to be validated in larger prospective cohort studies. The measurement of
EAT is operator-dependent and inter-observer variations may occur;
although we observed good inter-observer correlation. Also measuring
EAT-T in obese and those with sub-optimal echo windows is a challenge,
these patients were excluded from this study. Also, this was a
hospital-based study and may not reflect the normal population. However,
a CT scan-based study to show correlation with CAD may not be feasible
in normal population.