Cardiovascular Risk Score (SCORE2) Predicts The Incidence and Severity of Cardiac Damage After Polytrauma: How to Identify At-Risk Patients?

Abstract

Objective:

Cardiac damage predicts poor outcomes in polytrauma (PT). In older patients, cardiovascular risk factors may predispose to post-traumatic cardiac dysfunction. This study examined whether cardiovascular risk correlates with cardiac damage and influences clinical outcomes in PT.

Methods:

This study at a German Level 1 Trauma Centre enrolled 59 PT patients upon emergency room admission. Blood samples were taken at the emergency room, 24, 48, 72, 96 hours, and 10 days to assess cardiac damage via troponin T and N-terminal pro-B-type natriuretic peptide. Transthoracic echocardiography (TTE) was performed at 24/48 hours. Cardiovascular risk was evaluated using the Systematic Coronary Risk Evaluation (SCORE)2 algorithm. Subgroup analysis compared cardiac damage in patients with high (SCORE2 >7.5%) versus low risk, and assessed the additional impact of chest trauma.

Results:

Arrhythmias were observed in 39% of patients, whereas acute repolarization disorder occurred in nearly 19%. TTE revealed wall motion abnormalities in 12%, diastolic dysfunction in 10%, and right ventricular dysfunction in 5%. SCORE2 and lipoprotein(a) significantly correlated with serum levels of troponin T and N-terminal pro-B-type natriuretic peptide. SCORE2 values were associated with nonsurvival, wall motion disorders, diastolic dysfunction, and relaxation disorders (P < 0.05). A higher incidence of arrhythmias, diastolic dysfunction, and relaxation disorders was observed in the subgroup of high-risk patients with chest trauma. Patients in the high-risk group without chest trauma showed higher nonsurvival rates (50%), which may be strongly influenced by a history of myocardial infarction.

Conclusions:

Cardiovascular risk was significantly associated with cardiac damage markers, TTE abnormalities, and increased mortality. A history of myocardial infarction was associated with higher mortality in PT patients with an elevated SCORE2 risk.

INTRODUCTION

Trauma is one of the leading causes of death among the younger, working-age population (1,2). Cardiac damage, often associated with chest trauma, is a known predictor of poor outcomes following polytrauma (PT) (3). However, beyond blunt chest trauma, existing cardiac comorbidities and risk factors (such as hypertension, hypercholesterolemia, pre-existing heart disease, or smoking) may also predispose individuals to post-traumatic cardiac damage. Accordingly, an earlier study identified patients with cardiac comorbidities, characterized by higher concentrations of cardiac damage markers, as well as increased body mass index and elevated initial blood glucose levels, as a distinct subgroup of PT patients (4).

In an aging population, the prevalence of cardiovascular risk factors is rising, leading to an expected—and already observable—increase in the number of older trauma patients with multiple comorbidities arriving routinely in trauma centers (5). The mean age of these patients has risen from 47.7 years (2011) to 55.9 years (2021) (6), and the proportion of patients aged 60 years or older has been described in the literature to increase from 23% (2002) to 40% (2017) (n = 27,049 patients) (7). In older PT patients, 23% were reported to have coronary artery disease, while hypertension was shown in 60% and diabetes in 9% of patients (8,9). Next to comorbidities, the age of PT patients has been shown to have independent prognostic value for trauma outcome (10). Additionally, geriatric patients requiring intubation, blood transfusions, sustained head, cervical spine, or chest trauma have been found to have an increased risk of mortality (8).

However, the common cardiac comorbidities are not only prevalent in geriatric patients, and serve as risk factors for cardiovascular diseases (CVDs) such as myocardial infarction (MI) and heart failure. To identify people at higher risk of CVD the algorithm, known as the Systematic Coronary Risk Evaluation (SCORE) model has been previously developed (11) and further optimized in SCORE2 (12). This SCORE2 estimates the 10 years of fatal and nonfatal CVD in European individuals aged 40–69 years, who have no prior history of CVD or diabetes. It includes the parameters: age, smoking, systolic blood pressure, and total and high-density lipoprotein (HDL) cholesterol (12). In addition, elevated serum levels of lipoprotein (a) (Lp(a)) have been identified as a causal and independent risk factor for CVDs and are estimated to be 90% genetically determined. According to the literature, 1 in 5 people is considered at high risk for atherosclerotic CVD and aortic valve stenosis due to elevated Lp(a) levels (13).

