Archive for October, 2011

Human coronary circulation stands  unique among  others as it is a   life-sustaining circulation.It is  considered   a great  medical achievement   to visualise   the right and left coronary artery  system by coronary angiogram.  Actually  what we see is   only  a  fraction   of  the surface area  of  coronary circulation . The surface area of  epicardial coronary arteries   constitutes  less than 5 % of entire coronary vascular tree .

This  is the reason  normal coronary angiogram can never mean normal  coronary circulation !

This huge gap in our perception is the single important factor  that  explains the vagaries  of modern coronary care .

This also  make any coronary  scenario  a  reality .

“A patient with normal coronary angiogram getting a myocardial infarction the next day and a severe triple vessel disease living comfortably with medical management”

So ,  it is essentially a   false  sense of  scientific accomplishment   by the  cardiac scientists  at  least in the  of coronary circulatory physiology.

There are innumerable channels of micro vessels traversing across the heart, sharing , bridging , branching, penetrating  and  perfusing the muscle mass.They can be anatomicaly patent , physiologically non patent .They can be recruited by hemodynamic stress . It is also influenzed by  favirable growth milleu and hormonal and neural stimuli.

What determines the extent of these invisible circulation ?


An in vitro heart with special catheters showing the true extent of coronary circulation: Courtesy http://eurheartj.oxfordjournals.org/content/28/3/278.full.pdf+html

Why many cardiologists   do not give due credit  the   coronary collateral  circulation  ?

Right from the days  of  Levine in 1970s( Who made a seminal contribution  about coronary collateral)  the  utility value of  coronary  collateral  circulation   was  never able to convince the cardiology professionals .

It has been our traditional  teaching ( without much evidence of course  !) coronary collateral circulation  is not effective to support blood flow during exercise . This fact has been  disproved  many times . Coronary collateral circulation was indeed useful in limiting damage in ACS and  relieve symptoms in stable angina.It helps  in reverse remodeling and provided electrical stabilty as well in post MI population.

Still  the concept  was  alienated  and   made   totally irrelevant  in the interventional  era  . Many   cardiologists  found well-developed collateral’s as an interference to their expertise and ego since it has a potential to alter the indication of PCI.They  continue to have  strong  scientific conviction (Pseudo ?)   that man made collaterals must always been superior to God made collaterals !

Whenever  some credible  reports emerge about  collateral circulation   being   equivalent to  revascularisation procedure , these concepts were  prematurely buried for some reason.

In the last decade there was a concern  about  performing  PCI in patients with well-developed collaterals  .The argument was , they tend to develop early stent occlusion and restenosis . It  was a genuine  query  raised by few thought leaders in the field as  collateralised vessels  suffer from  low flow states  after PCI ,   if the pre -existing collateral continue to function.

But then , few  studies countered this  , and   said PCI  is safe and  in fact may  fares well   in  patients  with  extensive collaterals .

In these  studies  interventionist’s  argument looked  amusing !  as they  seem to  define a  successful  PCI  as  not only to open the occluded vessel  but also  make sure to close  all functioning  collaterals  .(What a  a pity for our natural biological  angiogenic forces which had  worked  and  grown meticulously for months!)

Cardiac science in the current format,  makes   the future look  bleak for coronary a collateral circulation .With  early PCI  becoming a norm we will never ever allow the natural collaterals to  grow  ,  and even the  established collaterals  will have to face a stiff   fight  for survival  with  sophisticated coronary interventions .

Competing interest in the filed of  coronary collateral   research

While the basic scientists want  to  grow collaterals with angiogenesis ,  stem cells etc  interventionists   continue to  indulge in rampant angioplasties which  will suppress  collateral growth.

This implies we will struggle to  establish  the true  importance of  coronary collateral circulation .

Final message

Can it be an  effective form of revascularisation  ? 

