Feeds:
Posts
Comments

Stunning images in cardiology : Pulmonary atresia with VSD and MAPCA .

January 9, 2011 by dr s venkatesan

Great things happen in India nowadays  .Economy is growing    at  9% , the growth of  automobile industry is  fastest in the world. But in  scientific  research and development  it   has  been traditionally lagging behind . Things are set to change. The medical science , (If you want to call it as industry it is fine !)  especially  the imaging science is making rapid strides. The proliferation of  private and corporate hospitals and institutes   has helped us practice the latest .

Pulmonary atresia with VSD is a rare congenital disease where  there is partial or  total (chaotic  )pulmonary arterial blood supply .

When the pulmonary  artery becomes atretic , what will the lung do ?

It has to get perfused somehow ! It tries to snatch the  blood from the aorta  in whatever  possible manner . Depending on the severity of pulmonary atresia  , there  can be  a total anomalous pulmonary  arterial supply (Type 4 ) .Here , few twigs directly originate  from Aorta, few from branches of  Aorta  and sometimes bilateral  PDA etc .These are collectively called major arotopulmonary collateral  (MAPCAS) .In fact differentiating a PDA from a MAPCA can be extremely difficult .(It has only academic purpose though !)

Hither to ,  visualising  the  MAPCAS was a  huge  task . Aortogram with selective cannulation of MAPCA  was  neccessary.Now,  with the advent of  MDCT we can get some stunning  images  of these collaterals non invasively.

Why is visualizing and delineating MAPCA anatomy important ?

This will facilitate the surgeon to plan  the  unification of pulmonary  arterial flow    and reenginnering the pulmonary circulation  (with or with  out  conduits)

Here is a rare  publication originating from India  in  American journal of radiology  . An  exclusive   article  with  CT scan  images of the  defect .

Amrita  Institute , from  the southern   Indian  state of  Kerala (  also known as God’s  own country )  is doing a phenomenal  cardiology  work  especially  in pediatric cardiology.

Three cheers to the team which published this  master piece . With the courtesy of   AJR the link to the article is placed here.

Posted in Uncategorized | Tagged , , , , , , , , , , , , , , , | Leave a Comment »

Amazing echo videos from India

January 6, 2011 by dr s venkatesan

Rheumatic heart disease is rampant in India.  Advanced forms of mitral stenosis are  still common.

Critical mitral stenosis with LA clot formation is often seen.

But here is a  women in late twenties  presenting for the first time with syncope .

And what  you see inside is  not a fiction  . . .

Left atrial clot occupying the whole cavity ! Where is the blood bound for left ventricle ?

4 chamber view

Luckily the clot is   so  big and MVO is less than 1 sq cm. It is highly unlikely the LA clot can negotiate the orifice.

Small fragments can dislodge .This patient developed syncope whenever she bends and lie down at a particular position.

What needs to be done in this patient  ?

Can it be lysed ? No ,Emergency surgery is required with concomitant mitral valvotomy or mitral valve replacement.

Is there a temporary aortic filter available to prevent systemic emboli from heart  ?

Distal protection devices are  available only temporarily in the coronaries and  carotids during interventional procedures.There is no aortic protection devices  for LA,LV clots in high risk patients .  When IVC filters  are used  block a potential pulmonary   clot why not aortic filters  for preventing systemic emboli  ?

Why we have not thought about  this  . . . is  surprising . May be intensive anti coagulation is as effective .

Posted in cardiology -Therapeutics, echocardiography | Tagged , , , , | 1 Comment »

Please welcome “Coronary calcium ” in non obstructive CAD !

January 5, 2011 by dr s venkatesan

Some say medicine is a funny science . . .  it is true  at times. It will remain so , as long as we convert  a fact into a myth and a myth into a fact at our convenience . It  is  often   fueled  by the  whims and fancies of modern research  ! This phenomenon is happening in a regular  fashion  for  many decades now.

