Feeds:
Posts
Comments

Posts Tagged ‘ddd pacing’

Ignoring distal LBB disease in conduction system pacing: Is it pure science?

Posted in Uncategorized, tagged , , , , , , , , , , , on August 24, 2026|

The huge popularity of conduction system pacing (CSP) , especially the Left bundle branch Area Pacing (LBBAP) has been hailed as a paradigm shift in cardiac pacing. By utilising the native His-Purkinje network, CSP promises a physiological alternative to the dys-synchronous RV pacing. However, beneath this procedural enthusiasm lies a critical, clinical assumption .It is the disregard of distal LBB integrity. In our haste to bypass proximal blocks, the electrophysiology community has mastered the art of ignoring distal conduction system disease a practice that relies more on hope than long-term, evidence-based science.

The physiological basis of LBBAP  is based on capturing the main left bundle branch trunk or its proximal fascicles to downstream  distal healthy  Purkinje network1. In patients presenting with complete heart block , this approach looks fine , if the underlying pathology is strictly nodal or intra-Hisian. However, in progressive, degenerative conduction system disorders such as Lev’s or Lenègre’s disease fibrosis is rarely localized. It is a multi-level, diffuse process that tracks distally into the fascicles and terminal Purkinje ramifications2.

How, can we casually overlook the small but surely dangerous risk of progressive distal LBB disease in complete heart block, which can lead to unpredictable catastrophic events ? This electrical oversight finds a striking, parallel in historical pacing concepts. In patients with sinus node dysfunction (SND), the electrophysiology community long ago established that a standalone atrial lead (AAI pacing) is a clinical hazard3. The minor yet real risk of AV nodal disease progression (approximating 0.6% to 4.5% per year) almost universally mandates the placement of a backup ventricular lead, safely transitioning the strategy to dual-chamber (DDD) pacing4.

The current electrophysiology consensus downplays this distal disease , by invoking the physics of the virtual electrode. The argument is even if the localized nerve fibers directly contacting the lead tip degenerate over the subsequent decade, the high-programmed voltage outputs will maintain permanent myocardial capture, ensuring patient safety from asystole5. While this assumption satisfies the basic requirements of bradycardia support, it ignores a core fact.

Aprar from thew physiological uncertainty , there is also a  significant risk of procedural failure. Real-world registries reveal that approximately 5% to 15% of patients undergo acute on-table crossovers due to  septal calcification, anatomical variations, or an immediate functional failure to engage a viable conduction pathway7.

Conduction system pacing is undoubtedly a great addition to our EP armamentarium, but it must be practiced with  humility in the face of unproven long-term  putcome and procedural complexities. A clinical pragmatism is warranted. Conventional dual chamber (DDD) is backed by more than four decades of  randomized clinical evidence.9. Until we clarify the natural history of the chronically paced, diseased left bundle,  DDD pacing should remain  the standard of care.

References

  1. Huang W, Su L, Wu S, et al. A novel pacing strategy with low and stable threshold-left bundle branch pacing. Europace. 2019;21(3):471-477.
  2. Lev M. Anatomic, pathologic, and electrocardiographic correlations in the atrioventricular and distal conduction system. Prog Cardiovasc Dis. 1964;7(4):317-340.
    Andersen HR, Nielsen JC, Thomsen PE, et al. Long-term follow-up of patients paced in atrioventricular synchronous vs. single-chamber atrial mode for sick sinus syndrome. Lancet. 1997;350(9086):1210-1216.
  3. Brandt J, Anderson H, Fåhraeus T, et al. Natural history of AV conduction in patients with sick sinus syndrome as related to bilateral bundle branch block. Pacing Clin Electrophysiol. 1992;15(11 Pt 2):1914-1918.
  4. Vijayaraman P, Sharma PS, Cano Ó, et al. Comparison of Left Bundle Branch Area Pacing and His Bundle Pacing in Bradycardia Indications. JACC Clin Electrophysiol. 2021;7(11):1433-1442.
  5. Jastrzębski M, Kiełbasa G, Cano Ó, et al. Left bundle branch area pacing outcomes: the MELOS registry. Eur Heart J. 2022;43(40):4161-4173.
  6. Heckman LI, Luermans JG, Vos LM, et al. Left Bundle Branch Area Pacing: A Comprehensive Review of Technical Aspects, Clinical Outcomes, and Future Directions. J Clin Med. 2023;12(11):3611.
  7. Wijesuriya N, Niederer S, de Verteuil R, et al. Extraction of conduction system pacing leads: a systematic review and international survey. Europace. 2024;26(2):euae032.
  8. Wilkoff BL, Cook JR, Epstein AE, et al. Dual-chamber pacing or ventricular pacing in patients with an implantable defibrillator: the DAVID trial. JAMA. 2002;288(24):3115-3123.
  9. Khurshid S, Epstein AE, Verdino RJ, et al. Incidence and predictors of pacing-induced cardiomyopathy. Heart Rhythm. 2014;11(9):1618-1625.

