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A study shows that the number and volume of a brain lesion was lower in patients by implanting Embolic Cerebral Protection Devices. It reduces the rate of complications in patients during TAVR, cardiovascular diseases, etc. Visit Keystone Heart for detail information.nFor More Information:nhttp://www.keystoneheart.com/us/ninfo@keystoneheart.comn1 877 575 4433n

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brain emboli clinical consequences and brain

Brain Emboli

Clinical Consequences and Brain Injury

Kevin Abrams, MD.

Chief of Radiology

Medical Director of Neuroradiology

Baptist Hospital and Neuroscience Center, Miami, FL

Clinical Associate Professor of Radiology

FIU School of Medicine

why are we discussing brain lesions in cardiology
Why are We Discussing Brain Lesions in Cardiology?

Clinical Consequences and Brain Injury

clinical stroke after tavr at 30 days

Clinical Stroke After TAVR at 30 Days

  • VARC defined: 1.5-6% in recent RCTs
  • Confer 3- to 9-fold increased risk of mortality
  • AHA/ASA defined; Symptoms (ask the neurologist) + Brain MRI
  • Stroke range is 15-28%

30-day stroke rates in recent RCTs

Are we under-reporting stroke?

Clinical Consequences and Brain Injury

new ischemic lesions are present in a substantial

New Ischemic Lesions are Present in a Substantial Number of Patients Undergoing Cardiovascular Interventions with Diffusion weighted (DWI) MRI

TAVI

58-100%

CAS

20-70%

AVR

48%

Cardiac Cath

3-18%

CABG

18-42%

AF Ablation

7-42%

Clinical Consequences and Brain Injury

calcific aortic valve stenosis
Calcific Aortic Valve Stenosis

Primary source of embolic material following TAVI

Large irregular masses of dystrophic calcification prevent normal valve opening

Sizeable calcific deposits prevent normal valve function

Calcified stenotic aortic valve

Clinical Consequences and Brain Injury

most of the stroke events take place periprocedural
Most of the Stroke Events Take Place Periprocedural

PARTNER (Cohort A)

TAVI (32 Stroke Pts)

AVR (15 Stroke Pts)

41%

47%

59%

53%

Over 30 days post procedure

Over 30 days post procedure

Periprocedural

Periprocedural

Clinical Consequences and Brain Injury

tavi potential paths of cerebral emboli
TAVI: Potential Paths of Cerebral Emboli

Three aortic arch take-offstypically lead to the four arteries feeding the brain:

Right Carotid

Right Vertebral

Left Carotid

Left Vertebral

Layton KF et al. Bovine Aortic Arch Variant in Humans. AJNR 2006.

Clinical Consequences and Brain Injury

distribution of embolic lesions following tavi as assessed by dwi
Distribution of Embolic LesionsFollowing TAVI as Assessed by DWI

Equally distributed in all major cerebral vascular territories except ACA

27%

Cerebellum/Brainstem

Middle cerebral

Vascular Territories

38%

2%

Anterior Cerebral

Posterior Cerebral

33%

Arnold 2010, Wityk 2001.

Clinical Consequences and Brain Injury

clinical embolic stroke syndromes
Clinical Embolic Stroke Syndromes

Middle Cerebral Territory

Right Carotid

  • Left hemiparesis, face and arm more than leg
  • Left neglect

Vertebral, Basilar and Posterior Cerebral Artery Territories

Right Vertebral

  • Vertigo, falling to left
  • Diplopia (blurred vision)
  • Dysarthria (slurred speech)
  • Hemiparesis or quadriparesis
  • Hemisensory loss
  • Hemianopia or cortical blindness

Clinical Consequences and Brain Injury

clinical embolic stroke syndromes 1
Clinical Embolic Stroke Syndromes

Middle Cerebral Territory

Left Carotid

  • Right hemiparesis, face and arm more than leg
  • Aphasia, loss of expressive as well as receptive language

Vertebral, Basilar and Posterior Cerebral Artery Territories

Left Vertebral

  • Vertigo, falling to left
  • Diplopia, dysarthria
  • Hemiparesis or quadriparesis
  • Hemisensory loss
  • Hemianopia or cortical blindness

Clinical Consequences and Brain Injury

dwi lesions reversal and brain damage
DWI Lesions, Reversal and Brain Damage
  • 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 & metabolism 2012;32:50-56).
  • Transient or permanent resolution of initial DWI lesion depends on the duration of ischemia - 10 vs 30 min. Transient resolution of DWI lesion is associated with widespread neuronal necrosis; moreover, permanent resolution of DWI lesions even after 10 min 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 - 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.)

