Keystone Heart is focused on protecting the brain from emboli to reduce the risk of brain infarcts during TAVR.
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Why Care About Embolic Brain Lesions When We’re Talking About Cardiovascular Issues?

You may be wondering why it is important to discuss brain lesions in relation to TAVI and other cardiovascular procedures. Through our years of experience and research, we’ve learned embolic brain lesions and stroke during a TAVI procedure can permanently effect patients’ mental and physical health.

It is not just the threat of major stroke due to embolic material passing from the heart to the brain. It is much more insidious than that. Patients can also suffer from minor strokes and clinically covert strokes, which may lead to long term disability due to embolic material dislodged to the brain during cardiovascular procedures.

The long term consequences of milder clinical symptoms and new brain lesions can have a major impact on patients’ everyday living and quality of life especially when it comes to higher executive neurocognitive functioning. Some examples are memory loss, ability to focus, and/or change of personality.

Long Term Effects

Acute DWI lesion is generally a reliable signature of infarct core and represent mostly permanent brain damage -sustained reversal is infrequent (Campbell et al. J of Cerebral Blood Flow and metabolism 2012;32:50-56).

Transient or permanent resolution of initial DWI lesion depends on the duration of ischemia -10 min vs 30 min. Transient resolution of DWI lesion isassociated with widespread neuronal necrosis; moreover, permanent resolution of DWI lesions even after 10 minutes of ischemia does not indicate complete salvage of brain tissue from ischemic injury (Li et al. Stroke. 2000;31:946-954).

Based on histology and experimental studies on cerebral ischemia normalization of DWI does not imply that the tissue is normal and neurons already exhibit evidence of structural damage and stress. Other non-neuronal cell populations may partially compensate for altered fluid balances at the time of DWI reversal despite the presence of neuronal injury probably caused by delayed neuronal cell death by apoptosis (Ringer et al. Stroke. 2001;32:2362-2369).

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