Stress hyperglycaemia ratio is an independent predictor of in-hospital heart failure among patients with anterior ST-segment elevation myocardial infarction

doi:10.21203/rs.3.rs-5028884/v1

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Research Article

Stress hyperglycaemia ratio is an independent predictor of in-hospital heart failure among patients with anterior ST-segment elevation myocardial infarction

https://doi.org/10.21203/rs.3.rs-5028884/v1

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Background

Stress hyperglycaemia ratio (SHR) has been reported to be independently and significantly associated with various adverse cardiovascular events as well as mortality. Moreover, in-hospital heart failure following acute myocardial infarction has been demonstrated to account for majority of all heart failure (HF) cases with anterior myocardial infarction showing higher rates of HF. However, the association between SHR and in-hospital HF following an anterior ST-elevation myocardial infarction (STEMI) has not been reported earlier. Therefore, the present study aimed at identifying the relationship between SHR and in-hospital HF post STEMI.

Methods

In this retrospective study electronic health records of 512 patients who presented with anterior STEMI from 01 January 2022 to 31 January 2024 were analysed. Based on the development of in-hospital HF, the enrolled patients were stratified into two groups: Group I, comprising of 290 patients who developed in-hospital HF and Group II comprising of 222 patients who did not develop in-hospital HF. ROC and Multivariable logistic regression analyses were performed to assess the relationship between SHR and in-hospital HF.

Results

The results revealed that SHR is a significant independent predictor of in-hospital HF (OR: 3.53; 95%CI: 2.02–6.15; p < 0.001). Apart from SHR, the results also identified age, nosocomial pneumonia, ventricular fibrillation, LVEF, and NT-pro-BNP levels as other independent predictors. ROC analysis showed that SHR independently had a moderate discriminative power with AUC: 0.683, 95% CI 0.605–0.762; p = 0.04, which was almost comparable to the combined predictive value of other independent risk factors (AUC: 0.726, 95% CI 0.677–0.784). Noticeably, combining SHR and other identified independent predictors demonstrated a significant predictive power (AUC: 0.813, 95% CI 0.757–0.881; p = 0.01).

Conclusion

SHR is an independent predictor for in-hospital HF in anterior wall STEMI patients.

Stress hyperglycaemia ratio

anterior wall STEMI

In-hospital heart-failure

NT-pro-BNP

Nosocomial pneumonia

The most common sequalae of acute ST-elevation myocardial infarction (STEMI) is new-onset left ventricular systolic dysfunction that poses increased risks for sudden death and heat failure (HF). Although the use of primary percutaneous coronary intervention (pPCI) results in better prognosis [1, 2] as it can limit both the infarct size as well as preserve the left ventricular systolic function [3, 4]. However, previous studies have demonstrated that timely PCI in not helpful in preserving or maintaining heart function in all STEMI patients and despite successful pPCI, 4.7–8.6% of STEMI patients still experience significant depression in heart function [5, 6]. Despite the rapid advances in interventional and pharmacological treatment modalities, STEMI still is the leading cause of HF and mortality. As per an estimate the incidence of HF in patients with STEMI even after pPCI is 4.6%, 4.7%, and 5.1% at 1 month, 1 year, and at 2 years respectively[5]. Post-acute STEMI incidence of new-onset HF has been reported to range from 10%-45% [7–13]. Previous investigations have suggested that in-hospital HF after acute myocardial infarction (MI) is a major contributor for all HF cases [14]. Previous investigations studying the significant predictors of HF following STEMI have shown high heterogeneity among the study subjects in terms of type of acute MI (STEMI or non-STEMI), reperfusion modalities (thrombolysis, pPCI, and PCI after thrombolysis), exclusion of patients with cardiogenic shock, and infarct location[15–19]. Studies have demonstrated higher rates of HF [5, 16, 19], lower left-ventricular ejection fraction [20], and higher mortality [21] in patients with anterior MI compared to patients with other infarct locations.