The number one killer disease of heart  is  the atherosclerosis  . Atherosclerosis means hardening  of arteries. The advent of coronary  calcium score with CT scans ,  it became a craze among many physicians . (It was   replaced later  by 64 /128 slice MDCT with unprecedented  commercial over tones !)

How can we  conquer the atherosclerosis ?   when the enigma of calcium in coronary artery is yet  to be solved.

The next few decades will be crucial   as  we are  trying to find answer to the following question .

Is  coronary calcium  good ,  bad or neutral   in CAD  ?

This article in American journal article begins the new year 2011  with good news for people , who show some calcium in their plaques.

What makes a plaque vulnerable ?

Plaque contents , it’s distribution and consistency make it vulnerable. Soft spots  formed by   lipids   may  result in  plaque cracks and fissure.   Semi solid  , mixed  ,  gel like soft  plaques   are dangerously prone for  rupture . Oxidation of LDL,  LDL  liquefaction and tissue metalloprotinase , thickness of fibrin caps , all promote softening.  If none of above  mechanism is operative in a given patient , the   plaque becomes  stiff and hard.

Calcification is the ultimate in hardening . Calcified plaque  is resistant to mechanical deformation.If  stiff  plaques   are less vulnerable , hard plaques ( ie calcified  plaques ) must be least  vulnerable . Calcification   can be called an end result of coronary atherosclerosis.

So , calcified  coronary artery  can be referred to as  a failed  mission of  atherosclerosis .It is  equivalent to  death  of atherosclerosis and denotes the end process of this dreaded disease process.

Calcification tames atherosclerosis  in it’s own den

What is the implication of a stiff hard, sharp calcified plaque lining  (or even projecting ) in the coronary lumen ?

As this study has shown , calcium in the walls of coronary artery is innocuous  . Of course , calcium should not be dense and obstruct the blood flow . This will  require  intervention. Many  consider , calcium as  a foreign body in the coronary artery . But the prevalent understanding is ,  presence of non obstructive calcium  is often  a  non issue or in fact a welcome issue in some.

After all , millions of  human beings  happily roam around  with the hardest possible substance  lining their  coronary artery called  stents.

Caution about calcium

This article does not portray calcium as a healing molecule in  CAD . In  the realistic senseit is  too complex to make such a generalization.  The  message is  , calcified lesions are less likely to result in acute coronary  events than soft , non calcified lesions.

It is well known ,  calcium can be problematic for the interventional  cardiologists  .It makes life tough for them in deploying  stents. Calcium rich lesions exerts  radial force in a diagonally opposite direction and interferes with stent approximation.

It is also believed localised , sharp calcium crystals may tear a plaque  and cause   plaque dissections. This  happens if the calcium is lying in an eccentric fashion overhanging the shoulder region of the plaque   abutting a soft spot.

Final message

It is now clear ,  why calcium  score in CT scans  failed miserably to predict  high risk subsets of CAD. In spite of repeated studies  the researchers failed  to show a positive correlation .  The studies are flawed  as they  were trying to look for a positive correlation  which is non existent . In fact , the above study seems to suggest calcium  score may indeed  predict low risk individuals!

Posted in Cardiology - Clinical, Cardiology -unresolved questions, cardiology- coronary care, Cardiology-Coronary artery disese | Tagged , , , | 2 Comments »

How does LVH produce q waves in ECG ?

December 28, 2010 by dr s venkatesan

LVH is supposed to produce tall R waves . But , we know  often LVH is misdiagnosed as   myocardial infarction especially  anterior MI.  (With deep q waves*  in v1 to v3 and sometimes q in inferior leads as well)

Infarct tissue  is a  cluster of dead cells  , while  LVH is a bundle of live cells . How can the ECG produce similar changes  in both ?

One need to realise ,  ECG does not function  as  a tissue identifying  machine.  It’s job is to simply  tell which direction the current  is traveling with reference to the  recording electrode .

If it comes towards  the electrode ,  R  wave is recorded and  if it goes away Q is recorded.

