Abstract

JACC

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TCTAP A-025

Presenter

Arun Kochar

Authors

Asees Paul Singh1, Hiteshi Kc Chauhan2, Arun Kochar1, Pankaj Garg3

Affiliation

Fortis Hospital, India1, Fortis Healthcare Limited, India2, Garg Fistula Research Institute, India3
View Study Report
TCTAP A-025
Chronic Total Occlusion

Assessment of Coronary Collaterals and Its Clinical Determinants in Patients with Total/Subtotal Coronary Artery Occlusion – An Observational Study Conducted at a Tertiary Care Center in India

Asees Paul Singh1, Hiteshi Kc Chauhan2, Arun Kochar1, Pankaj Garg3

Fortis Hospital, India1, Fortis Healthcare Limited, India2, Garg Fistula Research Institute, India3

Background

Coronary collateral arteries develop and mature in response to ischemia caused by severe coronary stenosis or occlusion. However, the determinants of collateral formation and its role - especially in total/subtotal coronary occlusion - are poorly understood. A succinct insight into collateral formation and its determinants would be a step forward towards delineating future therapeutic strategies focused on the promotion of collateral growth and functionality.
Objectives:    1. To determine the role of conventional coronary risk factors in coronary collateral development.    2. To study the association of coronary collateral formation in patients with total / subtotal occlusion with clinical presentations,         coronary artery involved and grades of collaterals.

Methods

The coronary angiograms of 527 adult patients, who underwent this diagnostic procedure in the time period from June 2018 to July 2020 at our tertiary care center in India, were studied. 50 patients of this 527-patient cohort, who had subtotal and total coronary artery occlusions, were included in our study with the aforementioned objectives.

Results

Of these 50 patients, 37 were male and 13 were females. The baseline parameters, past medical history and clinical presentations are tabulated below.  Table 1: Baseline Parameters, Prior Medical History and Clinical Presentations in patients                with Coronary Artery Occlusion (N=50)
Variables Values
Baseline Parameters
Age, mean (SD) 54.14 ¡¾ 7.45 years
Male, n (%) 37 (74)
Female, n (%) 13 (26)
Medical History, n (%)
Diabetes Mellitus 15 (30)
Hypertension 10 (20)
Smoking 7 (14)
Prior CAD 6 (12)
Multifactorial                                       4 (8)
No risk factors 5 (10)
Clinical Presentation, n (%)  
STEMI 24 (48)
NSTEMI 6 (12)
UA 5 (10)
CSA 15 (30)
 
 Table 2: Association of Grades of Collaterals with Risk Factors and Clinical Presentation
Variables Inadequate Collaterals(n) AdequateCollaterals(n) P value
Diabetes mellitus 14 1 0.003
Hypertension 3 7 0.02
Smoking 6 1 0.16
Prior CAD - 3 0.02
STEMI 20 4 0.003
NSTEMI 3 3 0.51
UA 4 1 0.38
CSA 2 7 0.007
 88 % of patients had single artery occlusion. The artery most commonly occluded was the Left Anterior Descending [LAD], followed by the Right Coronary Artery [RCA] and the Left Circumflex [LCx]. In LAD artery occlusion, RCA was the major contributor as collateral artery. LAD artery was the major contributor as collaterals in both LCX and RCA type of occlusion. The incidence of collaterals in males as compared with female patients showed no significant difference. There was a lower prevalence of adequate collaterals in diabetic patients and higher prevalence of adequate collaterals in patients with hypertension. There was no significant variation in collateral grades in patients with normal left ventricular [LV] function as compared with those with abnormal LV function. The most common grade of collaterals observed was grade 1 in half of this cohort. Inadequate collaterals were seen in 83 % of patients with STEMI. Adequate collaterals were observed in 77 % of patients with CSA and 66 % with recurrent CAD.

Conclusion

Diabetics have a lower prevalence of adequate collaterals. Adequate collateral formation is seen in patients with hypertension. Patients with chronic stable angina and with prior CAD show a significant prevalence of adequate collaterals, suggesting that ischemia could be responsible for the induction of collateral growth. We need larger studies on collateral formation and its determinants, so that future therapeutic strategies can target the promotion of collateral growth and functionality.