Received 2023-07-23

Revised 2023-08-04

Accepted 2023-08-27

Introduction

Coronary artery disease (CAD) is a major health concern leading to over 17.8 million deaths annually [1]. The underlying cause of CAD is atherosclerotic cardiovascular disease, which is associated with acute coronary syndrome (ACS) including ST-segment elevation myocardial infarction (STEMI), non-ST-segment elevation myocardial infarction (NSTEMI), and unstable angina. Atherosclerotic plaque rupture constitutes the major underlying cause of STEMI since its major components are, endothelial cells, leukocytes, and intimal smooth muscle cells [2].

Inflammation and lipid accumulation play a substantial role in the development of atherosclerosis and cardiovascular disease [3]. Chronic inflammation is associated with an increase in inflammatory mediators, cytokines, and adhesion molecules. This inflammatory response is closely related to the formation, progression, and rupture of atherosclerotic plaques [4]. Furthermore, the absorption of low-density lipoprotein (LDL-c) by macrophages in the vessel wall leads to the release of inflammatory cytokines and necrosis of the atherosclerotic plaque [5].

Monocytes play a critical role in the development and progression of atherosclerosis, and their number can be a predictor of heart events [6]. In inflammatory or pro-thrombotic states, monocytes can express tissue factors and become pro-coagulants [7]. Additionally, activated monocytes release circulatory pre-inflammatory cytokines that can damage the elastic layer and cause atherosclerotic plaque rupture [8]. In contrast, high-density lipoprotein (HDL-c) has anti-inflammatory, antioxidant, and anti-thrombotic effects. The low level of HDL-c in patients is associated with an increased hospital mortality risk following myocardial infarction (MI). HDL-c protects endothelial cells from inflammation and oxidative stress by controlling the activation and proliferation of monocytes and preventing their absorption into the artery wall. It has also been shown that HDL-c, as an anti-atherosclerotic agent, can inhibit the expression of tissue factor in monocytes by preventing P38 mitogen-activated protein kinase activation and inhibiting phosphoinositide 3-kinase (PI3K) [9, 10]. It is hypothesized that there is a relation between the number of monocytes, the low HDL-c levels, and the progression of atherosclerosis and consequently cardiovascular accidents. Previous studies have found that regression of coronary atherosclerotic plaques after treatment with pravastatin is associated with increases in serum HDL-c and decreases in peripheral blood monocyte counts [11]. This has led to the introduction of the monocyte-to-high-density lipoprotein ratio (MHR) as a novel cardiovascular biomarker that may be more effective than individual measurements of monocyte count and HDL-c levels in predicting both short-term and long-term outcomes of CAD [12, 13]. Several studies have shown that MHR during hospitalization in ACS patients is significantly associated with C-reactive protein (CRP) and other inflammatory indices, and patients with higher MHR are at higher risk of in-hospital death, major adverse cardiovascular events (MACEs), and stent thrombosis [7, 14-16]. Given these findings, this research was designed to assess the correlation between the admission MHR values, in-hospital mortality, and MACE in patients who had experienced STEMI and undergone primary percutaneous coronary intervention (PCI).

Materials and Methods

This retrospective cross-sectional study analyzed the medical records of patients with a diagnosis of STEMI who underwent primary PCI between March 2021 and March 2022 at Madani Training and Research Hospital, Tabriz, Iran. Patients who presented within 12 hours of the onset of symptoms (typical chest pain lasting for more than 30 minutes) and had ST-segment elevation of 1 mm or greater in at least two consecutive leads were included in the study. Subjects with clinical signs of heart failure (HF), history of MI, active cancer, hematological proliferative disorders, active hepatobiliary diseases, chronic antihyperlipidemic treatment, active infection, chronic inflammatory disease, receiving steroid therapy, autoimmune disease, and those without a recorded measurement of admission laboratory parameters including cholesterol levels before PCI were excluded from this study. In this study, patients were divided into two groups according to the median of their admission MHR.

Data regarding clinical and demographic properties and laboratory parameters were obtained from medical records. The study protocol was approved by the local ethics committee. This study was approved by a regional research ethics committee under the code IR.TBZMED.REC.1401.794.

Statistical Analysis

Data were reported as mean ± standard deviation (SD) or median (interquartile range) for parametric variables and percentages for categorical variables. The normality of continuous variables was confirmed by the Kolmogorov-Smirnov tests. Differences between groups were determined using the Mann-Whitney U test or independent t-test, as applicable; categorical variables were tested using Chi-square or Fisher exact tests, as applicable. Receiver operating characteristic curves were generated to determine MHR cutoff values for in-hospital mortality and MACEs. Univariate and multivariate binary logistic regression analyses were performed to identify independent predictors of in-hospital mortality and MACEs. Significance was set at P < 0.05. All statistical calculations were performed using SPSS software (version 16.0 for Windows, SPSS, Inc., Chicago, IL).

