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What is protected left main disease ? How good is the protection ? If good , why should it need another protection ?

Posted in Uncategorized on September 15, 2009| 7 Comments »

Left main disease  is an important subset of CAD , and it has special interest for the interventionist. Traditionally cardiologist have   a fear to touch this lesion , as they thought a sudden occlusion within this vessel is life threatening   . Later on as  they gained experience  it was thought  we could intervene safely at least in protected left main . Subsequently  it was realised this fear was largely unfounded  , after all  the proximal LAD is equally  dangerous and we spend hours together inside an LAD ! .Now we have technology and expertise to do successful PCI any where in LM. And  unfortunately , the same expertise is not applied in selecting the ideal patients who will benefit the most . LMD has become a glorified indication for PCI.

The terminology of protected and unprotected LMD is in vogue for many years . Unfortunately it do not convey a uniform meaning . In next few minutes ,  I shall share  my views on the nuances of protected and unprotected LMD .

The term   protected was  not  coined by  cardiovascular physiologists   but by   interventional  cardiologists . Hence it connotes a  anatomical  meaning rather than physiological.  Protected LMD  meant there must be a at least one  graft to either LAD or circumflex . And this graft should be functional . The presence of this graft is supposed to increase the comfort levels of the interventionist as well as  the patient.

A left main coronary artery disease angiographically  can be  classified  as

Common types of Left main lesion

  • Asymptomatic , non flow limiting , angiographically insignificant disease(< than50%)
  • Ostial
  • Ostio proximal
  • Shaft : Mid, distal or diffuse Left main
  • Bifurcation

Unprotected left main

  • All the above lesions
  • Non functional GABG grafts ( eg: LIMA occlusion makes LAD unprotected)

Protected left main

  • Post CABG  with atleast one functional graft to LAD /LCX
  • ? Left main   with total  LAD and very good LAD collaterals from RCA /LCX

Partially protected Leftmain

It could mean any of the following,     Left main Plus  .  . .

  1. Incomplete occlusion of single  LIMA graft
  2. Occlusion of  SVG-LCX and patent LAD-LIMA
  3. Occlusion of LIMA-  LAD graft but patent SVG-LCX  graft
  4. Patent LIMA-LAD  but a  critical  LM / LCX  bifurcation lesion with no grafts for LCX*

The above 3  situations may demand a  PCI .But logic would  suggest one would try to open up the partially occluded graft rather than open the left main . Of course the decision involves status of RCA .

*The only indication for a  PCI  in protected  LMD could be 4

Unusual ( Crazy !) questions  about  left main disease

Can left main be protected by collateral circulation ?

It is very common to find Left main   bifurcation  lesion   with LAD having  very good collaterals from RCA sometimes filling up to proximal  LAD .This can be considered   “protected left main equivalent”

As on today , cardiologists would rather   believe  a surgeon’s graft  rather than a naturally grown  collateral from RCA however extensive it may be !

But logics and real case experience would indicate in a patient  with LMD and an  extensively collateralised LAD can in fact be  considered a protected left main.

If a  left main is well protected by a functional LAD graft , why should we do a PCI for left main at all ?

This question was risen in one of our cath conferences , a patient   who had functioning  LIMA to  LAD graft.His   RCA had a functioning  venous graft  and his circumflex had a partially functioning  graft.The left main had a near total  obstruction and the proximal  LAD was  faintly visible .

Since the  patient  had class  2 angina Options were discussed .He  satisfied  the  current criteria of protected LMD .Just because he fulfils the criteria of protected left main , he  does not  become eligible for  left main    PCI .  After all he is having this LMD for many years. Protecting again the left main which is already protected is not a big deal in terms  of outcome .  Double protection is waste of resource at additional risk. It was decided to attempt a PCI to SVG graft to LCX. If it does n’t work leave him with medical management.

Does  every patient  after a CABG   has a high chances of developing LMD ?

