This study has demonstrated that the identification of arterial calcification on admission CT scans of injured patients is possible. Calcification was common, and around three-quarters of trauma patients over the age of 45 years displayed evidence of atherosclerotic cardiovascular disease. The presence of arterial calcium was associated with a tendency towards lower survival, although an increase in the distribution and severity of arterial calcification was not generally associated with in-hospital mortality following injury.
Establishing the prevalence of cardiovascular disease in trauma was previously limited by difficulties in identifying asymptomatic individuals. In the general population, multiple studies have demonstrated an association between high coronary artery calcium scores (CACS) with an increased risk of adverse cardiac events, both in symptomatic and subclinical heart disease [13–17]. CACS is predictive of all-cause mortality in patients with heart disease [18, 19], and provide cardiac screening assessments in other conditions including HIV [20] and aortic aneurysms [21]. Calcification of the abdominal aorta may be an independent predictor of cardiovascular events [22], whilst calcium in the thoracic aorta, carotids and iliac arteries on CT has been associated with increased long term mortality in healthy subjects [11]. Arterial calcification on CT is therefore likely to represents a suitable marker of cardiovascular disease in trauma patients.
Isolated levels of CAC were not generally predictive of survival and only patients with severe CACS had higher death rates. Some previous studies have shown an association between cardiac co-morbidities with poor outcome following trauma [1–3]. Given the incidence of cardiovascular disease within the study cohort, the lack of significance of association of coronary calcification with mortality was unexpected. Previous studies, however, have examined injured patients with symptomatic heart disease whereas our study population also included asymptomatic subjects. This might suggest it is only symptomatic heart disease which leads to poorer outcome in trauma.
In contrast, an independent association of SMA calcium with mortality was demonstrated. CIA calcification also showed a tendency towards increased mortality. CIA was the most frequently calcified vessel, however, and may simply be a marker of advanced systemic calcification. This has been suggested in research in non-trauma patients and an association between CIA calcium and long-term mortality has been revealed in healthy subjects [11]. Conversely, SMA calcification was rare, perhaps suggesting SMA disease is more discriminatory than that of the CIA, and that the location of calcification is related to outcome.
The relationship between arterial calcification and all-cause mortality as opposed to cardiovascular mortality is not understood. An association with higher levels of inflammatory mediators leading to a chronic inflammatory state has been suggested [23] whilst atherosclerosis may be linked with reduced innate and acquired immune function [24]. Mesenteric ischaemic reperfusion injury is known to play a role in the development of the systemic inflammatory response syndrome (SIRS) [25] and the number of SIRS variables present on admission predicts mortality in trauma [26]. It is possible that SMA atherosclerosis increases the ischaemia-reperfusion injury from the GI tract after trauma leading to increased incidence or severity of organ dysfunction. To this end, arterial stiffness is known to lead to end organ damage and poorer outcomes [27]. Research has revealed markers indicative of arterial stiffness (including central pulse pressure and carotid-femoral pulse wave velocity) have a positive association with both thoracic and aortic calcification [28]. Consequently, this detrimental relationship between adverse arterial haemodynamics, atherosclerosis and end organ perfusion may be a factor in the underlying pathophysiology of our findings. Nevertheless, the role of mesenteric atherosclerosis and arterial stiffness in post-traumatic inflammation and organ dysfunction require further study, including the use of echocardiography to examine whether left ventricular changes resulting from adverse arterial haemodynamics are seen in patients with increased SMA calcification.
This study is subject to limitations. Firstly, its retrospective nature may have led to inaccurate documentation of patient characteristics and outcomes, and restricted the availability of wide datasets and clinical features. In particular, a smoking history was not possible to ascertain, in spite of the potential significance of this information. Conclusions were derived from the presence of absence of calcium, or score estimates, but not objectively calculated values. Although it was an aim of this study to determine whether calcium score assessments could be made and applied, it means that the findings can only be generalised. However, formal calcium scoring of non-cardiac CTs is not possible, and so it would have been unfeasible to objectively measure calcium scores in this study. Our analyses were also limited to a single centre and may have been underpowered given few numbers in certain sub-groups. Finally, evidence on the prognostic value of arterial calcification on mortality has often followed up patients over many years. It would be valuable in future studies, therefore, to analyse whether arterial calcification is more predictive of the higher longer-term death rates seen in trauma patients.