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The ECG and the myocardium in subarachnoid haemorrhage

Dr. Timothy G Costello

St. Vincent's Hospital, Melbourne

Subarachnoid haemorrhage is frequently accompanied by significant cardiovascular abnormalities. These include in particular myocardial dysfunction and injury which in a high percentage of cases will manifest as a variety of ECG abnormalities 1 , some of which may be indistinguishable from those seen in association with an episode of severe myocardial ischaemia and/or infarction. When the neuroanaesthetist is presented with this clinical/electrocardiographic picture, it may pose a management dilemma in the preparation of these patients for surgery 2 . A particular clinical variety of myocardial dysfunction, that of Transient Left Ventricular Apical Ballooning (TLVAB) may present a further problem in clinical care 3 . This self limiting syndrome needs to be identified and distinguished from the more serious dysfunction resulting from associated atherosclerotic ischaemic heart disease as therapeutic approaches to the two entities may be very different. Recent clinical research by Zaroff et al 4 has highlighted a further distinct clinical group of patients who present with cardiac injury following an episode of SAH. He has identified two subgroups of patients who present with specific adrenoreceptor polymorphisms or genetic subtypes which will predispose these patients to the problems of reduced cardiac output (LVEF) and myocardial drainage (Troponin increase). The identification of these patients via genotyping may advance the understanding of management of their cardiac injury when presenting with SAH.
  1. Jain R, Deveikis J, Thompson B.G. Management of patients with stunned myocardium associated subarachnoid haemorrhage. Am. J. Neuroradiol. 2004;25:126-9
  2. Priebe HJ. Aneurysmal Subarachnoid Haemorrhage and the Anaesthetist, Br. J. Anaesth.(2007) 99 (1):102-18
  3. Hessell EA. The Brain and the Heart. Cardiovascular Anaesthesia 2206; 103 (3): 522 -6
  4. Zaroff JG et al. Adrenoreceptor Polymorphisms and the risk of Cardiac Injury and Dysfunction after Subarachnoid Hemorrhage. Stroke 2006; 37:1680 - 5
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