Clinical prognostic value of elevated CK-MB in severe multiple trauma patients with nonmyocardial contusion

doi:10.21203/rs.3.rs-2752343/v1

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Clinical prognostic value of elevated CK-MB in severe multiple trauma patients with nonmyocardial contusion

https://doi.org/10.21203/rs.3.rs-2752343/v1

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Background: Unintentional injury was the leading cause of death and disability among individuals younger than 49 years globally in 2019. However, the association between serum CK-MB levels and clinical value in polytrauma patients with nonmyocardial contusion remains unclear.

Methods: This was a single-center, retrospective study. Demographic and clinical data were extracted from the Hospital Information System (HIS) at the Third Xiangya Hospital of Central South University. A total of 287 patients were included in the study. Patients were divided into a normal group (CK-MB ≤25 U/L) and an abnormal group (CK-MB >25 U/L) based on a low CK-MB level. Further clinical and follow- up data were analyzed by using univariate and multivariate logistic regression.Finally, disease-free survival and overall survival were calculated by the Kaplan– Meier method.

Results: Multivariate logistic regression demonstrated that CK-MB (OR: 1.023, 95% CI: 1.006-1.040) was an independent risk factor for predicting in-hospital mortality in polytrauma patients with nonmyocardial contusion. Compared with normal CK-MB levels, CK-MB elevation was associated with a longer length of ICU stay (7.38±13.13 vs. 3.16±5.86 days, P =0.004) and total length of hospital stay (24.73±23.04 vs.

18.29±14.63 days, P =0.015) and was more likely to result in arrhythmia during hospitalization (19.29% vs. 10%, P =0.048). Moreover, the follow-up data showed that patients with CK-MB elevation were more likely to have cardiopalmus after discharge (15.00% vs. 5.68%, P =0.027).

Conclusion: Our findings suggested that elevated CK-MB played an important role in the prognosis of polytrauma patients with nonmyocardial contusion, and a higher level of CK-MB indicated a poor prognosis.

Creatine kinase-MB (CK-MB)

polytraumas

nonmyocardial contusion

long-term prognosis

risk markers

Unintentional injury, including trauma, was the leading cause of death and disability among individuals younger than 49 years globally in 2019 ^{[1, 2]}.

Approximately 5.8 million deaths are caused by trauma every year, among which the mortality rate of severe trauma patients can reach 8.5% ^[3]. Recent studies have focused on potential preventable risk factors for in-hospital mortality in polytrauma patients ^{[4, 5]}, including the plasma lactate level, the blood glucose level, and base excess, have been confirmed to predict the short-term prognosis in polytrauma patients ^{[6, 7]}. However, there is limited research exploring risk markers and long-term survival after polytraumas.

CK-MB is a cardiac injury biomarker widely used in the assessment of adult patients. In clinical practice, CK-MB plays an essential role in the diagnosis of acute coronary syndrome ^[8]. Moreover, an elevated serum level of CK-MB is associated with poor prognosis of COVID-19 ^{[9, 10]} and provides a predictive value for contrast- induced acute kidney injury among myocardial infarction patients ^[11]. In addition, studies have also found that CK-MB is associated with the in-hospital mortality of polytrauma patients ^{[4, 12]}. However, due to the limitations of the above studies, the association between serum CK-MB levels and short-term prognosis and long-term prognosis in polytrauma patients with nonmyocardial contusion remains unclear.

Therefore, this study aimed to explore the impact of elevated CK-MB on the short-term and long-term prognosis of polytrauma patients with nonmyocardial contusion.