In infarction it is obvious the dead cells  form a distinct electrically inert  window so that the  muscle  mass located in the opposite pole  (If viable ) will record  q waves.

In LVH  how the  direction of  current get reversed ?

We know,  cardiac muscle  is made  up of not only myocytes , it is enriched with, fibroblasts, interstitial cells, collagen and other extracellular matrix .These non contractile cells have little electrical energy to show off.  In physiological LVH there is  not much proliferation of interstitium . It simply  reflects hypertrophy of  individual contractile units. It robustly produce good quality electricity and the ECG inscribes a tall r waves

Causes of  physiological LVH include

  • Athletic heart
  • Many of the hypertensive patients
  • Early stages of Aortic stenosis
  • Any LVH due to increased loading conditions( In the initial stages )

Pathological LVH

Here  LVH  is predominately  due to  proliferation of fibroblasts  and interstitial cells  .This interferes with the alignment of sarcomeres of myocytes. When the  architecture of contractile units  are  altered ,  it finds difficult to generate good quality action potentials  . Since the ECG is the summation of action potentials  ,  it gets distorted  with local delay,   notch ,slur etc . Ultimately it many  cases q waves are inscribed .

Th  q waves ,  gets amplified by the fibrotic process which is  technically dead cells for the ECG machine at least !.

Note: Pathological LVH grows well with excellent nourishment from ACE gene dependent growth factors. In fact , who will develop pathological LVH  (and who will not  )  is  predetermined by our ancestral genes.  (Other wise called fate or destiny  !)

Conditions  causing pathological q waves

  • About 10% of  LVH due HT can manifest q waves
  • HOCM
  • Late stages of Aortic stenosis
  • Some cases of Diabetic HT combination
  • HT with CKD

* There is one more cause for q in LVH .This is technical .   As  the  heart rotates counterclockwise ,  septal activity instead of  recording a r wave  ,  merges  with the s wave mimicking q waves. In fact this could be very common cause for labeling LVH as MI.

Final message

Q waves are not sacred to diagnose MI.It can be generated  even by live myocytes  when it behaves like an  electrically dead ones.

Posted in Uncategorized | Tagged , , , , , , , , | 1 Comment »

How to calculate pulmonary vascular resistance without even touching a catheter ?

December 27, 2010 by dr s venkatesan

Calculating the pulmonary vascular  resistance (PVR)  has been a  big head ache for all those involved in pediatric and (for many )in adult cardiology as well  . The complex formulas , the delicate  oximeter samples, the catheters, a sick child , an arrhythmia prone right ventricle , restless staff  nurses , and  finally the mathematics  !  all make it a dreaded exercise .

Echo is a great physiological tool  . . . It is now been used  over 50 years . It is our earnest belief ,   Doppler can measure the flow and pressure any where within the heart   however dynamic  the chambers may be !

Then ,why can’t  we have a simple formula  by  this  non invasive method  to calculate PVR  ?

Yes ,  Dr Abbas et all  from the desert hospital  of Arizona  raised  this question and  reported a new equation to calculate PVR.

Their  hypothesis is as simple as this . . .

  • Pressure     =    Resistance X Flow
  • Resistance = Pressure /Flow

Pulmonary vascular resistance = PA Pressure/PA FLOW

Substitute PA pressure with TR jet

Substitute PA flow by   RVOT VTI (  Velocity time integral )

And  we  get

PVR = TR Jet velocity/ RVOT VTI x  10

This  is the simplest way to arrive at PVR at the bedside .

An example

Is it validated ?

Yes .

Then,why it is not being followed widely ?

It is  a  too  simple  method to  use   !  That  is  the biggest excuse ! We are tuned  to  think  ,  a  complex parameter can not be measured in a  simple manner  .  Any thing simple must be  wrong !

But the reality is  . . .

Cath calculations are   much more  complex with so many variables   which  can  get terribly wrong .