Acute hyperglycaemia in response to physiological stress because of an acute illness has been associated with significantly higher risks of morbidity and mortality in critically ill patients[22–26]. Studies have reported this correlation between stress hyperglycaemia and morbidity and mortality irrespective of prior status of diabetes and can be more significant in non-diabetic subjects [22–24]. Recently a novel indicator of relative hyperglycaemic status, the stress hyperglycaemia ratio (SHR) has been proposed [27]. It is defined as random glucose levels at admission divided by the estimated average glucose levels using glycosylated haemoglobin (HbA1c). It has been demonstrated that SHR is a better marker of stress hyperglycaemia and a significant predictor of critical illness compared to absolute hyperglycaemia in patients with acute illness[27]. Previous studies have shown a significant association between SHR and poor prognosis in acute coronary syndrome (ACS) patients [28–30]. However, these studies have primarily focussed on unstable angina and non-STEMI [28]. Furthermore, the association between SHR and HF in STEMI patients treated with PCI remains unexplored, therefore necessitating an investigation.

Since in-hospital HF after acute MI has been demonstrated to account for majority of all HF cases [14], and anterior MI showing higher rates of HF [5, 16, 19], and mortality [21], the present study is therefore aimed at assessing the significance of SHR (calculated from HbA1c) in predicting in-hospital HF in anterior STEMI patients undergoing PCI.

Study design and setting

This retrospective study was conducted at Prince Faisal-Bin-Khalid Cardiac Centre, Abha, Kingdom of Saud Arabia.

Study subjects and duration

From 01 January 2022 to 31 January 2024, the electronic health records (EHR’s) of a total of 600 patients with anterior wall STEMI were perused. Out of 600, only 512 patients met our set inclusion / exclusion criteria, hence were finally enrolled. Amongst the enrolled 512 patients, 290 with in-hospital heart failure (HF) were included in Group I, and 222 patients who had not developed in-hospital heart failure were included in Group II. The study was approved by the ethics committee at King Khalid University (HAPO-06-B-001), Abha, Saudi Arabia vide approval number ECM# 2024 − 1901 and carried out in-line with the 2013 revision of the principles of Declaration of Helsinki[31]. Written consent was obtained from each subject enrolled.

Inclusion Criteria

Patients were only included in the study if: (1) they had been diagnosed with acute anterior wall STEMI (2) Underwent primary percutaneous intervention (pPCI) within 1.5 hours of symptom onset.

Exclusion Criteria

Exclusion criteria were: (1) Any history of previous myocardial infarction, congenital heart disease, cardiomyopathy, chronic heart failure, or severe valvular disease (2) Incomplete clinical data.

Data and Definitions

The following clinical variables were recorded for all patients enrolled: (1) age, gender, smoking status, heart rate, systolic blood pressure, diastolic blood pressure, and past medical history (Diabetes, hypertension, past myocardial infarction (MI) (2) Laboratory variates (WBC, blood sugar, glycosylated haemoglobin (HBA1c), serum creatinine, cystatin C, low density lipoprotein (LDL), biomarkers (highest peak from repeated samples during hospitalization)- creatine kinase, creatine kinase-MB, N-Terminal pro- brain natriuretic peptide (NT-pro BNP), and cardiac troponin I (3) In-hospital complications- Atrial Fibrillation (AF), ventricular fibrillation (VF), sustained ventricular tachycardia, and nosocomial pneumonia (NP) (4) data from first transthoracic echocardiography-left ventricular ejection fraction(LVEF), left ventricular end diastolic diameter, left atrial diameter, mitral and aortic regurgitation, left ventricular diastolic dysfunction, and regional wall motion abnormality (RWMA) of left ventricular wall (5) Coronary angiographic data- pre-procedural thrombolysis in myocardial infarction (TIMI) flow grade in the left anterior descending artery (LAD), left circumflex artery (LCX), and right coronary artery (RCA), post-procedural TIMI flow grade < 3 in infarct related artery, lesions in the proximal part of LAD, single vessel disease, three vessel diseases, and total artery occlusion.

The diagnosis of acute STEMI was confirmed as per the criteria established by the European Society of Cardiology[32]. The infarct region was detected by electrocardiogram and confirmed by angiography. In-hospital HF was defined as documented evidence of dyspnoea upon exertion or fluid retention, and in patients with Killip class ≥ II upon signs of HF like rales, jugular venous distention, or pulmonary edema and was only confirmed once excluding other conditions that can cause similar signs and symptoms. Patients were stratified to one of the Killip classes, as per the set criteria[33]. Stress hyperglycaemia ratio (SHR) was calculated as, SHR = (Fasting blood glucose (FBG) (mmol/L)) / (1.59×HbA1c (%)—2.59) [28]. The decision of using fasting glucose (FBG) instead of admission glucose (ABG) levels as the numerator in the above equation was grounded in its comparatively better prognostic significance in patients with acute cardiovascular disease [34, 35]. It has also been reported to be insensitivity to food or other sugar infusions, and limited inter-individual variability [36,37 ]. P-value < 0.05

