P Milsom

Capture of intracardiac material

minimising potential systemic emboliPaget Milsom

Green Lane Cardiothoracic Surgical Unitat

Auckland City Hospital

other significant contributors

S Mitchell A Barber A Merry L Blakey L Tippett S Hach

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Disclosure Form

I have had a financial interest with Dual Vent Circuit Ltd.

This could be perceived as a conflict of interest in the content of the subject of this program.

However the presentation is evidence based and balanced.

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Brain damage - talk outline

MagnitudeCostEtiology

Reduction methods

Trials and reportsNew approach to microemboli reductionReducing Brain Injury in Cardiac Surgery

Relating structural damage to functional outcome

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CABG brain damage - magnitudeRisk of Stroke

• CABG (0.6% - 5.2%)

• Valves (4.2% - 13%) Nussmeier, Jan 96

6.1% adverse neurological event Type 1 & 2

50% severe ↑ mortality and hospital stay

Roach, NEJM Dec 96

60% cognitive defects @ 8 days50% persisting @ 1 year

Taylor, Annal Thorac Surg 1998

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Incidence CNS perioperative injury↑ Complexity surgery → ↑ Adverse outcome

Newman Lancet;2006: 368:694

CABGNon vented 9/486 (1.9%)Vented 58/1549 (3.7%) p < 0.05

1.95 risk ratio 1.8% (0.07 - 3.7%) absolute risk

Roach, Personal communication 1999Combined procedures

16% adverse cerebral outcometype 1 8.4%type 2 7.3%

Wolman Stroke;1999;30:514

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Cost of Cerebral Event

D Hill 1999

174100Total Care Cost (%)

11.13.4Hosp Mort (%)

11.67.0Hosp LOS (days)

131.944.0ICU LOS (hrs)

StrokeNo Stroke

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Etiology of Brain Injury

Known Risk factors for CVABypass TimeAortic atheromaIABP usageDiabetesHistory of hypertensionHistory of pulmonary diseaseUnstable angina↑ age

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Etiology of Brain Injury

Major Risk factors for CVA

Embolism

Hypotension on bypass

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Increased Embolisation = ↑ Risk Neurological Deficit

43> 10008.6< 200Pugsley199435≥ 600< 30Clark 199570≥ 174

30< 106Stump 1996Neurological DeficitEmboli count

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Microemboli Release

80% released after x-clamp removal

continues for 28 mins following establishment of physiological flows

Tingleff et al Ann Thorac Surg 95

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Circuit Operates at Point of Maximum Embolisation

0

200

400

600

800

1000

start stable Up to34ºC

34 - 37ºC pumpwean

workingheart

Med

ian

Embo

li C

ount

CPB Rewarming

Ann Thorac Surg 1998;66:785-91

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New Approach to Microemboli Reduction

Circuit diverts total output of weaning heart

to CPB venous resivoir

↓

Emboli removed by CPB circuit prior to x-clamp removal

Milsom P, Mitchell S, Ann Thorac Surg 1998;66:785-91

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Surgical Considerations with Dual Vent Circuit

Surgical registrar manages root pressure by the variable resistor

De-airing time ≤ conventional methods.

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Microemboli CountConventional v's Milsom Circuit

0

500

1000

1500

2000

5 Surgeons PM Conventional PM Dual Vent Nonvented CABG

Med

ian

Embo

li C

ount

1749 1580

101 9

Ann Thorac Surg 1998;66:785-91

N=58 N=16

N=14 N=4

P Milsom 219AVR + 2 CABG1435AVR130MVR + Tricuspid12

208AVR117AVR + 2 CABG106AVR + 1 CABG90MVR818AVR + 1 CABG7

865AVR62AVR5

167AVR + 1 CABG4562AVR3363MVR2652AVR1IMAProcedurePatient No.

Index of Microembolic Activity after Aortic Declamping

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Summary

Minimises emboliat the time of maximum emboli release

Potentially minimises neurological damage

Dual Vent Circuit

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Reducing Brain Injury in Cardiac Surgery

Paget Milsom, Alan Barber, Alan Merry, Linda Blakey, Lynette Tippett, Sylvia Hach

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Primary Hypothesis

Dual Vent Circuit (DVC)

creates less

DW MRI brain damage (vol)

than

conventional “de-airing”

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Material & Methods

Registered trial Funded jointly by: NHF & Neurological Soc

Cardiac valve surgery patients +/- CABG

150 Prospective randomized - Only the surgical team unblinded to the intervention

√

Post-op 6 wks

Primary endpoint

√√DW MRI (ischaemic volume)

Reliability change index

√Neuropsych testsConsensus statement for assessment after Cardiac Surgery

√MMSE >24 mRS < 2NIHSS

√√√Neurological ExamChangePost-op ≤ 7 daysPre-op>18 years neurologically intact

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The controversy over the relationship between imaging and neuropsych testing

FORKohn 2002Toner 1994Restrepro 2002

AGAINSTVanninen 1998Bendszus 2002Knipp x 4 2004 → 09

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Results

Cohort

40 patients

26 men aged 63yrs (SD 12 yrs)

post-op imaging

37 with (36MRI + 1CT)

3 without (pacemaker, declined, early discharge)

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Pre-op

72 h post-op

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Early post-op results

Images:37 Scans (36 DWI 1CT)16 patient with ischemic lesions

16 / 37 43%13 small < 1cm33 confluent lesions 8 %

Clinical:2 strokes 5.0%

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Patients with and without post-operative ischemia on diffusion weighted MRI

0.0432:195:11CABG+valve : Valve0.14411:1012:4AV:MV/TV0.3672(9)3(19)Diabetes mellitus (%) 0.4834(19)4(25)Dyslipidaemia (%)0.2727 (33)3 (19)Atrial Fibrillation (%)0.1034(19)7(44)IHD (%)0.4958(38)7(44)Hypertension n(%)0.32310.613.5Length of stay (days)0.345144.0158.4CPB time (mins)0.6675.86.5EuroScore0.24059.665.2Age mean (SD)0.58914:711:5Male:Female

PDWI lesion absent

DWI lesion present

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Late Follow-up Procedures

Neuropsych

Neurological

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6 Week Results

Neurocognitive measurement 35 patientsRCI assesseddeficit = ↓ 1 ≥ measure

22 significant decline in ≥ 1 measure 63%

12 significant decline in ≥ 2 measure 34%

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6 Week Results

32 patients combined NP and MRI imaging

15 Patients new DWI lesions

all ↓ > 1 NP measure 100%

17 Patients no DWI lesion

only 6 ↓ > 1 NP measure 35%p<0.0001

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Patients with and without post-operative ischemia or neuropsychological decline

0.00237.49(4 →350)

DWI lesion / absence

0.1036.370.0785.00(0.83 →30)

CABG+valve : Valve

0.3511.010.3041.01CPB time0.6890.970.6381.04EuroScore0.1500.370.8900.91Gender/male0.1021.040.2491.03Age

PORPORPredictor variable

Neuropsychological outcome

DWI outcome

Logistic regression

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The burden of ischaemic damage resulting in decrease ≥ 2 neurocognative measures

6/8 (75%) patients multiple lesions or single lesion 1cm3

2/7 (29%) solitary lesion

3/17 (18%) no lesionp = 0.001

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Conclusions

Minimising brain emboli is a purposeful endeavor

as

Cognitive decline is linked to brain ischemia

and furthermore the

Volume of MRI damage is associated with the magnitude of cognitive decline