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Archive for November, 2011

What is a coronary risk factor ?

Right from the days of  Framingham study we have conferred a privileged   place   to  few  cardiac  risk factors.

they are

  • Diabetes mellites
  • Hypertension
  • Hyperlipidemia
  • Smoking
  • Obesity

They are referred to as conventional risk factors .  What is the convention ?  Do they deserve  the  cult  status they enjoy ?

Today we also have a  cluster  of non conventional risk factors like , Lip (a) , low HDL, Homocystenemia , CRP , Apo B etc . Currently ,  in any large cohort of CAD  up to 30 %  do not exhibit even a single conventional risk factor  . This is a huge number .Hence   we tend to give more importance to genetic make up and mental stress etc  .The search is still  on for newer risk factors .

Why some research  findings are difficult to comprehend ?

It is because we are yet to  decode the  intricacies  of  human biology  fully . Our knowledge is so superficial  , as we chase  a pseudo scientific  proofs   for  a  presumed  hypothesis.  The classical example is the concept called good cholesterol (HDL) and reverse cholesterol transport which  is never based on solid scientific foundations.

Take the sorry story of  Torcetrapib

Many consider  low HDL  as an independent CAD risk factor to be a  myth  or else why should we miserably fail  to have any positive effect of  increasing the HDL  levels by pharmacological means . (One argument is physiological  and natural elevation of  HDL  would still be beneficial  . But the issue is still wrapped in a statistical mystery

This  paper from  JAMA   adds further insight into our ignorance about  the  genesis of CAD .

The data is from  NRMI registry.

The statistics  reveal  a stunning fact .In  the overall CAD cohort ,  patients  with no major risk factors  experience  highest mortality and the ones with maximum   risk factors have least mortality ! What a shocker of a study ?

http://jama.ama-assn.org/content/306/19/2120

This  paper  would bring  jitters to the population ,  but in the real sense it sends an important message .

A significant population develop CAD without any  known risk factors.(14.5% in NRMI registry )

If a person develops  a CAD without any major risk factor  ,  it seems  . . . it is not at all a  good news   !  rather we need to introspect , why  without any risk factor he or she has suffered CAD ,

One inference is  their vascular system is more vulnerable ! Some hidden factors are operating . How to manage such  patients  without any target to intervene ?   A diabetic dyslipidemic smoker has a   definite  therapeutic target  .

What about these   lesser  humans  who   develop   CAD without any known risk factors  ? They  tend to suffer more !

Is  CAD  due to DM/SHT  is better than  others  ? This study seems to say so ” Known devils are better than unknown ones ”

Final message

Unlearning is an   “essential and fundamental”  component of   scientific learning .  In this progressive scientific world , this applies  most to   medical profession  than any other field !

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Exertion and  acute coronary syndrome (ACS) has a tricky relationship. On the one  hand, it  would  appear they are not related at all  as only a miniscule of patients   give history of recent severe exertion prior to ACS   , while  few others  tell us  a clear- tale of   unaccustomed  exertion ,  just prior to the onset of chest pain.

Here is case history  of a  man  who was rushed to our  ER from  Madras central station ( Our hospital is located just opposite to it !  )

A  48 year bank officer  was  about to board  a train to Patna   . It was a rainy  November  evening ,  his car got struck in traffic .He along with  his family members were rushing to catch the rain  .He had  to run fast with his heavy luggage  .Even as they boarded  the train successfully and occupied their  seats  ,   within minutes  he  developed intense chest pain and sweating . The distressed family de-boarded the train and was rushed to our hospital  . Yes  you guessed it right   . . . he  was showing an extensive ST elevation  in anterior leads on arrival.

So what  has  happened ?  What is the coronary hemo-dynamics during heavy unusual physical exertion ?

The above patient did  not have any obvious risk factor . He vaguely recalled ,   one if his family doctors telling him ,  he had borderline high BP and was never prescribed a  drug . His wife told us  he has been a emotionally  liable individual .