2.1 Patient selection

Polytrauma patient data were collected through the Hospital Information System (HIS) at the Third Xiangya Hospital of Central South University from January 2019 to December 2021. Further clinical information confirmation and clinical follow-up data were collected by communication with the patients. The eligibility criteria in this

study included the following: (1) ISS > 16; (2) length of hospital stay > 24 hours; (3) age ≥ 18 years; and (4) complete clinical data. The exclusion criteria included the following: (1) age < 18 years; (2) comorbidity with coronary artery disease, myocardial infarction, heart valve disease, congestive heart failure, and arrhythmia;

(3) comorbidity with malignant tumors; (4) length of hospital stay < 24 hours; (5) period from injury to admission > 24 hours; (6) cardiac contusion was found by CT or MRI scans; (7) missing data regarding CK-MB values; and (8) troponin values that were negative at admission and within 24 hours. This retrospective study was supported by the Institutional Review Board of Third Xiangya Hospital, Central South University (No. 22200), and due to the retrospective nature of the study, the requirement for informed consent was waived. A flow chart of our research is shown in Fig. 1.

2.2 Data collection

The demographics of our study included age, sex, and comorbidity of diabetes and hypertension. The first record of vital signs was collected while admitted to the emergency department and included temperature, respiratory rate, heart rate, systolic blood pressure, diastolic blood pressure, and peripheral capillary oxygen saturation (SP02). The injury severity score (ISS), APACHE-II score, sequential organ failure assessment (SOFA) score, and Glasgow Coma Scale (GCS) score were calculated for each patient within 24 hours after admission to the emergency department. The first record of laboratory data was collected within 72 hours after admission to the emergency department and included white blood cell (WBC), neutrophil (NEU), red blood cell (RBC), hemoglobin, hematocrit, platelet, blood urea nitrogen (BUN), serum creatinine, uric acid, total bilirubin, albumin, creatine kinase (CK), CK-MB, lactate dehydrogenase (LDH), myoglobin, serum level of sodium, potassium, chloride, calcium, pondus hydrogenii (PH), PaO2 (partial pressure of arterial oxygen)/FiO2 (fraction of inspired oxygen), PaO2, partial pressure of arterial carbon dioxide (PaCO2), base excess, bicarbonate radical, arterial lactate level, d-dimer, prothrombin time (PT), activated partial thromboplastin time (APTT), and international normalized ratio (INR) values. The interventions within 72 hours after

admission included mechanical ventilation, continuous renal replacement therapy (CRRT), diuretics use, cardiac agent use, vasopressor use (including dobutamine, dopamine, epinephrine, norepinephrine, and phenylephrine use) and bronchoscopy.

2.3 Follow-up and outcomes

The enrolled patients were followed every 3 months for the first year and then every 12 months thereafter. We supplemented the follow-ups with our outpatient system or communicated with patients by telephone. All patients were monitored until May 31, 2022, or death. The short-term outcomes were the in-hospital mortality, length of ICU stay, total length of hospital stay, and incidence of arrhythmia. The long-term outcomes were overall mortality and incidence of cardiopalmus.

2.4 Statistical analyses

The counting data are described as percentages (%), and measurement data are shown as the mean ± standard deviation (SD). The chi-squared test or Fisher’s exact test was used to evaluate the comparison of counting data, and Student’s t test or one-way ANOVA was used for the comparison of continuous variables. Multiple imputation (mi) was conducted for missing data interpolation (missing data < 20%). Univariate and multivariate logistic regression were performed to identify the potential independent predictors for in-hospital mortality and CK-MB elevation (forward- stepwise, likelihood). Disease-free survival (DFS) was defined as living without any symptoms of cardiopalmus. Disease-free survival (DFS) and overall survival (OS) were calculated by the Kaplan–Meier method, and differences between Kaplan–Meier curves were investigated by the log-rank test. Statistical analyses were performed using Stata v.16.0 (Stata Corporation, College Station, Texas). The P value was considered statistically significant below the 5% level.