The present study aims to investigate the association between cardiac comorbidities and the development of cardiac damage after trauma in PT patients. We hypothesized that a high cardiovascular risk, as quantified by the SCORE2 algorithm, as well as pre-existing cardiovascular and other comorbid conditions, is independently associated with poorer clinical outcomes in PT patients, including an increased incidence of in-hospital cardiac complications and mortality. Building on this hypothesis, we sought to determine whether early assessment using an established heart-specific risk profile in the emergency department could improve the prediction of subsequent cardiac complications or myocardial injury following PT. Furthermore, we aimed to externally validate this cardiac risk score in PT patients and evaluate its potential to enhance early risk stratification and clinical decision-making. Therefore, we assessed the occurrence of cardiac damage in PT patients using a combination of cardiac damage biomarkers and transthoracic echocardiography (TTE), as previously described (14). The cardiovascular risk profile of PT patients was estimated via SCORE2 and the assessment of Lp(a) levels. In addition, the cumulative effect of increased cardiovascular risk (SCORE2 >7.5%) and the presence of chest trauma (accounts for up to 25% of traumatic deaths (15)) were investigated. Identifying specific cardiac comorbidities as risk factors for cardiac damage after PT—and thereby recognizing “at-risk” patients early—will ultimately enable trauma surgeons to optimize monitoring, therapy, and improve patient outcomes.

MATERIAL AND METHODS

Ethical approval

Ethical approval was obtained from the local ethics committee (Approval ID: 89/19). Written informed consent was obtained from all participants or their legal guardian, if meeting the inclusion criteria.

Study design

This investigation was designed as a prospective observational study conducted at a level-1 trauma center in Germany. The patient collective in the present study is a prospective observational cohort with availability-based inclusion. The study population consisted of PT patients of legal age with an injury severity score (ISS) ≥16. Patients who were transferred to our clinic as secondary referrals, had isolated TBI, or were unable to undergo TTE within the first 48 hours due to personnel or technical limitations were excluded. Additionally, patients who did not survive the emergency room (ER) phase or the first 24 hours, or who had an initially fatal prognosis, were excluded from the analysis immediately after the initial diagnostic workup in the ER. The final study cohort comprised 59 patients.

Sample collection

Venous blood samples were collected at six predefined time points: upon arrival in the ER, at 24, 48, 96 hours, and 10 days post-admission. Blood collection was performed as part of routine diagnostic procedures, and samples underwent standard clinical laboratory analysis. Additionally, aliquots were kept on ice, and plasma/serum was isolated by centrifugation at 3500 × g for 15 minutes at 4°C, following the NTF Biobank protocol (16) for biomarker analysis. Clinical and demographic data were extracted from electronic patient records.

Cardiac biomarkers

Serum concentrations of cardiac damage biomarkers—troponin T (TnT) and N-terminal pro-B-type natriuretic peptide (NT-proBNP)—were quantified using high-sensitivity electrochemiluminescence immunoassays (Roche Diagnostics, Rotkreuz, Switzerland).

Lipoprotein A enzyme-linked immunosorbent assay (ELISA)

To analyze the genetic predisposition of CVDs in polytraumatized patients, the Lp(a) concentrations were measured in serum samples collected at ER using Human LPA ELISA kit (LSBio, Eching, Germany).

Fibroblast growth factor 23 (FGF-23) ELISA

As FGF-23 is described as a biomarker of right ventricular dysfunction (17), FGF-23 serum levels were quantified in the ER-samples via a DuoSet ELISA (R&D Systems, Abingdon, UK).

SCORE2

Cardiac risk factors for PT patients were calculated with the SCORE2 algorithm using blood pressure at arrival (first measured blood pressure), HDL/cholesterol concentrations, sex, age, and smoking (12) via the online tool of the Swiss Arteriosclerosis Association (https://agla.ch/de/rechner-und-tools/esc-score2-rechner). SCORE2 >7.5% was entitled in the analysis as “high-risk” and was compared with the “low-risk” group.

Transthoracic echocardiography

All echocardiographic examinations were conducted in collaboration with the Department of Cardiology, adhering to the echocardiography standards set forth by the German Centre for Cardiovascular Research. Upon admission to the intensive care unit, TTE was performed at two time points (24 and 48 hours) by a board-certified cardiologist. A consistent set of ultrasound devices was used throughout the study (Manufacturer: GE HealthCare; Models: Venue Go R2 and Vivid iq, Frankfurt, Germany). Echocardiographic assessment included evaluation of left ventricular ejection fraction (EF), left ventricular end-diastolic diameter (LVEDD), tricuspid annular plane systolic excursion (TAPSE), and systolic pulmonary artery pressure (sPAP). Further, all the echocardiograms (ECGs) conducted during the in-hospital stay were analyzed by cardiologists.

Statistical analysis

All statistical analyses were conducted using GraphPad Prism 9 (Dotmatics, San Diego, California). Group comparisons involving more than two groups were performed using the Kruskal–Wallis test followed by Dunn’s multiple comparisons test. For comparisons between two groups, the Mann–Whitney U test was utilized. Correlation analyses were conducted using Spearman’s rank correlation coefficient. Statistical significance was defined as a P value ≤0.05. Data are presented as mean ± standard error of the mean.