It is well  known  , sudden exertion in an  emotional  milieu   would  result  in  intense  adrenergic drive  . (Here the emotion was anxiety/ fear of missing the train )  Adrenergic drive was  amplified with the  isometric exercise (heavy suitcases ) ,   shoots the intra  coronary blood pressure (normal 45-60mmhg)  into  dangerous spikes . (By the way , what happened to  coronary auto regulation  ?) . We also  realise simple raise  of  intra coronary pressure alone is not sufficient  .These patient  will  harbor at least some degree of  atherosclerosis  which face a  shearing stress and give way /tear  or fissure resulting in  a sudden substrate for intra coronary  thrombosis.  Some of them may manifest  only  as coronary vasospasm  .When sustained  it can also result in a full-blown acute coronary syndrome.

The concept of trigger vs risk factor

One should remember  both physical and mental exertion   act  mainly as a  trigger (They are not  major risk factors  like DM/HT/Smoking /Dyslipedemia) . All that is required ,  for  this   vulnerable population  to fire  is a trigger.  Physical exertion ( especially  isometric)  when  associated with  emotionally charged  brain  sends a  perfect  invitation  for an impending  ACS !

Another example  for untoward  effects of  exertion

A middle aged man who had  impaired glucose intolerance and dyslipdemia  was referred for an  EST.He did complete  12 minutes of  Bruce  protocol  comfortably . But  on the same day evening  ,  he felt  uneasy  and came to our ER ,   only to record a full blown STEMI .

These events may be rare but if properly understood   these  patients can teach  us  few   lessons in the genesis of ACS and coronary hemodynamics .

Special  issues  about   exertion in post PCI patients

One of the purpose of doing  PCI  for CAD  is to improve the  functional  capacity  (and possibly to prevent future ACS) . Paradoxically ,  we  continue  to have  some apprehension about subjecting post PCI  patients  into early stress testing . (I remember reading some guidelines that advice us to  avoid stress testing strictly for 6 months post PCI  ! Is it true ?)

If a  cardioloigst  is  not too comfortable  putting their  patients  into a  treadmill  post PCI ,  it only implies they doubt their efficacy ! It   would  also imply  these  patients   should  not be allowed to exert to their full capacity in day to day  life events as well .(Attention  cardiologists   . . . Yeh  . . . we have a  fundematal problem on our hand !)

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Modern  day cardiology can do wonders. It can revive a sinking  patient in cardiogenic shock with IABP , LV  assist ,   multivessel angioplasty and bring back  life . On  the other  hand  , a young man with an infected mitral valve who is put on  intensive  antibiotic  regimen   , progressively deteriorates  throws an emboli into brain ,  raise his urea  creatinine  , cardiac   failure worsens and finally succumbs .

This is a clear case of failure  of medical therapy in infective endocarditis .  It is almost certain  surgery would have saved him .

Why  the delay ?

So the question that is been debated for so long is   “When to intervene with surgery in IE”  ?

While we show extreme  urgency for ACS , the same is not shown  with IE.This is going to change in the future .Thanks to the  EASE trial (Early surgery  in  endocarditis )  This land mark study from Korea  is likely to revolutionise  the way we will look into the  problem  of infective endocarditis. It was presented in the just concluded AHA annual scientific sessions  in Orlando

This was  our  observation  too . The issue was discussed in  the year 2008 .It reminds me ,  every  learned  thought or opinion is in fact a paper  but unfortunately modern science does not accept a  fact without evidence of a  study . Until then  it remains  as a crap !

I am glad  to note   genuine concepts will some day  get ratified . Kudos to the Korean team.It is a great study to do with  many ethical issues.

Click below to read the related article

Link to EASE Trial  http://www.theheart.org/article/1313215.do

Next question  on the cards

Should there be  a time window above which medical therapy should be   deemed (Doomed !) to have  failed  , so that the patient becomes a default candidate for surgery.

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  • Acute myocardial  infarction is the number one cardiac emergency .
  • About a million papers and articles are available in  medical literature about STEMI.
  • Management of STEMI when they present early is addressed by every text book.
  • It is  really surprising to note there is no  simple and  specific guidelines  to manage STEMI when they present late to the ER .
  • Such a scheme is vital for physicians,  as experience suggest almost 40 % of all STEMI arrive late and are ineligible for specific reperfusion strategies.

