Impact of the Stress Hyperglycemia Ratio on Heart Failure and Atherosclerotic Cardiovascular Events After Acute Myocardial Infarction

Abstract

Background: An acute hyperglycemic status is reportedly associated with poor prognosis in patients with acute cardiovascular diseases. Although the stress hyperglycemia ratio (SHR) is used to evaluate the hyperglycemic condition on admission, relationships between SHR and clinical outcomes, particularly heart failure (HF), remain uncertain in acute myocardial infarction (AMI).

Methods and Results: This retrospective multicenter study included 2,386 patients with AMI undergoing percutaneous coronary intervention. SHR was calculated using blood glucose and HbA1c levels. Co-primary endpoints included HF-related events (death, worsening HF, and hospitalization for HF) and major adverse cardiovascular events (MACE; death, recurrent AMI, and ischemic stroke) during the index hospitalization and after discharge. The mean (±SD) SHR was 1.30±0.51; HF events and MACE occurred in 680 (28.5%) and 233 (9.8%) patients during hospitalization, respectively. SHR was independently associated with in-hospital HF events and MACE. Of 2,017 patients who survived to discharge, 195 (9.7%) and 214 (10.6%) experienced HF events and MACE, respectively, over a median follow-up of 536 days. The risk of HF events was higher in patients with a high (>1.45) SHR than in those with SHR ≤1.45; there was no significant difference in MACE rates after discharge between these 2 groups.

Conclusions: In AMI patients, SHR was predictive of in-hospital outcomes, including HF events and MACE, whereas after discharge a higher SHR was associated with higher HF risks, but not MACE.

Acute hyperglycemia is a relative increase in blood glucose levels in response to critical conditions, including acute myocardial infarction (AMI), which may represent poor diabetic control and can be caused by inflammation and neurohormonal dysfunction during severe illness.¹ The transient hyperglycemia is reportedly associated with poor short- and long-term prognosis in patients with AMI.² However, the blood glucose level on admission does not necessarily reflect the acute hyperglycemic state, which could be affected by chronic glucose levels.³ The stress hyperglycemia ratio (SHR), an index calculated from admission blood glucose (BG) and HbA1c levels, was developed to normalize the acute increase in glucose levels in relation to background glycemic status.⁴ The prognostic value of the SHR has been reported in patients with AMI for predicting subsequent major adverse cardiovascular events (MACE) and mortality.^3,5–9 However, whether higher SHR is associated with heart failure (HF) events, one of the most common clinical complications after AMI,^10,11 remains unclear. The aim of this study was to evaluate the prognostic value of SHR for HF events and MACE after AMI in current clinical practice.

Methods

Study Design

This was a retrospective multicenter registry study conducted at 4 tertiary referral hospitals in Japan (Chiba University Hospital, Eastern Chiba Medical Center, Chiba Emergency and Psychiatric Medical Center, and Chiba Aoba Municipal Hospital).^12–19 From January 2012 to December 2021, a total of 2,485 patients with AMI, including ST-segment elevation myocardial infarction and non-ST-segment elevation myocardial infarction, primarily underwent percutaneous coronary intervention (PCI) within 48 h after admission at the 4 hospitals according to local standard practice, including the predominant use of dual antiplatelet therapy, intracoronary imaging, and contemporary drug-eluting stents.^20–26 AMI was defined based on the fourth universal definition of myocardial infarction.²⁷ After excluding patients with missing BG and HbA1c data (n=99), 2,386 patients were included in the present study (Figure 1).

Figure 1.

Study flow. AMI, acute myocardial infarction; BG, blood glucose; HF, heart failure; MACE, major adverse cardiovascular events; PCI, percutaneous coronary intervention.

This study was performed in accordance with the Declaration of Helsinki and was approved by the ethics committee of each participating hospital. Informed consent for this study was obtained on an opt-out basis.

Assessment of Hyperglycemia

In the present study, non-fasting BG and HbA1c levels were measured on admission for AMI. SHR was defined as the ratio of acute to estimated average BG levels.⁴ An acute BG level was obtained as the non-fasting BG level on admission, and the average BG level was estimated using the formula (1.59 × HbA1c [%]) − 2.59. Thus, SHR was calculated by dividing the acute BG level (mmol/L) by the estimated average BG level (mmol/L).⁴ Diabetes was defined as a previous diagnosis of diabetes or the previous use of glucose-lowering medications, or HbA1c ≥6.5%.²⁸

Outcomes

Follow-up data were obtained from medical records at each hospital. The co-primary endpoints of this study were HF events and MACE during hospitalization for AMI and after discharge. HF events during hospitalization were defined as a composite of all-cause death and worsening HF that was adjudicated by the use of intravenous diuretics (e.g., furosemide) and vasopressors or inotropes (e.g., norepinephrine and dobutamine).^29–31 HF events after discharge were defined as a composite of all-cause death and HF rehospitalization. MACE during hospitalization and after discharge were defined as a composite of all-cause death, recurrent AMI, and ischemic stroke, according to the consensus document.³² Clinical outcomes after discharge were evaluated in patients who survived to discharge and had follow-up information (Figure 1). The primary interest of this study was the relationship between SHR and both HF events and MACE.

