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Posts Tagged ‘hypertrophic obstructive cardiomyopathy’

In HCM every myocyte is  genetically made  defective . Myofibrils are in disarray every where . Still , can we identify some vulnerable zones that acts as arrhythmic  focus ? If that is possible , we  have a opportunity to abate that focus .

In HOCM  , which is the most stressed area ? LVOT ?  Septum, ? When we say stress , it can mean either mechanical or electrical .

VENTRICULAR TACHYCARDIA 002

Does electrical instability involve the same zone as mechanical stress ?

How often VT originate from LVOT in HCM ?  For this we have good clinical model _, the patients who underwent alcohol septal ablation.

What happens to the incidence of VT  post septal  ablation  ?

“It is reported  post septal ablation the incidence of SCD  becomes  equal to general population” (Read the paper below )

If that is true , it is obvious the  arrhythmic  focus is also ablated along with LVOT myocardium .

Outcome of HOCM after alcohol septal ablation

Though many studies claim  so !  It  fails to convince us  .  HOCM is a diffuse disease of  myocardium.  Even a cluster of myocyte disarray  with fibrosis   can be a future focus  irrespective of it’s location .

However ,  it is always possible relieving the mechanical stress of the LV can definitely reduce the likelihood of an electrical event .(Even if the arrhythmic focus is intact elsewhere !)

* We know RVOT is  developmentally arrhythmia prone zone . We also know HCM involves RVOT (After all ,  IVS  is legally shared by both ventricles !  ) . Some of  the monomorphic  VTs with LBBB morphology may originate from RVOT in HCM .

Management of recurrent VT in HOCM

  • Drugs (Amiodarone/ Calclum blockers/ Beta blockers/Disopyramide)
  • ICD- (Probably mainstay  )
  • Very rarely ablation (If localised focus is well documented )

Reference

1.A case report for successful ablation of  VT in HOCM   http://www.ncbi.nlm.nih.gov/pubmed/9255687

2.http://www.ncbi.nlm.nih.gov/pubmed/23076968

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Hypertrophic cardiomyopathy (HCM) manifests   with or without obstruction. Obstructive HCM ,  (ie HOCM)  is more often symptomatic .However , the risk of arrhythmias, sudden death, and some degree of diastolic dysfunction are common in both.

ECG, clinical examination are generally  not sensitive to identify obstruction in HCM  .Echocardiogram is the easiest  way to identify  the obstruction (gradients> 3o mmhg across LVOT are considered significant ).LV angiogram ,MRI, CT scans are rarely necessary today.

However , the following clinical clues will help us  to suspect significant obstruction in HCM

History

  • Class  2 or  3 dyspnea.
  • Exertional syncope
  • Exertional angina

Pulse

  • Pulsus bisferiens (Two peaks in systole )

LV apex

  • Sustained , double apical impulse  often indicate obstruction.
  • Presence of Mitral regurgitation ( 20% can have  MR without obstruction due to intrinsic abnormalities of  mitral valve )

* It should  be realised , valsalva induced MR /LVOTO  may occur in many of the non obstructive HCM.

What happens to  clinical signs of obstruction with medical therapy(Beta blockers etc)

One would expect these signs to regress or disappear, but it rarely happens. The pulse , the  murmur show  little change .  This implies , the main mechanism of beneficial effect could be in  heart rate  reduction , and  improvement in the   diastolic properties of left ventricle.

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