a b s t r a c t

Subject: The aim of this study was to compare the predictive values of modified shock index (MSI) and Shock Index for 7-day outcome in patients with ST-segment elevation myocardial infarction .

Methods: This retrospective study included 160 consecutive patients with STEMI and emergency percutaneous coronary intervention. The Blood pressure and heart rate (HR) measured at emergency department were used to calculate SI (HR/systolic BP) and MSI (HR/mean artery pressure). The Major adverse cardiac events included all-cause mortality, Life-threatening arrhythmias, cardiogenic shock, and Killip class within 7 days.

Results: Forty-nine patients had increased MSI (>=1.4), whereas 72 had increased SI (>=0.7). Except the parame- ters on BP and HR, other parameters were similar between the normal and increased SI groups. However, the in- creased MSI group had significantly higher age (69.0 +- 13.0 years vs 63.9 +- 12.9 years, P = .025) than the normal MSI group. The 7-day all-cause mortality was 8.8%, and MACE rate was 24.4% in this study. Both increased SI and increased MSI predicted higher MACE rates. However, the odds ratios of increased MSI for all-cause mortality (6.8 vs 3.4), cardiogenic shock (3.0 vs 1.6), life-threatening arrhythmias (9.1 vs 4.6), and MACE (6.8 vs 3.4) were higher than those of increased SI. Modified shock index and SI were independent factor for MACE, but the odds ratio of MSI was higher than of SI (3.05 vs 1.07).

Conclusions: Both SI and MSI in emergency department could predict the all-cause mortality and MACE rates within 7 days in patients with STEMI, but MSI may be more accurate than SI.

(C) 2015

Introduction

Shock Index is a simple index, defined as the ratio of heart rate (HR) and systolic blood pressure (SBP). It has been demonstrated as a useful predictor for hospital mortality among adult patients with trauma [1-3]. Shock index is better not only than SBP, diastolic blood pressure , and HR alone but also than some risk stratifi- cation systems, for example, SI is more useful than the Triage Sort (TSO) for secondary triage in a mass-casualty situation [4].

? Competing interests: The authors declare no competing interests.

?? This work was supported by a grant from the National High Technology research and development Program of China (863 Program, No. 2012AA02A516) and the Ministry of Chinese Education Innovation Team Development Plan (IRT1141).

* Corresponding author. No 1 Minded Road, Nanchang, Jiangxi, China 330006 Tel./fax: +86 791 86262262.

E-mail addresses: [email protected] (Q. Shangguan), [email protected] (J. Xu), [email protected] (H. Su), [email protected] (J. Li), [email protected] (W. Wang), [email protected] (K. Hong), [email protected] (X. Cheng).

¹ Contributed equally.

In addition to trauma, SI could predict the risk of short- and long-term mortality for other nontrauma diseases, such as pulmonary embolism and aortic dissection. In patients with pulmonary embolism, SI could provide information to stratify the risk of short- and long-term mortal- ity [5]. In patients with acute pulmonary embolism, Toosi et al [6] found that an elevated SI was associated with increased Inhospital mortality, independent of echocardiographic findings. Meanwhile, in the patients with aortic dissection, a significant linear correlation was found between the ratio of false/true lumen and the SI [7]. Therefore, the use- fulness of SI is beyond to trauma and hemorrhagic diseases.

In clinical, the risk stratification for the patients with ST-segment elevation myocardial infarction is very important to identify those patients who are relatively more serious. Risk assessment pro- vides an opportunity to integrate various patient characteristics into a semiquantitative score that can convey an overall estimate of a patient’s prognosis; can dictate the acuity, intensity, and location of care; and can provide the patient and family with a more informed sense of potential outcome [8]. At present, several systems of risk stratification such as Thrombolysis in Myocardial Infarction and Globle Register Acute coronary events (GRACE) are used, but the sophisticated calcula- tion usually makes them inconvenient to operate at bedside in daily

http://dx.doi.org/10.1016/j.ajem.2015.04.066

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Q. Shangguan et al. / American Journal of Emergency Medicine 33 (2015) 1072–1075 1073

clinical practice [9,10]. Recently, Huang et al [11] suggested that admis- sion SI of 0.7 or greater is a useful predictor for Short-term outcomes in the patients with STEMI. Other studies also indicated that an SI of 0.8 of greater is a novel predictor for inhospital and long-term mortality in the patients with STEMI [12,13]. These results provided a simple index for risk stratification in the patients with STEMI.