RESULTS

A total of 59 PT patients were included in the study, with a mean ISS of 26.9 ± 10.2 and a mean age of 54.7 ± 19.7 years. During the in-hospital course, 18.6% succumbed to their injuries. Chest trauma was observed in 61% of the cohort, whereas signs of myocardial contusion (contusio cordis) were identified in only 7.8% of cases. Contusion cordis was defined by the presence of at least one of the following objective findings: 1) new electrocardiographic abnormalities, 2) elevation of high-sensitivity cardiac TnT above 50 pg/mL, or 3) new echocardiographic abnormalities. A detailed overview of patient demographics and trauma mechanisms is presented in Table 1. To further evaluate comorbidities and cardiovascular risk profiles in this trauma population, the patients’ cardiovascular risk SCORE2 and the American Society of Anaesthesiologists (ASA) Physical Status Classification were assessed. The mean calculated pre-existing cardiovascular risk was 8.6%, and the average ASA score was 3.2 (Table 1). In addition, the pre-existing cardiac conditions were documented: angina pectoris within the preceding 4 weeks was reported in 5.1% of patients, and a history of MI in 8.4% of cases.

Table 1.

Demographics and clinical data of polytraumatized patients cohort

Demographics parameters	Values
Sex	15 females (25.4%): 44 males (74.6%)
Age	54.7 ± 19.7 years
ISS (Injury Severity Score)	26.8 ± 10.2
Nonsurvivors	11 (18.6%): 4 TBI (limitation of therapy), 4 cardiac complications, 2 unknown, 1 sepsis
Chest trauma	36 (61.0%)
Sternal fracture	8 (13.6%)
Contusio cordis	4 (7.8%)
AISChest	1.9 ± 1.6
AISChest >2	42.5%
OIS (Organ Injury Scale)	1.6 ± 1.6
ASA (American Society of Anaesthesiologists) Physical Status System	3.2 ± 1.1
SCORE2	8.6 ± 9.6 %
Angina pectoris within the last 4 weeks	3 (5.1%)
Previous acute myocardial infarction	5 (8.5%)
Trauma mechanism	Traffic accident (as) -Cyclist: 3 (5.1%) -Pedestrian: 7 (11.9%) -Car driver: 6 (10.2%) -Motorcyclist: 6 (10.2%) Fall from ≥3 m: 13 (22%) Fall from <3 m: 10 (16.9%) Staircase fall: 5 (8.5%) Work accident: 4 (6.8%) Hit by a subway/tram: 3 (5.1%) Knife attack: 1 (1.7%) Others: 1 (1.7%)

AIS, Abbreviated Injury Scale; SCORE, Systematic Coronary Risk Evaluation.

To investigate potential genetic predisposition to CVD, serum levels of Lp(a) were measured using ELISA. None of the patients demonstrated elevated genetic cardiovascular risk, defined as Lp(a) concentrations exceeding 30 mg/dL (Table 2).

Table 2.

Percentage of patients with serum levels of troponin T, NT-proBNP, and lipoprotein(a) above the normal threshold during the 10-day observation period

Percentage of patients with:	Time point after trauma
	ER	24 hours	48h	72 hours	96 hours	Day 10
Troponin T >50 pg/mL	15.5%	39.65%	29.3%	13.8%	15.5%	3.5%
NT-proBNP >125 pg/mL	22.4%	46.6%	55.2%	51.7%	32.8%	15.5%
Lipoprotein A >30 mg/dL	0%	n.a.	n.a.	n.a.	n.a.	n.a.

n.a., not available; NT-proBNP, N-terminal pro-B-type natriuretic peptide.

Cardiac damage was assessed via several biomarkers, and Table 2 presents the percentage of patients with serum levels of TnT, NT-proBNP, and Lp(a) exceeding the normal reference values. On day 1 post-trauma, 39.65% of patients showed elevated TnT levels, while at the same time the NT-proBNP levels were exceeded in 46.6% of patients (Table 2).

To evaluate the occurrence of functional cardiac damage, we conducted TTE in our PT patients within the first 24 and 48 hours after trauma (Table 3). The results showed that in our patient cohort, the right ventricular function was slightly impaired (demonstrated by reduced TAPSE values, as well as slightly increased sPAP values), while the left ventricular function measured by the EF was preserved. We further evaluated ECG signs of arrhythmia and myocardial ischemia: arrhythmias were observed in 38.9% of patients, while ST-segment elevations/deviations were present in 18.6% of cases during the 10-day observation period (Table 3).

Table 3.