The following  flow  chart is  exclusively meant for usage in STEMI when they  arrive late >12 hours .

This is a personalised version based on working in one of the oldest CCU in  Asia which handles  about  2000 acute coronary syndromes every year with a mortality rate of 6-7 %  Hope one can bear with it !

Please click on the chart for a high resolution Image

Comments are welcome

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Third heart sound is a unique heart sound  because its   perfect physiology  to hear it  in the young  ,  while the same may denote  serious LV dysfunction in patients with myocardial disease.

It is a low pitched  early diastolic sound usually correspond to  the end of rapid filling phase.The mechanism of genesis of this sound has been debated for many years .(Still I think it is unsettled !)

We know genesis of intracardiac sound is contributed  by three factors

  • The blood flow
  • The valve motion
  • The myocardial contractile and  relaxyl  property

The above  three is collectively  called cardio-hemic system . When this system vibrates heart sounds are generated .In  the genesis of S3 all the three may be important . The only difference is ,  in physiological S3 the valvular and hemic component play a major role . In pathological S3 the  myocardial component has a pivotal  role .The distended LV facilitates chest wall impact during the rapid filling phase . It is now  accepted  LV S3 is  generated outside the LV  . It  was proved elegantly by Shaver et all with sound recording on either side of  LV /Chest wall.

It is to be emphasized  the mechanism of genesis of S3 is diagonally opposite in  physiology vs  pathological  S3 in some conditions . Rapid AV filling  can  rarely be  responsible for pathological  S3  associated with severe LV dysfunction , while chest wall  impact can contribute in both physiological as well as pathological S 3 .

 One can understand the complexity of genesis of  S 3  , as  there are  too many  determinants  that contribute in  varying degree of acoustics.

Factors determining the intensity of S3 is complex 

  1. Age,
  2. Atrial pressure,
  3. Rapidity of  flow across the atrio-ventricular valve,
  4.  Rate of early  diastolic relaxation 
  5.  Distensibility of the ventricle,
  6.  Blood  volume,
  7. Ventricular cavity size,
  8.  Diastolic momentum of the  heart,
  9. Degree of contact (coupling) with the chest wall, thickness
  10. Character of the chest wall
  11.  The position of the  patient.

 

It is ironical, pathological   S3 which is a  diastolic  sound  though ,  still  its genesis  is largely  determined by the systolic function of the heart .This mystery is partially solved as we recognise  now ,  LV S3 is equally common in  severe degrees of diastolic dysfunction. In fact ,  while we were studying the relationship  of LVS3 in DCM  , it  has strongly predicted the  presence of   severe restrictive pattern in them .

 

 

 Reference

1.Multimedia of S3

http://www.inovise.com/learn/s3causes.html

2.Importance of  S3 in cardiology NEJM 2001 article

http://www.nejm.org/doi/pdf/10.1056/NEJMoa010641

3.Chest wall impact theory of S3  by Shaver

Shaver JA, Salerni R. Auscultation of the heart. In: Hurst, ed. Heart. 8th ed. New York, NY: McGraw-Hill, Inc; 1994:291.

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Mitral regurgitation is  one of  the most common lesion of rheumatic heart disease .Mechanism of MR in acute rheumatic fever is different from chronic rheumatic heart disease.

Acute Rheumatic fever

The following mechanisms contribute to MR of acute rheumatic fever

  1. Edema of leaflets (Carey Coombs murmur )
  2. Valvulitis
  3. Small verrucous  vegetations (See Image )
  4. Acute LV dilatation in fulminant cardiac failure.

