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Archive for June, 2010

It is a well known  cardiac auscultatory  sign,   S 1  becomes  variable in intensity with the onset of atrial fibrillation.

In physiology , the intensity of S 1 is determined by many factors.

  1. The valve morphology(Thickness, Calcium , Rigidity )
  2. Valve mobility
  3. PR interval
  4. Force of LV contraction
  5. Preceding RR interval (4 and 5 are inter related)
  6. Insulation and auditory factors (Thick chest wall  etc)

How does atrial fibrillation modify the intensity of  S1 ?

It is to be noted , atrial fibrillation alters only one  of the above factors, namely the RR interval which becomes irregular.

The mix of short and long RR intervals  occurs at random  . A short RR interval, results in a relatively softer S1  and vice versa . The mechanism is directly attributable  to the degree of LV filling and subsequent change in force of contraction .

Many times , at fast ventricular  rates (Say >150) the distinction between short- long cycles is  negligible in terms of net cardiac cycle.

If  the RR interval , is too prolonged there can be an  inverse relationship  with s 1 intensity .It gets  muffled as the  mitral valve floats back  to it’s  orifice and a partial or even complete  closure occurs , making  force of LV contraction irrelevant in the genesis of S1 .

The vanishing act of PR interval  in atrial fibrillation.

It does not require great brains  to  understand ,  if P waves are absent ,  PR interval must also be absent !

If PR interval is absent ,  there  can be no  influence of it on the first heart sound. Logic demands  absence of PR interval must have some sort of  influence on the intensity of S1. As far as i know cardiology  literature has not answered this query.

What are the two types of S 1 variation ?

Experince  has shown us , the variation of S1 can be of two types*.

Sequence 1 : Varying between , Loud -Louder- Loudest -pounding

Sequence 2: Varying between , Loud -Normal – soft -Muffled

* Applicable only for those with shrewed ears !

S 1 intensity with reference to underlying pathology : Valvular vs Non valvular atrial fibrillation

It is obvious the impact of  varying RR interval on  the intensity of S1 will directly depend upon the underlying pathology. The  intensity of   S1  in  non valvular AF (Like , lone AF, Thyrotoxic AF, Hypoxic  AF ,Ischemic AF etc)  are  more vulnerable to  changing   RR interval .

In rheumatic heart disease , the influence of valve morphology , rigidness, calcification and presence  of MR  generally prevail over the  impact  of changing RR interval .So,  in a case of tight mitral stenosis  and AF  it  is expected the sequence 1 is more common .

In lone AF or AF due to CAD , sequence  2 is more likely *  Associated LV dysfunction , and ischemic   MR may further dampen the intensity of  S1 .

Clinical implication

Hearing  few occasional  loud  S1 in AF , is an indirect indication that underlying LV function is good,  as it reflects the force of  LV contraction .

Silent AF

Some hearts are notoriously silent even in the midst of AF. If  the silence is not  due to obesity  or  other insulation defects,  it suggests a sinister diagnosis ,  like severely  dysfunctional ventricle  like  DCM etc.

As a corollary, it is often noticed ,  palpitations* are , often not  felt  by patients with dysfunctional  ventricles  in spite of atrial fibrillation. (As loud S 1 is rare with dysfunctional ventricle)

*Palpitation is a symptom that equates to Dp/Dt of ventricles.

What  happens to mid diastolic murmur in AF ?

The murmur length  varies  linearly with reference  to RR interval. The pre systolic  accentuation disappears ,but   pre-systolic component may persist .

Final message

Simple, bed side auscultation during atrial fibrillation can give us vital clues about the etiology, and the  underlying LV function .  Let us not be ashamed to talk about clinical cardiology  . . .at least in the bed side !

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Bifurcation lesions and ostial lesions  continue to  challenge the expertise of   interventional cardiologists.

Variety of techniques have been described. Geo positioning of a ostial lesions ,  exactly on the rim of ostium  is required  . This is very difficult in  many patients  , as stent migration either into side branch or protrusion into the main branch is common. Both reduce  optimal  PCI outcome  .

Here is a innovative  technique   described  first by  Szab0 in 2005 TCT conference .

Highlights of the technique

  • It is a twin guide  wire technique.
  • The Circumflex guide  wire  is threaded over the most proximal strut  of  balloon mounted  LAD stent .
  • The guidewire makes sure the LAD stent move beyond the LAD ostium .
  • Of course some technical limitation is  there, this seems to be a good option at least in some deserving  LAD ostial or LCX ostial lesions

Technical hitch

The balloon and stent is to be manhandled prior to deployment.  We are little awry to do it

The review article in the journal  Eurointervention

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Japanese cardiovascular society publishes this journal  called as  “Circulation  journal” It has some great articles in every Issue .The Impact  factor is consistently rising.