My personal  inference  is   coronary collateral  circulation  “would and should”  have  a definite role  in at- least  some of the subsets  with chronic coronary  syndromes. If we think otherwise . . .    it’s against the principle of  natural biological science .

A good  collateral   system with optimal medical management  can save not only our  patient’s  lives but also  their hard earned currencies !


Here is a rare article in European heart   journal that discuses coronary collateral circulation  . Let us welcome such wonderful  reviews which keep the interest alive on the filed.


Read Full Post »

Is there  an  anginal equivalent  in cerebral circulation ?

Coronary Ischemia produce  angina . . . Cerebral  ischemia do not produce  corresponding   ischemic cerebral pain ! Why ?

Exertional angina  is the dominant  event when coronary artery is  stenosed  . When cerebral artery is stenosed   exertional  head ache do not occur .  So , how does brain respond to  exertional  ischemia ? (EST is also  a stress  to our  cerebral circulation  .  If only we record  EEGs  during treadmill we will  know the truth !)

But in the clinical setting  ,  we are not only surprised by lack of head ache during cerebral  ischemia   , even  exertional   giddiness  is not a common presentation . Instead ,  brain  primarily   respond to ischemia  with focal neurological  deficit instead  of  generating  pain within the skull. This is often referred  to as TIAs .

But,  chronic ischemia  has its effect in the form of lacunar  infarct with its  clinical counter part  – vascular  dementia.

Electrical rhythm  disturbance   like   Ischemic cerebral  arrhythmia are also  known to occur .

The reason for these coronary vs cerebral stenosis behavior is  not clear . Number of possible explanations can be offered.

  1. Paradoxically ,   in spite  of  brain  being a central neurological  command , by itself  has less pain receptors  especially to ischemia
  2. The hypoxic threshold for cerebral cells may exceed many fold to  that of myocytes.
  3. Cerebral  auto-regulation is more developed than coronary regulation.
  4. The circle of  Willis  , though   do not help  much when individual  cerebral arteries are  occluded  suddenly , it does  play  a role in balancing cerebral circulation  at times of chronic  low flow states and  ischemia .
  5. Finally , even in physiology  many of us are comfortable with  little  brain function. One estimate says we  hardly  use   2-3 % of  brain’s processing power (Like our computer  CPU) .Hence  intellectual , deterioration  are  very  late  phenomenon of cerebral ischemia.



How often head ache occur in  acute stroke ?

It occurs in less than 15 %  in acute ischemia .( In chronic ischemia it is very rare ? non existent ?)

The exact source of pain is not clear .

A stretch induced pain , dull infarct zone pain, cerebral edema induced transient  ICT may also contribute .


It  was a real surprise ,  when I found this journal exclusive for  head aches !


What is the mechanism of vascular head ache ?

It is ironical  ,  more often an excess blood flow by inappropriate vasodilatation that cause many episodes of vascular head ache . These confirm the complexities of  ischemic vs non ischemic pain within the brain .

Read Full Post »

The answer to this  seemingly innocuous  question is not  that simple at all.  We know ,sinus tachycardia is  a common expression of thyroid  excess while  sinus bradycardia is the  hall-mark of thyroid depletion. So  obviously ,  the first thing that would  strike us  is ,  there must be  something  cooking between thyroxine and the SA node .

We realised much later , there is no direct action of thyroid hormone on the SA node instead it has a crucial interaction with adrenergic system which   has the major influence on chronotropy.

Click on the image for flash Animation (Courtesy Mcgraw Hill )

How does thyroid interact with adrenergic system ?

Thyroxine (T4)  is an inactive molecule , it has to get converted to  T3 for its action. This conversion takes place inside target cells like myocytes, pacemaker cells  (of course  it has action  on virtually any metabolically active cell !  )

The most important point to remember is , unlike catecholamines the thyroid receptors are located  in the surface of  the nucleus  inside the cell , instead of cell membrane . Surprisingly T4 does not require any specialised transporter to enter the cell.It simply diffuses into the bi-lipid layer of cell membrane as T4 is immensely lipid soluble.  . After entering the cell in the cytoplasm it gets converted into  T 3.