3.1 CK-MB as an independent risk factor to predict in-hospital mortality in polytrauma patients

A total of 287 patients were ultimately enrolled in our study. First, all variables were analyzed by conducting univariate and multivariate logistic regression to identify the risk factors for in-hospital mortality (Table 1). The results showed that the vital signs of temperature (OR: 0.054, 95% CI: 0.007–0.422) and respiratory rate (OR: 0.752, 95% CI: 0.635–0.891) while admitted to the emergency department, CK-MB (OR: 1.023, 95% CI: 1.006–1.040), myoglobin (OR: 1.001, 95% CI: 1.000-1.002), and

Table 1

Univariate and multivariate logistic regression for in-hospital mortality in severe multiple-trauma patients.
Characteristics	Univariate	P-value	Multivariate	P-value
Characteristics	OR (95% CI)	P-value	OR (95% CI)	P-value
Demographics
Age	0.995(0.957–1.034)	0.790
Gender (male to female)	1.639(0.488–5.505)	0.424
Score systems
ISS score	1.145(1.071–1.223)	< 0.001
GCS score	0.736(0.650–0.833)	< 0.001
SOFA score	1.367(1.204–1.554)	< 0.001
APECHE-II	1.187(1.106–1.274)	< 0.001
Vital sign
Temperature	0.110(0.024–0.498)	0.004	0.031(0.001–0.844)	0.039
Respiratory rate	0.829(0.713–0.962)	0.014	0.701(0.513–0.957)	0.026
Heart rate	1.017(0.991–1.044)	0.197
Systolic pressure	0.960(0.939–0.987)	0.003	1.002(0.927–1.084)	0.951
Diastolic pressure	0.946(0.909–0.986)	0.008	1.000(0.892–1.122)	0.994
SPO2	0.926(0.858–1.001)	0.051
Comorbidity
Hypertension	0.446(0.057–3.518)	0.444
Diabetes	2.300(0.272–19.458)	0.445
Laboratory data
WBC	1.078(1.002–1.160)	0.044	1.045 (0.934–1.170)	0.443
NEU	0.977(0.928–1.029)	0.385
RBC	0.963(0.466–1.991)	0.919
Hemoglobin	0.984(0.963–1.006)	0.154
Hematocrit	0.966(0.896–1.041)	0.368
Platelet	0.999(0.990–1.007)	0.740
Blood urea nitrogen	1.050(0.928–1.187)	0.438
Serum creatinine	1.003(0.999–1.008)	0.167
Uric acid	1.001(0.999–1.002)	0.360
Total bilirubin	1.014(0.968–1.063)	0.551
Albumin	0.949(0.868–1.039)	0.257
CK-MB	1.025(1.014–1.035)	< 0.001	1.025(1.001–1.049)	0.039
LDH	1.001(1.000-1.002)	0.056
Myoglobin	1.001(1.000-1.002)	0.008	1.001(1.000-1.002)	0.073
Sodium	1.080(0.914–1.276)	0.336
Potassium	1.026(0.855–1.232)	0.782
Chloride	1.067(0.955–1.192)	0.250
Calcium	0.398(0.055–2.891)	0.362
PH	0.698 (0.277–1.761)	0.447
PaO2/FiO2	0.999(0.996–1.002)	0.542
PaO2	0.992 (0.975–1.009)	0.352
PaCO2	1.039(0.990–1.091)	0.124
Base excess	0.790(0.703–0.888)	< 0.001	1.639(0.360–7.463)	0.523
Bicarbonate radical	0.707(0.602–0.830)	< 0.001	0.354(0.046–2.740)	0.320
Lactate	1.442(1.183–1.757)	< 0.001	0.973(0.544–1.742)	0.927
D-dimer	1.032(0.987–1.080)	0.166
PT	1.421(1.099–1.829)	0.007	0.726(0.400-1.318)	0.293
APTT	1.050(0.962–1.146)	0.277
INR	2.380(0.070-80.556)	0.629
Treatment
Mechanical ventilation	21.98(2.817-171.485)	0.003	2.919(0.158–53.852)	0.471
CRRT	25.818(3.322-200.637)	0.002	5.989(0.311-152.955)	0.235
Diuretics used	5.250(1.694–16.270)	0.004	4.023(0.406–39.871)	0.234
Cardiac agents used	2.896(0.335–25.052)	0.334
Vasopressor used	44.262(5.644-347.115)	< 0.001	3.876(0.236–63.527)	0.342
Bronchoscope	4.714(1.513–14.693)	0.008	8.386(0.739–95.130)	0.086

diuretic use (OR: 4.729, 95% CI: 1.462–15.293) were independent risk factors for predicting in-hospital mortality in polytrauma patients with noncardiac contusion, but other myocardial enzymes, including CK and LDH, had no predictive value (Table 1).