* Note  : Acute rheumatic fever in its first episode can never  cause stenosis  however fulminant the fever may be  .There is no acute mitral stenosis .But ,  during recurrence and reactivation some amount of stenotic process may occur.  Still ,  recurrence and reactivation are more often related to significant MR rather than MS. ( Isolated mitral stenotic lesions  rarely  give h/o recurrent rheumatic fever )

Chronic rheumatic  heart disease

As the mitral valve gets progressively damaged  any combination of MS or MR occur .The following mechanism are involved in  the genesis of MR. (Pathology of Mitral stenosis is not discussed here)

  1. Chordal shortening, tethering , pulling , prevent proper co-optation
  2. Chordal lengthening
  3. Chordal disruption (Minor > Major )
  4. Prolapse of either AML or PML (Not both ,unlike myxamatous MVPS)
  5. Infective endocardits  of  leaflet
  6. Perforations of  leaflet
  7. Annular  dilatation
  8. Fibrosis of posteromedial/Antero-lateral   pap muscle(Rare )
  9. Left atrial pathology

* The direction and the  width of MR jet is  related to the mechanism of MR.

If there is chordal shortening due to fibrosis  of mitral valve  co -optation plane is altered . The degree of chordal shortening , pap muscle fibrosis (rare)  symmetry of chordal involvement determine the MR.

Rheumatic mitral valve prolapse

  • This could be  more common than we realise.
  • It can be true or pseudo.
  • True prolapse occur due to chordal weakening or lengthening .
  • In chordal disruption the leaflet tips usually become flail

Since rheumatic process fixes the PML first , the AML   appear to overshoot the plane of PML and   appear as prolapse.(Pseudo )

The sail like AML commonly  directs the jet posteriorly and laterally .(Murmur conducted to axilla and back )

It is rare for PML to prolapse in RHD , if  it does occur ,  it directs the jet anteriorly (murmur conducted to aortic area mimic AS !)

It is rare to see a  perfect  central jet in RHD  . presence of  Central jet is a good sign to consider mitral valve repair.

Myocardial involvement in RHD.

Even though rheumatic fever is a classical  example for  pan-carditis , it is surprising   to note (Of course fortunately !)   how  myocardium escapes in the  chronic process of RHD.

Is it really true  ,  myocardium do not get involved in chronic RHD ?

Clinical cardiologists rarely discuss this issue. Pathogists indeed have documented significant lesions within myocardium  . Involvement of left atrial myocardium and  rarely  ventricular myocardium in the sub mitral  zone  can influence the  degree of  MR

* Even in acute rheumatic fever with fulminant carditis , myocardial involvement is  disputed by many  ! . My belief is ,  there will   definitely a subset  in   both acute and  chronic  forms of   RHD   , in which myocardium  gets  involved . In our institute LV dysfunction associated with RHD occur in  up to  5 % of  RHD population .

Importance of knowing the mechanism of MR

Two aspects  appear important

1. Is there a potentially  reversible component in pathology so that we can  wait  before intervention  ?

I have seen children referred for mitral valve replacement due to severe MR  . In due course   MR regress by the time they reach the tertiary center (waiting period included ) At least one child i remember,  the MV surgery was canceled  due to spontaneous regression MR.

It was later found the MR was  more of valve inflammation than degeneration .

* Always think about the possibility of reversible rheumatic MR  in every severe isolated  MR in children (Do not apply this rule in adults or in combined MS or MR  )  Do a ESR, ASO and start an  intensive anti inflammatory therapy  , aspirin with strict penicillin prophylaxis .With this  one can definitely postpone the surgery  in few cases  and  may avoid it altogether !

2. Surgical implication

If we could delineate  the  exact pathology of MR   it will facilitate  the   repair . Annular  reduction and  neo  chordae  etc . Of course ,the surgery could be  very  difficult in scarred mitral valves ,  Dr Sampath kumar *of AIIMS  New delhi , India  would  feel other wise !

*A pioneer in mitral valve repair in chronic  RHD (See reference 2 )

Questions  that need  answers

How is balloon/Surgery  related injury different from rheumatic process ?

Why is  rheumatic  mitral vale  prone for bacterial infection ?

What is the relationship  between  extent of  aortic valve involvement and  degree of mitral valve involvement in RHD ?

Reference

1.http://circ.ahajournals.org/content/94/1/73.full?sid=10599470-3563-4c38-b688-c5fc8c032f96

2. http://icvts.ctsnetjournals.org/cgi/reprint/5/4/356

Books

There two popular books exclusively  for cardiac pathology

1.Silver

2. Renu Virmani

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