Myocardial damage in patients with SAH

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Myocardial damage in patients with SAH

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After SAH

• 27-100 patient ? EKG change
• 40 patient ? CK-MB cardiac Troponin I ?
• 10 patient ? lethal arrhythmia (ventricular
  tachycardia, ventricular fibrillation, torsades
  de pointes)
• 10 patient ? left ventricular (LV) wall motion
  abnormalities by cardiac echo a subset of these
  patients will have irreversible myocardial
  damage, but most regain LV function in several
  weeks

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History

• 1903, Cushing cardiac effects of intracranial
  hemorrhage (alterations in blood pressure and
  cardiac rhythm)
• 1947, Byer et al ECG changes in a patient with
  subarachnoid hemorrhage (SAH)
• 1954 cerebral T wave in patient with SAH

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EKG change after SAH

• large and inverted T waves ("cerebral T waves")
• prolonged QT intervals
• Marked QT prolongation, sometimes with deep, wide
  T-wave inversions, may occur with intracranial
  bleeds, particularly subarachnoid hemorrhage
  ("CVA T-wave" pattern)
• Others ST segment alterations, Q waves

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Prolonged QT intervals

• most common stroke-related EKG abnormality (in
  71 of patients with SAH )
• QT prolonged ?serious ventricular arrhythmias
  including sudden death torsade de pointes

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T wave abnormalities

• The suggestion that these abnormalities are
  neurally induced is supported by the observation
  that inverted T waves may normalize if brain
  death occurs.
• Furthermore, inverted or flat T waves have been
  reported in 55 percent of patients with
  subarachnoid hemorrhage, but autopsy studies of
  these patients have failed to reveal any
  underlying cardiac abnormality.

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Pathophysiology

• The pathophysiology of cardiac injury after SAH
  remains controversial.
• Coronary artery disease (CAD) and coronary
  vasospasm as possible mechanisms?
• 1. some SAH patients have ECG and
  echocardiographic findings ? no angiographic
  evidence of CAD or vasospasm
• 2. myocardial ischemia secondary to excessive
  tachycardia and/or hypertension

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• Catecholamine hypothesis?
• 1. A series of autopsy studies in patients with
  SAH (with/without EKG change) ? petechial
  subendocardial hemorrhage, and histologically,
  myocardial cell cytoplasm with dense eosinophilic
  transverse bands
• Similar lesion
• 1.patient with pheochromocytoma
  2.experimental animals with infusion of
  catecholamines and stimulation stellate ganglion

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• 2. Patterns of LV wall motion abnormalities in
  SAH patients are atypical of CAD but may
  correlate with the distribution of myocardial
  sympathetic nerve terminals
• 3. Myocardial injury is most likely the result of
  a centrally mediated release of catecholamines
  due to hypoperfusion of the posterior
  hypothalamus.

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Predictors of neurocardiogenic injury after SAH

• cTnI is much more sensitive than CK-MB (100
  compared with 29) in the detection of left
  ventricular dysfunction in patients with SAH.
• An elevated level of cTnI is a good indicator of
  left ventricular dysfunction in patients with
  SAH.

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• The degree of neurological injury as measured by
  the Hunt-Hess grade is a strong, independent
  predictor of myocardial necrosis after SAH. This
  finding supports the hypothesis that cardiac
  injury after SAH is a neurally mediated process.

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Hunt-Hess score

• Grade 1 Asymptomatic or mild headache and slight
  nuchal rigidity
• Grade 2 Moderate to severe headache, stiff neck,
  no neurologic deficit except cranial nerve palsy
• Grade 3 Drowsy or confused, mild focal
  neurologic deficit
• Grade 4 Stupor, moderate or severe hemiparesis
• Grade 5 Deep coma, decerebrate posturing
• The grade is advanced one level for the presence
  of serious systemic disease (hypertension,
  diabetes, severe arteriosclerosis, chronic
  pulmonary disease) or vasospasm on angiography

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Conclusion

• If EKG abnormalities develop during
  hospitalization, the heart of a patient with SAH
  who has brain death is not accepted as a donor
  organ because of the possibility of cardiac
  abnormalities.
• This cardiac dysfunction was reversible and
  should not necessarily preclude these patients
  from undergoing operative interventions or
  becoming heart donors.

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References

• 1. Stroke. 2004 35 548-552
• 2. Circulation. 2005 112(21)3314-3319
• 3. J. Neurosurg. 2003 98741-746
• 4. UpToDate
• 5. Harrisons Principle of Internal Medicine,
• 16th edition, chapter 210

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