Results

A total number of 652 patients (378 males, 58% and 275 females,42%); with a median age of 68 years old (interquartile range (IQR) : 57-77) were included in the study. Among patients, 93 (14.3%) experienced MACEs. Out of the encountered events, 27 (4.1%) had ventricular tachycardia/ventricular fibrillation, 24 (3.7%) showed reinfarction, 6 (0.9%) had cardiopulmonary arrest, 3 (0.5%) had torsades de pointes and pulmonary embolism, and 37 (5.7%) expired during hospital follow-up.

Patients were categorized into two groups according to the median of their admission MHR: Group 1 (n=326) had an MHR lower than 15.59, and Group 2 (n=326) had an MHR higher than 15.59. The comparison of baseline, clinical, and laboratory parameters between groups is summarized in Table-1.

The serum levels of white blood cells (WBC), neutrophils, lymphocytes, monocytes, and MHR values were significantly higher in group 2 compared to group 1 (P<0.001). The serum hemoglobin level was significantly lower in group 2 compared to group 1 (P<0.001). The frequency of patients with a smoking history, Killip>1, and multiple vessel disease were significantly higher in group 2 compared to group 1 (32.2% vs. 19.9%, 81.9% vs. 79.8%, 79.4% vs. 68.1%; P< 0.001, P=0.05 and P<0.01 respectively). Patients in group 1 had higher values of left ventricular ejection fraction (LVEF) compared to group 2 (P=0.05). The in-hospital mortality rates and MACE were significantly higher in group 2 compared to group 1 (29% vs. 8%, 61% vs. 32%; P<0.001 and P=0.001). Other parameters were not significantly different between groups.

In the ROC curve analysis, MHR levels on admission above 16.1 predicted in-hospital mortality with a sensitivity of 75.7% and a specificity of 53.5% (area under the curve: 0.715; P<0.001, Figure-1), levels above 17.96 predicted MACE with a sensitivity of 60.2% and a specificity of 59.7% (area under the curve: 0.622; P<0.001, Figure-2).

Univariate and multivariate regression analyses were performed to examine the possible predictors of in-hospital mortality in the study population. In univariate regression analysis, BMI, MHR, Killip>1 and >1 vessel disease correlated with in-hospital mortality. In multivariate regression analysis, BMI, Killip>1, and MHR (OR 1.05, 95% CI 1.02-1.08, P=0.002) independently predicted in-hospital mortality (Table-2).

Univariate and multivariate regression analyses were also conducted to analyze the possible predictors of MACE in the study population. In the univariate regression analysis, age, BMI, Cr, troponin, Killip>1, LVEF, and MHR were correlated with MACE. In the multivariate regression analysis, age, BMI, troponin, LVEF, and MHR (OR 1.05, 95% CI 1.02-1.08, P<0.001) independently predicted MACE (Table-3).

Discussion

In this study, by analyzing the correlation between hospital admission MHR and in-hospital mortality and MACE in patients with STEMI who underwent primary PCI, we found that BMI, Killip>1, and MHR values were independently associated with in-hospital mortality, while age, BMI, troponin, LVEF, and MHR levels independently predicted MACE.

Atherosclerosis and plaque rupture due to STEMI are strongly associated with inflammation, which can be promoted by circulating monocytes. Oxidative stress and inflammation have been related to atherosclerotic progression and have become important factors in predicting adverse CAD outcomes [17-20]. Monocyte activation is an early step in the beginning of the atherosclerosis process, as evidenced by an increased count of circulating monocytes that is a predictor of plaque development. Endothelial cell dysfunction is the first stage of plaque development with mononuclear cells including monocytes and T lymphocytes attaching themselves to the endothelium. These cells in subendothelial space mature into macrophages and differentiate into foam cells by absorbing oxidized and other LDL-c. Foam cells release proinflammatory cytokines and tissue factor that increases the local inflammatory response, digests the internal elastic lamina and results in thrombus formation and ACS [21-24]. Tissue factor expression has been shown to increase following PCI, further demonstrating the pivotal role of monocytes in inflammation, thrombosis, and endothelial dysfunction [25]. Therefore, it is evident that macrophages and their precursor cells, monocytes, are key players in all stages of atherosclerosis and their involvement can lead to STEMI.