What is accelerated atherosclerosis of Left main following LAD /LCX  grafts ? It is  true  left main  has high risk of  accelerated atherosclerosis and it   undergoes  gradual obstruction once the LAD and LCX is grafted.This is due to low flow across the native left main as distal grafts maintain the flow . This is all the more likely in good bulk of patients who had undergone  CABG  where   LMD  was the indication .

A typical scenario

A left main patient   who undergoes a CABG  a follow up for a suspected  angina  angio after 5 years show the  totally  or near totally occluded native left main . Sudden   Visualisation of worsened leftmain disease    makes this patient eligible for  a  PCI as he fulfills the criteria for  protected leftmain .

Final message

A well protected left main  with a good  functioning graft especially to LAD   most often do not require a fresh revascularisation  procedure  irrespective of the tightness of left main disease . Most of such patients will be candidates for medical therapy .Contrary   to the popular belief ,   left main  intervention   could  be    confined  to   ” unprotected LMD   rather than well protected LMD” as the  potential benefits are more .Further interventional resources need not be wasted in giving second alternate protective channel  for an already protected vessel !

Of  course it should be remembered  in any given patient  with  protected or unprotected  LMD  the indication for  revascualrisation  is based on  the severity of lesion , symptoms,  LV function ,  residual ischemia, viability  etc .

Suggestions  , comments  and  corrections  welcome

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What are critical differences between complete heart block and AV dissociation ?

Posted in Cardiology - Clinical, cardiology -ECG, Cardiology-Arrhythmias, tagged , , , , , , , , , , , , , , on September 13, 2009| 3 Comments »

CHB and AV dissociation are often confused with one another . While CHB is an important cause for AVD , there are distinct differences  which have clinical implications. This table is an attempt to simpify the understanding of the two. Corections and suggestions welcome.

This is a high resolution image , to read better  right click on the table  copy image and open in any image viewer

complete-heart-block-chb-av-dissociation-avd-va-associationn-va-block-sinus-node-dysfunction-ecg-ep-study-interfernce-avd-aivr

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How the presence of atrial fibrillation influence the effectiveness of CRT therapy ?

Posted in Cardiology - Electrophysiology -Pacemaker, Uncategorized, tagged , , , , on September 12, 2009| Leave a Comment »

Atrial fibrillation and CHF are close companions. Either it   precipitates  CHF  or  follows it.In advanced heart failure of any etiology  the incidence of AF can be up to 40% .Medical therapy of AF is fairly effective in patients with normal LV function  .But when associated with refractory cardiac failure  it becomes  too complex to control .

Currently CRT with ICD  is becoming the standard OF care for advanced CHF. The efficacy of CRT is being rigorously being assessed . Even as the controversy  about  the wideness of QRS is being settled , the issue of optimal  timing of CRT has risen  . Now ,  the MADIT-CRT has answered this issue “Earlier it  is better , it can be  indicated even for  class 1 patients”

While MADIT -CRT will increase the number of CRT implants , we  have no clear cut answer for the  efficacy of CRT in patients with AF .( Of course , the MUSTIC and CARE HF sub group analysis suggested AF has no significant impact on CRT efficacy )

atrial fibrillation crt cardiac resynchronisation therapy icd madit crt care chf

Why is AF important in CRT ?

There are two issues that need analysis

  1. A patient who  has chronic AF at the time of CRT
  2. Development of  new onset AF after CRT implantation.

Impact of AF during CRT

  • Inter atrial synchrony is lost. ( Significance not clear . . . makes AF permanent)
  • AV synchrony is lost
  • Rapid AV conduction : May trigger   too much of Bivi pacing if sensed by LV lead

Presence of AF at the time of CRT gives us an opportunity to tackle this issue.

How to tackle  sudden AF induced CRT response ?

There are variety of algorithms available to

  • Ventricular sense response
  • Conducted AF response
  • Atrial tracking recovery

In dual chamber pacing mode switching converts DDD into VVI  .This happens  at the cost of loss of AV synchrony .This may have profound implication in CRT .

Then the big question comes  . What is the use  of  having Intraventricular  and interventricular  synchrony without AV synchrony ?