In last year, a new index, modified shock index (MSI), is created as the ratio of HR and mean artery pressure (MAP) [12] because DBP is an undeniable parameter when determining clinical severity. Some studies have found that MSI is a better predictor than SI for the outcome in adult patients with trauma [14,15]. However, the predictive value of MSI has not been evaluated in the patients with STEMI. This study was to identify whether MSI is better than SI for predicting the short-term outcomes in the patients with STEMI.

Patients and methods

This retrospective study included 160 consecutive patients with acute STEMI attended to the emergency department (ED) in our hospital from September 2013 to October 2014. The including criteria are arriving in the ED within 12 hours after symptom onset, diagnosis of STEMI, and received emergency percutaneous coronary intervention (PCI) later. ST-segment elevation myocardial infarction was defined as follows: chest pain or equivalent symptoms in combination with dynamic electrocardiographic changes consistent with STEMI (in the presence of ST elevation N 0.1 mV in >=2 extremity leads, N 0.2 mV in

>=2 precordial leads, or accompanying with Left bundle branch block morphology) and increased serum biochemical markers of cardiac ne- crosis, including creatine kinase-MB and troponin I. The excluding criteria were atrial fibrillation and obvious arrhythmia at blood pressure (BP) measurement.

Age, sex, and histories of myocardial infarction, hypertension, diabetes, and heart failure were obtained. Fasting blood glucose, results of coronary angiography, and Killip classes were also recorded [16].

All patients received standard medication therapy according to the detection of physicians under the guidelines for the management of STEMI, including antiplatelet and anticoagulation, statins, angiotensin- converting enzyme inhibitor or angiotensin receptor antagonists, nitrates, ?-blockers, calcium channel blockers [8,17,18]. The use of vascular active drugs including dopamine, adrenaline, noradrenaline, metaraminat, and isoprenaline was recorded.

SI and MSI

The BP and HR measured (Comen C50 Multi-parameter Patient Monitor, Shenzhen COMEN Medical Instruments CO, Shenzhen, China) at ED were used to calculate SI and MSI. Blood pressure and HR were measured twice with 1-minute interval, and their average was used as final value.

Shock index is the ratio of HR to SBP.

Modified shock index is the ratio of HR to mean blood pressure (MAP). Here, MAP = [(DBP x 2) + SBP]/3.

The cutoff value of SI was referred as 0.7 in the study by Huang et al [11], whereas the cutoff value of MSI was determined as 1.4 on the receiver operating characteristic curve. The C-statistic of MSI of 1.4 was 0.690.

Major adverse cardiac events

In this study, Major adverse cardiac events include all-cause mortality, life-threatening arrhythmias (LTA), cardiogenic shock, and heart failure within 7 days. The all-cause mortality was defined death caused by any reason; cardiogenic shock was defined as persistent hypo- tension (SBP b 90 mm Hg) that did not respond to fluid titration and re- quirement of an intra-aortic balloon pump or intravenous inotropic therapy. Heart failure was diagnosed on the Killip class of II or more. Life-threatening arrhythmias included sustained ventricular tachycardia and ventricular fibrillation in hospitalization [8,18].