Clinical Consequences and Brain Injury

each new dwi lesion matters 10 may 2013 vol 340 science
Each New DWI Lesion Matters10 MAY 2013 VOL 340 SCIENCE
  • Each 1-mm3 voxel of Brain Tissue contains:
    • at least 80,000 neurons
    • Each neuron may be connected to up to 10,000 other neurons
    • 4.5 million synapses
  • At 294.7 mm3 on median lesion volume (the median volume of new DWI lesions post TAVR in US, Lansky et al London Valve 2015)

Each patient lost on average during his unprotected TAVR procedure:

• Over 20 Million Neurons • Over 1 Billion synapses

Clinical Consequences and Brain Injury

measuring cognition
Measuring Cognition
    • Attention / Processing Speed
  • Visuospatial Abilities
    • Perception (match shapes)
    • Construction (arrange blocks to form complex pattern)
  • Memory
    • Implicit
      • Procedural (riding a bike)
    • Explicit
      • Episodic (I went to the store this morning)
      • Semantic (who was the first president?)
  • Language
    • Naming
    • Vocabulary
    • Fluency (name as many words as you can in 60 seconds)
  • “Executive Functioning”

Clinical Consequences and Brain Injury

measuring cognition 1
Measuring Cognition

Executive functioning

  • Organization
  • Strategy Development
  • Mental flexibility
  • Abstract Thought
  • Working Memory
  • Inhibition
  • Complex Sequencing

RED

  • BLUE
  • YELLOW
  • GREEN

RED

  • GREEN
  • BLUE
  • YELLOW

Clinical Consequences and Brain Injury

cerebral reserve
Cerebral Reserve
  • The brain’s ability to compensate in the face of an insult (e.g. clinically overt stroke, trauma) or multiple insults (new clinically silent lesions) over time and refers to the amount of brain damage the brain can sustain before overt clinical symptoms are manifest (Staff, Neuroimaging Clinics of North America 2012)
  • Any periproceduralstroke in all patient populations will add to the ischemic burden of the brain now and in the future thus decreasing the cerebral reserve (K Abrams 2013)

Clinical Consequences and Brain Injury

cerebral reserve 1
Cerebral Reserve
  • Infarcts are associated with brain volume reduction, but, importantly, also with detectably lower cognition (Blum et al, Neurology, Nov 2012)
  • Cognitive decline relates directly to loss of brain substance with progression of lesion burden (Schmidt et al, Annals of Neurology 2005)
    • therefore brain infarcts will ultimately affect cognition

It All Adds Up

Clinical Consequences and Brain Injury

neurocognitive decline
Neurocognitive Decline

Most studies with complete neurocognitive battery examining the association between…

DEMENTIA

NEUROCOGNITIVE DECLINE

BRAIN INFARCTS

show a consistent link between the three

Clinical Consequences and Brain Injury

new dwi lesions and neurocognitive nc function

New DWI Lesions and NeuroCognitive (NC) Function

Clinical Consequences and Brain Injury

18

long term clinical consequences of silent mri lesions and brain pathology
Long Term Clinical Consequences of “Silent” MRI Lesions and Brain Pathology
  • Large population-based studies demonstrate associations between MRI lesions and cognitive decline, clinical stroke, and mortality (Vermeer et al Lancet Neurol 2007;6:611-9)
  • There is increasing evidence that cumulative burden of ischemic brain injury causes neuropsychological deficits or aggravates vascular dementia (Bendszus Lancet Neurol 2006:5;364-72)
  • Dementia is a cumulative effect of “multiple hits” and brain infarcts; more than 50% of those with dementia have multiple pathologies on autopsy, whereas among those without dementia over 80% have single or no pathology (Tatemichi Stroke 1994;25:1915-9)
  • The presence of silent brain infarcts at base line more than doubled the risk of dementia, are associated with worse performance on neuropsychological tests and a steeper decline in global cognitive function.
  • Silent thalamic infarcts are associated with a decline in memory performance, and nonthalamic infarcts with a decline in psychomotor speed. (Vermeer et al 2003:348;1215-1222)
  • In addition, patients with Atrial Fibrillation have an increased risk of dementia, excess mortality and neurocognitive impairment due to many factors including pre-existing microinfarcts and reduced brain volume (Kwok et al Neurology 2011;76:914-922, Santangeli et al Heart Rhythm 2012;9:1761-1768)

Clinical Consequences and Brain Injury

conclusion
Conclusion

A “silent” infarct is still an infarct whether random or iatrogenic

Until someone proves these DWI lesions are somehow beneficial to the patient, we need to take steps to prevent them from occurring

Clinical Consequences and Brain Injury

is cerebral protection necessary
Is Cerebral Protection Necessary?

Absolutely!

Clinical Consequences and Brain Injury