When nothing works .The best strategy is ( Rather deemed to be best ! )

  • To ablate the  AV node  pace  the atrium and ventricle  (RV & LV)  .

Note : Ablation of AV node and putting a dual chamber pacing can never guarantee a physiological pacing as the atrium continues to fibrillate and AV synchrony is rarely there .

Final message

For CRT is to be successful , there should be maximal Bi-Vi capturing , of course this capture has to optimally timed , and must reverse the three pathological asynchronies , namely intraventricular , Interventricular  and  atrio  ventricular  asynchronies.

It is obvious , presence of AF complicates the issue as it demands  constant monitoring and programming of the device (Of course  now most  of them are automated) . It may   require  knocking down of AV node , which  not only carries a risk of SCD *  ,  it also make these  patients   permanently  dependent   on the RV pacing  . This  adds on ,  another  risk ,  for an  acute complication   if the RV lead fails for some reason.

Reference :

*Sudden death after radiofrequency ablation of the atrioventricular node in patients with atrial fibrillation
Journal of the American College of Cardiology, Volume 40, Issue 1, Pages 105-110
C.Ozcan

EP experts generally take  too much liberty in adopting this  strategy for the simple reason it solves the nuisance of atrial impulses  interfering with   ventricular  leads  function that result in  inappropriate ventricular capture fusion or ultimately poor BiVi pacing . But it is not an easy decision  atleast for the patient ! This article , emphasises the dangers involved in ablate and pace strategy for uncontrolled AF.

Further reading

  • Fung, J. W H, Yip, G. W K, Yu, C.-M. (2008). Does atrial fibrillation preclude biventricular pacing?. Heart 94: 826-827 [Full Text]
  • Khadjooi, K, Foley, P W, Chalil, S, Anthony, J, Smith, R E A, Frenneaux, M P, Leyva, F (2008). Long-term effects of cardiac resynchronisation therapy in patients with atrial fibrillation. Heart 94: 879-883 [Abstract]
  • Buck, S., Rienstra, M., Maass, A. H., Nieuwland, W., Van Veldhuisen, D. J., Van Gelder, I. C. (2008). Cardiac resynchronization therapy in patients with heart failure and atrial fibrillation: importance of new-onset atrial fibrillation and total atrial conduction time. Europace 10: 558-565 [Abstract] [Full Text]

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How paroxysmal nocturnal dyspnea differ form orthopnea ?

Posted in Cardiology - Clinical, Tutorial in clinical cardiology, tagged , , , , on September 11, 2009| 1 Comment »

orthopnea paroxysmal nocturnal dyspnea pnd www.drsvenkatesan.com

Some Infrequently asked questions in (iFAQ) in PND

What gives relief from PND?

The classical description is, the patient wakes up from sleep. sits up, often to stand up, and go to the nearest window and try to breathe fast and an episode of dyspnea settles down in a few minutes. The relief is completely in many unless the ongoing trigger and baseline cardiac defect overwhelms the reserve mechanism.

What is the hemodynamics behind relief?

Since symptoms are due to sudden unexpected congestion during sleep, assuming erect posture slows down the venous return of 400 ml instantly. It is equivalent to an IV diuretic push. Further standing up (even sitting up is sufficient)  brings the left atrium in its natural superior position, compared to LV. The gravitational forces emerge* and aid in LV filling and improve stroke volume and relieve the congestion backlog. Apart from this two more factors contribute. V/Q mismatch improves as more lungs get perfusion in an erect posture . Finally seeking the window is spontaneous, in search for better fractional oxygen content from the atmosphere. (One more related question. How do pillows give relief of dyspnea in acute LVF? Few of the above mechanism operates)

*Postural changes in LA mean pressure is a complex topic of physics involving lungs, pulmonary circulation, and LA mean pressure.

Is basal rales mandatory during episodes of PND?

Yes. Most will have. But it should be emphasized in orthopnea patients, rales are rare since it takes some time for lung congestion take place. If rales appear immediately after lying down it may Indicate severely compromised LV function.

