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Myocardial creatine kinase isoenzyme in serum after subarachnoid haemorrhage

Insights

Elevated myocardial isoenzyme of creatine kinase (MB CK) in subarachnoid hemorrhage patients may indicate cerebral ischemia. This finding could aid in surgical timing and prognosis assessment.

Area of Science:

  • Neurology
  • Cardiology
  • Biochemistry

Background:

  • Subarachnoid hemorrhage (SAH) can lead to serious neurological complications.
  • Cardiac involvement following SAH is recognized but not fully understood.
  • Creatine kinase isoenzymes, particularly MB CK, are markers of cardiac injury.

Purpose of the Study:

  • To investigate the presence and significance of myocardial isoenzyme of creatine kinase (MB CK) in patients with acute subarachnoid hemorrhage.
  • To explore the association between elevated MB CK levels and neurological complications like cerebral ischemia and arterial spasm.
  • To evaluate the potential of MB CK as an early indicator for surgical intervention and long-term prognosis in SAH patients.

Main Methods:

  • Serum samples were collected from 16 patients with acute subarachnoid hemorrhage.
  • Levels of myocardial isoenzyme of creatine kinase (MB CK) were measured in patient sera.
  • Cerebral angiography was performed to detect intracranial arterial spasm.
  • Neurological deficits were assessed and correlated with MB CK levels and angiographic findings.

Main Results:

  • Elevated MB CK levels were detected in the serum of 7 out of 16 patients (43.75%) with acute subarachnoid hemorrhage.
  • All patients with elevated MB CK showed either intracranial arterial spasm or a focal reversible neurological deficit.
  • These deficits were not attributable to direct pressure from hematoma or aneurysm.

Conclusions:

  • The presence of MB CK in SAH patients may serve as a biomarker for cerebral ischemia.
  • MB CK levels could be valuable in optimizing surgical timing and predicting long-term prognosis.
  • Sympathetic nervous system activation might be a common pathway linking myocardial MB CK release and intracranial arterial spasm in SAH.

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