The irony  about this  hypothetical  science of PVR is ,  we do not know  which is  gold the standard ?   In fact , none can be  a standard .  So ,  to label PVR  derived by echo ,  as an   inferior modality  can not be accepted  .It is all the more funny ,  as  we are  trying to  define a new  formula    with  the help of   flawed and battered   parameter  namely  the cath derived PVR .

Final message

Abbas’s  formula  is  indeed a  realistic way of arriving at PVR by echocardiogram. If only we measure it routinely  /serially in as many patients as we can , a new data base  will  be created .Which can later be  proven as a fact.It is suggested every cath lab should try to validate this formula.

Link to full text article : Courtesy of JACC

Abbas AE, Fortuin FD, Schiller NB, Appleton CP, Moreno CA, Lester SJ. A simple method for noninvasive estimation of pulmonary vascular resistance. J Am Coll Cardiol 2003;41:1021-7.

Posted in Cardiology - Clinical, cardiology -Therapeutics, Cardiology -unresolved questions, echocardiography | Tagged , , , , , , , | Leave a Comment »

Medical communications : Signals too weak !

December 23, 2010 by dr s venkatesan

Doctors are obsessed  with science .  Science is man-made , often , the quality of which is far from perfect (Apart from scientific inaccuracies , personal and commercial conflicts creep in )  .Hence  ,  patients   may not get  the true benefits of genuine science  today . This has a huge moral and economic implications .

The entire life time savings  of  our population , is threatened to be consumed by the vagaries of modern medicine. A recent WHO  report  reveals  , the  major cause for  poverty  is attributable to  the frivolous and  greedy   modern health care delivery system. Many times,  bulk of the nation’s wealth is  being  spent on  prolonging the final   few  months  of     lives(Often unproductive ! )  of their fellow citizens.

The irony is ,  many of these expenditures have questionable benefits.

  • A simple car is prone for fewer errors but it still serves it’s purpose .A hybrid car which switches between hydrogen, petrol and electricity  is obviously vested with numerous unexpected issues.
  • An ordinary  cell phone is easy to operate,  while an Andorid 2.2 phone  is loaded with great  applications  ,  but the  original purpose of a phone  ,  namely communicating with others is often   compromised.
  • Modern medicine  is a monster machine  with  thousands of  visible and invisible switches . The funny thing is most of us do not even know jobs assigned to these switches .Worst of  all , these controls  can self ignite  or put off  on its own . One can imagine . . .  the potential errors  from this monster controlled by a  minuscule master of medicine .

Does your patient aware of all those uncertainties ! Why is it so difficult for us to communicate  the above facts to our patients ? Mankind can benefit ,    if we put across the  following  doctrine to our public domain.

A medical  non  intervention can be as safe  as  an  intervention ,  but one has to accept the occasional complications  arising out of a  non intervention . In this context  it should be  realised  ,  we never hesitate to  accept the   consequence of  a  modern  intervention.

Why and how our  mind is readily accepting even deaths  during an  inappropriate procedure , while we struggle to accept  even a temporary set back  for not doing a needy intervention.

What is the solution ? We need to uncomplicate  medicine . . . simplify them .When doctors intervene with common sense as a weapon  to tackle the  scientific excesses patient is bound to  benefit.

Don’t ask don’t tell  dogma   should be replaced by ‘”Tell  without asking” .Be transparent about the limitation  of science.

Documenting and adhering to protocols is satisfying for upholders of science , but one should realize being unscientific also   can help our patients many times.

When your hospital protocol says check for hypoxia in every patient  with dyspnea ,  mind you it may land your patient to a totally   unwarranted  ventilator assistance for a very transient hypoxia reported your fellow over phone.

Here is an article that reveals ,   how a  few oral words of   advice could help  both financially and academically in critical care.

http://chestjournal.chestpubs.org/content/138/6/1475.abstract

 

Final message

William Osler said   ” Lesser is better” in medical  communication  . It may not apply today.

Did Osler  was  referring to  falsehoods in medicine ? , Then ,  probably he  is 100 %  is right . . . for the current times !