PND vs Orthopnea: Which is a reproducible symptom?

Obviously orthopnea. PND can never predict which day its going to come as there is CNS component to the circuit in triggering this. (REM sleep, Dreams etc)

How many episodes of PND can occur in one night?

Usually one. Because PND requires a time lag of at least few hours.Usually, these patients will not sleep thereafter or the usual wake-up time ensues.

Can episodes of PND be prevented?

Since its a volume-dependent pulmonary hemodynamic stress, a diuretic at dusk will prevent these episodes in many.

What is the sensitivity of PND for predicting heart disease?

It has low sensitivity( <30% ) but up to 75% specificity to diagnose heart disease.(Class 3 Non-Expert Evidence)

Is PND sign of advanced heart disease?

No.It has very low sensitivity to predict severity of heart disease.

Can PND and Orthopnea occur at same patient at same time a same day ?

Orthopnea has no time lag.It occurs immediately hence it is obviously more severe. Many of these patients, however, do get into sleep after some time as some sort of compensation or adaptation to neural signals of dyspnea take place.

These patients, later on, can get into the same cycle of PND . However, as heart disease (as in cardiomyopathy ) worsens the pulmonary interstitium shows some reactive fibrotic changes resist water logging in the lungs.

Since PND and orthopnea share a close relationship in terms of pathophysiology, we cluster it together in symptomatology. However, they are temporally separated in most patients in natural history.

PND : is it equivalent to acute heart failure?

Yes, it can be called so (If it is due to heart disease*) . It fulfills all criteria of cardiac failure. LV/LA filling pressure raised, forward output (Cardiac Index may still be normal ) .PND is a transient, acute, left-sided failure that results in acute oxygen debt for the body which is self-corrected usually.

* In volume overloaded, CKD patients PND can occur

What is the relationship between RV dysfunction to PND /Orthopnea?

There is a complex fluid regulatory mechanism in the failing heart. The lung can be congested if and only if the RV function is adequate enough to flood the lungs and at the same time LV function matches it with its inadequacy resulting in persistent congestion. In other words, a very high RVEDP is protective against pulmonary edema (However the patient will feel the dyspneic still due to hypoxia /VP VQ etc !)

Its prudent to give importance to PND/Orthopnea with reference to the balance of RV and LV function. One may recall why pericardial disease where right heart filling is impeded rarely lead to lung congestion.

Can PND be associated with Angina ?

Yes, it can but generally its not. Angina occurs due to nocturnal sub-endocardial Ischemia. This combination occurs in critical Aortic valve disease.(Both AS/AR)

Is PND a cardiac emergency?

Difficult question. Most times, no. Since its self-limiting especially if the patient knows he is going to settle with his past experience. But it can trigger dangerous events in severely compromised hearts.As expected, the first episode creates much panic and invariably elicits an emergency alert.

PND has sinister significance if is due to nocturnal ACS.Its a sign of ischemic LVF and requires immediate care.

Which is the most benign form of PND and Orthopnea ?

Students should know, medicine is a funny science. PND as a symptom is benign in some, while it denotes impending death in others.

Benign PND : Obese men, women, in pregnancy may experience terrifying dyspnea at night when they turn around or stretch. This is due to the upward movement of the diaphragm encroaching lung space.

If you record mitral inflow Doppler filling pattern during an episode of PND what will you find?

It’s quite simple logic. You do it yourself and find it as a learning exercise.(Please don’t make the patient suffer by doing echo at times of distress. One of your colleagues to attend to him as you simultaneously do an echo for academic purpose)

Try calculating LVEDP with various echo formulas.

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Why ECG evidence for AV dissociation does not occur in majority of patients with ventricular tachycardia ?

Posted in Uncategorized, tagged on September 10, 2009| 2 Comments »

AV dissociation is the specific marker for diagnosing VT. Evidence for AV dissociation manifest in many ways in ECG. *Random p waves unrelated to qrs complexes , fusion beats , capture beats are  the common features that help us diagnose AV dissociation. Unfortunately these  occur only in about  40 % of patients  with VT.(Fusion beats in VT are also  called as Dressler’s beat)

For clinical features of AV dissociation follow this link

What is the normal AV association ?