Statistical Analysis

All statistical analysis was performed using R[38] scripting language and the accompanying R studio [39] (Version 1.2.5033, Orange Blossom). Sample size calculation was done using Cochran’s equation [40]. Continuous variables with Gaussian distribution were reported as mean ± standard deviation (SD), whereas continuous variables with non-Gaussian distribution were reported as median (interquartile interval), and categorical data in numbers and percentages (%). Continuous variables following Gaussian distribution were compared using student’s t-test, whereas continuous variables with non-Gaussian distribution were compared using Mann-Whitney U-test. Chi-Square tests were used to compare categorical variables. The odds ratio (OR) and confidence interval (CI) were obtained by multivariable logistic regression. Variates with p < 0.05 in univariate analysis were considered significant and hence were included in multivariable logistic regression analysis to uncover independent predictors (p < 0.05). The predictive value of each significant independent predictor was assessed utilizing the area under receiver operating characteristic curve (AUROC).

Baseline characteristics of the study cohort

This study involved a total of 512 anterior-wall STEMI patients. The mean age of the study population was 62 ± 14.2. The study cohort was predominantly male (79.8%). The study subjects were stratified into two groups: one comprising of subjects who developed in-hospital HF (Group I) and the other comprising of subjects not developing in-hospital HF (Group II). The primary analysis of data extracted (demographic, clinical, echocardiographic, and angiographic characteristics of the enrolled study subjects) revealed that subjects in Group I in comparison to subjects in Group II presented with older age (p < 0.001), increased heart rate (p < 0.001), higher fasting blood glucose (p < 0.001), higher glycated hemoglobin (HbA1c) (p = .001), higher SHR (p < 0.001), low blood pressure, low LVEF (p < 0.001), new-onset AF (p < 0.001), VF (p < 0.001), ventricular tachycardia (p < 0.001), NP (p < 0.001), increased left-ventricular end-diastolic diameter, mitral regurgitation (p < 0.001), regional-wall motion abnormality (RWMA) in apical (p = 0.010), anterior (p < 0.001) and rest of the left-ventricular wall (p < 0.001), higher WBC count, higher serum creatinine (p < 0.001), higher cystatin C levels (p < 0.001), increased fibrinogen levels, higher peaks of D-dimer (p < 0.001) and NT-pro-BNP (p < 0.001). Additionally, 3-vessel disease, pre-procedural TIMI flow grade ≤ 1 in LCX and RCA, post-procedural TIMI flow grade ≥ 3 in infarct-related artery were significantly associated with the in-hospital HF (Table 1).