Statistical analysis

All statistical analyses were carried out using the SPSS statistical soft- ware, version 19.0 (SPSS Inc, Chicago, IL).The data were presented with mean +- SD or median and interquartile range for continuous variables and were compared by analysis of variance and Bonferroni correction if the data had normal distribution, otherwise by Wilcoxon Signed Rank Test. Categorical variables presented as percentage were compared by the Pearson ?² test.

multiple logistic regression analysis was performed for 7-day MACE

[12]. The dependent variables were SI of 0.7 or greater (or MSI >=1.4), age, sex (male, 1; female, 2), the history of old myocardial infarction (yes, 1; no, 2), diabetes (yes, 1; no, 2), hypertension (yes, 1; no, 2), stroke (yes, 1; no, 2), and the levels of blood blood glucose. P values were statistically significant at b .05.

Table 1

The general information of the studies patients and the comparison between 2 groups divided on SI of 0.7 or more or MSI of 1.4 or more

Variable	All (n = 160)	SI b0.7 (n = 88)	SI >=0.7 (n = 72)	P	MSI b 1.4 (n = 111)	MSI >=1.4 (n = 49)	P
Age (y)	65.5 +- 13.1	64.5 +- 13.0	66.6 +- 13.4	N.05	63.9 +- 12.9	69.0 +- 13.0	b.01
Male	132 (82.5%)	73 (83.0%)	59 (81.9%)	N.05	92 (82.9%)	40 (81.6%)	N.05
History of MI	3 (1.9%)	1 (1.81%)	2 (2.8%)	N.05	2 (1.8%)	1 (2.0%)	N.05
Diabetes mellitus	32 (20%)	17 (19.3%)	15 (20.8%)	N.05	22 (19.8%)	10 (20.4%)	N.05
Hypertension	92 (57.5%)	54 (61.4%)	38 (52.8%)	N.05	68 (61.3%)	24 (49.0%)	N.05
History of stroke	10 (6.3%)	5 (5.7%)	5 (6.9%)	N.05	7 (6.3%)	3 (6.1%)	N.05
Onset to admission intervals (h)a	5.0 (4.0, 8.0)	5.0 (4.0, 7.5)	5.0 (4.0, 8.0)	N.05	5.0 (4.0, 7.5)	5.25 (4.0, 8.0)	N.05
SBP (mm Hg)	119.1 +- 24.9	130.6 +- 23.5	105.1 +- 18.7	b.01	126.7 +- 23.4	101.9 +- 18.9	b.01
DBP (mm Hg)	73.2 +- 14.9	77.1 +- 14.3	68.5 +- 14.1	b.01	76.8 +- 13.7	65.0 +- 14.3	b.01
MAP (mm Hg)	64.1 +- 12.2	69.2 +- 11.6	57.8 +- 9.9	b.01	67.8 +- 11.3	55.6 +- 9.8	b.01
Heart rate (beat/min)a	77 (68, 90)	71 (61, 78)	90 (79, 102)	b.01	72 (64, 81)	93 (84, 107)	b.01
Killip class				N.05			N.05
I	139 (86.9%)	78 (88.6%)	61 (84.7%)		100 (90.1%)	39 (79.6%)
II	15 (9.4%)	8 (9.1%)	7 (9.7%)		9 (8.1%)	6 (12.2%)
III	2 (1.3%)	0	2 (2.8%)		0	2 (4.1%)
IV	4 (2.5%)	2 (2.3%)	2 (2.8%)		2 (1.8%)	2 (4.1%)
Blood sugar (mmol/L)a culprit vessel	6.2 (5.2, 7.7)	6.4 (5.2, 7.7)	5.9 (5.2, 7.4)	N.05	6.1 (5.2, 7.3)	6.7 (5.3, 8.3)	N.05
anterior descending artery	81 (50.6%)	46 (52.3%)	35 (48.6%)	N.05	60 (54.1%)	21 (42.9%)	N.05
Left circumflex branch	18 (10.6%)	7 (8.0%)	10 (13.9%)	N.05	8 (7.2%)	9 (18.4%)	.050
Right coronary artery	62 (38.8%)	35 (39.8%)	27 (37.5%)	N.05	43 (37.8%)	19 (38.8%)	N.05

Data are presented as mean +- SD, number (percentage), or median (25th, 75th percentiles).