In  normal physiology ,  even though atria are passive , powerless chambers  in terms of mechanical activity  ,  it reigns  supreme control over ventricle and   dominates   electrically  . In fact , the atrium  and the AV node together ,    dictates when the ventricle has to contract and at what rate  .  So,  in normal human  beings in  sinus rhythm ,  there is a complete AV  association   where both chambers live in a perfect harmony.

What is VA association ?

The atrium and ventricles are  not only related   antegradelyy it  also  has a concealed  retrograde  relationship , (which is often pure electrical ! ) called VA conduction .The conduction velocity and the refractory period of VA  junction is  variable .The AV junctional refractory period is determined by the penetrating power of both atrial and ventricular impulses .

What is complete AV dissociation ?

For complete AV dissociation to occur there should be no physiologically or electrically  linked relationship between the atria and ventricle.For it  to occur the atrial impulse has to get  blocked  in AV junction .

This block can   either be functional  or organic,   partial or total , persistent  or intermittent

This occurs in   primarily in   AV junctional pathology like CHB  etc, that result  in complete AV dissociation . The next major cause for AV dissociation , is   by an  interference from  an accelerated lower pacemaker as in ventricular tachycardia or accelerated idioventricular rhythm .

What does the atria do when the ventricle  starts  contracting rapidly and  independently as in ventricular tachycardia ?

When the ventricle , starts firing independently at a rate of > 200 each of the impulse and  tries to  traverse  the AV junction retrograde . At the same time , the sinus impulse which does it’s normal routine job  by beating around 70/beat ,   faces an  unusual interference on its normal downward journey by  the pathological bombardment  from  the upcoming  ventricular impulse .What happens when both these wave fronts  meet head on . (The hither to perfect harmonical  relationship becomes  a rivalry for the electrical control of heart.)

Sadly , the ventricle mostly succeeds  in the race and  most of the   ventricular impulses    retrogradely  enter  the AV  junction and colludes with  the incoming atrial impulses. When this happens , the AV dissociation is said  to occur. The important point here is,  many times if the retrograde VA conduction is fast and optimally timed , it can cross the AV node without difficulty  and reach the atria  and  subsequently  even    depolarise  the SA node   and  reset  it  . If the VT is persistently conducting  retrograde  it can suppress the SA node as long as the VT is there. This makes a P wave becoming totally absent.  (Note of caution : If you say VT as one of the causes of absent P wave you may be failed in your cardiology board , but this remains a fact !)

So the atrial  depolarisation  and contraction During VT is a complex one. It depends  mainly on the  intensity of the  upcoming    electrical wave front   from the ventricle  . The distance traveled by this wave front  determines  the location of  p waves .It may be in one of the following ways .

  • P waves can be totally absent
  • P wave may occur antegrade
  • On the QRS
  • Over the T wave

In effect the P wave can  literally be any where   in the given strip of  VT

When does a fusion  beat occur ?  When does a capture occur ?

This again is determined by the AV  junctional refractory period. If it permits ,  an   occasional atrial impulse may sneak through the AV junction and capture the ventricle . This is capture beat. Capture beats   are usually narrow qrs  . So in a wide qrs tachycardia  if we note  an occasional narrow or relatively narrow  qrs complex it could denote a VT.

If the atrial impulse after crossing the AV junction   collides with the   upcoming ventricular  impulse  the surface ECG inscribes  a fusion beat. An incomplete capture beat is a fusion beat. It is a combination of two qrs complex one activated from above , one from below .The width of the fusion beat may be wide , narrow or intermediate.

So the evidence for AV dissociation  in surface ECG  is rarely  manifested  if the VT is successfully  traverse  the AV junction and   reset  the SA node  or keep it in a semi depolarised state  .This could be clinically important  some times , the SA node takes time to recover following  A DC shock especially in elderly

An episode of VT can unmask  a hidden sinus node dysfunction , as VT is technically similar to an atrial override pacing   of course  from  below .

