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The debate of rate control verses rhythm control in atrial fibrillation  goes on and on. The AFFIRM, RACE,PIAF, STAF the HOT CAFE all went against sinus rhythm in the last 10 years . This was one of the settled contoversies in cardiology . The conclusion was ventricular  rate control was no way inferior to rhythm control in patients with SHT, CAD population .This made the electrophyiologists wonder how can a natural rhythm fare bad ! . But the findings  were consistent .Rhythm control neither improved the quality of life nor  it reduced the incidence of stroke. The later finding was very surprising but the explanation was convincing as stroke in elderly was more related to SHT, CAD, DM etc than  AF itself. The source of emboli in ischemic stroke could come any where distal to LA .The big assumtion that all strokes in elderly  should come from LA appendage or the body  of LA was  premature and  wrong. What prevented stroke in AF was not restoration of SR but administration of oral anticoagulants with adequate INR.(2-3)

Having failed to document superiority in elderly  population   , the  logic machine  strongly suggested restoring SR  in patients with CHF,  will atleast provide hemodynamic and also survival  benefit .

And thus came the AF-CHF trial  published in NEJM 2008

Alas !  AF-CHF  also found there is no useful purpose of restoring sinus rhythm in patients  with atrial fibrillation and cardiac failure. In fact patients in SR fared little worse !

 Why . . .  why . . . why ?

Should we ask the seemingly absurd question !

Is sinus rhythm poorly tolerated by cardiac failure  patients ?

It is some times possible atrial fibrillation by itself could be a mechanism to amplify the  cardiac reserve by which it provides a  relatively high ventricular rate to improve the cardiac index  . Even though the optimal ventricular rate in AF is around 80-90 at times of need it has to increase to 120-130. Patients in class 3 CHF and AF often achieve this in times of demand .This is not possible in patients who are getting rhythm control drugs and further patients in SR can  not increase the HR suddenly from 80 -130  .

So is this a  wild imagination !   AF could be a safety valve mechanism in CHF to increase the HR . Where the atria come to the rescue of ventricle like a rate adaptive pacemaker .

The other logical* ! argument is that  there  is nothing wrong with restoring  SR , but the  methods to achieve and  maintain SR  is too cumbersome and results in adverse outcome .The currently available  drugs are too toxic for the purpose  .

If we have a simple and safe way to restore SR in these patients it should always be superior to AF .

But it is a well  known fact  that , whatever be the rhythm or rate the ultimate outcome will be dictated by the LV function, mitral valve function etc.

 Read abstract of AF-CHF

Rhythm Control versus Rate Control for Atrial Fibrillation and Heart Failure

Denis Roy, M.D., Mario Talajic, M.D., Stanley Nattel, M.D., ., for the Atrial Fibrillation and Congestive Heart Failure Investigators

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Rhythm Control versus Rate Control for Atrial Fibrillation and Heart Failure

Denis Roy, M.D., Mario Talajic, M.D., Stanley Nattel, M.D.,  the Atrial Fibrillation and Congestive Heart Failure Investigators* –>ABSTRACT

Background It is common practice to restore and maintain sinus rhythm in patients with atrial fibrillation and heart failure. This approach is based in part on data indicating that atrial fibrillation is a predictor of death in patients with heart failure and suggesting that the suppression of atrial fibrillation may favorably affect the outcome. However, the benefits and risks of this approach have not been adequately studied. Methods We conducted a multicenter, randomized trial comparing the maintenance of sinus rhythm (rhythm control) with control of the ventricular rate (rate control) in patients with a left ventricular ejection fraction of 35% or less, symptoms of congestive heart failure, and a history of atrial fibrillation. The primary outcome was the time to death from cardiovascular causes.
Results A total of 1376 patients were enrolled (682 in the rhythm-control group and 694 in the rate-control group) and were followed for a mean of 37 months. Of these patients, 182 (27%) in the rhythm-control group died from cardiovascular causes, as compared with 175 (25%) in the rate-control group (hazard ratio in the rhythm-control group, 1.06; 95% confidence interval, 0.86 to 1.30; P=0.59 by the log-rank test). Secondary outcomes were similar in the two groups, including death from any cause (32% in the rhythm-control group and 33% in the rate-control group), stroke (3% and 4%, respectively), worsening heart failure (28% and 31%), and the composite of death from cardiovascular causes, stroke, or worsening heart failure (43% and 46%). There were also no significant differences favoring either strategy in any predefined subgroup.
Conclusions In patients with atrial fibrillation and congestive heart failure, a routine strategy of rhythm control does not reduce the rate of death from cardiovascular causes, as compared with a rate-control strategy.
 