Table 1

Baseline demographic and patient characteristics stratified by in-hospital HF
Variate	Group I (n = 290)	Group II (n = 222)	p-value
Demographic and clinical variates
Age (years), mean ± SD	65.2 ± 9.6	57.6 ± 10.5	< 0.001
Male, n (%)	218 (75)	191 (86)	0.002
Hypertensive, n (%)	154 (53)	107 (48)	0.262
Diabetic, n (%)	96 (33)	58 (26)	0.086
Smoker, n (%)	142 (49)	118 (53)	0.370
SBP (mmHg), mean ± SD	129.6 ± 23.7	135.32 ± 22.6	0.005
DBP (mmHg), mean ± SD	77.3 ± 14.8	80.4 ± 14.9	0.019
HR (bpm), median (Q1, Q3)	87(74,101)	81(72, 93)	< 0.001
New-onset Atrial Fibrillation, n (%)	26 (9)	7 (3)	0.006
Sustained Ventricular Tachycardia, n (%)	18 (6)	1 (0.4)	< 0.001
Ventricular Fibrillation, n (%)	35 (12)	7 (3)	< 0.001
Nosocomial Pneumonia, n (%)	73 (25)	9 (4)	< 0.001
Laboratory variates
Fasting Blood Glucose, mmol/L	9.29 ± 4.10	6.02 ± 1.64	< 0.001
HbA1c (%), mean ± SD	6.98 ± 1.81	6.43 ± 1.38	0.001
SHR, median (Q1, Q3)	0.98(0.87, 1.19)	0.72(0.61, 0.83)	< 0.001
WBC (10⁹/L), median (Q1, Q3)	11.8(8.6, 15.6)	10.6(7.5, 10.9)	0.031
LDL (mmol/L), (mean ± SD)	3.6 ± 1.3	3.4 ± 1.2	0.072
Cystatin C (mg/L), median (Q1, Q3)	1.2(1.0, 1.7)	1.0(0.8, 1.3)	< 0.001
Serum Creatinine (µmol/L), median (IQR interval)	83.0(68.6, 112)	75.2(61.0, 86.8)	< 0.001
Peak CK (IU/L), median (Q1, Q3)	1006.3(268.5, 2898)	1012.7(278.0, 2383.2)	0.623
Peak CK-MB (IU/L)	90.2(32.2, 271.0)	83.4(34.7, 200.6)	0.415
Fibrinogen (g/L), mean ± SD	4.2 ± 1.6	3.9 ± 1.1	0.017
Peak D-dimer (µg/mL), median (Q1, Q3)	1143(541.2, 1696.3)	500(287.2, 1478)	< 0.001
Peak Troponin I (µg/L), mean ± SD	18.8 ± 16.9	16.7 ± 15.3)	0.147
Peak NT-pro-BNP (pg/mL), median (Q1, Q3)	2168(887, 4937)	693(313, 2158)	< 0.001
Echocardiographic variates
LVEF (%), median (Q1, Q3)	45(38, 56)	56(49, 60)	< 0.001
RWMA
Apex, n(%)	201(69)	129(58)	0.010
Anterior wall, n(%)	250(86)	164(74)	< 0.001
Rest of anterior wall, n(%)	154(53)	82(37)	< 0.001

Table 1

continued
Variate	Group I (n = 290)	Group II (n = 222)	p-value
Left-ventricular diastolic dysfunction, n(%)	119(41)	80(36)	0.250
Left-atrial diameter (mm), median(Q1, Q3)	36(31, 39)	35(32, 40)	0.121
Left-ventricular end-diastolic diameter (mm), Median(Q1, Q3)	46(41, 49)	45(43, 48)	0.041
Mitral regurgitation, n(%)	116(40)	56(25)	< 0.001
Coronary-angiographic variates
Pre-procedural TIMI flow grade ≤ 1 in
LAD, n(%)	148(51)	109(49)	0.654
LCX, n(%)	27 (9)	7(3)	0.006
RCA, n(%)	32(11)	11(5)	0.015
1-vessel disease, n(%)	87(30)	89(40)	0.018
3-vessel disease, n(%)	119(41)	66(30)	0.010
Presence of lesion in proximal LAD, n(%)	215(74)	154(69)	0.213
Total artery occlusion, n(%)	139(48)	102(46)	0.653
Post-procedural TIMI flow grade < 3, n(%)	29(10)	11(5)	0.037

SBP, systolic blood pressure; DBP, diastolic blood pressure; HR, heart rate; HbA1c, glycosylated haemoglobin; SHR, stress hyperglycaemia ratio; WBC, white blood cells; LDL, low density lipoprotein; CK, creatine kinase; CK-MB, creatine kinase-myocardial band; NT-pro-BNP, N-terminal pro-brain natriuretic peptide; LVEF, left-ventricular ejection fraction; RWMA, regional-wall motion abnormality; TIMI, thrombolysis in myocardial infarction; LAD, left-anterior descending artery; LCX, left-circumflex artery; RCA, right-coronary artery; mean ± SD, mean ± standard deviation; p < 0.05, significant.

Association of SHR and in-hospital heart failure post anterior-wall STEMI

To find the association between SHR and in-hospital HF following anterior-wall STEMI, parameters with statistically significant differences between the two groups were further analysed with univariate and multivariate logistic regression analyses, with in-hospital HF as dependent variable. The results revealed that stress hyperglycaemia ratio (SHR) is a significant independent predictor of in-hospital HF (OR: 3.53; 95%CI: 2.02–6.15; p < 0.001), as presented in Table 2.

Table 2

Association of SHR with in-hospital HF after anterior-wall STEMI
SHR ≥ 0.85	OR	95%CI	\(\:P\)
SHR (unadjusted)	4.38	2.60–9.27	0.001
SHR (adjusted)*	3.53	2.02–6.15	< 0.001

*, adjusted for age, gender, left-ventricular ejection fraction, ventricular fibrillation, nosocomial pneumonia, and N-terminal pro-brain natriuretic peptide levels; p < 0.05, significant.

