Systemic Immune-Inflammatory Index as a Determinant of Atherosclerotic Burden and High-Risk Patients with Acute Coronary Syndromes

Gur, Demet Ozkaramanli; Efe, Muhammet Mucip; Alpsoy, Seref; Akyüz, Aydın; Uslu, Nurullah; Çelikkol, Aliye; Gur, Ozcan

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Original Article • Arq. Bras. Cardiol. 119 (3) • Sept 2022 • https://doi.org/10.36660/abc.20210416 copy

Systemic Immune-Inflammatory Index as a Determinant of Atherosclerotic Burden and High-Risk Patients with Acute Coronary Syndromes

Authorship SCIMAGO INSTITUTIONS RANKINGS

Abstract

Background

Systemic immune-inflammatory index (SII), which is derived from neutrophil, platelet and lymphocyte counts, represents the homeostatic balance among inflammatory, immune and thrombotic status. The systemic immune-inflammatory index is superior to indices such as neutrophil-lymphocyte ratio in predicting prognosis in various malignancies, while it is shown to predict future cardiac events better than traditional risk factors after coronary intervention.

Objectives

Herein, we aimed to evaluate the relationship of the systemic immune-inflammatory index with atherosclerotic burden and in-hospital complications in acute coronary syndrome patients.

Methods

The clinical outcomes, such as extent of myocardial damage, atherosclerotic burden, bleeding, acute kidney injury, duration of hospital stay and in-hospital mortality, were evaluated in a retrospective cohort of 309 consecutive acute coronary syndrome patients. The systemic immune-inflammatory index was calculated as (Platelet X Neutrophil)/Lymphocyte count on admission. Study population was categorized into tertiles with regard to systemic immune-inflammatory index. A p value of <0.05 was considered statistically significant.

Results

The highest systemic immune-inflammatory index values were within ST elevation myocardial infarction patients (641.4 in unstable angina pectoris, 843.0 in non-ST elevation myocardial infarction patients and 996.0 in ST elevation myocardial infarction patients; p=0.004). Maximal troponin concentration (0.94 vs. 1.26 vs. 3; p<0.001), number of diseased vessels (1 vs. 2 vs. 2; p<0.001), the SYNTAX (synergy between percutaneous coronary intervention with taxus and coronary artery bypass grafting) score (9 vs. 14 vs. 17.5; p<0.001) and duration of hospital stay (2 vs. 2 vs. 3; p<0.001) also increased with increasing SII_tertile(tertile1 vs. tertile 2 vs. tertile 3). Systemic immune-inflammatory index was an independent predictor of SYNTAX score (ß: 0.232 [0.001 to 0.003]; p<0.001), extent of myocardial damage (ß: 0.152 [0 to 0.001]; p=0.005) and duration of hospital stay (ß: 0.168 [0.0 to 0.001]; p=0.003).

Conclusions

This study has demonstrated that the systemic immune-inflammatory index, a simple hematological index, is a marker of atherosclerotic burden and longer hospital stay on well-known risk factors in high risk acute coronary syndrome patients.

Inflammation; Acute Coronary Syndrome; Coronary Artery Disease

Variable	Total n=309	SII Tertile 1 n=103	SII Tertile 2 n=103	SII Tertile 3 n=103	1 vs. 2 p value	2 vs. 3 p value	1 vs. 3 p value
Age, years	64.5±12.1	62.8±11.8	65.1±13.1	65.5±11.2	0.500	1.00	0.306
Female gender, n (%)	82 (26.5)	25 (24.3)	32 (31.1)	25 (24.3)	0.350	0.350	1.00
UAP, n (%)	53 (17.2)	27 (26.2)	17 (16.5)	9 (8.7)	0.125	0.141	0.002
NSTEMI, n (%)	113 (36.6)	36 (35)	46 (44.7)	31 (30.1)	0.200	0.043	0.552
STEMI, n (%)	143 (46.3)	40 (38.8)	40 (38.8)	63 (61.2)	1.00	0.002	0.002
Diabetes mellitus, n (%)	123 (39.8)	36 (35)	40 (38.8)	47 (45.6)	0.665	0.397	0.155
Hypertension, n(%)	117 (37.9)	43 (41.7)	33 (32)	41 (39.8)	0.194	0.309	0.887
Hyperlipidemia, n (%)	125 (40.5)	42 (40.8)	36 (35)	47 (45.6)	0.473	0.155	0.574
Hemoglobin, g/dL	13.5±1	13.8±1.8	13.2±1.8	13.3±1.8	0.047	1.00	0.075
White blood cells, 103/µL	9.9±2.7	9.1±2.7	9.5±2.3	11.4±2.5	0.571	<0.001	<0.001
Neutrophil count, 103/µL	6.8 (3.54)	5.1 (2.37)	6.7 (2.5)	8.8 (3.03)	<0.001	<0.001	<0.001
Lymphocyte count, 103/µL	1.84 (1.1)	2.3 (1.12)	1.8 (0.89)	1.3 (0.75)	<0.001	<0.001	<0.001
Monocyte count, 103/µL	0.63 (0.36)	0.7 (0.36)	0.6 (0.31)	0.6 (0.39)	0.163	0.893	0.341
Platelet count, 103/µL	238 (96)	207 (75.75)	241 (75.00)	278 (116.75)	0.001	<0.001	<0.001
C-reactive protein, mg/L	4.55 (8.63)	3.8 (8.1)	4.7 (8.1)	5.4 (10.8)	0.651	0.262	0.271
Urea, mg/dL	34 (15)	32 (13)	33.5 (15)	36 (17.1)	0.469	0.082	0.038
Creatinine, mg/dL	0.93 (0.32)	0.93 (0.28)	0.91 (0.33)	0.94 (0.38)	0.984	0.694	0.854
SII	835 (860.09)	462 (194.51)	833 (252.9)	2055 (935.7)	<0.001	<0.001	<0.001

Outcome	SII Tertile 1 n=103	SII Tertile 2 n=103	SII Tertile 3 n=103	1 vs 2 p value	2 vs 3 p value	1 vs 3 p value
Number of diseased vessels	1 (1)	2 (2)	2 (2)	0.013	1.00	0.011
Atherosclerotic burden or SYNTAX Score	9 (11)	14 (11.5)	17.5 (11)	0.022	0.002	<0.001
Extent of myocardial damage or Maximal troponin, ng/L	0.94 (2.06)	1.26 (3.61)	3 (4.02)	0.434	0.002	<0.001
Hospital stay, days	2 (1)	2 (1)	3 (3)	0.709	<0.001	0.026
Bleeding, n(%)	27 (26.2)	22 (21.4)	32 (31.1)	0.257*	0.157*	0.538*
Acute kidney injury, n(%)	18 (17.5)	17 (16.5)	22 (21.4)	1.00*	0.477*	0.598*
In-hospital mortality, n(%)	5 (4.9)	8 (7.8)	9 (8.7)	0.568*	1.00*	0.407*

		SII			NLR		PLR
		r_s	p		r_s	p	r_s	p
UAP	SYNTAX	0.300	0.031		0.266	0.054	0.145	0.299
NSTEMI	SYNTAX	0.345	<0.001		0.236	0.011	0.183	0.045
STEMI	SYNTAX	0.471		<0.001	0.456	<0.001	0.387	<0.001

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[1] Mailing Address: Demet Ozkaramanli Gur • Namik Kemal University Faculty of Medicine Department of Cardiology, Tekirdag 59000 – Turkey. E-mail: dozkarm@yahoo.com