Final message

During VT , electrophysiologically  there must be a dissociation between  the atrial  and ventricular contraction.But the evidence  for which is not manifested in surface ECG in the majorty.The primary reason for this,  due to  the  intact  VA  conduction  that    result in  retrograde VA  association.This  makes the  classical findings of   AV dissociation a redundant or invisible  one .

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Can you diagnose AV dissociation without looking at ECG ?

Posted in Cardiology - Clinical, cardiology -ECG, tagged , , , , , , , , , on September 9, 2009| Leave a Comment »

AV dissociation is  common clinical situation that can occur  during both    bradyarrhythmias  and tachyarrhythmias .

Bradycardias

  • Complete heart block
  • During pacemaker rhythms

Tachycardias

  • Accelerated junctional  rhythm
  • Idioventricular  rhythm
  • Ventricular  tachycardia

AV dissociation is essentially an  ECG diagnosis. But it is associated with some  clinical  signs   ,which can be detected by an astute physician in the bedside. At rapid heart rates  it may be really difficult at times to recognise theses findings, but a  cardiology fellow should look for these whenever they encounter AV dissociation  in ECG.

  1. Varying pulse volume
  2. Varying korotkoff  sounds during BP measurement.
  3. Cannon a waves in JVP
  4. Varying intensity of first heart sound on auscultation
  5. Mitral regurtitant murmur may be heard
  6. Hypotension in compromised hearts

What is the mechanism of clinical signs of AV dissociation ?

During AV dissociation , the atrial and ventricular contractions occur  out of phase  and the sequential contraction  is lost. So atrial contractions  might  occur with a closed AV valves .  This result in reflux of blood into the neck resulting in cannon waves . It may be visible only in few beats as the retrograde conduction VA conduction , is highly variable.

Further , only some atrial beats contribute for ventricular filling some do not.This results  in varying LV volumes and this  could result in changing pulse volume.Occasionally the ventricular and atrial   contraction occur simultaneously  .When this happens ,  some amount of blood  reguritates through the open tricuspid valve and mitral valve  which result in MR or TR .

Clinical utility

This could be important , in differentiating  the perennial  issue   of decoding the   wide qrs  VT from  SVT with  aberrancy .A rapid clinical assessment  here could  aid in the diagnosis  of VT  by  identifying  AV dissociation  . An experienced cardiologists will realise even in a given  ECG  with VT  identifying or ruling out  AV dissociation is not always a  pleasant excercise !

In this era of  high tech gadget  oriented cardiology is it not too much  to call for clinical   recognition of  this  entity ?

Definitely not , if  we know Wencke bach  recognised  the classical type 1 2nd degree  AV block in late 19th century even before the ECG machine was  invented ,

Simply by looking at the neck , by carefully observing progressive prolongation of  distance between a and c waves and subsequent dropping of c waves . Amazing isn’t it ?

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Great cardiology websites: May be the best (free!) source for learning ECG !

Posted in Great websites in cardiology, tagged , , , , , on September 9, 2009| Leave a Comment »

This learning resource is  a must read for all cardiology fellows

Frank G. Yanowitz, M.D
Professor of Medicine
University of Utah School of Medicine
Medical Director, ECG Department
LDS Hospital Salt Lake City, Utah

Click the link to reach the master teacher

yanowitz great cardiology ecg website


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Conveniently forgotten studies in CRT : The importance of diastolic wall motion defect in cardiac failure !

Posted in cardiology -ECG, Cardiology -Interventional -PCI, cardiology -Therapeutics, Uncategorized on September 8, 2009| Leave a Comment »

The   failing heart  enlarges progressively and  attain a globular shape . What  looks  for the  naked eye  as a simple global hypokinesia of LV  , when  analysed  ,  reveal multiple  forms regional desynchronisation .This is especially true if the QRS complex is wide.