3.2 Predictive factors associated with CK-MB elevation

We assumed that there were any variables associated with the elevation of CK- MB. Patients were divided into a normal group (CK-MB ≤ 25 U/L) and an abnormal group (CK-MB > 25 U/L) based on the low CK-MB level. Table 2 shows that Abbreviated Injury Score (AIS)-Thorax, AIS-Abdomen, AIS-Limb, GCS score, SOFA score, APACHE-II score, respiratory rate, heart rate, systolic pressure, diastolic pressure, SPO2, WBC, blood urea nitrogen, hemoglobin, albumin, CK, LDH, myoglobin, sodium, base excess, bicarbonate radical, lactate, D-dimer, PT, APTT, INR, mechanical ventilation, diuretic use, and vasopressor use were associated with the elevation of CK-MB (P < 0.05). Next, multivariate logistic regression was conducted, and the results indicated that AIS-Abdomen, myoglobin, CK, and APACHE-II were independent predictive factors associated with CK-MB elevation, indicating that CK-MB was associated with myocardial enzymes and the severity of polytrauma (Table 3).

Table 2

໿Clinical and epidemiological characteristics of the 299 patients studied.
Variable	Total	Abnormal group	Normal group	P value
Variable	(n = 299)	(n = 209)	(n = 90)	P value
Demographics
Age (years)	51.57 ± 14.20	51.76 ± 14.34	51.11 ± 13.93	0.717
Gender, male (%)	234(78.26)	169(80.86)	65(72.22)	0.097
Score systems
ISS score	24.67 ± 7.32	25.96 ± 7.92	21.68 ± 4.45	< 0.001
AIS (Head and neck)	1.66 ± 1.54	1.59 ± 1.53	1.82 ± 1.58	0.240
AIS (Face)	0.54 ± 0.85	0.54 ± 0.84	0.56 ± 0.88	0.794
AIS (Thorax)	3.04 ± 1.21	3.23 ± 1.11	2.61 ± 1.33	< 0.001
AIS (Abdomen)	1.60 ± 1.42	1.80 ± 1.41	1.13 ± 1.33	< 0.001
AIS (Limb)	1.44 ± 1.30	1.56 ± 1.30	1.18 ± 1.29	0.022
AIS (External)	1.15 ± 0.49	1.16 ± 0.49	1.12 ± 0.52	0.749
GCS score	13.82 ± 2.88	13.47 ± 3.28	14.63 ± 1.29	0.001
SOFA score	3.37 ± 3.11	3.89 ± 3.38	2.17 ± 1.92	< 0.001
APECHE-II	8.14 ± 6.00	9.24 ± 6.45	5.58 ± 3.74	< 0.001
Vital sign
Temperature (℃)	36.62 ± 0.38	36.59 ± 0.40	36.68 ± 0.31	0.076
Respiratory rate (/min)	20.66 ± 3.50	20.94 ± 3.90	20.00 ± 2.24	0.033
Heart rate (/min)	90.48 ± 20.67	92.58 ± 21.75	85.60 ± 17.03	0.007
Systolic pressure (mmHg)	117.27 ± 28.45	112.23 ± 27.27	128.99 ± 27.81	< 0.001
Diastolic pressure (mmHg)	72.28 ± 16.87	70.48 ± 17.21	76.47 ± 15.31	0.005
SPO2 (%)	95.23 ± 4.48	94.72 ± 4.99	96.43 ± 2.64	0.002
Comorbidity
Hypertension (%)	46(15.38)	27(12.92)	19(21.11)	0.072
Diabetes (%)	11(3.68)	8(3.83)	3(3.33)	0.835
Laboratory data