Functional data from TTE, summary of echocardiography and ECG findings

	Within the first 24 hours	48 hours after trauma
Echocardiography
Wall movement disorder (n (%))	4 (6.8%)	7 (11.9%)
Ejections fraction (%)	62 ± 6.9	61.6 ± 7.9
Left ventricular end-diastolic diameter (LVEDD)	47.8 ± 6.8 mm	46.7 ± 7.4 mm
Right ventricular dysfunction (n, (%))	3 (5.1%)	2 (3.4 %)
Diastolic dysfunction (n (%))	5 (8.5%)	6 (10.2%)
Relaxation disorder	4 (6.8%)	6 (10.2%)
Tricuspid annular plane systolic excursion (TAPSE)	23.2 ± 4.6 mm	27.2 ± 6.3 mm
Systolic Pulmonary Arterial Pressure (sPAP)	26.2 ± 10.4 mmHg	27.9 ± 11.8 mmHg
Pericardial effusion (n (%))	5 (8.5%)	2 (3.4%)
Pleural effusion (n (%))	7 (11.9%)	9 (15.3%)
Chest drainage (n (%))	3 (5.1%)	3 (5.1%)
ECG findings
Arrhythmia (bradykardia, VHF, tachykardia) (n (%))	23 (38.9%)
Acute ischemia/repolarization disorder, e.g., ST-segment elevations/deviations (n (%))	11 (18.6%)
Others (n (%))	Myocarditis: 1 (1.7%) Signs of pulmonary artery embolism: 5 (8.5%) Need for stent implantation: 1 (1.7%) T-negativation: 3 (5.1%) New onset of atrial fibrillation: 1 (1.7%)

ECG, electrocardiogram; TTE, transthoracic echocardiography

To analyze the association between cardiac comorbidities and the development of cardiac damage in PT patients, a correlation analysis was conducted between the SCORE2, cardiac damage markers, and functional TTE data. The results of this analysis showed a significant positive correlation between SCORE2 and NT-proBNP levels measured at ER and on day 1, as well as a negative correlation with creatine kinase (CK)-MB levels at both time points (Figure 1). Additionally, Lp(a) concentrations were found to be negatively associated with TnT at day 1 (r = −0.43; P < 0.01), NT-proBNP levels at the ER (r = −0.37; P < 0.05), and CK-MB at day 1 (r = −0.44; P < 0.01).

Fig. 1.

Correlation between cardiovascular risk parameters and cardiac damage markers. A significant positive correlation between SCORE2 and NT-proBNP levels measured at the emergency room (ER) (A) and on day 1 (d1) (B) was observed in polytrauma patients. A negative correlation between SCORE2 and CK-MB levels at ER (C) and day 1 (D). CK-MB, creatine kinase MB; ER, emergency room; NT-proBNP, N-terminal pro-B-type natriuretic peptide; SCORE, Systematic Coronary Risk Evaluation.

Pre-existing cardiac risk profile and the clinical outcome of PT patients

Based on the observed correlation between post-trauma cardiac damage markers and cardiac risk factors, we hypothesized that the pre-existing cardiac risk profile may influence both the overall outcome of PT patients and, more specifically, the occurrence of cardiac damage following PT. To test this hypothesis, we subdivided the patients into two groups based on their cardiovascular risk profile: low risk (SCORE2 <7.5%) and high risk (SCORE2 >7.5 %), and compared the clinical outcomes and cardiac damage between these groups.

In the high-risk PT patients’ group, 34.8% were non-survivors, while only 6.1% died in the low-risk group. Beyond the overall impaired outcome, the occurrence of TTE-detected changes in cardiac function was also shown in the high-risk group of patients. A higher incidence of wall movement disorders (13% vs. 3%), relaxation disorders (13% vs. 0%), as well as diastolic dysfunction (13% vs. 3.0%) was observed in this group compared to the low-risk group. In general, the proportion of patients with arrhythmias was high in both groups—approximately 40% (Table 4).

Table 4.

Comparison of outcomes and functional cardiac parameters among high- and low-cardiac risk groups of polytrauma patients

Demography and clinical findings	High-risk group (SCORE2 >7.5%) n = 23	Low-risk group (SCORE2 <7.5%) n = 33
Sex (female:male)	5:18	9:24
Age	71.5 ± 10 years	41.5 ± 14.5 years
Chest trauma	60%	63.63%
Sternal fracture	8.7%	12.1%
Contusion cordis	8.7%	6.1%
Nonsurvival	34.8%	6.1%
Wall movement disorder 24 hours (48 hours)	13.0% (21.7 %)	3.0% (6.1%)
Right ventricular dysfunction 24 hours (48 hours)	4.3% (0 %)	6.1 % (6.1%)
Relaxation disorder 24 hours (48 hours)	13.0% (17.4 %)	0% (3.0%)
Diastolic dysfunction 24 hours (48 hours)	13.0% (13.0 %)	3.0% (6.1%)
Pericardial effusion 24 hours (48 hours)	4.3% (4.3 %)	9.1% (9.1%)
Pleural effusion 24 hours (48 hours)	8.7% (8.7 %)	15.2% (21.2%)
Chest tube 24 hours (48 hours)	8.7% (8.7 %)	3.0% (3.0%)
Arrhythmia	39.1%	42.4%
Acute ischemia in ECG	8. 7%	27.3%

ECG, electrocardiogram; SCORE, Systematic Coronary Risk Evaluation.

