Original Contribution
Ischemic-appearing electrocardiographic changes predict myocardial injury in patients with intracerebral hemorrhage,☆☆,

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Abstract

Objectives

Myocardial injury is common among patients with intracerebral hemorrhage (ICH). However, it is challenging for emergency physicians to recognize acute myocardial injury in this population, as electrocardiographic (ECG) abnormalities are common in this setting. Our objective is to examine whether ischemic-appearing ECG changes predict subsequent myocardial injury in the context of ICH.

Methods

Consecutive patients with primary ICH presenting to a single academic center were prospectively enrolled. Electrocardiograms were retrospectively reviewed by 3 independent readers. Anatomical areas of ischemia were defined as I and aVL; II, III, and aVF; V1 to V4; and V5 and V6. Medical record review identified myocardial injury, defined as troponin I or T elevation (cutoff 1.5 and 0.1 ng/mL, respectively), within 30 days.

Results

Between 1998 and 2004, 218 patients presented directly to our emergency department and did not have a do-not-resuscitate/do-not-intubate order; arrival ECGs and troponin levels were available for 206 patients. Ischemic-appearing changes were noted in 41% of patients, and myocardial injury was noted in 12% of patients. Ischemic-appearing changes were more common in patients with subsequent injury (64% vs 37%; P = .02). After multivariable analysis controlling for age and cardiac risk factors, ischemic-appearing ECG changes independently predicted myocardial injury (odds ratio, 3.2; 95% confidence interval, 1.3-8.2). In an exploratory analysis, ischemic-appearing ECG changes in leads I and aVL as well as V5 and V6 were more specific for myocardial injury (P = .002 and P = .03, respectively).

Conclusion

In conclusion, although a range of ECG abnormalities can occur after ICH, the finding of ischemic-appearing changes in an anatomical distribution can help predict which patients are having true myocardial injury.

Introduction

Intracerebral hemorrhage (ICH) accounts for 4% to 15% of cases of acute stroke and is the most fatal form of this disease [1], [2], [3]. Although no specific therapy has been demonstrated to improve outcome, clinical practice commonly includes treatments aimed at minimizing damage from the hematoma, minimizing the risk of ongoing bleeding, and preventing complications of the disease [4]. That admission to a stroke unit provides benefit [5] and that less aggressive care leads to worse outcome [6] suggest that, at least, some treatments in current use improve outcome.

Many clinical trials, both past and ongoing, exclude patients with concomitant myocardial ischemia [7], [8], [9], [10], [11]. Hemostatic therapy in particular is associated with an increased risk of cardiac events, although it is notable that many ICH patients suffer such events anyway [8]. It can be challenging to recognize acute myocardial “injury” in patients with ICH as electrocardiographic (ECG) abnormalities are common in this setting, possibly reflecting neurocardiogenic influences [12], [13], [14], [15], [16], [17], [18], [19]. Indeed, the incidence of ischemic-appearing ECG changes in patients with ICH has been reported to be 14% to 35% [12], [13], [19], [20]. For an example see Fig. 1.

The question, then, is whether an abnormal ECG finding on presentation in a patient with ICH should be considered as representing true myocardial injury. The answer has implications for blood pressure management, use of hemostatic therapy, medications used for anticoagulation reversal, and extent of a cardiac workup performed during hospitalization. The current literature that pertains to ischemic-appearing ECG changes in patients with ICH is limited, mostly describing the prevalence of ECG abnormalities without addressing their value in diagnosing acute cardiac events [12], [13], [19], [20]. It has been suggested that neurocardiogenic influences characterized by increased sympathetic nervous system activity on the heart are responsible for the observed ECG changes after acute intracranial events including ICH [21], [22]. Alternatively, ICH and coronary artery disease have common risk factors, and myocardial injury could occur in patients with ICH because of progression of concomitant coexisting coronary artery disease.

We hypothesized that ECG abnormalities on presentation that meet criteria for myocardial ischemia and present in a coronary anatomical distribution predict myocardial injury in patients with ICH.

Section snippets

Study design

This was a retrospective review of data collected as part of a prospective cohort study of primary ICH outcome. Since 1994, consecutive patients with ICH presenting to Massachusetts General Hospital have been registered into a database and followed up prospectively [23], [24], [25]. Patients were identified by systematic review of emergency department (ED) logs; hospital discharge diagnoses; and lists of all admissions to the neurology, neurosurgery, and internal medicine services. Demographic

Results

There were 218 patients with primary ICH who presented initially to our ED and did not have a do-not-resuscitate order during the study period. Twelve patients were excluded for unavailable initial ECGs or unavailable troponin I or T, leaving a study population of 206 patients (94%). Troponin I or T levels were determined in 177 patients (86%) on ED arrival, 181 patients (88%) by day 1, and 191 patients (93%) by day 2. One hundred fifty patients (73%) received serial troponin I or T testing.

Discussion

Overall, we found that ischemic-appearing ECG changes on arrival were observed in 41% of patients with ICH and that such changes independently predict myocardial injury. Therefore, clinicians faced with such changes should not disregard these findings as nonspecific in the setting of ICH but, rather, consider such patients as having true myocardial injury.

The first account in the Western literature of an association between acute stroke and ECG changes appeared in 1947 [30]. Since then, many

Limitations

Our study has several limitations. The most important limitation to this study is its retrospective design. Care was not standardized across the cohort, and not all initial ECGs were available. In addition, serial cardiac enzymes were sent at the discretion of the clinical care team rather than in a controlled fashion. It is possible that some patients would have developed troponin elevations later in their course but that these went unmeasured, leading us to underestimate the frequency of

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  • Presentation information: Abstract presented at SAEM Annual Meeting, Chicago, IL, May 2007.

    ☆☆

    Conflicts of Interest Disclosure: Dr Joshua N. Goldstein has received consulting fees from CSL Behring.

    This study is funded by the National Institute of Neurological Disorders and Stroke (NIH K23NS059774).

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