In contrast, HDL-c has well-known anti-inflammatory, antioxidant, and antithrombotic effects, particularly through suppressing monocyte activities and interrupting the differentiation of monocytes to macrophages, thus restricting the inflammatory response. HDL-c can also reduce the expression of adhesion molecules preventing monocyte recruitment to arterial walls [26, 27]. In addition, research has shown that an increased level of HDL-c is associated with reduced extramedullary monocytepoiesis in ACSs, suppressing the production of various chemokines, and thus interrupting the monocyte production and differentiation process from the spleen - a major source of monocytes in ACS. Consequently, lower levels of HDL-c and LDL-c have been reported as independent predictors of mortality in ACSs and other clinical illness diseases [28, 29].

In our study, serum cholesterol levels were lower in the MACE (+) group although this was not statistically significant and did not correlate with mortality and MACE in multivariate analysis. Nonetheless, HDL-c’s various effects highlight the importance of its role in cardiovascular diseases. MHR has emerged as an important indicator of inflammatory status and adverse cardiovascular outcomes, with its pioneering study conducted by Kanbay et al. [30]. They reported an association between increased MHR and the presence of cardiovascular comorbidities in chronic kidney disease patients [31]. After that, Canpolat et al. found that patients with pre-ablation high MHR values increased the risk of AF recurrence after ablation. Moreover, a study by MHR demonstrated that MHR was a significant predictor of stent thrombosis, mortality, and in-hospital MACE in patients with STEMI [32]. The association of monocytes and systemic inflammation, as well as the inhibitory effect of serum HDL-c on monocyte activation, suggested that an increased MHR may be predictive of adverse cardiovascular events in STEMI patients. Consequently, the monocyte-to-HDL-c ratio has been used as a new marker to predict clinical outcomes in several studies [16, 33].

We also concluded that MHR is effective in predicting mortality and MACEs. In our study, receiver operating characteristic curve analysis revealed that MHR greater than 16.1 is a cutoff value for mortality and MHR greater than 17.96 is a cutoff value for MACE. The results of multiple studies also have illustrated that high MHR was associated with in-hospital mortality among STEMI patients who underwent primary PCI [16, 30, 33] . The levels of various laboratory parameters related to inflammation have been studied in individuals with cardiovascular disease and were found to be able to predict mortality and MACE. Furthermore, the admission troponin I level was identified as a predictor of negative cardiovascular outcomes. Our research revealed that higher admission troponin I levels were independently related to MACE.

Conclusion

In this study demonstrated that admission MHR was an independent predictor of in-hospital mortality and MACE in patients with STEMI who underwent primary PCI. The results of this study suggest that MHR may be a useful biomarker for predicting adverse cardiovascular outcomes in patients with STEMI. Moreover, MHR can provide clinicians with additional information to facilitate the personalization of treatment strategies in these patients.

Conflict of Interest

The authors declare that there is no conflict of interest.

GMJ Copyright© 2023, Galen Medical Journal. This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/) Email:info@gmj.ir

 Correspondence to: Hamid Sedigh, Cardiovascular Research Center, Shahid Madani Heart Hospital, Tabriz University of Medical Sciences, Daneshgah St., Tabriz, Iran. Telephone Number: +984133373958 Email Address: hamidsedigh1368@gmail.com

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Table 1. Comparison of Demographic, Clinical, and Laboratory Parameters between Groups According to Admission MHR

Variables	Group 1 n=326 MHR<15.59	Group 2 n=326 MHR>15.59	P-value
Demographic
Age (years)	67.5 (55-77)	69(60-78)	0.01
Male, n (%)	189 (58)	189 (58)	1
BMI, kg/m2	24.2 (21.5-26.5)	24.2 (21.6-26.7)	0.26
Diabetes mellitus, n (%)	102 (31.3)	105 (32.2)	0.8
Hypertension, n (%)	144 (44.2)	165 (50.6)	0.1
Hyperlipidemia, n (%)	138 (42.3)	156 (47.9)	0.15
Coronary syndrome, n (%)	92 (28.2)	86 (26.4)	0.59
Family history of CAD, n (%)	104 (31.9)	98 (30.1)	0.61
Smoking, n (%)	65 (19.9)	105 (32.2)	<0.001
SBP (mmHg)	110 (100-110)	110 (100-115)	0.52
DBP (mmHg)	70 (60-70)	70 (60-75)	0.63
HR (bpm)	84 (77-93)	85 (77-92)	0.78
Laboratory parameters
Hemoglobin (mg/dl)	14.6 (12.8-15.9)	13.8 (12-15.5)	<0.001
Platelet (/mm3)	220 (140.6-292.2)	211 (148.3-308.2)	0.51
WBC (103 mL)	9.2 (6.9-13.2)	15.1 (10.6-19.1)	<0.001
Neutrophil (103 mL)	1.5 (0.9-3.6)	3.5 (1.75-5.72)	<0.001
Lymphocyte (103 mL)	6.5 (4.4-9.4)	9.6 (6.56-12.8)	<0.001
Monocyte (103 mL)	0.39 (0.27-0.49)	0.98(0.79-1.23)	<0.001
Total cholesterol (mg/dl)	185 (179-191)	186 (179-193)	0.35
Triglyceride (mg/dl)	170.33±16.15	170±17.01	0.8
LDL (mg/dl)	126 (120-136)	128 (119-137)	0.46
HDL (mg/dl)	41 (39-44)	41 (38-43)	0.07
VLDL (mg/dl)	15 (13-16)	15 (14-16)	0.83
MHR	9.65 (6.88-12.62)	23.6 (19.4-29.7)	<0.001
Creatinine, mg/dL	1.1 (0.9-1.3)	1.09 (0.9-1.3)	0.84
Troponin I, ng/mL	6.5 (5.37-9.6)	6.5 (5.5-8.3)	0.85
CRP, mg/L	3.3 (2.6-4.1)	3.3 (2.5-3.9)	0.31
Killip class>1, n (%)	260 (79.8)	267 (81.9)	0.05
Angiographic characteristics
Culprit artery, n (%)
LAD	216 (66.3)	202 (62)	0.25
CX	134 (41.1)	137 (42)	0.81
RCA	137 (42)	134 (41.1)	0.81
Multiple-vessel disease, n (%)	222 (68.1)	259 (79.4)	<0.001
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Continues of Table 1. Comparison of Demographic, Clinical, and Laboratory Parameters between Groups According to Admission MHR

