Archive for July, 2012

A 38 year old man presented with  acute breathlessness  and chest pain .His ECG is  posted  below . The ER in charge   medical officer promptly handed over the patient to   STEMI  alert    group (This is how  cardiologists are   referred to !   in one of the leading corporate hospital in India )

Note Atrial fibrillation , ST segment elevation, in pre-cardial leads

A team of  white coated  humans  in  various  gender and ages  swarmed the patient . ECGs and text where shared  among  the  STEMI alert group  through  I pad 3 which transmitted  HD  quality ST elevation with a  retinal  precision . A senior consultant   insisted   to shift the patient to cath lab direct  . Since he had  signs of cardiac failure , one of  the wise Junior fellow wanted  to correct the failure with Nitroglycerine  and  Dobutamine before rushing him to cath lab . Hence he was put on hold in the side room of ICU .

Echo examination showed LVH and wall motion defect could not  either confirmed or ruled out .  Initial  Troponin was negative . In the mean time the bio chemistry results came. He had a creatinine of  5.2 and Potassium of 6 meq . Hence the patient was diverted to Nephrology unit  and  dialysis was done. The next day morning  his ECG   looked like this .

It  may  sound a  pessimistic , but  still I would consider   the above  episode  is  a rare  example of appropriate care happening  ! This patient was diverted in a timely fashion from cardiology  care  to the  Nephrology . Please note , it is not the  the  clinical acumen that   helped  here.  If  he had  not presented with  LVF   he would have been a victim of inappropriate care  and landed on the cath-lab table directly  !

Final message

Every moment in clinical medicine is important , especially during the genesis of  diagnosis.  Where the patient lands  . . . in a frighteningly  large  hospital is as important  as the disease process itself. In this scientifically arrogant medial atmosphere  most of us, are  tuned  to view every problem as their own  ! This is  the default mode of modern medical  thinking process . How faulty  we are ?

The future is worrisome  as the field of  Internal medicine is  at risk of dying a premature death (or is it dead already !)

By the  way  what is the mechanism of ST elevation and Tall T waves in hyper-kalemia ?

Many factors contribute .

  1. Is it a true ST elevation  ? There is reason to believe   the tall T waves drag the fag end of ST segment along with it .
  2. Next is  related to QT interval . Hypo-kalemia widens while hypo-kalemia does  the opposite .(  though not classically) .
  3. When QT is shortened the segment gets squeezed in within a limited space ,  in order to accommodate the  ST segment it   gets rolled up and elevated . (Like an up sloping ST segment  in extreme tachycardia during stress  testing)
  4. Whatever  be the mechanism it is something to do with potassium ion flux .Transient intra-cellualr hyper-kalemia.
  5. Another possibility is diffuse uremic peri-carditis , which is a common accompaniment  of renal failure.In fact this patient did have a peri-cardial rub

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Doppler Mitral Inflow velocity profile   is the key to  assess LV diastolic function . The ratio between  E and A has become most popular parameter .

In the absence of atrial contraction what shall we do ?

The answer is simple .  We have 2 D parameters of LV diastolic function.

LA dimension ( > 30 % basal dimension which is  usually >  4 cm  ) is a most specific marker of diastolic dysfunction in the absence of   mitral regurgitation or stenosis.

The only available  velocity E wave profile  can help .A short  E deceleration time in a short cycle  would suggest  significant diastolic dysfunction.High amplitude   E  wave  > 2  M/sec in the absence of MR  will suggest diastolic dysfunction .

Curiously  ,   it can be  assumed    an episode of   lone AF  per-se   ,  be an indicator of diastolic stress for the left atrium .

After all ,  why should a person all of a sudden develop an episode of AF .(Hypoxia, Ischemia ,  excluded )

Other parameters.

Mitral annular velocities / E propagation velocity   / E/E’  are other tissue Doppler parameters  can be used.

Pulmonary venous flow velocity is  largely not useful  (Since A reversal does not occur )

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Medical science and commerce grow hand in hand .  Many believe   the field  of   medicine has  ceased to be a pure  science long ago . Both are mutually inclusive . We have no other option ! If there is no commercial interest   . . .Who will fund cardiology research ?  Then  . . . How are you going to  develop a biological pacemaker or  the  eagerly  awaited  total artificial heart ?

Without involvement of the commercial forces ,  no break through is possible . If you take medical science  , majority of growth has occurred by the motivational force of  medical industry  . Here is an  exclusive website for sub specialty called cardiopulmonary business .

But do we  have  the  medical research in safe hands ?

Why  a  hastily  developed  cardiac  device enter  the human domain and recalled within 2 years  fearing grave Injury   ?