It is generally divided into three groups

  • Intraventricular desynchrony (IV)
  • Ventriculo-Ventriculo desynchrony(VV)
  • Atrio ventriculo  desynchrony(AV)

In our search for improving CHF mortality and morbidity  ,  we have  stumbled upon this concept of restoring the lost synchrony of the heart. Cardiac resynchronisation therapy  has become ( Rather projected to become !)  a  great modality for patients  with cardiac failure.It was   initially advocated only   for severe forms of cardiac failure  , now  advised even for class 1 CHF. (CRT-MADIT 2009)

Restoring  the lost  synchrony  by rewiring the cardiac conducting system with multiple leads and optimally timed pacing increases the effectiveness of cardiac contractility.It can improve EF, and also regress mitral regurgitation.

The above concept was perfect on paper , but was very difficult to replicate on real patients. CRT was ineffective in 30% of patients.   Many had partial  effect. Few had adverse effect .

The reason for the poor efficacy  is  technical in many .  Identifying the optimal  sites for  positioning  the leads  and the futility of such an  exercise as the LV epicardial  lead is pre- selected by the patients coronary venous anatomy are the major issues.An electrically ideal site for pacing  can  contain a  mechanically dysfunctional scar.   While these  technical issues may  be addressed  in due course  what worries us is the conceptual flaws.

Emerging  facts indicate timing of asynchrony could be vitally important.

  • Systolic   synchrony
  • Diastolic synchrony

What is the incidence desynchrony with reference to the cardiac cycle ?

CRT resynchronisation

One major reason that was overlooked totally was the presumption cardiac dysynchrony occur only during systole. It is a less recognised fact is the ventricular relaxation is not uniform and synchronous.A  failing ventricle can not be expected to relax  systematically and coherently  for the simple reason the myocytic calcium reuptake into the sarcoplasmic reticulum  is grossly impaired. This  is directly responsible for the diastolic dysfunction observed in dilated cardiomyopathy . If this impairment occur uniformly throughout the  left ventricle it can be termed global diastolic dysfunction which is little easier to correct .But what really happens is  the  defect in calcium reuptake occurs in a random fashion with lot of regional variation. This is called regional diastolic wall motion defect or regional diastolic dysfunction.The above mechanisms result in the typical restrictive filling pattern of many of the advanced  patients with DCM . CRT as a concept should need to address this issue.

How to diagnose Diastolic WMD?

The  fact  is  ,we have not  mastered the quantification of systolic WMD as yet. It may take years before decoding the  nuances  of diastolic wall motion defects. At least we need to know such a thing exists.Tissue  doppler strain rates ,  velocity vector imaging could be useful tools. As such they are not clinical tools.

Final message

crt cardiac resynchronisation asynchrony echocardiography

Cardiac resynchronisation as a concept is good on paper . Heart need to be synchronous both during systole and diastole .This becomes especially important in an advanced stages of  heart failure. Without proper follow up  and potential adverse effects of CRT on diastolic WMD ,   CRT concept    has  miles to travel !  . Some  pessimistic thinking   cardiologists ( Me . . . !)   would even argue  it as a case of prematurely released device into the  patient domain. Of course there is  lot of  scientifc data that  will vouch for its beneficial effects .(The latest being from the prestigious NEJM ,  CRT-MADIT) but it has to prove it’s worth in individual patients. Physicians must exercise caution  before embarking on heroic  attempts to provide resynchrony of failing hearts .

Reference

This study from France published in JACC 2005  by Iris Schuster,

http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109705021005/fulltext

Coming soon

ICDs are better bet than CRT

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Why LVH does not occur in all patients with systemic hypertension ? ?

Posted in Cardiology -Mechnisms of disease, Hypertension, Infrequently asked questions in cardiology (iFAQs), tagged , , , , , on September 7, 2009| Leave a Comment »

Left ventricular  hypertrophy (LVH) is one of the most common  structural heart disease.Systemic hypertension, aortic valve disease are responsible for the bulk of the cases .Some  of the LVH occur due to cardiomyopathy (HCM/Non HCM variants).Athlete’s heart is a physiological response to exercise and  it  is largely a normal entity.