This T 3 is attracted towards the nucleus. Once  it is attached to nucleus , it brings about  changes in the gene configuration and  through  messenger RNA results in new protein generation . These cellular  elements are vital for maintaining the  ionic channels and ports and anti-ports.Among these the most important is adrenergic receptor molecule , an its  signal system namely the GTP/Adenyl cyclase/Cyclic AMP units in the cell membrane .

Thyroxine is a physiological hormone  required to maintain these adrenergic  receptor complex on day-to-day basis. (It can be called as cell servicing hormone )

The circulating catecholamine’s  action is  heavily  influenced by the thyroid hormone status.   Sympathetic  nervous system is the live wire for human biological system.  So , when thyroid is in excess the entire metabolism of  cell is increased and vice versa happens.With the close interaction with adrenergic system  , one can understand how thyroid excess causes anxiety state and depletion causes  depression.

Coming back to heart ,

  • Thyroid hormone   up-regulates  beta receptors in cell membrane and augments the action of epinephrine and  result  sinus  tachycardia .It can have positive inotropic action as well (Hyperdynamic  state )
  • Aguments intracardiac  conduction.
  • The action of thyroid hormone on heart can well extend to the pathological phase, where in it can cause multiple ventricular ectopics and atrial fibrillation. (Note the striking similarities between  these arrhythmias   and   adrenergic  arrhythmias !)

What is time frame for  thyroid  hormone action ?

Obviously thyroid hormone can not  have a rapid onset action  since it invites the nuclear synthesis  (Like steroid hormones)  it may take few weeks time for thyroid hormone to express its effects.

How does beta blockers exert its action in thyrotoxicosis ?

This occurs in two ways.

  • The beta blockers occupy the adversely up-regulated dense  beta receptors of cell membrane and  prevents excess adrenergic  action.
  • There is some evidence beta blockers prevent conversion of T4  into T3 .This seems to be less important than its direct sympathetic blockade.

For effective control of thyrotoxicosis one need to administer beta blocker in combination with anti-thyroid drugs.

Will calcium blockers be effective in controlling the tachycardia of thyrotoxicosis ?

No it is not . It may  reduce the heart rate a little but never to the extent of beta blocker. This is another  indirect evidence for  the interaction between thyroxine and adrenergic system.

If thyroid hormone is able to potentate the circulating catecholamine action why not it be used as a

positive Inotropic in cardiac failure ?

A very valid question.  It was tried by many researchers especially in dilated cardiomyopathy. .For some reason it has not worked well , except in patients with  associated with hypothyroid  state.I personally believe thyroid hormone must have  a major role  in chronic heart failure in spite of the fact  we have  proposed sympathetic blockade as concept for regulating cardiac failure.

Read Full Post »

Human coronary artery anatomy would  rank  top among  all human biological mysteries. The variations in their branching pattern is next only to palmar creases and cerebral gyri !

The left coronary artery can divide in to two , three  or even four branches occasionally.The trifurcation  occurs in upto 20 % of population .The ramus intermedious  can some times be a major division .Usually it supports the diagonal or OM territory.

It is very rare to see a ramus  take a long course . Here  is a patient whose LAD is small  which  falls  short of LV apex . Sensing this , the ramus travels all the way to apex and support the LAD in distress !

RAO caudal view shows the Ramus reaching all the way to LV apex! Note the diminutive LAD and absence of true OMs from LCX.

* Technically  this can  also be  referred to as a rare form of dual LAD system .

Read Full Post »

Second heart sound in TOF is often single and loud . It is often  best heard in left 2nd intercostal space as well as on right 2nd  space.