^a Median (25th, 75th percentiles).

1074 Q. Shangguan et al. / American Journal of Emergency Medicine 33 (2015) 1072–1075

Table 2

The percentages of 7-day outcomes in the 4 groups stratified by SI and MSI

Outcome	All patients (n = 160)	MSI				SI
		b 1.4 (n = 111)	>=1.4 (n = 49)	P		b 0.7 (n = 88)	>=0.7 (n = 72)	P
MACE	39 (24.4%)	17 (15.3%)	22 (44.9%)	b.01		13 (14.8%)	26 (36.1%)	b.01
Killip classes	20 (12.5%)	10 (9.0%)	10 (20.4%)	b.05		6 (6.8%)	14 (19.4%)	b.05
Cardiogenic shock	9 (5.6%)	4 (3.6%)	5 (10.2%)	N.05		4 (4.5%)	5 (6.9%)	N.05
LTA	9 (5.6%)	2 (1.8%)	7 (14.3%)	b.01		2 (2.3%)	7 (9.7%)	b.05
All-cause mortality	14 (8.8%)	4 (3.6%)	10 (20.4%)	b.01		4 (4.5%)	10 (13.9%)	b.05

Results

Based on optimizing the sum of sensitivity and specificity by receiver operating characteristic curve analysis, the optimal cutoff value of MSI for predicting MACE was 1.4 in this study.

The sensitivity of MSI of 1.4 or greater was lower (56.4% vs 66.7%) than that of SI of 0.7 or greater, but specificity was higher (77.7% vs 62.0%) in this study.

Table 1 shows the general information of 4 groups divided by SI less than 0.7 or 0.7 or greater and MSI less than 1.4 or 1.4 or greater. On MSI, 111 patients had normal and 49 had increased MSI. Although on SI, 88 patients had normal and 72 had increased SI. The median (25th, 75th percentiles) of SI was 0.9 (0.8, 1.0) in the increased MSI group.

Except the parameters on BP and HR, other parameters were similar between the normal SI and increased SI groups. However, the increased MSI group had significantly higher age (69.0 +- 13.0 years vs 63.9 +- 12.9 years, P = .025) and percentage of left circumflex branch (P = .05) as culprit vessel (Table 1).

Meanwhile, the increased MSI group had significantly higher age than the increased SI group (69.0 +- 13.0 years vs 66.6 +- 13.4 years, P = .334).

The 7-day all-cause mortality was 8.8%, and MACE rate was 24.4% in this study. Both increased SI and MSI groups had higher MACE rates. The increased SI group had significantly higher all-cause mortality (13.9% vs 4.5%, P b .05) and MACE rate (36.1% vs 14.8%, P b .05) than the normal SI group. On MSI, these differences were more obvious (all-cause mortality 20.4% vs 3.6%, P b .05; MACE rate 44.9% vs 15.3%, P b .05) (Table 2).

The odds ratios (ORs) of MSI of 1.4 or more for all-cause mortality (6.8 vs 3.4), cardiogenic shock (3.0 vs 1.6), and LTA (9.1 vs 4.6) as well as MACE (6.8 vs 3.4) were higher than those for SI of 0.7 or more, except Killip classes (Table 3).

Multifactor analysis showed that, in addition to MSI or SI, age and blood glucose level were the independent factors for the 7-day MACE (Table 4).

Discussion

Shock index is known as hemodynamic stability predictor. Its predicting value for the outcome has been fully demonstrated in the patients with trauma [1-4]. Recently, some studies further showed that a new index, MSI, in the ED is a more valuable marker for predicting the mortality rate than SI alone in adult patients with trauma [14].