Statistical Analysis

Statistical analyses were performed using R (R Foundation for Statistical Computing, Vienna, Austria). Data are presented as the mean±SD, median with interquartile range (IQR), or as frequencies with percentages. Continuous variables were analyzed using Student’s t-test, and categorical variables were evaluated using Fisher’s exact test. Kaplan-Meier analysis with the log-rank test was performed to estimate HF event- and MACE-free survival after discharge according to SHR using a cut-off value of 1.45. Because no established threshold of SHR has been reported, receiver operating characteristics (ROC) curve analysis was used to identify the best cut-off value of SHR to predict all-cause mortality. Multivariate analyses were performed using logistic regression and the Cox proportional hazards models to estimate unadjusted and adjusted odds ratios and hazard ratios with corresponding 95% confidence intervals (CIs). Factors with P<0.01 in univariable analysis for both HF events and MACE were included in the multivariable models, although cardiogenic shock (CS) and cardiac arrest, as well as BG, HbA1c, and SHR were not simultaneously included in the multivariable analysis because of the confounding effect. P<0.05 was considered statistically significant.

Results

Of the 2,386 patients with AMI who underwent PCI, 890 (37.3%) had diabetes; the mean SHR of these 890 patients was 1.30±0.51. During hospitalization and after discharge, 312 (13.1%) patients died, and ROC curve analysis showed that SHR was predictive of all-cause mortality, with the best cut-off value of 1.45 (area under the curve 0.641; 95% CI 0.603–0.678), which was the same value as the upper quartile of SHR. Patient characteristics are presented in Table 1. During hospitalization, HF events and MACE occurred in 680 (28.5%) and 233 (9.8%) patients, respectively (Table 2). Overall, similar trends were found in the characteristics of patients who developed HF events and MACE compared with those without such outcome events, including older age, lower body mass index, a higher prevalence of diabetes, lower left ventricular ejection fraction, and more severe clinical presentations (CS and cardiac arrest), impaired renal function, and a lower hemoglobin level (Table 1). In addition, levels of BG, HbAlc, and SHR were significantly higher in patients with HF events and/or MACE than their counterparts without these events (Table 1). Baseline characteristics according to SHR are also listed in Supplementary Table 1. Patients with SHR >1.45 had significantly higher rates of in-hospital HF events and MACE than their counterparts (Table 2).

Table 1.

Baseline Characteristics for In-Hospital HF Events and MACE

	All (n=2,386)	HF events			MACE
		No (n=1,706)	Yes (n=680)	P value	No (n=2,153)	Yes (n=233)	P value
Age (years)	68.0±12.5	66.6±12.6	71.5±11.6	<0.001	67.7±12.6	71.1±11.8	<0.001
Male sex	1,842 (77.2)	1,334 (78.2)	508 (74.7)	0.074	1,665 (77.3)	177 (76.0)	0.623
BMI (kg/m2)	24.3±3.8	24.6±3.8	23.7±3.8	<0.001	24.4±3.8	23.7±4.1	0.013
Hypertension	1,635 (68.5)	1,182 (69.3)	453 (66.6)	0.205	1,496 (69.5)	139 (59.7)	0.003
Diabetes	890 (37.3)	590 (34.6)	300 (44.1)	<0.001	780 (36.2)	110 (47.2)	0.001
Dyslipidemia	1,518 (63.6)	1,132 (66.4)	386 (56.8)	<0.001	1,394 (64.7)	124 (53.2)	0.001
Current smoker	858 (36.0)	648 (38.0)	210 (30.9)	0.001	781 (36.3)	77 (33.0)	0.351
Previous MI	182 (7.6)	128 (7.5)	54 (7.9)	0.733	161 (7.5)	21 (9.0)	0.435
Previous HF	54 (2.3)	18 (1.1)	36 (5.3)	<0.001	44 (2.0)	10 (4.3)	0.037
LVEF (%)	47.5±12.8	51.2±10.7	37.5±12.5	<0.001	48.8±12.0	33.5±13.0	<0.001
Clinical presentation
STEMI	1,678 (70.3)	1,144 (67.1)	534 (78.5)	<0.001	1,503 (69.8)	175 (75.1)	0.097
Cardiogenic shock	349 (10.4)	73 (4.3)	276 (40.6)	<0.001	221 (10.3)	128 (54.9)	<0.001
Cardiac arrest	227 (9.5)	64 (3.8)	163 (24.0)	<0.001	153 (7.1)	74 (31.8)	<0.001
eGFR (mL/min/1.73 m2)	64.5±24.3	69.3±22.6	52.3±23.9	<0.001	66.3±23.6	48.2±24.5	<0.001
Hemoglobin (g/dL)	13.9±2.2	14.2±2.0	13.1±2.5	<0.001	14.0±2.1	12.8±2.6	<0.001
Glucose (mmol/L)	9.97±3.84	8.95±3.79	12.51±6.40	<0.001	9.54±4.50	13.89±6.80	<0.001
HbA1c (%)	6.45±1.45	6.41±1.41	6.55±1.55	0.024	6.42±1.42	6.72±1.70	0.002
SHR	1.30±0.51	1.18±0.35	1.61±0.71	<0.001	1.25±0.46	1.74±0.76	<0.001

