The present study identified that AIP, one
of the new biochemical markers associated with
atherosclerosis, has an independent inverse association
with well-developed coronary collaterals. Although the
TyG index differed significantly between the groups,
it had no independent association with coronary
collateral development.
The AIP is a new lipid index superior to
low-density lipoprotein (LDL)-cholesterol (LDL-C), HDL-C, total cholesterol, and triglyceride in
predicting CAD.[24] Atherogenic index of plasma is
a substitute for small dense (sd) LDL particles and
is inversely proportional to LDL-C particle size.[25]
The rise in AIP indicates a decrease in LDL particle
diameter and an increase in sdLDL, which favors the
formation of foam cells and atherosclerotic plaque
development.[26] Atherogenic index of plasma is
independently associated with CTO and is thought
to predict the presence and severity of CTO.[27]
High-density lipoprotein cholesterol has
cardioprotective effects and improves endothelial
function through its anti-inflammatory and
antioxidative effects; in addition, it modulates
monocyte activation, adhesion, and migration.[28,29]
In the present study, HDL-C level was found close to
statistical significance in the well-developed collateral
group. The HDL-C level might have contributed to
well collateral development.
Studies have shown that the TyG index is superior
to HOMA-IR (homeostatic model assessment for
insulin resistance) in assessing insulin resistance
and can be used to predict CAD and adverse
cardiovascular events.[30-32] Insulin resistance can
directly or indirectly contribute to ventricular
and vascular dysfunction due to attenuated
proinf lammatory response and aggravated
atherosclerotic plaque.[33,34] Furthermore, insulin
resistance can alter systemic lipid metabolism,
leading to dyslipidemia and even accelerating the
rupture of fragile plaques by aggravating vascular
endothelial damage and inflammation.[35] However,
in the current study, although its relationship with
collateral development was significant, it was not
detected as an independent variable.
Monocyte-lymphocyte ratio, a novel marker of
systemic inflammation, is an independent risk factor
for CAD and predicts lesion severity.[36] Increased
MLR favors body inflammation and oxidative
stress, accelerates the formation of foam cells and
endothelial damage, suppresses immune responses,
and aggregates coronary plaque development.[37,38]
In the present study, its relationship with collateral
development had no statistical significance.
Melidonis et al.[39] more frequently detected thirddegree
collateral circulation following complete
occlusion of the LAD and right coronary arteries.
In the current study, well-developed collaterals were
observed much more in the LAD artery CTO cases. We thought that this might be due to the size of
the myocardial jeopardy area, which is influential
in collateral development, and the ischemic stimulus
that it created. We considered that the higher the
total number of occlusions and the number of lesions
above 50%, the greater the collateral development as
a factor affecting the size of the myocardial jeopardy
area.
The relatively small study population and the
single-center design may limit the interpretation
of results. The study’s cross-sectional nature limits
the direct relationship between cause and effect.
More extensive and prospective studies are needed to
confirm this relationship.
In conclusion, the use of AIP, one of the new
biochemical markers associated with atherosclerosis
in patients with CTO, should be at the forefront in
predicting poor collateral development. Furthermore,
the use of TyG would be beneficial, but MLR was
not appropriate. Compared to these parameters, the
AIP, which is noninvasive and easily accessible, can
help predict the degree of collateral development the
best, but more comprehensive randomized controlled
studies are needed.
Ethics Committee Approval: The study protocol was
approved by the Recep Tayyip Erdoğan University Faculty of
Medicine Ethics Committee (Date/no: 18.05.2022/40465587-
050.01.04-443). The study was conducted in accordance with
the principles of the Declaration of Helsinki.
Patient Consent for Publication: A written informed
consent was obtained from each patient.
Data Sharing Statement: The data that support the
findings of this study are available from the corresponding
author upon reasonable request.
Author Contributions: Idea/concept: N.E.; Literature
review: A.G.Ö.; Analysis and interpretation: A.E.; Data
collection: M.M.Ö.; Materials: M.Ö.; Design/control:
C.A.
Conflict of Interest: The authors declared no conflicts
of interest with respect to the authorship and/or publication
of this article.
Funding: The authors received no financial support for
the research and/or authorship of this article.