To assess post-traumatic cardiac damage in more detail, we compared serum levels of cardiac damage biomarkers among both groups over a 10-day period. There was no significant difference in TnT levels between the two groups (Fig. 2A). Nevertheless, a consistent trend toward higher concentrations was observed in the high-risk group. CK levels were significantly elevated in the low-risk group between 24 and 96 hours post-trauma (Fig. 2B), and CK-MB levels were significantly higher at 48 hours in this group (Fig. 2C). Patients in the high-risk group exhibited significantly higher NT-proBNP levels both at ER admission and at 24 hours post-trauma as compared with the low-risk group (Fig. 1E). Interleukin-6 (IL-6), a pro-inflammatory cytokine and marker of systemic inflammatory response, was also quantified in both groups; however, no significant difference was found (Fig. 2D).

Fig. 2.

Serum levels of cardiac damage, heart failure, and inflammation biomarkers in high-risk (SCORE2 >7.5 %) and low-risk (SCORE2 <7.5) groups of polytrauma patients. A, Concentrations of cardiac damage maker troponin T in the high-risk (SCORE2 >7.5%, n = 23) and low-risk (SCORE2 <7.5%, n = 33) groups at the emergency room (ER), 24, 48, 72, 96 hours, and 10 days after trauma. B, Creatine kinase (CK) concentrations measured via ELISA in both trauma patient groups. C, Concentrations of the muscle-brain (MB) creatine kinase isoenzyme (CK-MB) in the two groups of PT patients. D, Concentrations of the pro-inflammatory cytokine IL-6 are not altered between the risk groups. E, The heart failure marker NT-proBNP is significantly increased in patients with high cardiovascular risk at the ER and 24 hours after trauma. *P ≤ 0.05; **P ≤ 0.01, ****P ≤ 0.0001. CK-MB, creatine kinase MB; ELISA, enzyme-linked immunosorbent assay; ER, emergency room; NT-proBNP, N-terminal pro-B-type natriuretic peptide; PT, polytrauma; SCORE, Systematic Coronary Risk Evaluation.

To further investigate the potential influence of pre-traumatic cardiovascular risk on post-traumatic cardiac function, we assessed the ventricular performance using a combination of circulating biomarkers and echocardiographic parameters and compared the data among both groups (Fig. 3). No significant differences were observed in the levels of FGF-23, a proposed marker of right ventricular dysfunction (Fig. 3A) among both groups of patients. Similarly, TAPSE remained similar at both 24 hours (Fig. 3B) and 48 hours post-trauma time points (Fig. 3C), when comparing the high-risk and the low-risk groups. Left ventricular function, evaluated via EF at 24 and 48 hours following trauma, demonstrated a trend toward reduction in the high-risk group; however, these differences did not reach statistical significance. At 48 hours post-trauma, LVEDD—an indicator of ventricular remodeling—was significantly elevated in the high-risk group, suggesting a modest degree of left ventricular dilatation in these patients (Fig. 3H).

Fig. 3.

Evaluation of cardiac function in high- and low-risk groups of polytrauma patients. Right ventricular function: A, Serum levels of fibroblast growth factor 23 (FGF-23) as a marker of right ventricular dysfunction are not altered between the high cardiovascular risk and the low-risk groups. Tricuspid annular plane systolic excursion (TAPSE) at day 1 (B) and day 2 (C) is not altered in high-risk versus low-risk polytrauma patients. Left ventricular function: Ejection fraction (EF, in %) was compared between both groups at day 1 (D) and day 2 (E), and a slight decrease was found in the high cardiovascular risk group. Left ventricular end-diastolic diameter (LVEDD) at day 1 (F) and day 2 (H) was significantly increased in the low-risk group. *P ≤ 0.05. EF, ejection fraction.

To determine whether the observed differences could be attributed to the differences in damage severity between subgroups, we assessed it with several established trauma scoring systems. Initially, the ASA physical status classification was applied to evaluate patients’ pre-trauma physical conditions and perioperative risk. No significant differences were detected between the high- and low-cardiovascular risk groups (Fig. 4A). Similarly, trauma-specific scores, including the Abbreviated Injury Scale for the chest (Fig. 4B) and the Organ Injury Scale (Fig. 3C), revealed no statistically significant differences between both groups. Overall injury severity, assessed via ISS, was comparable between the groups (Fig. 4D). Finally, the levels of Lp(a)—a genetic cardiovascular risk factor—were elevated in the high-risk group, as shown in Figure 4E.

Fig. 4.

The trauma burden is comparable in high- and low- cardiovascular risk groups of polytrauma patients. A, The American Society of Anesthesiologists (ASA) physical status classification showed no significant differences between groups, indicating comparable preoperative physical status and perioperative risk. B, The Abbreviated Injury Scale (AIS) for thoracic injuries did not differ significantly between the high-risk and low-risk groups. C, Similarly, the Organ Injury Scale (OIS) revealed no intergroup differences. D, The Injury Severity Score (ISS) was also comparable between both groups. E, A trend toward elevated Lipoprotein A (Lp(a)) levels was observed in patients with a high cardiovascular risk, although this did not reach statistical significance.