Postamble

This opinion letter is being sent to EURO PACE journal : Expecting a fast tracked rejection letter within a week or two .(Based on my past experience) They view these type of articles as destructive criticism I was told by one editor. Some one please clarify me, the difference between a constructive and a destructive critic, please)

.

Read Full Post »

What are the mechanisms of mitral regurgitation in HOCM ?

Posted in Uncategorized, tagged , , , , , , , , , , , on August 12, 2011| Leave a Comment »

Hypertrophic cardiomyopathy(HOCM)  is a relatively common inherited myocardial disease.Since it predominately involves  LV myocardium and we know LV muscle mass is an integral part of  mitral valve apparatus , it is natural HOCM  has a major  impact on   mitral valve function .

The mechanism  of MR in HOCM is attributed to the following .

  • Asymmetric septal hypertrophy (ASH ) related abnormal pap muscle alignment (Geometric distortion  )
  • Exaggerated SAM(AML  is attracted towards LVOT with every systole that tend to  keep the mitral  valve  unguarded and MR results)*
  • Intrinsic abnormalities of mitral valve.
  • Associated MVPS
  • VPDs and Non-sustained VT can result in transient MR
  •  Pacemaker mediated MR (DDD pacemaker was used to induce desynchrony of LVOT vs LV free wall .This  concept  is almost a failed  one now !)
  • End stage HOCM -Left ventricular dilatation

* This mechanism is considered less important ,  as SAM is almost universal in HOCM  but MR occurs in less than 20%  patients with HOCM.

Eccentric MR vs central MR

In HOCM the MR is more often eccentric .This is understandable as the primary mechanism is related to faulty angle of pap ,muscle vs leaflet attachment.

If SAM is primary mechanism jet is directed posterior.

Murmur of MR in  HOCM

Is rarely pansytolic as the mechanism of MR begins to operate well after the systole starts .

Many times it is difficult to differentiate LVOT murmur from MR murmur . Th ever confusing and tentative  maneuvers might help in few shrewd cardiologists.

Issues  during echocardiogram

Very often MR jets are mistaken for LVOT gradient.Ideally two gradients in isolation (or  overlapping each other)  one bell shaped other dagger shaped must be documented.

Please note : LVOT jet is different from MR jet in size, shape, timing and site of maximum signal . Still it is often be confused with one other. Most common reason for this is technical .A careful apical 4 chamber view with well opened LVOT will reduce the error . Never record a HOCM echo without ECG gating . The MR jet may be very trivial in color flow but doppler will still pick the signal well . Realise ,for hemodyanmic reasons MR jet must be always more than LVOT jet.Finally if you get a report a LVOT gradient > 100mmhg in HOCM suspect it to be MR ! More often your suspicion will prove to be right !

Can mitral regurgitation occur in non obstructive HCM ?

Yes , in few . This is due to intrinsic abnormalities of mitral valve .

What happens to MR with surgical correction ? Can medical management  regress the MR ?

It is expected to regress.But many patients don’t. Effect of beta blockers   on MR severity is not studied well.

Management

  • Most cases of MR  do not require specific intervention.Just reassure them.
  • Correction of LVOT obstruction is expected to relieve MR considerably.
  • Intensive beta blocker or calcium blocker can regress the MR.(Negative inotropy)
  • Mitral valve repair may be necessary in few  with re-engineering of pap and chordae .
  • Mitral valve replacement should be a last resort. It  may be highly tempting  .But restraint is warranted. Much  damage has been done by showing undue haste in replacing mitral valve in HOCM

Final message

It needs to be realized whatever we do  for the HOCM patients , the ultimate outcome is determined by the quantum myocardial disarray  the patient has inherited from their parents.The myectomy , the alcohol ablation, mitral valve repair,  DDD pacing , beta blockers all are palliative. Except a few  , most HOCM patients generally live their natural history .

Read Full Post »