Abstract

Subarachnoid hemorrhage (SAH) is one of the deadliest types of strokes with high rates of morbidity and permanent injury. Fluctuations in the levels of cerebral metabolites following SAH can be indicators of brain injury severity. Specifically, the changes in the levels of key metabolites involved in cellular metabolism, lactate and pyruvate, can be used as a biomarker for patient prognosis and tailor treatment to an individual’s needs. Here, clinical research is reviewed on the usefulness of cerebral lactate and pyruvate measurements as a predictive tool for SAH outcomes and their potential to guide a precision medicine approach to treatment.

Highlights

  • Subarachnoid hemorrhage (SAH) is one of the deadliest types of stroke [1]

  • This review aims to summarize how changes in brain energy production, represented as the changes in the levels of lactate, pyruvate, and the lactate-pyruvate ratio (LPR), have been shown to reflect the extent of injury after SAH, and can correlate with clinical events and patient outcomes

  • Elevated cerebrospinal fluid (CSF) pyruvate concentration is strongly associated with poor grade SAH (WFNS ≥ III)

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Summary

Introduction

Subarachnoid hemorrhage (SAH) is one of the deadliest types of stroke [1]. It comprises 2% to 5%. Pyruvate produced through cytosolic glycolysis is converted into acetyl-CoA by the enzyme complex pyruvate dehydrogenase (PDH) enters the mitochondrial citric acid cycle to produce ATP In anaerobic conditions such as hypoxia or ischemia, oxidation cannot occur and the accumulation of cofactors results in the inhibition of PDH activity. The measurement of lactate and pyruvate levels can potentially predict the occurrence of secondary events, such as vasospasm and DCI, and may guide targeted therapeutic management of patients with SAH in an effort to reduce mortality and morbidity. Glucose supply to neurons (purple cell) is decreased and the absence of oxygen causes pyruvate metabolism to shift towards lactate production and less efficient ATP production to meet cellular energy demands.

Metabolic Mechanisms Underlying Disturbed Energy Metabolism in SAH
Lactate and Pyruvate after SAH
Relevant Results
Brain Hemodynamics and Lactate and Pyruvate
Association of Lactate and Pyruvate with Secondary Complications and Events
Conclusions
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