Please do not get confused with AHA’s  “Circulation”

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There are thousands of forums for medical science.

Most are aimed at research.  Few are available  to scrutinize  research.

Cardiac safety research consortium

This one from Duke university ,  is a great beginning in collaboration with FDA .

Let us welcome , this whole heartedly and wish all success in it’s motto !

Namely , exposing all safety issues in the modern cardiac therapeutics .

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Learning (and of course unlearning! )  is a continuing process in the field of medicine. . We have exclusive  medical universities for various specialties . The popularity of  radial access for doing coronary interventions is progressing very fast and  the  femoral puncture technique  is expected soon to become   extinct !

Here comes a virtual on-line university for mastering radial artery interventions.

I wonder  , they issue a  Master’s degree  on the subject !

Thanks to Terumo for  initiating the concept .

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This article is in response to the prevalent belief  about  primary PCI for STEMI   endorsed by world cardiology forums. (Caution: A highly personalized version)

Time window in STEMI

  • Is the window half-opened  or half closed ?
  • Is it open at all ?
  • Or ,does it open only for primary PCI  ,and tend to close down  bluntly for thrombolysis

Modern medicine   grew faster than our thoughts .We have witnessed the audacity of advising  arm-chair treatment  for MI  till later half of   last century . Now we are talking about  air dropping of patients   over the  cath lab  roofs  for primary PCI.

Still ,we have not conquered the STEMI. While ,  we have learnt to “defy  deathin many patients  with cardiogenic shock , we continue to lose patients(“Invite death “)  in  some innocuous forms  of ACS due to procedural  complications  and inappropriate ( rather ignorant !) case selection.

Note : The ignorance  is not in   individual physician mind ,   it is prevalent in the whole cardiology knowledge pool.

The  crux of the issue for modern medicine is ,  how to reduce risk  in patients who are at  high risk and how not to convert a low risk patient into a high risk patient by the frightening medical gadgets.

In other  words ,  arm chair treatment for STEMI was  not (Still it is not !) a dustbin management . It has a potential to save  70 lives  out of 100. What many would  consider it as  ,  nothing but  the natural history of MI .

Medical management of STEMI is ridiculous !

That’s what a section of  cardiologists try to project by distorting the already flawed evidence base in cardiology. Some think it is equal  to no treatment. Here we fail to realise, even doing none has potential to save 70 lifes out of 100 in STEMI who reach the hospital.

Out of the  remaining , 10 lives   are saved by aspirin heparin (ISIS 2) and the concept of coronary  care . Another  7  lives are saved by thrombolysis (GUSTO,GISSI) . PCI  is shown to save saves one more life (PAMI).The remaining 6-7 % will die in CCU  irrespective of what we do .

Of course , now medical management has vastly improved since those days  .  A  thrombolysed ,  heparinsed ,  aspirinised ,  stanised  with adequately antagonized   adrenergic ,  angiotensin system   and   a proper coronary care ( That takes care electrical  short-circuiting  of heart)   will score  over interventional approach in vast majority of STEMI patients.

Now comes the real challenge . . .

When those 70 patients who are likely to survive  , “even a arm-chair treatment“, and the 20 other patients  who will  do a wonderful recovery with CCU care ,  enter  the cath lab  some times in wee hours of morning  . . .what happens  ?

What are the chances  of   a patient  who would otherwise be saved by an arm-chair treatment be  killed by vagaries of  cath lab  violence  ?(With due apologies ,statistics reveal  for every competent cath-lab   there are at least  10  incompetent  ones  world over !)

In the parlance of criminology , a hard core criminal may escape from  legal or illegal shoot out  but an innocent should  not die in cross fire , similarly ,  a cardiogenic shock patient with recurrent  VF  is  afford to lose his  life , but it is  a major medical crime to  lose a simple branch vessel  STEMI (PDA,OM,RCA )  to die in the cath lab,  whom in all probability  would have survived  the arm chair treatment.

Why this pessimistic view against primary PCI  ?

Yes, because  it  has potential to save  many lives  !

Time and again ,  we have  witnessed  lose of   many lifes  in many  popular hospitals in  India ,  where a   low risk MI  was  immediately  converted  to a high risk MI  after an primary  PCI with number of complications .

I strongly believe I have saved 100s of patients  with  low risk MIs by not  doing  for primary  PCI in the last  two decades.

*The argument that PCI confers better LV function and longterm  beneficial effect is also not very convincing for low risk MIs .This will be addressed separately

The demise of comparative efficacy research.

Primary PCI is superior to thrombolysis  : It is agreed , it may be  fact in academic sense .