Table 3

The comparison of ORs for outcomes between MSI of 1.4 or more and SI of 0.7 or more

At first, the present study demonstrated that SI of 0.7 or greater is a useful predictor for 7-day outcomes in the patients with STEMI. This re- sult was concomitant with that from a study of 7187 patients with STEMI, in which SI of 0.7 or greater indicated greater 7- and 30-day all-cause mortality and MACE as the TIMI risk score (11). Other studies also showed that SI of 0.8 or more is strong independent predictor of short-term and/or long-term outcome in patients with STEMI [12,13].

Second, the present study firstly demonstrated that MSI (>=1.4) is a better predictor than SI (>=0.7) for 7-day all-cause mortality and MACE in the patients with STEMI, as increased MSI predicted higher rates for all-cause mortality (20.4% vs 13.9%) and MACE (44.9% vs 36.1%) as compared with increased SI. Furthermore, the ORs of MSI of 1.4 or more for all-cause mortality (6.8 vs 3.4), cardiogenic shock (3.0 vs 1.6), and LTA (9.1 vs 4.6) as well as MACE (6.8 vs 3.4) were higher

than those of SI of 0.7 or more, except from for Killip classes. Meanwhile, the O^R s of MSI was also higher than that of SI (3.05 vs 2.61 ).

As the calculation of MSI uses MAP from SBP and DBP, MSI could more correctly reflect myocardial perfusion and systemic vascular resis- tance [14]; its higher predicting power in the patients with STEMI is easily to be understood

Third, the present study demonstrated that increased MSI was an independent factor for the 7-day MACE. Furthermore, the O^R s of MSI was higher than that of age (3.05 vs 1.07). These results indicated that

the poorer outcome in the increased MSI groups is not because of the older age, as the older patients may have higher SBP and lower DBP and then had higher MSI. Thus, MSI per se is a useful predictor.

In addition, another independent actor was blood glucose level. This finding is concomitant with the wide-accepted concept that Admission hyperglycemia is an independent predictor in patients with STEMI undergoing Primary PCI [8,19].

Clinical implication

Although several systems have been used for risk stratification in the patients with STEMI, such as TIMI and GRACE, the sophisticated calcula- tion usually makes them inconvenient to operate at bedside in daily clinical practice [9,10]. Our results suggest that MSI of 1.4 or greater could be used for risk stratification in the patients with STEMI, although a large, more sufficient study is required to demonstrate these findings in the future.

Limitations

The number of the studied patients in this study was small. Mean- while, only 7-day outcomes were analyzed. Moreover, the SI and MSI after PCI and treatment were not evaluated.

Table 4

MSI >=1.4 (49/160) SI >=0.7 (72/160)

OR 95% CI OR 95% CI

MACE Killip classes	4.5 2.6	2.1-9.7 1.0-6.7	3.3 3.3	1.5-7.0 1.2-9.1		P	O^R	95% CI		P	O^R	95% CI
Cardiogenic shock	3.0	0.8-11.9	1.6	0.4-6.0	Age	b.01	1.07	1.03-1.12		b.01	1.08	1.03-1.13
LTA	9.1	1.8-45.5	4.6	0.9-23.0	SI or MSI	b.05	3.05	1.19-7.82		b.05	2.61	1.03-6.65
All-cause mortality	6.8	2.0-23.1	3.4	1.0-11.3	Glucose	b.05	1.18	1.03-1.36		b.05	1.18	1.02-1.36

The independent factors for the 7-day MACE on MSI of 1.4 or more or SI of 0.7 or more MSI SI

Q. Shangguan et al. / American Journal of Emergency Medicine 33 (2015) 1072–1075 1075

Singh et al [15] pointed out that MSI of 0.7 or greater also predicts poor outcome in patients with trauma. This study only divided the patients into 2 groups by a cut point of MSI of 1.4 as the MSI less than

0.7 was only seen in 2 cases without 7-day MACE. Therefore, the value of MSI less than 0.7 in the patients with STEMI is unclear now.

Conclusions

Both SI and MSI measured in ED could predict the all-cause mortality and MACE within 7 days in patients with STEMI and received PCI, but MSI may more accurately predict 7-day mortality and MACE than SI.

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