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Module 1 EP > Molecular control of Pacemaking > Flashcards

Molecular control of Pacemaking Flashcards

1
Q

AP of the PMC

A
  • Depolarise on hyper polarisation due to HCN (If channels)
  • Upstroke is slower as no rapid Na channels (Nav1.5)
  • Repolarisation is more constant (not like VCM’s plateau)
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2
Q

Origin of the nodes

A
  • Believed to be remnants of primary myocardium
  • Possibly derived from 1st HF
  • Repression of contractile phenotype differentiation
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3
Q

Repression of Chamber Myocardium differentiation

A
  • Tbx18, Tbx3
  • Isl1
  • Shox2
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4
Q

Induction of Chamber Myocardium

A
  • Tbx5, Tbx20
  • Nkx2.5
  • Nav1.5 expression for rapid
    depolarisation
  • Pitx2 (suppresses PMP)
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5
Q

Development of the SAN

  • Where
  • Molecular queues in morphology
A
  • On the right, between IVC and SVC

Head
- Compact area containing centre (Tbx18)

Tail
- More fragmented, more fibroblasts (Nkx2.5)

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6
Q

The 2nd HF in PMC origin

A
  • Posterior and anterior compartments
  • Signalling with BMPs, FGFs, nodal, TBx5, Nkx2.5, Isl1
  • Isl1 expression maintain most primitive stage of differentiation
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7
Q

Electrical mapping of PM centre in development

A
  • In linear HT, comes from left side
  • Left side centre maintained after looping
  • Cells recruited to IFT, migrate to AV junction
  • PM program seals fate of cells once in the right position
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8
Q

PMCs and the 3rd HF

A
  • PMCs originate on the right side, far from the 1st HF
  • Unique, posterior position
  • Wnt8 specifies 3rd HF
    (Crescent inhibits this)
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9
Q

The PMP

  • Initiators
  • Promotor (expansion, specification)
  • Suppression
A
  • Shox2 and Isl1
  • Tbx18
  • Pitx2
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10
Q

PMC Channel and GJ expression

A
  • HCN4, Hcn1 and Hcn2
  • Cav1.3 and Cav3.1
  • Cx30.2 (slow conducting Cx)
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11
Q

Working CM expression

A
  • Nppa, Nppb (BNP and ANP)
  • Cx43, Cx40 (fast Cx)
  • Scn5 (Nav1.5)
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12
Q

Non-PMCs of node region

A
  • Lots more collagen and fibroblasts than myocytes
  • Transitional cells with some properties of PMC and WMC (Nav1.5)
  • Conduct AP to crista terminalis (first WMC to depolarise)
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13
Q

PMCs of the node

A
  • Myocytes are small and thin
  • Elongated spindle, spindle or spider shape
  • Poor electrical coupling between cells
    (few GJ, slow Cx)
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14
Q

Elongated Spindle and Spider PMCs

A

Elongated spindle
- Possibly link the SAN to surrounding atrial myocardium

Spider
- Possibly where the AP is first produced

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15
Q

HCN4, Nav1.5 and Cx43 in the SAN and WCMs

A
  • HCN4 mostly in centre, some in periphery, none in WCMs

- Nav1.5 and Cx43 in WCMs, some in periphery but none in centre of SAN

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16
Q

SAN vs atrial ion channels and pumps

A

Atria

  • Nav1.5
  • RyR (relatively more)

SAN
- HCN4

17
Q

Currents of SAN AP

A

Phase 4:

  • I(f) initially
  • then I(Ca-t)
  • then I(Ca-l)

Phase 0:
I(Ca-l)

Phase 3:
- I(K)

18
Q

Currents of VCM AP

A

Phase 4:
- I(K)

Phase 0:

  • I(Na)
  • I(Ca-t)
  • I(Ca-l)

Phase 1:

  • I(K-to)
  • I(Ca-l)

Phase 2:
- I(Ca-l)

Phase 3:
- IK1

19
Q

SAN vs VCM AP

  • Amplitude
  • Depolarisation
  • GJs
A

Amplitude:
- Small vs Large

If:
- Present vs Absent

Nav1.5
- Absent vs Present

GJs
- Sparse/slow vs Abundant/fast

20
Q

Channels of the PM potential

A
  • HCN4
  • RyR
  • T-type Ca
  • (Nav1.5)
  • Blocking any of these slows heart rate
  • Redundancy, loss of no one current can silence the PM potential
21
Q

Interconnected Clocks

A
  1. Ion flux across the cell membrane
  2. Ca storage and release from SR
    - ‘clocked’ release of SR Ca make NCX efflux Ca
    - Na influx causes depolarisation
    - depolarisation causes Ca influx
    - Ca content of SR influences NCX behaviour by leaking
22
Q

Sick Sinus Syndrom

  • Who gets it
  • What is it
  • How common?
  • What is cause?
A
  • Disease of the elderly
  • Bradyarrhythmia due to dysfunction of SAN
  • Reason for 50% of implanted PMs
  • Mutations in HCN4 or SCN5a*
  • Nav1.5 believed to be important in conducting AP from SAN to WCMs
23
Q

The Biological PM

A
  1. Cell therapy (SCs)
  2. Hybrid therapy (SCs + Hcn2)
  3. Gene therapy (Tbx18 viral transduction)*
  • Could reduce need for implanted devices
  • most promising

Module 1 EP (12 decks)

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