Posted in bio ethics, medical quotes | Tagged , , , , | Leave a Comment »

How to lose the golden hour in STEMI ? The curious helicopter ride to the cath lab !

December 22, 2010 by dr s venkatesan

STEMI is an cardiovascular emergency . We alert  instantly the services  of  911/108/1066 . What we fail to realise is , the  physician’s thought process  should also  be equally fast  . Before dispatching  a STEMI patient by ‘air mail” to the nearest cath lab ,   spend few thought full moments ! We have  a simple and   equally effective option  ,(If not superior )  of revascularisation  , right in your clinic or hospital ! Use it liberally , it is not a inferior treatment !

This article  is from the prestigious  journal  “Annals of emergency medicine” .It confirms a longstanding doubt regarding the efficacy of  air lifting of STEMI patients.

A shocking observation . . . is . . .  many of those patients who are air lifted  for primary PCI   receive none of revascularisation  modalities !  Learn  how  many  of our patients have a futile helicopter ride in the golden hour of STEMI  !

Final message

Even airdropping of STEMI patients to cath lab for primary PCI is not  enough in this unique   race against time  . So , in the management of STEMI ,  we need lots of non -medical  sense* !  .Please judge    “the delay”   due to transfer carefully   and  always consider administering  the thrombolytic agent  when a patient  with STEMI  arrives   within 30 minutes.

A definite primary thromolysis (Within 30 minutes ) is  often  better than a PPCI  (Potential primary  PCI), which  may  or may not materialize in time  !)

*Please  realise  even  inclement weather  and traffic jams can have a impact on coronary patency !

See  comment about this article in Heart wire

What next ?   On site  mobile cathlab ?

Posted in Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions | Tagged , , | Leave a Comment »

Coronary arteries showing exemplary friendship !

December 18, 2010 by dr s venkatesan

Sharing and caring for  others  is the  unique human nature . Some believe this is  now gradually   becoming  rare in human domain ,   but still  found in plenty among  animal species. While modern human  likes to live independently  wants to stand on his own legs  our  biological system still  think differently .

A 40-year-old man with diabetes and hypertension with class 3 angina had this angiogram

RCA to LAD collaterals

A different view

RCA to LAD in RAO caudal view

See , how a  pair of  human coronary arteries  mutually  help   their  colleague  at times of distress !

The astonishing observation is ,  the  RCA even as its suffering  with  a severe,   long segment disease it  helps out-of-the-way ,  with a long arm  of  support to  the entire LAD . While , the LCX reciprocates  the RCA by sending  thank you twigs to distal RCA

LCX sending reciprocating twigs to RCA

By the way , this patient was referred  for CABG after an   intense  debate in the cath meeting  .The argument ranged from medical management /PCI/CABG.

The key question were

  • How good is the collateral’s and what  are the chances of  graft flow  exceeding the collateral  blood flow ?
  • What is the effect of CABG on the existing collateral’s ?

Final message

Coronary arteries  has unique sense of sharing and friendship at times of vascular crises.

This is the fundamental basis for   coronary collateral circulation .

Posted in Cardiology -unresolved questions, cardiology-Anatomy, Uncategorized | Tagged , , , , , , , , | Leave a Comment »

Land mark reviews in cardiology : How to choose an ideal coronary intervention in unstable angina ?

December 18, 2010 by dr s venkatesan

Cleveland clinic is a leading centre for cardiac care .Major technological breakthrough occurs from this institute than any other place. Thousands of articles come out every year. Some articles , get global attention and make  a huge impact. These are usually related to a new hi- tech modality like CRT devices or percutaneous aortic valve deployment etc ,etc.

                                                Some articles , which are very important  may not get the due  attention . Journal editorial boards often  have a scorecard called impact factor .That is ,   how  a  journal  is  impacting the practice habits of  medical professionals . Ideally we need to have to grade individual   articles with impact factor .Many articles may not have any significant  impact  however good the impact factor of the journal.