Unless indicated otherwise, data are given as the mean±SD or n (%). BMI, body mass index; eGFR, estimated glomerular filtration rate; HF, heart failure; LVEF, left ventricular ejection fraction; MACE, major adverse cardiovascular events; MI, myocardial infarction; SHR, stress hyperglycemia ratio; STEMI, ST-elevation myocardial infarction.

Table 2.

In-Hospital Clinical Outcomes

	All (n=2,386)	SHR ≤1.45 (n=1,793)	SHR >1.45 (n=593)	P value
HF events	680 (28.5)	356 (19.9)	324 (54.6)	<0.001
MACE	233 (9.8)	100 (5.6)	133 (22.4)	<0.001
All-cause death	184 (7.7)	68 (3.8)	116 (19.6)	<0.001
Worsening HF	647 (27.1)	342 (19.1)	305 (51.4)	<0.001
Recurrent MI	31 (1.3)	23 (1.3)	8 (1.3)	0.837
Ischemic stroke	43 (1.8)	23 (1.3)	20 (3.4)	0.002

Unless indicated otherwise, data are given as n (%). Abbreviations as in Table 1.

Multivariable analysis identified SHR as a factor significantly associated with both HF events and MACE during hospitalization (Table 3). In-hospital clinical outcomes in patients with and without diabetes and CS were further evaluated, and higher SHR was associated with HF events after discharge regardless of diabetes (Supplementary Table 2), whereas the prognostic value of SHR >1.45 for in-hospital outcomes was more evident in patients with CS (Supplementary Table 3).

Table 3.

Multivariable Logistic Regression Analysis for In-Hospital HF Events and MACE

	HF events		MACE
	OR (95% CI)	P value	OR (95% CI)	P value
Age	1.020 (1.010–1.040)	<0.001	1.010 (0.989–1.020)	0.483
BMI	0.992 (0.957–1.030)	0.682	0.999 (0.950–1.050)	0.975
Diabetes	1.200 (0.932–1.550)	0.157	1.080 (0.752–1.550)	0.683
Dyslipidemia	0.877 (0.680–1.130)	0.312	0.933 (0.652–1.340)	0.706
LVEF	0.910 (0.899–0.921)	<0.001	0.934 (0.920–0.948)	<0.001
Cardiogenic shock	6.870 (4.710–10.00)	<0.001	3.310 (2.210–4.950)	<0.001
eGFR	0.986 (0.981–0.992)	<0.001	0.988 (0.980–0.996)	0.003
Hemoglobin	0.855 (0.801–0.911)	<0.001	0.867 (0.796–0.943)	<0.001
SHR >1.45	1.830 (1.380–2.410)	<0.001	1.510 (1.030–2.210)	0.034

CI, confidence interval; OR, odds ratio. Other abbreviations as in Table 1.