How many patients with SHT develop LVH ?

It is surprising to note , not every patient with SHT develop LVH .In fact estimates suggest only  about 30-40% of chronic  hypertensive individuals develop SHT .

What are the determinants of LVH in SHT ?

  • Magnitude of systolic pressure
  • Magnitude of diastolic pressure
  • Pulse pressure
  • Duration of SHT
  • Age
  • Gender
  • Body  weight/Obesity
  • Effect of treatment

While any of the above factors may operate in determining LVH

none of the above are important than this

“Genetic susceptibility ”

The myosin isoforms are determined by the genes .The re expression of   fetal isoforms in adults is responsible for LVH in many .This is determined by the genetic homogeneity

LVH  in  renal disease

Secondary hypertension due to renal dysfunction is a major determinant of LVH. This is espcially true if the pateints are dialysis dependent.The mechanism are not clear .

Diabetes and SHT :  LVH  friendly forces

When diabetes alone and SHT alone is less likely to result in LVH the combination of these two entities greatly increase the likely hood of LVH.DM induced microangitis amplifies the after load effect of HT and result in early LVH.Further this LVH is different from pure forms of hypertensive LVH  in that the interstitium goes for hypertrophy and in some cases neovascualrisation. In hypertensive LVH it is predominately myocyte hypertrophy  with little interstitial  proliferation. this has important therapeutic implication as any drug which reduce the blood pressure can regress pure myocytic hypertrophy, while in diabetic LVH  regression is difficult to achieve .

Lipid levels inversely related to LVH ?

There is no consistent relation between lipids and LVH .Occasional reports suggest a negative correlation.

Which LVH is associated with diastolic dysfunction ?

It is a well known fact , LVH has major effect on LV diastolic function.But it is also a fact only some forms of LVH develop this. Now it is clear only if the interstitial hypertrophy occur  diastolic dysfunction is manifested.  Even as the as the hypertrophied  myocyte  continue to  relax  the interstitium do not have molecular mechanisms to relax .Hence, as discussed earlier , diabetic hypertensive patient often  develop diastolic dysfunction .

Final message

LVH is not a simple expression of raised after load.It has major  non hemodynamic determinants which if identified , could have important therapeutic implication.

Coming soon . . .

Can  coronary artery  disease induce LVH in the absence of SHT or DM ?

//

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What is Brody effect in ECG ?

Posted in Cardiology - Clinical, cardiology -ECG, tagged , , , , , , , , , , , , , , on September 7, 2009| Leave a Comment »

The quantum of electrical energy reaching the surface of the chest wall varies widely .It depends upon myocardial mass, proximity to the chest wall  and the thickness of chest wall.

Apart from this ,  the amount of blood within the left ventricle also determine the QRS voltage of ECG.

In dilated LV due to a regurgitant lesion , the LVEDV is increased . Since  blood is a very good conductor of  electricity , it amplifies the transmural  activation front and results  in high voltage QRS complex.This is referred to as Brody’s effect.

Where else , we  can  visualise the Brody effect  ?

During excercise stress testing , when  the heart rate and   the  LV diastolic volume increases .There is  a significant increase in QRS  voltage in leads facing LV, especially V5 and V6.

This is  usually a benign response in healthy individuals. However in patients  with preexisting CAD and LV dysfunction an  increase in R wave amplitude may  be a marker of  exercise induced LV dilatation  which  could  predict an adverse outcome .

Is there  a reversed Brody effect , where Q waves get deepened on exercise ?

This has not been described in literature , but it is seen often in patients with post MI stress testing .Q gets deepened .If the q gets minimised* it could indicate presence of significant viable tissue  , as it gets recruited during the excercise induced positive inotrpism mediated by   catecholamine .Lengthening or deepening of Q indicate less viable tissue.

*Study in progress : Will  be referenced shortly .

Brody effect is a complex phenomenon.

Advanced readers follow the link for illustration on Brody effect

http://www.bem.fi/book/18/18.htm

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