This is primarily due

  1. Presence of  pulmonary stenosis  and  resultant reduced pulmonary blood flow makes P2 soft or absent .Hence  A2 becomes loud by default.
  2. In tune with any  cono -truncal anomaly  , aortic root  is  anteriorly  malposed  in TOF. This brings the aorta  closer to chest wall  (Nullifying the  aquastic insulation  of main  pulmonary trunk  ) and results in a  booming aortic  second heart sound.
  3. Increased flow across  aortic valve . In cyanotic heart disease with reduced pulmonary blood flow aortic flow is augmented and may even result in dilatation of aorta . A large aorta with increased flow is perfect setting  for  generating a loud A2  . It  is common to hear a  aortic ejection click as well in these situations .

When you hear a single  second heart sound at  the base  of heart  , how do you recognise it to be   A2  or P2 ?

Will be answered shortly.

Read Full Post »

Gynecologists  do have  interactions with cardiologists  frequently  in their day to day practice.In fact ,  in any big hospitals cardiologist consult  invariably happen every day . In our institute  fellows visit the maternity ward almost daily to give opinion   about a cardiac issues .  These are mainly emergencies like  breathless   rheumatic heart  patient  in labor , A DVT to R/O pulmonary embolism,  women  with prosthetic valve waiting for delivery, and a  women with LV dysfunction posted for hysterectomy  etc.

While it is common  for  our  Gynec colleagues to call us in  emergencies ,   and we do have a cardiac clinic every week ,  it is rare to discuss broad based practice  issues. There is little inter departmental  brain storming sessions.

Here is an excellent initiative from  European union where they have  created consensus document for reducing  cardiac risk  in peri menopausal  women.(http://eurheartj.oxfordjournals.org/content/28/16/2028.full.pdf+html)

The beauty of this document lies in the succinct practice points written in every  page .

In India , even though premier bodies like cardiological  society of  India  exits it rarely  considers bringing about such guidelines  in collaboration with other scientific bodies . ( To be  more precise  . . .they  do not have their own guidelines either ! )

I believe , FOGSI  (Federation of Obstetrics and gynecologists society of India ) is doing a much better job and they have created exclusive guidelines in O & G.

Read Full Post »

Q : Beta blockers reduce  blood pressure mainly through

  1. Reduction in Heart rate
  2. Reduction in cardiac output
  3. Negative Inotropic action
  4. Vascular sensitization to circulating catecholamines
  5. Blocks  Renin secretion and  reduce vascular tone.

Answer : (May be  4 as well !)

Our understanding of beta blocker’s  action  in SHT has changed considerably over the years .The  negative inotropic action on the myocardium  attributed for BP reduction ,  is no longer considered  important . Now we know , beta blockers can  reduce peripheral vascular resistance significantly.(There were days , we presumed  the opposite to be  true ,  ie when beta blockers are blocked , alpha action will overshoot to cause excess vascular resistance ! ) This  is more of  perceived fear.  This concept was never proved convincingly even in the  dreaded  Prinzmetal  angina* where beta blockers are  relatively contraindicated for fear of  aggravating vasospasm.

*Note : This is may  still be valid in selected few  who  show a  tendency for  Raynaud  phenomenon especially in peripheral vascular  system.

Additional  factors   influencing  beta blockers in SHT

  • Suppression  of  central adrenergic drive  ,  modulation of   brain stem vasomotor centre  are aslo considered vital . This action is linearly related to the ability of beta blockers to cross the blood brain barrier which is more with lipophilic drugs like metoprolol.
  • The role of beta blocker in isolated systolic hypertension in elderly  is unique.Here it reduces the myocardial dp/dt (ie contractility )  and hence help them prevent  systolic spikes of pressure and the resultant  stroke.
  • The newer  vasodilating beta blockers  like Nebivolol, (Nitric oxide mediated ?)  and Carvidilol may have additional advantage in controlling BP.
  • It needs to be appreciated , beta blockers combine well with  diuretics like  hydrochlorthaizide  .This  makes it easier to control severe forms of HT  especially volume dependent ones in  both young and elderly. (SHEP trial )

Final message

The modification of vascular response to catecholamines  is  the single most important mechanism of reduction of blood pressure.