Of the 2,386 patients with AMI who underwent PCI, 2,017 were included in the follow-up outcome assessment (Figure 1; Supplementary Table 4). Over a median follow-up period of 536 days (IQR 349–1,306 days) after discharge, HF events and MACE occurred in 195 (9.7%) and 214 (10.6%) patients, respectively (Table 4). Kaplan-Meier analysis demonstrated that patients with SHR >1.45 had an increased risk of HF events compared with those with SHR ≤1.45, whereas the incidence of MACE after discharge did not differ significantly between the 2 groups (Figure 2). These findings were consistent regardless of the presence of diabetes (Figure 3), whereas patients with SHR >1.45 had an increased risk of clinical events after discharge, particularly those without CS (Supplementary Figure). Multivariable analysis showed that SHR was a significant factor associated with HF events after discharge (in addition to age, left ventricular ejection fraction, renal function, and anemia), but not with MACE (Table 5).

Table 4.

Clinical Outcomes After Discharge

	All (n=2,017)	SHR ≤1.45 (n=1,606)	SHR >1.45 (n=411)	P value
Follow-up (days)	536 [349–1,306]	544 [353–1,293]	518 [309–1,343]	0.321
HF events	195 (9.7)	131 (8.2)	64 (15.6)	<0.001
MACE	214 (10.6)	160 (10.0)	54 (13.1)	0.072
All-cause death	128 (6.3)	91 (5.7)	37 (9.0)	0.017
HF rehospitalization	85 (4.2)	54 (3.4)	31 (7.5)	<0.001
Recurrent MI	65 (3.2)	52 (3.2)	13 (3.2)	1.000
Ischemic stroke	42 (2.1)	35 (2.2)	7 (1.7)	0.699

Unless indicated otherwise, data are given as the median [interquartile range] or n (%). Abbreviations as in Table 1.

Figure 2.

Probability of freedom from heart failure (HF) events and major adverse cardiovascular events (MACE) after discharge using a stress hyperglycemia ratio (SHR) cut-off value of 1.45.

Figure 3.

Probability of freedom from heart failure (HF) events and major adverse cardiovascular events (MACE) after discharge in patients with and without diabetes using a stress hyperglycemia ratio (SHR) cut-off value of 1.45.

Table 5.

Cox Proportional Hazards Analysis for HF Events and MACE After Discharge

	HF events		MACE
	HR (95% CI)	P value	HR (95% CI)	P value
Age	1.026 (1.010–1.043)	0.002	1.007 (0.993–1.022)	0.325
Hypertension	1.332 (0.949–1.869)	0.168	1.332 (0.949–1.869)	0.098
Current smoker	0.979 (0.679–1.412)	0.909	0.843 (0.600–1.184)	0.324
Previous HF	1.690 (0.874–3.267)	0.119	2.122 (1.097–4.104)	0.025
LVEF	0.965 (0.954–0.976)	<0.001	0.992 (0.981–1.003)	0.137
eGFR	0.991 (0.985–0.998)	0.011	0.989 (0.983–0.995)	<0.001
Hemoglobin	0.832 (0.776–0.892)	<0.001	0.882 (0.824–0.944)	<0.001
SHR >1.45	1.625 (1.191–2.217)	0.002	1.167 (0.847–1.601)	0.346

HR, hazard ratio. Other abbreviations as in Tables 1,3.

Discussion

The present study demonstrated that in patients with AMI undergoing PCI, SHR predicted clinical outcomes during hospitalization and after discharge. For in-hospital outcomes, a higher SHR was associated with both HF events and MACE, whereas after discharge SHR was only predictive of HF events. These findings suggest that SHR, an index for evaluating acute and transient hyperglycemia, may be useful for stratifying the risk of clinical outcomes, particularly for HF-related events, in acute and chronic phases.

Stress-Induced Hyperglycemia in Myocardial Infarction

Acute hyperglycemia, typically evaluated with a transient elevation of BG, is an indicator of adverse outcomes in patients with cardiovascular disease.³³ A decreased insulin level and increased levels of catecholamines, steroids, and glucagon secondary to activation of the sympathetic nervous system as a physiological response to stress induce hyperglycemia, leading to oxidative stress and endothelial dysfunction.³⁴ In addition, greater glucose fluctuation may be associated with coronary flow impairment and microvascular dysfunction,^35,36 resulting in a poor prognosis, along with severe patient conditions. Guidelines indicate BG levels on admission of >11 and >10 mmol/L as cut-off values for defining acute hyperglycemia, regardless of diabetic status.^37–39 Previous studies showed that stress-induced hyperglycemia was found in 20–50% of patients with AMI on admission,^33,40 with stress-induced hyperglycemia well known to be associated with poor outcomes after AMI.² An elevated BG level is a strong predictor, although hyperglycemia on admission may reflect not only a stress-induced reaction but also chronic poor diabetic control.³ In this context, Roberts et al. developed the SHR to accurately estimate acute hyperglycemia representing a transient physiological response to an intercurrent illness.⁴ In their original study, Roberts et al. reported that multivariable analysis revealed SHR was an independent predictor of death and admission to the intensive care unit, whereas BG level alone was not,⁴ theoretically supporting the use of SHR when estimating “true” stress-induced hyperglycemia. To date, numerous studies have demonstrated that a higher SHR is associated with worse outcomes, particularly for MACE, in patients with AMI and/or PCI.^3,5–9,35 However, the prognostic value of SHR for HF events and the cut-off value remain to be established.

