The present study indicates that the duration of hypotension during ED resuscitation period is independently associated with the incidence of myocardial injury in patients with severe trauma. In addition, the duration of hypotension is independently associated with MACE and in-hospital mortality.
In the non-cardiac surgery setting, several large observational cohort studies already reported an association between hypotension and myocardial injury. Van Waes and colleagues analyzed a cohort of 890 prospective vascular surgery patients and found out that a decrease of 40% from preoperatively measured mean arterial blood pressure was associated with postoperative myocardial injury when the duration of hypotension was longer than 30 min (relative risk = 1.8 with a 99% confidence interval of 1.2–2.6) . A large retrospective analysis of more than 53,000 non-cardiac surgery patients supports these findings and showed that mean arterial pressure < 65 mmHg was significantly related to both myocardial and acute kidney injury . A further study by Abbott and coworkers investigated the relationship between intraoperative heart rate and systolic blood pressure with myocardial injury [15, 16]. This secondary analysis of the VISION study revealed that low blood pressure defined as systolic blood pressure < 100 mmHg with a co-existing elevated heart rate > 100 beats per minute was more strongly associated with myocardial injury compared with decreased systolic blood pressure < 100 mmHg alone (OR 1.42 [95% CI 1.15–1.76] versus OR 1.20 [95% CI 1.03–1.40]) .
The existing evidence in this context resulted in a consensus statement on intraoperative blood pressure for elective surgery  which summarizes that during adult non-cardiac surgery, decreased systolic arterial pressure < 100 mmHg and MAP < 60–70 mmHg may be associated with organ injury, e.g. myocardial injury.
We performed multiple sensitivity analyses to better characterize the association between hypotension and myocardial injury. Hypotension, defined by the duration of MAP < 65 mmHg was always associated with myocardial injury (either at presentation or based on peak hsTnT within 72 h after trauma). However, regarding systolic blood pressure with a cutoff < 90 mmHg, only the absolute duration of hypotension was associated with myocardial injury at presentation. All other sensitivity analyses for Sys < 90 mmHg showed no significant association. This could be explained by various reasons. In terms of the analyses using peak hsTnT as endpoint, there was a relevant selection bias in the measurement of follow-up troponins. In addition, it may be possible that the measurement of systolic blood pressure was more inaccurate than the measurement of MAP in this cohort. In the future, it should be investigated whether this discrepancy between MAP and systolic blood pressure can be reproduced.
With regard to hypotension and outcome, patients with severe trauma represent a special cohort because guidelines advocate permissive hypotension for bleeding control before surgical treatment is available. In severely injured patients with active bleeding, current guidelines recommend maintaining mean arterial pressure around 65 mmHg . In line with these recommendations, our findings suggest that protracted hypotension < 65 mmHg is associated with myocardial injury and other adverse events.
Next to hypotension, various other mechanisms of myocardial injury in severe trauma patients have been proposed. One frequently postulated pathomechanism is direct mechanical trauma, causing cardiac contusion or “bruising” with consecutive cell death [18, 19]. However, recent studies indicated that troponin is also elevated in patients without blunt cardiac chest trauma. Edouard et al. investigated 17 trauma patients without chest trauma and could reveal significantly increased troponin levels in this cohort . In several experimental trauma models, myocardial injury followed ischemia–reperfusion injury, inflammation and hemorrhagic shock [21,22,23] and it was interpreted to result from physiological stress. Martin et al. retrospectively investigated 1081 trauma patients admitted to the ICU. Severe chest trauma (defined as AIS ≥ 3) was not independently associated with increased troponin levels, and the authors concluded physiological stress played an essential role in the pathogenesis of myocardial injury in severe trauma patients . Moreover, they identified that hypotension was more common in the group with high troponin levels, however, without quantifying the strength of the association or its independence.
The finding of the association between hypotension and in-hospital mortality in the present study is in line with previous data from a large cohort. Kim et al. retrospectively investigated 17,406 patients and could show that hypotension was associated with increased mortality in patients with trauma .
Strengths and limitations
A strength of this study is that we investigated a broad cohort of patients with severe trauma. Especially, we included all types of injuries taking into account mechanisms of troponin release other than chest trauma. Second, although we performed a retrospective analysis, our data are based on a prospectively constituted database which ensures high data quality. This is also applicable for blood pressure values which were recorded permanently and automatically. On the other hand, our broad inclusion criteria could also be seen as a limitation as the cohort of patients in whom permissive hypotension is recommended is narrow. Due to the retrospective nature of the study, it is not possible for us to comprehend which patients really received permissive hypotension with the aim to control bleeding and which patients were hypotensive because of other reasons, e.g. induction of anesthesia.
There are further limitations to the present study: we could only analyze blood pressure values in the resuscitation room as pre-hospital documentation was not available. Thus, blood pressure and troponin measurements were performed simultaneously and hypotension in the course of resuscitation period may have been influenced by events and/or interventions after hsTnT measurement. However, there were several considerations serving as a basis for the decision to choose initial hsTnT as the primary endpoint of this analysis: first, in contrast to follow-up troponin measurements, baseline troponin data were almost complete and as troponin is measured routinely in our resuscitation room, data could be regarded as representative without any selection bias. Second, our decision was based on the assumption that patients with a longer period of hypotension during resuscitation period may also have had hypotension before entering the hospital. Third, we analyzed relevant secondary endpoints that occurred after resuscitation period (MACE and mortality) that were also independently associated with hypotension which emphasizes our findings. Finally, we performed additional analyses using peak hsTnT values as endpoint. Although selection bias might be present, these data help to understand our results. It is important to mention that we conducted a retrospective study. However, most patient characteristics correspond to the current literature so that our cohort may be regarded as representative.