Effect of chest trauma on post-traumatic cardiac dysfunction and clinical outcome in high-risk group of patients

In the final part of the analysis, the high-risk group (SCORE2 >7.5%) was subdivided based on the presence (+TXT) or absence (–TXT) of chest trauma to assess whether chest trauma increases the risk of cardiac dysfunction and contributes to worse outcomes. Overall nonsurvival was higher in patients without chest trauma (−TXT group), which may be strongly influenced by the fact that 30% of these patients had a history of MI. Notably, diastolic dysfunction (23.1% vs. 0%) and relaxation disorder (30.8% vs. 0%) 48 hours post-trauma were also observed only in this group. As expected, chest tube insertion was only necessary for patients with chest trauma. Finally, the incidence of arrhythmia was notably higher in the TXT+ group, affecting 46.2% of patients, compared with 30% in the group without chest trauma (Table 5). Results can be compared with patients with low cardiac risk presented in Figure S1, http://links.lww.com/SHK/C873 and Table S1, http://links.lww.com/SHK/C874.

Table 5.

Comparison of outcomes and functional cardiac parameters among high cardiac risk patients with (+TXT) and without (−TXT) chest trauma

Demography and clinical findings	+TXT group (n = 13)	−TXT group (n = 10)
Sex (female:male)	1:12	4:6
Age	67.8 ± 9.4 years	77.1 ± 8.1 years
Contusion cordis	7.7%	10%
Angina pectoris within the last 4 weeks	7.7%	10%
Acute myocardial infarction	7.7%	30%
Nonsurvival (with previous myocardial infarction)	23.1% (-)	50% (30%)
Wall movement disorder 24 hours (48 hours)	15.4% (15.4%)	10% (20%)
Right ventricular dysfunction 24 hours (48 hours)	0% (0%)	10% (0%)
Relaxation disorder 24 hours (48 hours)	15.4% (30.8%)	10% (0%)
Diastolic dysfunction 24 hours (48 hours)	15.4% (23.1%)	10% (0%)
Pericardial effusion 24 hours (48 hours)	7.7% (7.7%)	0% (0%)
Pleural effusion 24 hours (48 hours)	7.7% (15.4%)	10% (0%)
Chest tube 24 hours (48 hours)	15.4% (15.4%)	0% (0%)
Arrhythmia (in the overall stay in the hospital)	46.2%	30%
Acute ischemia in ECG	7.7%	10%

ECG, electrocardiogram.

We also evaluated systemic biomarkers of cardiac damage in high-risk patients stratified by the presence or absence of thoracic trauma. The concentrations of cardiac TnT showed no statistically significant differences between the +TXT and −TXT subgroups; however, the levels trended to be consistently higher in the −TXT group across all time points (Fig. 5A). In contrast, CK levels were significantly elevated in the TXT group at 48 hours post-trauma (Fig. 5B), while CK-MB was significantly increased at 24 hours in the same subgroup (Fig. 5C). Serum concentrations of IL-6 remained comparable over time between the two groups (Fig. 5D). Interestingly, NT-proBNP levels were significantly higher in the −TXT patients at admission (ER), as well as at 24 and 48 hours post-trauma (Fig. 5E).

Fig. 5.

Serum levels of cardiac damage, heart failure, and inflammation biomarkers in high cardiovascular risk patients (SCORE2 > 7.5%) with (+TXT) and without (–TXT) thoracic trauma. A, Temporal profile of cardiac troponin T concentrations in patients with (+TXT, n = 13) and without (−TXT, n = 10) chest trauma. B, Serum levels of creatine kinase (CK), quantified via ELISA, did not differ significantly between the two subgroups. C, Creatine kinase-MB (CK-MB) isoenzyme levels in +TXT and −TXT groups. D, Concentrations of interleukin-6 (IL-6), a key pro-inflammatory cytokine, showed no statistically significant differences between the groups. E, The levels of N-terminal pro-B-type natriuretic peptide (NT-proBNP), a marker of heart failure, were significantly elevated in patients without thoracic trauma. *P ≤ 0.05; **P ≤ 0.01; ***P ≤ 0.001. ELISA, enzyme-linked immunosorbent assay.

To determine whether thoracic trauma exacerbates the risk of cardiac dysfunction following PT, we assessed right and left ventricular functions in +TXT and −TXT groups. Plasma concentrations of FGF-23 were elevated in the +TXT group; however, this difference did not reach statistical significance (Fig. 6A). TAPSE showed no significant alteration between the groups (Fig. 6, B and C). sPAP, a surrogate marker for right ventricular afterload/pulmonary hypertension, was assessed at 24 and 48 hours post-injury, and the values were comparable between the groups. sPAP values at 48 hours exceeded the upper limit of the normal physiological range (17–25 mmHg) in both groups (data not shown, because of low sample size). EF was not affected by the presence or absence of chest trauma (Fig. 6, D and E). Similarly, LVEDD remained within the normal range and showed no significant intergroup differences (Fig. 6, F and G). Results can be compared with patients with low cardiac risk presented in Figure S2, http://links.lww.com/SHK/C875.