This may be a direct consequence  of  1.  Blockade of  vascular  adrenergic receptors . Indirectly  through suppression of  Rennin secretion.

Read Full Post »

Instent restenosis is a  common problem.

Diffuse long segment instent restenosis is somewhat rare.

We  encountered one such patient who had diffuse instent restenosis of RCA.

ISR is ssupposed to be rare in DES, but here ISR occured with a Cypher stent  one year following implantation

He presented with angina which  was relieved  by plain baloon angioplasty.

 link to a  related article in  this  site  regarding the mangementof ISR.

Read Full Post »

We know primary PCI is a race against time  both for the  patient  and his  physician.

What is the upper limit for this unique race where the stakes  are high   and it involves  human lives  and  big  corporate  warfares  ?

  1. 6 hours
  2. 12 hours
  3. 24 hours
  4. 36 hours
  5. 54 hours
  6. Time does not matter . You can do a PCI as late as possible as long as  patient has sufficient insurance coverage and we have the expertise

Answer :

Please note there is  only one exception  . Cardiogenic  shock has been given a extended  lease of time window (Which can be technically up to  54 hours ) . PCI can be performed   if the onset of shock  is   within 36 hours  of STEMI  and to be performed within  18 hours after the onset ! )

* Even though we  have a  well set criteria for re-perfusion which bans primary PCI to be performed after 12 hours , cardiologists have enough technicalities to overcome this hurdle and keep doing the futile pPCI well after 12hours.

How they are   able to indulge in these futilities   without  any ethical issue ?

The answer  is very simple. Instead of calling it as primary PCI they refer to it as delayed PCI or rescue PCI !  Strict time specific guidelines are only for primary PCI . By changing the terminologies they   make a mockery of the concept of time window which  is vital for any intervention for STEMI !

Read Full Post »

Success of primary PCI is defined by  different yardsticks  by  different  cardiologists  , in different  institutions !  But , for the patient and his family,  getting  discharged   alive with out symptoms is a huge  success !

They  do not bother  even if they are charged  Rs 3-4 lakh for their stay ,  as they  believe  surviving  a heart attack  is a God’s grace   rendered thorough the hands of  the doctor.

But we know  the real success lies elsewhere. Cardiologist’s   perception of   success of  pPCI   should be based on scientific concepts. Unfortunately many  physicians  continue to  think like  their patients  . This  tendency to get self gratification  with a patient’s  frame of  mind is  common  and  needs  introspection .

This is esepcailly  true for primary PCI . It came with big fanfare  a decade ago . Soon ,many cardiologists developed  a habit  of criticizing   the  practice thrombolysis for STEMI .If primary PCI is such a superior modality  every patient   should be prevented from significant  myocardial damage following  STEMI .

Primary PCI  may be the the most logical method  still , for reverting the STEMI process  . But “A properly performed  primary PCI  as a  concept ” lies  mainly  on paper ,  not  been  replicated in real world for various reasons.

Please remember , a successful primary PCI

  • Is  not restoring TIMI 3 flow  in IRA
  • Is not relieving  the  angina
  • Is not discharging a  patient in stable condition

Even if  . . .  we accomplish each one of the above  . . .   if   the patient  carries  home  anything  equal  to ,  or more than moderate LV dysfunction ,  primary PCI  has  deemed to have failed.

Final message

What is the reality  check ?  In one  of  the  preliminary analysis   out of 20 randomly selected  patients  who have undergone STEMI*   within 12 hours  , significant LV dysfunction  was present in  12  patients making it pPCI only 40 % successful   in real world  .( Which  would struggle to beat the outcome of  promptly administered fibrinolysis )

* Primary PCI done in state of the art institutes .

Read Full Post »

Older Posts »