Apart from SHR, the other independent predictors of in-hospital HF identified by multivariate logistic regression are presented in Table 3.

Table 3

Other Independent Predictors of in-hospital HF based on Multivariate Logistic Regression NP, nosocomial pneumonia; SHR, stress hyperglycaemia ratio; LVEF, left-ventricular ejection fraction; NT-pro-BNP, N-terminal pro-brain natriuretic peptide; p < 0.05, significant.
Independent Predictor	OR	95% CI	p-value
Age (≥ 63 Years)	1.02	0.96–1.10	0.037
NP	3.48	2.12–8.87	< 0.001
Ventricular Fibrillation	4.32	2.18–10.36	< 0.001
LVEF (< 50%)	1.08	0.89–1.15	0.024
Peak NT-pro-BNP (≥ 832 pg/mL)	1.04	0.91–1.21	0.010

Cut-off value and predictive power of SHR

Using Youden’s index [41], the optimal cut-off value of SHR was calculated to be 0.85. Furthermore, the ROC curve analysis (Fig. 1) showed that SHR independently (Model 2) had a moderate predictive potential for in-hospital HF in anterior wall STEMI undergoing PCI (AUC: 0.683, 95% CI 0.605–0.762), which was almost comparable to the combined predictive value of other independent risk factors (Model 1) (AUC: 0.726, 95% CI 0.677–0.784). Noticeably, Model 3 (a composite of Model 1 and Model 2) demonstrated a significant predictive power (AUC: 0.813, 95% CI 0.757–0.881) compared to Model 1 alone (Table 4).

Table 4

AUROC for Model 1, Model 2, and Model 3
Predictive factors	AUROC (95% CI)	p-value
Model 1 (Age + NP + VF + LVEF + NT-pro-BNP)	0.726 (0.677–0.784)	Reference
Model 2 (SHR)	0.683 (0.605–0.762)	0.04
Model 3 (Model 1 + Model 2)	0.813 (0.757–0.881)	0.01

NP, nosocomial pneumonia; VF, ventricular fibrillation; LVEF, left-ventricular ejection fraction; NT-pro-BNP, N-terminal pro-brain natriuretic peptide; SHR, stress hyperglycaemia ratio; p < 0.05, significant.

To our knowledge this is the first study to investigate the impact of SHR calculated from glycosylated haemoglobin (HbA1c) on in-hospital HF following an anterior wall STEMI. The results strongly suggest that apart from conventional risk parameters-age, VF, nosocomial pneumonia, LVEF, and NT-pro-BNP levels, SHR is an independent predictor of in-hospital HF in patients with anterior wall STEMI (OR: 3.53, 95% CI: 2.02–6.15, p < 0.001). It has been suggested that the hypothalamic-pituitary-adrenal axis is responsible for stress hyperglycaemia by elevating cortisol and adrenaline secretion[42]. Pro-inflammatory cytokines-interleukin-1, interleukin-6, and tumor necrosis factor-α have been suggested to be responsible for impairment of insulin secretion and insulin resistance, and stress hyperglycaemia has been reported to be responsible for overexpression of these pro-inflammatory cytokines [36, 37, 43], thereby indicating a transitive relationship between stress hyperglycaemia and insulin resistance. Moreover, hypercoagulable state may be attributed to stress induced hyperglycaemia as it contributes to increased thrombogenic activity [44, 45]. Earlier investigations have shown significant associations between increased SHR and lager thrombus burden and decreased TIMI flow grade in angiography[46, 47]. The results of the present study are partially in line with various earlier studies. Stress hyperglycaemia has been reported to be a significant predictor of poor prognosis in acute coronary syndrome (ACS) patients in general and acute myocardial patients in particular [23, 28, 29, 30]. Stress hyperglycaemia has not only been established as a significant indicator of the severity of an acute emergent condition, but it has also been demonstrated to complicate and catalyse obstruction in microvasculature[48], weaken endothelial vasodilatory mechanisms[49], hinder platelet nitric oxide response[50], and augment vascular damage. However, admission blood glucose levels do not truly reflect the stress state as the actual stress hyperglycaemic state is masked by the chronic glucose levels [51]. Hence, as a sequel to the previous argument, Roberts et al. [52], proposed SHR as an indicator of real stress hyperglycaemia by filtering out the chronic glycaemic state from the absolute hyperglycaemia on admission. They further proved that SHR is a robust and better biomarker of critical disease than hyperglycaemia on admission.