Fig. 6.

Assessment of cardiac function by transthoracic echocardiography (TTE) in high cardiovascular risk patients (SCORE2 >7.5%) with (+TXT, n = 13) and without (−TXT, n = 10) thoracic trauma. Right ventricular function assessment (A–C): A, Systemic levels of fibroblast growth factor 23 (FGF-23), a biomarker of right ventricular dysfunction, were not significantly different between the +TXT and −TXT groups. Tricuspid annular plane systolic excursion (TAPSE), assessed on days 1 (B) and 2 (C) post-trauma, remained unaltered regardless of thoracic trauma status. Left ventricular function assessment (D–G): Ejection fraction (EF, %) measured on days 1 (D) and 2 (E) post-trauma did not differ between the +TXT and −TXT subgroups. Left ventricular end-diastolic diameter (LVEDD), evaluated as an indicator of ventricular remodeling, also showed no significant differences at day 1 (F) or 2 (G) between the two groups.

Finally, the general physical status of patients assessed by the ASA did not differ between both groups (Fig. 7A). As expected, Abbreviated Injury Scale for the chest (Fig. 7B) and Organ Injury Scale (Fig. 7C) were significantly higher in the group of patients with chest trauma. The CVD genetic risk factor Lp(a) showed no substantial difference between +TXT and −TXT groups (Fig. 7D). Similarly, the presence of thoracic trauma did not affect overall injury severity (Fig. 7E). Results can be compared with patients withlow cardiac risk presented in Figure S3, http://links.lww.com/SHK/C876.

Fig. 7.

Comparison of trauma severity and Lp(a) concentrations in high-risk polytrauma patients (SCORE2 > 7.5%) with (+TXT, n = 13) and without (−TXT, n = 10) thoracic trauma. A, The American Society of Anesthesiologists (ASA) physical status score showed no significant difference between the groups, indicating comparable baseline physical health and perioperative risk. The Abbreviated Injury Scale (AIS) for thoracic injuries (B) and the Organ Injury Scale (OIS) (C) were both significantly higher in the +TXT group due to the presence of chest trauma. Lipoprotein(a) [Lp(a)] concentrations (D) and Injury Severity Score (ISS) (E) were similar across both groups, suggesting a comparable systemic injury burden and genetic cardiovascular risk profile.***P ≤ 0.001; ****P ≤ 0.0001.

DISCUSSION

This study evaluated cardiovascular risk in PT patients, hypothesizing that higher risk correlates with increased susceptibility to cardiac damage and poorer outcomes. We applied the SCORE2 algorithm to estimate 10-year risk based on age, smoking, blood pressure, total cholesterol, and HDL (12). Because cardiac comorbidities in PT patients may have an endogenous, hereditary origin as well, we assessed the levels of Lp(a)—a biomarker well established in cardiovascular research but not commonly used in PT studies. Given that plasma Lp(a) concentration is mostly (90%) genetically determined (18), and that lifestyle (diet and physical activity) has little to no influence on its level (18,19), its inclusion could allow assessment of inherited cardiovascular risk factors in our patient population. Our data showed that none of the individuals in the present cohort exhibited Lp(a) levels within or above the high-risk range (30–50 mg/dL), suggesting that this specific cardiovascular risk factor was likely not a major contributor in our trauma patients’ population.

Our data showed that there is a positive correlation between SCORE2 and cardiac damage markers NT-proBNP levels, and a negative correlation of SCORE2 with CK-MB. The association between SCORE2 and NT-proBNP, seen also in our previous study (14), supports our hypothesis that patients with a higher cardiovascular risk profile are more susceptible to post-traumatic cardiac damage. In accordance with our findings, NT-proBNP and cardiac risk assessed via a simple scoring system (American University of Beirut cardiovascular risk index) were used in the literature to predict postoperative morbidity after noncardiac surgery and showed comparable predictive values (20).

To further clarify the influence of cardiovascular risk on post-traumatic cardiac damage, we divided patients into high- and low-risk groups based on their SCORE2 values and compared the extent of cardiac damage between them. The 7.5% threshold for SCORE2 was chosen as a cutoff point between both groups based on European Society of Cardiology guidelines (21). We found that patients in the high-risk group suffer stronger cardiac damage as indicated by higher NT-proBNP levels both at admission and 24 hours post-trauma. NT-proBNP is a well-standardized marker of heart failure (22) and is described in the literature as a potential marker of post-traumatic cardiac impairment, as it correlates with cardiac index and is associated with multiorgan dysfunction after PT (23). Serum NT-proBNP has also been described to help for predicting mortality in patients with major trauma (24). Notably, the acute and gold-standard cardiac damage marker TnT was only by trend increased in the high-risk group. In contrast, CK and CK-MB levels were significantly higher in patients with a low SCORE2 risk, which may be explained by the low specificity of these markers and the influence of muscle damage on their release. In addition, we measured FGF-23, a biomarker recently associated with right ventricular dysfunction in pulmonary hypertension, where elevated levels correlate with increased right ventricular diameter and reduced TAPSE (17). In our study, FGF-23 levels were elevated in “cardiac” high-risk trauma patients, though not significantly.

