static.livemedia.gr€¦ · k.gatzoulis, et al, ann noninvasive electrocard 1999, 4:115. snd csnrt...

TTT - NCS

• Establishing the diagnosis of NCS

• Avoid unnecessary additional andexpensive testing

• Clarify the VVS reaction pattern

• Potential role for selecting appropriatetherapy

• Prognostic tool?

TTT - Limitations

• Sensitivity, Specificity, Reproducibility

• Methodology varies in different EPLaboratories

• Drug provocation frequently required

• Positive responses in other cardiovasculardiseases associated with syncope

K.Gatzoulis, et al, Ann Noninvasive Electrocard 1999, 4:115

SND

CSNRT >525 msec

Chronotropic response to atropine or ISO <90 bpm

SACT >140 msec

IHR: 118.1 - (0.57 X age) + SD p Atropine / BB

NIECG markers / SUO

ΧΡΟΝΟΣ ΑΝΑΝΗΨΕΩΣ ΦΛΕΒΟΚΟΜΒΟΥ

AVNCD

HV >60 msec

ERP of the AVN >450 msec

Weckenbach and 2:1 AVB at CL >500 and 400 msecrespectively

Split His activity

EPS markers / SUO

Sub-Hisian block on atrial pace Non preexisting bi or trifascicular block an atrial

pace

VT / VF induction group

VT (sustained monomorphic)

Long runs of NSVT (>18 beats occasionally lastingup to 15 sec and associated with presyncopesymptoms) were noted but not consideredabnormal responses

VF or polymorphic VT degenerating into VFinduction

EPS markers / SUO

Others

Symptomatic SVT induction requiringcardioversion or overderive pace termination

CSM with >3.0 sec pauses

BT ERP (delta wave) <250 msec

EPS markers / SUO

K.Gatzoulis, P.Toutouzas, Drugs 2001

421 pts with SUO and 12 lead ECG and 24 HM

+ECG /+24 HM

+ECG /-24 HM

-ECG /+24 HM

SUO / EPSDesign

EPS SVD AVNCD VT/VF Others (ie SVT, HR-WPW, HCSS)

-ECG /-24 HM

K . Gatzoulis et al, Ann Noninvasive Electrocardiol, 2009

K . Gatzoulis et al, Ann Noninvasive Electrocardiol, 2009

K . Gatzoulis et al, Ann Noninvasive Electrocardiol, 2009

K . Gatzoulis et al, Ann Noninvasive Electrocardiol, 2009

K . Gatzoulis et al, Ann Noninvasive Electrocardiol, 2009

K . Gatzoulis et al, Ann Noninvasive Electrocardiol, 2009

1st AVB

OR 3.07, CI: 1.54 – 6.10, p=0.001

LAH

OR 0.56, CI: 0.17 – 1.81, p=NS

RBBB

OR 1.52, CI: 0.52 – 4.79, p=NS

LBBB

OR 2.83, CI: 1.10 – 7.22, p=0.029

1st AVB + LAH

OR 4.63, CI: 1.84 – 11.63, p=0.001

1st AVB + LPH

OR 4.63, CI: 1.84 – 11.63, p=0.001

RBBB + LAH

OR 4.63, CI: 1.84 – 11.63, p=0.001

1st AVB, RBBB, LAH

OR 8.63, CI: 3.01 – 24.71, p<0.001

An extremely high risk combination

LBBB, 1st AVB, left axis deviation

K . Gatzoulis et al, Ann Noninvasive Electrocardiol, 2009

Sinus bradycardia, 50 bpm

• Markers of abnormal substrate of structural heartdisease

• Markers of abnormal repolarization

• Markers of abnormal autonomic balance

• Inducibility on Programmed Ventricular Stimulation

• LVEF• QRS duration• LBBB• Late Potentials on SAECG• VPBs• NSVT

• Heart Rate Variability• Heart Rate Turbulence• Decelaration Capacity• Baroreceptor Sensitivity• Heart rate

• QT duration• QTc duration• QT dispersion• QTc dispersion• QT dynamics (QT/RR)• T wave alternans

69 post-MI patients (mean LVEF: 46±4.5%, males:96, age:65)42 DCM Syncope: 36

Presyncope: 26Asymptomatic with NSVT: 49

PVSSustained VT 23/69 post MISustained VT 8/42 DCMPolymorphic VT 5/42

After 52.3 months follow up: ICD activation: 12/23 post MI8/10 DCM

Absence of SCD in non-inducible patients.

Thank you