Experience has taught us , academics rarely succeeds in the bed side.

“superiority studies can never be equated  with comparable efficacy”

Only the  questions remain . . .

  • Where  is comparative efficacy  studies in STEMI ?(Read NEJM article )
  • Why we have not developed a risk based model  when formulating guidelines for   primary PCI ?
  • Is primary PCI for a PDA /D1/OM infarct worth same as PCI for left main ?
  • Is high volume center guarantee  best outcomes ?

Who is preventing comparative efficacy studies ?

Primary PCI : Still  struggling !

This study from the archives  of internal medicine tells   us , we are still scratching  the tips  of  iceberg (Iceberg  ? or Is it something else ?)  of  primary  PCI

Even a  pessimistic approach can be  more scientific  than a optimistic  !

When WHO can be influenzed and make a pseudo emergency pandemic  and pharma companies  make a quick 10 billion bucks  ,  Realise how easy  it is  for the   smaller ,  mainstream cardiology literature  to be  hijacked and contaminated .

Final message

Why we reverently follow the time window for thrombolysis,  while  we rarely apply it for PCI ?   This is  triumph of glamor over truth . The open artery hypothesis remains   in a  hypothetical state with no solid proof  for over 2o years since it was proposed.

Apply your mind in every  patient , do a conscious decision  to either thrombolyse  ,  PCI or none . All the three are  equally powerful approaches in tackling a STEMI , depending upon the time they present .Remember , the third modality of therapy comes free of cost !

Never think ,   just because  some one  has  an access to a sophisticated cath lab 24/7   , has a iberty to overlook the  concept of time window  !

Remember  you can’t  resuscitate   dead myocytes , however advanced your enthusiasm and   interventions are !

Realise , common sense is the most uncommon sense in this hyped up human infested planet.

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VSD is  the leading  cause  of   congential heart disease .

  • The natural history is wide open , from totally asymptomatic  , incidentally detected in   childhood to a fulminant cardiac failure  and death in early  infancy .
  • Many small VSDs get closed by year 10. None of the large VSDs close spontaneously.Few of the moderate sized VSD may get closed.
  • The site of the VSD is a major determinant of spontaneous closure. Muscular  VSDs are more likely to get closed .Of course many of the membranous VSD have  at least a rim formed by a adjoining muscular septum
  • Associated defects, RVOT obstruction and late onset AR also has a  influence  on the natural history.
  • Progressive PHT  leading onto   Eisenmenger  syndrome  occurs  has become a diagnostic curiosity in many countries .

It  is natural to expect  the VSDs   to share a  close relationship with  the conduction system which   fights for  “equal rights”  to occupy the inter ventricular  septum  , (In spite of   a defective septum ! )

How often we see conduction defect in VSDs ?

It is  rather surprising  to note   conduction  defects are not  common in VSDs .In fact it can be termed  rare . How  this is  posssible ?   VSDs , however large it maybe   ,  usually spares the conduction system . This is simply due to the fact , developmentally the two systems  , ventricular septum and the electrical  system  of the heart comes from different embryological focus and and are simply anchored together.

If the IVS is not formed properly ,the bundle  of His and it ‘ s major right and left branches  are  simply displaced  and not are  destroyed  ,  they  tend to occupy  one of the rims of VSD

*Further, a VSD located peripherally and distally towards the apex has little impact on the conduction tissue as it has already fanned out and small little twigs are affected ,while central , proximal,  and basal VSDs  can have more significance .

Classically ,  it has  major  significance   for the  surgeons than cardiologists  , as post operative blocks are more common than the preoperative blocks !

What are the  changes to the conduction system in various VSDs ?

Membranous VSD

  • Migration  of  A-V node   posteriorly toward crux of heart *
  • His bundle  courses  along  the  posteroinferior rim of defect

* This makes sure the compact AV node never comes into picture of VSD . It  also it explains the  rairty of   complete heart block  due to mechanical damage  to the  AV node  by the  VSD jet

How to avoid  injury during surgery ?

Sutures  are  made a few millimeters from postero-inferior rim,  Do not penetrate  the septum.  Suture along  RV side  of the  septum  as the  His bundle  is  often located on the  LV side of muscular septum.

RV approach to close VSDs,  make  postoperative RBBB a common issue but generally it has no great clinical significance

Location of conduction defect in various  VSDs

  • Membranous VSD  –  Conduction tissue runs along posteroinferior border of defect
    Muscular VSD
  • (Especailly with Inlet extension)  – conduction tissue is anterosuperior to defect
  • AV canal defects . This is the only type of VSD where serious defects of conduction occur  .Interruptions can also occur in the AV node.

Coming  soon . . .

Where  will the conduction system run in single ventricle where there is no IVS ?

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