Next to cardiac damage markers, we further analyzed functional cardiac damage in both groups of patients by means of TTE. In the high-risk PT patients, we observed a higher ratio of patients exhibiting wall movement disorders, relaxation disorders, and diastolic dysfunction. Similar to our previous study (14), we found a significant association between elevated SCORE2 values and impaired myocardial relaxation. This is consistent with the CVD literature, which describes a strong correlation between SCORE2 and cardiac functional changes such as left ventricular hypertrophy, diastolic dysfunction, and increased left atrial volume (25). Overall, these findings confirm the prognostic relevance of the SCORE2 risk stratification tool in the PT setting.

As chest trauma is a well-known cause of blunt cardiac injury and is responsible for up to 25% of trauma-related deaths, we also analyzed its effect on post-traumatic cardiac damage in the high-risk group (SCORE2 >7.5%) (15). Supporting this, patients with thoracic trauma showed higher rates of diastolic dysfunction and impaired relaxation 48 hours after trauma. Surprisingly, we found that the mortality rate was higher in the group of patients without chest trauma, which could be explained by a higher ratio (30% vs. 7.7%) of patients with a history of prior MI in this group. It is well established that patients with a recent MI before surgery have a significantly increased risk of major adverse cardiac events and all-cause mortality within the first postoperative year (26). These findings indicate that prior MI may be a more pertinent determinant of post-traumatic cardiac dysfunction than the presence of thoracic trauma itself.

Based on these important findings, several recommendations can be proposed. First, calculating SCORE2 in the emergency department may help physicians identify patients at increased risk for post-traumatic cardiac complications, thereby prompting earlier, focused diagnostic evaluation-such as cardiac MRI or serial ECG monitoring. In general, scoring systems always played a decisive role in PT and can be used to increase the quality of care (27). Second, existing PT guidelines could be updated to recommend additional TTE in patients with elevated SCORE2 values. Currently, the S3 PT guidelines advise the following diagnostic algorithm of traumatic cardiac damage: measurements of systemic levels of cardiac damage markers (like troponin), performing a three-channel ECG, and, only when there are clinically suspicious findings, the conduction of TTE (28–30). However, given the observed association between elevated cardiovascular risk and myocardial dysfunction, it may be necessary to reconsider whether an abnormal cardiologic risk score alone should prompt at least one or serial cardiac TTE assessments. Early identification of “at-risk” patients could facilitate the timely use of the full range of diagnostic tools and potentially improve clinical outcomes.

This study has several limitations. One of them is the inability to definitively determine whether the observed cardiac functional impairments are solely trauma-related or partially reflect pre-existing CVD. Another limitation is the fact that we do not know whether the observed functional changes after trauma are transient or long-lasting. To further evaluate the long-term trajectory of cardiac function, the follow-up examinations and interviews with this cohort of trauma patients are planned. Finally, age represents an important potential confounder in the present analysis. Age is an integral component of the SCORE2 algorithm and therefore differs substantially between the low- and high-risk groups. At the same time, age itself is a well-established independent predictor of mortality following PT. Consequently, part of the observed association between higher SCORE2 risk categories and adverse outcomes may be attributable to age-related effects rather than cardiovascular risk alone. In addition, 36.3% of nonsurvivors sustained severe TBI. In these cases, treatment limitations were implemented after discussion with the patients’ relatives, based on the poor neurological prognosis, the presumed wishes of the patient, and advanced age. This may have further influenced mortality outcomes and should be considered when interpreting the results.

CONCLUSION

Cardiovascular risk, as assessed by the SCORE2 algorithm, demonstrated a significant association with cardiac damage biomarkers, echocardiographic abnormalities, and mortality in PT patients. The presence of thoracic trauma did not further increase the risk of cardiac damage, whereas a history of MI was associated with increased mortality among high-risk (SCORE2 >7.5%) PT patients. These findings highlight the potential prognostic value of incorporating cardiovascular risk assessment into the early evaluation of trauma patients. For the trauma context, it might be promising to develop a modified risk Score, which should include the presence of previous MI.

Supplementary Material

shk-66-079-s001.pdf ^{(326.1KB, pdf)}

shk-66-079-s002.pdf ^{(114.9KB, pdf)}

shk-66-079-s003.pdf ^{(296.6KB, pdf)}

shk-66-079-s004.pdf ^{(278.5KB, pdf)}