Asian Cardiovasc Thorac Ann 2008;16:e30-e31
© 2008 Asia Publishing EXchange Ltd
Reversal of Myocardial Dysfunction Due to Brain Injury
Jens Wippermann, MD,
Gerardus Bennink, PhD,
Thorsten Wittwer, MD,
Navid Madershahian, MD,
Christian Ortmann, MD1,
Thorsten Wahlers, PhD
Cardiothoracic Surgery, University Hospital Cologne
1 Institute of Forensic Medicine, University Hospital Jena, Germany
For reprint information contact: Jens Wippermann, MD Tel: 49 221 478 3707 Fax: 49 221 478 4186 Email: jens.wippermann{at}uk-koeln.de, Department of Cardiothoracic Surgery, University Hospital Cologne, Kerpener Str. 62, 50937 Cologne, Germany.
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ABSTRACT
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Severe myocardial dysfunction after blunt head injury is a rare but potentially lethal complication. We describe remarkable myocardial recovery after severe hemodynamic deterioration in a young man with brain injury, due to extracorporeal membrane oxygenation support. Because of the severity of brain damage, the patient succumbed after diagnosis of brain death. Postmortem histopathological examination of the heart showed severe myocardial necrosis.
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INTRODUCTION
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Cardiac injury may occur after many types of brain injury. Electrocardiographic changes and arrhythmias, such as torsade de pointes, have been described in patients with neurological injury.1 Left ventricular systolic dysfunction occurs in 10% of patients with subarachnoid hemorrhage.2 Elevation of serum cardiac troponin I and pathological evidence of contraction band necrosis in heart autopsies provide evidence of the development of myocardial necrosis in brain-injured patients.3,4 We describe actions to overcome the life-threatening situation caused by severe neurogenic cardiac injury.
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CASE REPORT
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A 39-year-old man was referred to our hospital after a road traffic accident. Computed tomography revealed extensive brain swelling, and emergency decompression by right temporal craniotomy was performed (Figure 1
). Twelve hours later, electrocardiographic changes revealed anterior myocardial ischemia with elevated cardiac enzymes. Cardiac troponin I increased to 2.3 ng · mL–1, and transesophageal echocardiography showed stunned left ventricle with an ejection fraction < 10%. This desperate hemodynamic situation was initially treated with inotropic support and insertion of an intraaortic balloon pump via the left femoral artery. Further deterioration could not be halted, and subsequently, a decision was made to support the patient with extracorporeal membrane oxygenation (ECMO). Institution of ECMO was started with a heparin-coated system and cannulas in the groin vessels. Being aware of the bleeding diatheses that can develop with ECMO, anticoagulation was monitored, with an activated clotting time of 130 sec. During 48 hours of ECMO support, improved left ventricular function was demonstrated, with better global contraction and increased ejection fraction of 50%. Unfortunately, on the 4th postoperative day, dilated non-responding pupils indicated brain death of the patient, which was confirmed by a neurologist. Postmortem histopathological specimens obtained from several areas of the heart showed severe ubiquitous coagulation and frequent contraction band necrosis of disseminated single and grouped cardiomyocytes. The inner and middle part of the cardiac wall was especially affected. Myocytes with contraction band necrosis showed hypercontracted eosinophilic cytoplasm, fragmentation into irregular transverse acidophilic bands, or a more diffuse granular appearance. All of these stages were positive for immunohistochemical detection of the terminal complement complex C5b-9 (Figure 2). The blood vessels showed no alterations.
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Figure 2. Immunohistochemical visualization of the terminal complement complex C5b-9 exhibiting cardiomyocytes with contraction band necrosis and coagulation necrosis (original magnification x100).
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DISCUSSION
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Cardiac injury and dysfunction after brain damage is a recognized but rare phenomenon. The most widely investigated form of neurocardiogenic injury is subarachnoid hemorrhage.2 The pathophysiology of cardiac injury after subarachnoid hemorrhage remains controversial. Historically, coronary artery disease and coronary vasospasm were proposed as possible mechanisms. However, some patients have electrocardiographic and echocardiographic findings suggestive of myocardial infarction, without angiographic evidence of coronary disease or vasospasm.2 It is well recognized that high sympathetic tone and elevated circulating levels of catecholamines can occur after traumatic head injury. However, animal models indicate that direct release of toxic levels of catecholamines into the myocardium by cardiac sympathetic nerve terminals is more likely to be the cause of neurocardiogenic injury than adrenal release of catecholamines into the systemic circulation.5
In our case, the initial clinical presentation after craniectomy was unclear. We did not suspect severe myocardial necrosis at that stage, but considered impeded coronary perfusion due to a ruptured vessel, dissection or hematoma. Because there was severe hemodynamic instability and deterioration, coronary angiography was abandoned. Extracorporeal membrane oxygenation was instituted as lifesaving therapy before awareness of the severity and outcome of the neurologic injury. In these circumstances, echocardiography can be helpful to clarify dysfunction of the heart in the presence of elevated cardiac enzymes. Catheter intervention with the aim of revascularizing the heart should be mentioned as an alternative option. However, as in this case of global hypokinesia and stunned left ventricle, pinpointing an isolated coronary stenosis as the culprit lesion is highly unlikely. In young patients with globally deteriorating heart function, which can be demonstrated by echocardiography, left heart catheterization does not appear to be mandatory.
Cardiac injury after brain injury is said to be reversible up to 48 hours. Therefore, we believe that the entire armamentarium of supportive strategies is justified to stabilize a deteriorating hemodynamic situation. Although the outcome of brain death was unfortunate in this young patient, it is important to stress the recovery potential of the myocardium, even in hearts with severe damage and necrotic areas.
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REFERENCES
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ABSTRACT
INTRODUCTION