In a retrospective study involving 905 STEMI patients, it was demonstrated that SHR was a strong predictor of no-reflow after primary PCI (pPCI) [53]. In another study on 1553 AMI patients, SHR has been reported to be a better prognostic indicator of in-hospital mortality [54] than absolute glucose levels on admission. Yang et al. [55], in a retrospective study involving 4362 subjects from the Catholic medical centre percutaneous coronary intervention (COACT) registry who underwent PCI, reported that the hazard ratio (HR) for upper SHR quartile (quartile 4) for long-term MACCE was 1.31 (95% CI 1.05–1.64) in comparison to lower SHR quartiles (quartiles 1–30). The present study also demonstrated that prior diabetic status has no influence on association of SHR and in-hospital HF following an anterior wall STEMI. This result is in line with an earlier study, wherein, a significant association was found between SHR and in-hospital death among patients following myocardial infarction (MI), irrespective of their prior diabetic status[29]. However, in a study SHR was shown to have no substantial association on all-cause mortality and cardiovascular death among non-diabetic ACS patients[56].

TIMI risk score [57, 58] is the most used prognosis stratification model for STEMI patients but despite all its strengths and significance some previous studies have reported that in majority of cases its predictive utility is limited[59, 60]. This may be attributable to the fact that the TIMI risk score model takes only cardiovascular risk factors into consideration and ignores the inclusion of all important metabolic factors. Hence, a few studies have suggested inclusion of SHR to the risk scoring system may aid in early risk profiling [30, 41]. The present study discovered that SHR is a significant independent risk and predictive factor for in-hospital HF post anterior wall STEMI. This assumes more importance given the ease and low cost associated with obtaining fasting blood glucose and HbA1c in clinical settings. The results of this study also demonstrate that integrating SHR with conventional risk factors augment the risk prognosis of in-hospital HF following an anterior wall STEMI. This is strongly indicative of including SHR as a significant predictive factor in constructing new prognostic models for STEMI in general.

Limitations

Single centre study, limited sample size, demographic component largely drawn from a particular geography (Aseer region, Kingdom of Saudi Arabia), might limit the generalization of the results. All these constitute the main limitations of this study.

SHR is an independent predictor for in-hospital HF in anterior wall STEMI patients treated with pPCI. Adding SHR to already established conventional risk factors (age, LVEF, NT-pro-BNP levels) for in-hospital HF significantly augments the discriminative ability of conventional risk factors.

Ethical Approval

This study was approved by the Research Ethics Committee at King Khalid University (HAPO-06-B-001) vide approval No: ECM# 2024-1901, and written informed consent was obtained from all the participants.

Consent for Publication

Not Applicable

Availability of Data

The data that support the findings of this study are available from the corresponding author upon reasonable request.

Conflict of Interest

None

Funding and Acknowledgements

The authors extend their appreciation to the Deanship of Scientific Research at King Khalid University, Abha, Saudi Arabia for funding this work through Large Group Project under grant number [RPG 2/562/44]

Zia-ul-Sabah, Javed Iqbal, Shahid Aziz, and Humayoun Khan Durrani majorly contributed to the conceptualization and Design. Saif Aboud M Alqahtani, Ayyub Ali Patel, and Imran Rangreze contributed towards data acquisition, analysis, and interpretation of data. Rasha Mirdad, Sara Shahrani, and Muad Ali Alfayea contributed to manuscript writing. All authors read and approved the final manuscript.

Acknowledgements

The authors extend their appreciation to the Deanship of Scientific Research at King Khalid University for encouragement and funding this work.

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Stress hyperglycaemia ratio is an independent predictor of in-hospital heart failure among patients with anterior ST-segment elevation myocardial infarction

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Abstract

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Introduction

Methods

Study design and setting

Study subjects and duration

Inclusion Criteria

Exclusion Criteria

Data and Definitions

Statistical Analysis

Results

Baseline characteristics of the study cohort

Association of SHR and in-hospital heart failure post anterior-wall STEMI

Cut-off value and predictive power of SHR

Discussion

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Conclusion

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