*WBC (10⁹/L)**	15.40 ± 6.47	16.16 ± 6.60	13.64 ± 5.85	0.002
NEU (%)	82.78 ± 9.32	83.18 ± 9.10	81.86 ± 9.80	0.260
RBC (*10¹²/L)	4.02 ± 0.76	4.03 ± 0.75	3.99 ± 0.80	0.680
Hemoglobin (g/L)	122.72 ± 23.89	120.97 ± 24.43	126.77 ± 22.19	0.054
Hematocrit (%)	39.24 ± 27.73	39.54 ± 32.92	38.55 ± 6.41	0.777
Platelet (*10⁹/L)	196.47 ± 66.07	194.87 ± 72.25	200.21 ± 48.98	0.522
Blood urea nitrogen	6.66 ± 3.08	6.95 ± 2.44	5.99 ± 4.14	0.013
Serum creatinine	78.97 ± 54.32	81.13 ± 30.75	73.96 ± 87.38	0.296
Uric acid	321.45 ± 206.78	324.98 ± 119.43	313.24 ± 331.27	0.653
Total bilirubin	13.53 ± 8.56	13.24 ± 9.14	14.18 ± 7.05	0.386
Albumin	37.78 ± 6.02	37.10 ± 6.42	39.37 ± 4.62	0.003
LDH	484.29 ± 387.86	544.90 ± 417.79	343.54 ± 259.08	< 0.001
Myoglobin	750.28 ± 764.52	933.98 ± 814.65	323.72 ± 377.92	< 0.001
Sodium	141.31 ± 3.34	141.62 ± 3.22	140.58 ± 3.50	0.013
Potassium	3.92 ± 2.10	3.97 ± 2.50	3.80 ± 0.39	0.542
Chloride	106.56 ± 4.83	106.43 ± 5.06	106.88 ± 4.28	0.466
Calcium	2.17 ± 0.84	2.13 ± 0.64	2.29 ± 1.17	0.122
PH	7.37 ± 0.31	7.36 ± 0.37	7.39 ± 0.11	0.421
PaO₂/FiO₂	393.49 ± 251.94	391.79 ± 283.58	397.44 ± 156.71	0.859
PaO₂	101.18 ± 43.86	99.71 ± 48.50	104.58 ± 30.45	0.379
PaCO₂	35.27 ± 6.83	35.06 ± 7.52	35.75 ± 4.86	0.426
Base excess	-3.37 ± 3.87	-3.83 ± 3.73	-2.31 ± 4.00	0.002
Bicarbonate radical	21.60 ± 2.98	21.20 ± 2.90	22.55 ± 2.96	< 0.001
Lactate	2.78 ± 2.19	2.99 ± 2.03	2.29 ± 2.48	0.012
D-dimer	11.19 ± 10.18	12.93 ± 10.80	7.16 ± 7.13	< 0.001
PT	12.23 ± 1.63	12.42 ± 1.73	11.80 ± 1.29	0.002
APTT	26.60 ± 5.51	27.08 ± 6.02	25.50 ± 3.90	0.023
INR	1.05 ± 0.14	1.07 ± 0.15	1.02 ± 0.12	0.010
Treatment
Mechanical ventilation, n (%)	113(37.79)	92(44.02)	21(23.33)	0.001
CRRT, n (%)	4(1.34)	2(0.96)	2(2.22)	0.586
Diuretics used, n (%)	59(19.73)	51(24.40)	8(8.89)	0.002
Cardiac agents used, n (%)	9(3.01)	6(2.87)	3(3.33)	0.830
Vasopressor used, n (%)	73(24.41)	64(30.62)	9(10.00)	< 0.001
Bronchoscope, n (%)	50(16.72)	39(18.66)	11(12.22)	0.171

Table 3

Short-term and long-term outcomes of the different groups
Outcomes	Abnormal group	Normal group	P value
Short-term Outcomes (n = 299)
In-hospital mortality, n, (%)	12(5.74)	1(1.11)	0.118
length of ICU stays(days)	7.55 ± 13.37	3.16 ± 5.86	0.003
Total length of hospital stays(days)	25.25 ± 23.72	18.29 ± 14.63	0.010
Incidence of arrhythmia, n, (%)	41(19.62)	9(10.00)	0.041
Long-term Outcomes (n = 279)
Overall mortality, n, (%)	10(5.24)	2(2.27)	0.257
Incidence of cardiopalmus, n, (%)	27(14.14)	5(5.68)	0.039