Here is an article,  which excellently depicts the principles of management of ACS.  It was published in 2003 JACC,  by Steven Nissen  from Cleveland,  Ohio .It deserves more attention . Every cardiologist , involved in ACS management should read this, especially the interventionist.

Link to article placed her with courtesey of JACC

Posted in Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology -Therapeutics, cardiology journals, cardiology- coronary care, Cardiology-Coronary artery disese, Cardiology-Land mark studies | Tagged , , , , , , , , , , , , , , | Leave a Comment »

Acute coronary syndrome is not a disease of heart !

December 18, 2010 by dr s venkatesan

Acute coronary syndrome  is primarily a disease of blood vessel , which perfuses  the heart.  It can even be a disorder of blood, often called vulnerable blood which predispose  for intra- coronary thrombus .

Mind you  , heart is an innocent bystander ! to the onslaught of  coronary atherosclerosis !

Hence , we  often use two terminologies .

CAD : Pure vascular (Coronary )  disease without  any structural and functional impairment of heart  ( No Angina, No myocardial damage ) Most of the asymptomatic plaques  , non flow limiting  lesions, incidentally detected by the modern coronary imaging gadgets  fall in this category.

When does  CAD becomes CAHD ?

CAHD : Coronary artery heart disease .Here not only the coronary artery is diseased , but it has it’s mission fulfilled   ie target organ either damaged structurally (STEMI, NSTEMI ) or functionally (EST positive , Chronic stable angina CSA )

Does the heart does any wrong to suffer from Acute coronary  syndrome  ?

No, it is simply not .The fault lies in one or more  of the following   .Generally at-least two these factors are enough to impede blood flow )  . They  combine to produce an ACS.

  • Blood defect
  • Vessel wall defect
  • Slowing of flow (Stasis)

This is called as Virchow’s triad   suggested over 100 years ago . Still valid in the era of per cutaneous  aortic valve implantation.

* The concept of de-linking  disorders of  coronary  vascular disease  from myocardial disease  is vital  in understanding the implications of current modalities of treatment. 

Even though we PCIs target the culprit ie blood vessel , it need to  realised , we  always fall short of real target . . .namely the heart . In coronary interventions  the catheters and wires roam around superficially over the heart  and they never even touch the heart .This is the reason PCIs are struggling to prove it’s  worthiness over medical therapy in many CAHD patients , which can reach deep  into the vessel, heart  and even every individual cells of heart.

Many (or . . . is it most ?)  Interventional  cardiologists have a bad  reputation for ” failing to look  look beyond the lesion” .  It is estimated  a vast  number  of cathlabs  and CABG theaters worldwide  are engaged in futile  attempt to restore coronary artery patency after a target organ damage is done .This is akin to building flyovers  to dead and closed highways .

Salvaging a coronary  artery and reliving a coronary obstruction is an entirely unrelated and futile  exercise to  a patient who has a problem  primarily in  musculature .

The much debated concept of  documenting  myocardial viability  , before revascularisation  died a premature death as the concept  by itself , was not viable commercially . (Viability studies   , tend to tie down the hands of device industry further , some  interventional   cardiologists began to see this concept  as an  interference to their freedom to adventure  )

Of-course , now  we have  other parameters  phenomenon  like  FFR estimation by Doppler , epicardial  -myocardial dissociation, slow  flow , no re-flow are  gaining importance.

Final message

ACS is primarily a disease of blood vessel but it’s impact is huge on heart. We need to look beyond the lesion .Restoring  a blood vessel  patency  to an ailing organ (Heart ) is not synonymous with total  cardiac intervention  and protection . There is lot more to cardiac physiology other than it’s blood flow. Heart muscle is a too complex organ to be controlled by few balloons and wires  which beat around the bush.

Posted in Cardiology -Interventional -PCI, cardiology -Therapeutics, Infrequently asked questions in cardiology (iFAQs) | Tagged , , , , , , , , , , , , | Leave a Comment »

« Newer Posts - Older Posts »