SHR and Outcomes

In the present study, a higher SHR was related to the increased risk of HF events rather than MACE, especially after discharge, regardless of diabetic status. Recently, the CORONOR registry from France reported that in patients with chronic coronary disease, HF hospitalization was more frequently observed over a median follow-up period of 4.9 years than ischemic events and major bleeding (8.1% vs. 6.3% and 3.1%, respectively).¹¹ In addition, this French registry demonstrated that the development of HF rather than ischemic events was linked to subsequent mortality in a greater magnitude.¹¹ Given that HF is one of the leading complications after AMI,^10,29 risk stratification for this outcome event may be clinically relevant. Importantly, some previous studies have indicated that the predictive value of SHR was weak or not significant for long-term mortality and MACE after AMI or PCI,^6,7 but our study identified SHR as an independent predictor of HF events after discharge. Because patients with an SHR >1.45 were more likely to have severe clinical presentations, including reduced left ventricular ejection fraction, CS, and cardiac arrest, than patients with an SHR ≤1.45 (Supplementary Table 1), acute hyperglycemia may be an indicator of large and life-threatening myocardial infarction, presumably resulting in HF events during hospitalization and after discharge. In addition, an acute hyperglycemic status is reportedly associated with inflammation, oxidative stress, and endothelial dysfunction, potentially leading to myocardial damage and HF outcomes.⁵ In the present study, a higher (>1.45) SHR was more frequently observed in patients with than without CS (66.8% vs. 17.7%), suggesting that SHR can reflect severely ill (stressed) conditions. Interestingly, although the presence of diabetes did not significantly affect the association of SHR with HF events, the prognostic value of higher SHR was evident, particularly in patients without CS presentation. Given the extremely high event rates in patients with AMI complicated by CS,⁴¹ SHR may not be helpful in in-hospital risk stratification. To predict future events, a simple cut-off value is useful in clinical practice, although the thresholds of SHR vary widely among studies, ranging from 1.08 to 1.68.^5,6,8,9 In the present study, we used 1.45 as the SHR cut-off value based on ROC curve analysis for mortality. However, some previous studies showed a U-shaped association between SHR and cardiovascular outcomes.³ Thus, future investigations are needed to define the best cut-off values of SHR for clinical use.

Although hyperglycemia is associated with worse outcomes, whether the intervention for BG levels conveys clinical benefits remains unclear. A recent randomized trial showed that tight BG control in patients in the intensive care unit did not result in a shorter length of stay in the intensive care unit and lower mortality.⁴² Currently, the guidelines only recommend frequent monitoring of BG levels in patients with hyperglycemia in acute coronary syndrome.³⁹ Even though currently available evidence suggests no effective therapeutic strategies in patients with stress-induced hyperglycemia, we believe that SHR is useful in stratifying patient risk after AMI.

Study Limitations

This study has some limitations. Because this was a retrospective study, the findings should be acknowledged as hypothesis generating. The main focus of the present study was to illustrate the prognostic value of SHR for HF events and MACE in patients with AMI; we did not address the diagnostic value of SHR relative to other glycemic metrics, such as BG and the glucose-HbA1c ratio.⁹ HF events during hospitalization and after discharge were not adjudicated with the same definition. In addition, data on the use of diabetic medications before admission and after discharge were not available in this study. Given the retrospective nature of the present study, no data on symptom onset to admission or balloon time were available.

Conclusions

SHR was predictive of in-hospital HF events and MACE, whereas after discharge a higher SHR was associated with an increased risk of HF, but not MACE, during long-term follow-up in patients with AMI. Further studies are warranted to clarify the prognostic value of SHR for HF events and whether SHR-guided diagnostic and therapeutic pathways are useful in clinical practice.

Sources of Funding

None.

Disclosures

Y.K. is a member of Circulation Journal’s Editorial Team.

IRB Information

This study was approved by the Ethics Committee at Chiba University Graduate School of Medicine (Approval no. 3933).

Supplementary Files

Please find supplementary file(s);

https://doi.org/10.1253/circj.CJ-24-0612

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