3.3 The predictive value of CK-MB elevation by subgroup analysis

The results of subgroup analysis showed that the in-hospital mortality OR for CK-MB elevation was 1.02 (95% CI: 1.01–1.04) (Fig. 2). Regardless of sex, age, ISS score and CK level, CK-MB elevation still had a potential predictive value for elevated in-hospital mortality in all patients. Moreover, CK-MB elevation seemed to have better predictive value at ages > 60 years (OR: 1.04, 95%: 1.01–1.07) compared

with patients at ages 40 to 60 years (OR: 1.02, 95%: 1.01–1.04) and those at ages < 40

years (OR: 1.01, 95%: 0.99–1.03).

3.4 The short-term and long-term outcomes of CK-MB elevation

Next, we explored the relationship between CK-MB elevation and clinical outcomes. The results confirmed that compared with normal CK-MB levels, CK-MB elevation was associated with a longer length of ICU stay (7.38 ± 13.13 vs. 3.16 ± 5.86 days, P = 0.004), a longer total length of hospital stay (24.73 ± 23.04 vs. 18.29 ± 14.63 days, P = 0.015), and a greater possibility of developing arrhythmia during hospitalization (19.29% vs. 10%, P = 0.048) (Table 4). A total of 276 live patients were followed up; of these patients, 8 patients were lost to follow-up (follow-up rate: 97.10%). Moreover, the follow-up data showed that patients with CK-MB elevation were more likely to have cardiopalmus after discharge (15.00% vs. 5.68%, P = 0.027) (Fig. 3). Interestingly, the CK-MB elevation group also exhibited a trend toward a poor prognosis, including higher in-hospital mortality (5.58% vs. 1.11%, P = 0.112) and lower overall survival after discharge (94.45% vs. 97.73%, P = 0.222).

Table 4

໿Independent Predictors of CK-MB elevation after admission in severe multiple trauma patients.
Predictors	B	SE	OR	95% CI	P value
AIS (Thorax)	2.77	0.196	1.454	1.116–1.895	0.006
AIS (Abdomen)	2.68	0.164	1.377	1.090–1.740	0.007
Myoglobin	5.15	0.001	1.002	1.001–1.003	< 0.001
D-dimer	2.89	0.021	1.059	1.019–1.101	0.004
Systolic pressure	-2.54	0.006	0.984	0.971–0.996	0.011
SPO2	-2.07	0.046	0.900	0.814–0.995	0.039

This was a retrospective study aimed to explore the clinical value of elevated CK-MB in severe polytrauma patients with nonmyocardial contusion. In this study, we confirmed that the CK-MB level was an independent risk factor for predicting in- hospital mortality. Subsequently, patients with elevated CK-MB were more likely to have cardiopalmus and tended to have a poor prognosis, including higher in-hospital mortality and lower overall survival after discharge.

Recent studies have indicated that serum CK-MB levels are widely associated with diagnosis, prognosis, and severity in many diseases ^[13–15]. Ilias Katsikis et al indicated that CPK levels and CPK-MM were significantly higher in ectopic pregnancy patients than in patients with intrauterine abortive gestation or regular pregnancies, while the CPK-MB relative ratio was decreased. A significant discriminatory ability was found for both increased total CPK levels and decreased CPK-MB relative ratios for the diagnosis of ectopic pregnancy ^[16]. Additionally,

Mehmet Bozbay et al found that pulmonary embolism patients with high CK-MB levels (> 31.5 U/L) had a higher in-hospital mortality after treatment with thrombolytic therapy; a CK-MB level of higher than 31.5 U/L had a sensitivity of 86.7% and specificity of 83.5% for predicting in-hospital mortality ^[17]. Another study found a significant association between serum CK-MB and the severity of disease among children with RV-infected gastroenteritis ^[18]. Similarly, elevated CK-MB levels were also associated with the prognosis and severity of trauma patients ^[19–21]. However, there are still limited studies focused on both short-term and long-term outcomes of CK-MB elevation in trauma patients, especially for those with nonmyocardial contusion.