 

 

 

 

 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 

 

 

 

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Pulse deficit is a clinical sign wherein , one is able to find a difference in count between heart beat (Apical beat or Heart sounds ) and  peripheral pulse .This occurs even as the heart is  contracting , the pulse is not reaching the periphery.This can occur in few clinical situations .

1 . Atrial fibrillation.

2. Very early diastolic  ventricular  ectopic beats

3. Some patients with Pacemaker.

The mechanism is  , the ventricular contractions are  too weak and unable to open the aortic valve  (Or opens feebly*)  , but at the same time they are good enough to close the mitral valve. To open the aortic valve it has to generate atleast 60-80 mmhg pressure , while mitral valve closes even  as LV generates  8-14mmhg  .(LV/LA pressure cross over). So intermitently the  second heart sound  is missed while S1 is retained,  producing more heart sounds and less pulse count in the periphery. The S1 is either felt or heard at the apex but the corresponding pulse is missing . Further , this intermittent absence of  S2  results in totally irregular S1 /S 2 relation.

 

 

Why some of the contractions of LV is too weak to open the aortic valve ?

Because the RR interval varies , the ventricular filling also varies , diastole duration is constantly changing some of the diastole are too short  and LV hardly gets filled , as the LV force of contraction is directly decided by the LVEDV and LV  fibre length these contractions are too weak.

Other published studies

There has been some doppler observations ,where there is a midventricular LV blood flow reversal in atrial fibrillation that could  explain the pulse deficit . Mechanism of production of pulse deficit in atrial fibrillation: assessment by blood flow dynamics

Second Department of Internal Medicine, Kagoshima University School of Medicine.

 http://www.ncbi.nlm.nih.gov/pubmed/3221309

What is the clinical significance of pulse deficit ?

Currently there is no great clinical significance of this phenomenon. But an astute clinician will pick up this sign and it may indicate underlying LV dysfunction. In patients with PPM,  pulse deficit  suggests  pacemaker malfunction .Some patients with cardiac tamponade &  pulsus paradoxus  systolic  blood pressure falls too low to make the pulse feeble or not palpable in the periphery .This situation may mimic a pulse deficit if not recognised.

Dr.S.Venkatesan ,Madras Medical College , Chennai, India

* What is the evidence for intermittent absence or feeble Aortic valve opening in Atrial fibrillation ? I could find this from the book written by Harvey Feigenbaum. whom we consider Father of Echocardiography

 

 

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Peer review of an article even in major journals never scrutinise the “Aim of  a study ” . However big is the journal,  they seem to bother only about the authors, materials, methods, and statistical analysis.  If only they peer review an article , right from the “Aim of the study” like ,

  • Who asks the research questions?
  • Who  defines the aim of the study ?
  • Who decides which drug to be compared with which drug ?
  • Who steers the steering commitee of a trial ?

If only , we could answer these questions without bias , pharma industry and their  regulators  would have ,  far more better image than what they have now !

A typical example for , the aim of the study  to be  wrong  , is  the “ONTARGET’ study on telmisartan.

Here they ( Who ? ) raised an inappropriate  question of     “Non inferiority” of one drug with other  without any  valid reason to compare these two drugs that will benefit the man kind !

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