LVEF, %	37.5 (30-50)	35 (25-45)	0.05
MACE, n (%)	32 (9.8)	61 (18.7)	0.001
Mortality, n (%)	8 (2.5)	29 (8.9)	<0.001

Data are expressed as median and interquartile range (IQR) for parametric variables and percentage for categorical variables.

Abbreviations: BMI: body mass index; CRP: C-reactive protein; CX: circumflex coronary artery; DBP: diastolic blood pressure; HDL: high density lipoprotein; HR: heart rate; RCA: right coronary artery; LAD: left anterior descending coronary artery; LDL: low-density lipoprotein; LVEF: left ventricular ejection fraction; MACE: major adverse cardiac events; MHR: monocyte-to-high-density lipoprotein; SBP: Systolic blood pressure; VLDL: very low-density lipoprotein; WBC: white blood cell.

Figure 2. ROC curve analysis showing the predictive cut-off value of MHR for in-hospital MACE. Abbreviations: MACE: major adverse cardiovascular events; MHR: monocyte to HDL ratio; ROC: receiver operating curve

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Table 2. Independent Predictors of Mortality According to the Univariate and Multivariate Regression

Analyses

Variables	Univariate			Multivariate
	OR	CI	P-value	OR	CI	P-value
Age (years)	1	0.97-1.02	0.97
Male, n (%)	0.59	0.3-1.16	0.13
BMI, kg/m2	1.44	1.31-1.58	<0.001	1.44	1.30-1.59	<0.001
MHR	1.06	1.04-1.09	<0.001	1.05	1.02-1.08	0.002
Creatinine, mg/dL	1.10	0.81-1.5	0.51
Troponin I, ng/mL	0.94	0.85-1.03	0.23
Killip class>1, n (%)	1.70	1.17-2.46	0.005	1.57	1.06-2.32	0.02
>1-vessel disease (multiple vessel diseases), n (%)	1.81	1.12-2.94	0.01	1.56	0.88-2.79	0.12
LVEF, %	0.97	0.94-1.004	0.08

Abbreviations: BMI: body mass index; CI: confidence interval; LVEF: left ventricular ejection fraction; MHR: monocyte-to-high-density lipoprotein; OR: odds ratio

Table 3. Independent Predictors of MACE According to the Univariate and Multivariate Regression Analyses

Variables	Univariate			Multivariate
	OR	CI	PV	OR	CI	PV
Age (years)	0.95	0.93-0.97	<0.001	0.94	0.92-0.97	<0.001
Male, n (%)	1.53	0.96-2.44	0.06
BMI, kg/m2	1.24	1.17-1.31	<0.001	1.28	1.2-1.37	<0.001
MHR	1.04	1.02-1.06	<0.001	1.05	1.02-1.08	<0.001
Creatinine, mg/dL	1.33	1.09-1.62	0.005	1.15	.87-1.52	0.32
Troponin I, ng/mL	1.18	1.13-1.24	<0.001	1.22	1.15-1.29	<0.001
Killip class>1, n (%)	1.29	1.02-1.62	0.03	1.30	0.98-1.72	0.06
>1-vessel disease (multiple vessel disease), n (%)	1.18	0.87-1.61	0.27
LVEF, %	0.94	0.92-0.96	<0.001	0.94	0.91-0.96	<0.001

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