In this study, we found that 69.90% of patients with ISS ≥ 16 exhibited elevated CK-MB, although no myocardial contusion was found by CT or MRI. Patients with elevated CK-MB had increased in-hospital as well as overall mortality. Similar results were also reported by Kovar FM ^[4] and Karakus A ^[20]. Moreover, we found that elevated CK-MB was associated with adverse outcomes after polytraumas, including a longer length of ICU stay, total length of hospital stay, and greater possibility of developing arrhythmia during hospitalization, which had not been reported previously. These results, with important clinical significance, suggest that CK-MB is a specifically significant short-term prognostic factor and provide a new direction for the management of severe polytrauma patients with nonmyocardial contusion.

CK-MB is released into blood serum when myocardial cells are injured. After a long history of augmented use, it has rapidly became the gold standard for identifying cardiac injury ^[22]. Many studies have evaluated the value of CK-MB in several diseases ^[23–25], but limited studies have found the predictive value of CK-MB in trauma. Two small-scale retrospective studies concluded that CK-MB plays a small role in identifying cardiac damage in trauma ^{[26, 27]}. Another study revealed the independent predictive value of CK-MB levels in trauma patients ^[20]. However, all previous studies failed to analyze severe and nonmyocardial polytrauma patients.

From our follow-up data, this research indicated that compared with the normal CK-MB group, the elevated CK-MB group was more prone to having cardiopalmus and higher mortality after discharge. In addition, the overall mortality showed an obvious downward trend with the extension of the follow-up period, especially after 20 months. We speculated that elevated CK-MB might reflect damage to internal organs, which appears to be consistent with the findings of Kovar FM et al. ^[4].

Regrettably, a short follow-up period contributed to the fact that there was no statistically significant link between elevated CK-MB and long-term outcomes of overall mortality. Therefore, a longer follow-up time is needed. In multivariate logistic regression, our results demonstrated that AIS-Thorax, AIS-Abdomen, myoglobin, D-dimer, systolic pressure, and SPO2 were independent predictive factors associated with CK-MB elevation. These findings might provide a direction for the mechanisms of CK-MB elevation in severe polytrauma patients with nonmyocardial contusion, including excitement of the sympathetic nerves, stress reactions, activation of the complement system, local and systemic inflammation, apoptosis, and organ dysfunction.

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Not applicable.

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Ethics approval and consent to participate：Not applicable.

Consent for publication：Not applicable.

Availability of data and materials：Not applicable.

Competing interests：The authors declare that they have no competing interests.

Funding: This study was supported by the Key Project of Hunan Provincial Science and Technology Innovation (No. 2020SK1010), the Wisdom Accumulation and Talent Cultivation Project of Central South University (No. YX202104) and Outstanding Youth Scientist Foundation of Hunan Province (No. 2022JJ10099).

Author Contributions: HD: follow-up, data curation, writing—original draft; QJ: data analysis, writing—review and editing, modification; CQ: writing—review and editing, data curation; LJC, CX: resources, writing—review and editing; SCZ: writing—review and editing, funding, modification, guidance.

Acknowledgments: Not applicable.

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Clinical prognostic value of elevated CK-MB in severe multiple trauma patients with nonmyocardial contusion

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Abstract

Figures

1. Introduction

2. Materials And Methods

2.1 Patient selection

2.2 Data collection

2.3 Follow-up and outcomes

2.4 Statistical analyses

3. Results

3.1 CK-MB as an independent risk factor to predict in-hospital mortality in polytrauma patients

3.2 Predictive factors associated with CK-MB elevation

3.3 The predictive value of CK-MB elevation by subgroup analysis

3.4 The short-term and long-term outcomes of CK-MB elevation

4. Discussion

Declarations

References

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