Why a drug known to cause serious side effect was purposefully  blinded with a hidden agenda  till the drug earns a  billion or two ?

What is in store for future generations  ?

When the profession is at the mercy of  forces other than  patient care as a primary aim  there is every reason for it  go awry and  become   a dangerous health hazard  . If any medical professional   who does not see this , as an important issue  for man kind ,  requires a rebooting for reality  !

Public should realise , what they often get  in the name of science  is  a huge  human body trial and victims of   biological  shopping  . It has   wide-ranging  Implication . It is ironical , we are in a piquant  situation , where   our bio-system   has to  fight not only against  the  diseases but also  the misplaced scientific methodology  and fraudulent practices.


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ICDs have revolutionizes the management of refractory VT   and in the  prevention of  sudden cardiac deaths in vulnerable population.Every year  100s of  thousand    ICDs are    implanted . Three  industry leaders are providing  state of  art  machines. The technology is evolving . Till recently , the  shocking leads of ICD has  a separate connectors  called DF1 .

Now,  we have all 4 leads incorporated into one lead  connector called  DF 4 . It has gained tremendous interest  among cardiologist and stand alone electro-physiologists  . The reason is simple  – Ease  of   implantation !

Does the  ease of implanting  do compromise   the  efficiency of ICD  system ?

I am surprised by this article . Here is an  excellent analysis by a truth seeking   electro-physiologist  about the   genuine issues of ICD implantation  especially to potential problems with  DF 4 interface .


A related article .


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A patient with  extensive anterior STEMI  presented 18 hours  after onset of  chest pain . He  was  other wise stable and free from angina but had persistent ST elevation (5mm in V 1 to V 5 ). He had a  total occlusion of LAD  with TIMI zero  flow . He had a  tight PDA lesion  as well . A bed side echo revealed LV EF  of 50% . The septum was hypo-kinetic but did not appear severely dysfunctional .

So , it was decided to open up the LAD. The moment  LAD was opened he developed severe acute LVF  /   flash pulmonary edema   .  Even after a 30 minutes of  heart (Fire )  fighting  he could not be resuscitated .

What is the mechanism of death here ? Expert  STEMI interventionist  from core  labs  may answer this !

An acute ischemic MR with myocardial disruption was suggested . Why it  was triggered after opening the IRA ?

Three mechanisms were discussed

  1. Re-perfusion injury
  2. Collateral  damage
  3. Physiological  de-stabilisation of  Contra -Lateral lesion (Remote lesions )

Re-perfusion Injury ?  How relevant it is in cath lab ?

Is re-perfusion injury  electrical  ,  mechanical or  both ?

In this particular patient even though there was a total LAD occlusion , the segments supplied   by  the LAD  was partially functional and  it was contributing to LV  pump function.  The moment  a trickle of   flow was established  , some thing happened and the whatever  little mechanical function  his LV  had  was also interrupted  . The LV came to standstill and the patient died .

If re-perfusion Injury is  simply an   electrical  event   like VF ,  it can be resuscitated . If it is mechanical  outcome is bad ! This is not a new concept  . It is  part of the  once famous  concept called myocardial stunning . There are  lots of reasons   for stunning  to be a  clinically relevant phenomenon .Unfortunately   if any cardiologist talks about it in 2012 ,  he is at risk of  labeled  as old fashioned !

Collateral damage.

One more mechanism which we feel that  might have contributed to death here  is   the  “collateral damage” .(This is not cross fire !)

We know collaterals can be recruited within 12 hours in many STEMI patients . In some  it can even salvage  significant mass of  myocardium . The acute collaterals to LAD may be interrupted  during primary PCI . Once you poke the lesion the coronary  vascular  bed which had dilated  (as a response to total occlusion ) may react with inappropriate vasoconstriction . This raises the local hydrostatic pressure (Myocardial edema)  and further impede  the   incoming  micro collateral flow . This a very  critical time  for the myocardium  where antegrade and retrograde flow are kept in a fine balance .

Interference with remote lesion Hemodynamics .

Another possibility  is  the  opening the  LAD lesion some how  impact on remote lesional  flow as well (PDA  in this patient  )

Please remember ,

Even a transient hypo- tension can have  devastating effect in  the  hemo -dynamics   of  non IRA  territory  especially if it harbors a critical lesion !

Final message

Coming to the title question  , Is no – flow better than  slow- flow in late presenters of STEMI ?

Common sense dictates whenever  an artery is obstructed  just get rid of it.  When  it  comes to the heart it must be done in an urgent basis That is the essence of primary angioplasty  . . .  agreed . But in this  patient  I believe ,  the  common sense  was proved wrong !

Truths are always hidden.  The  science of  myocardial re-perfusion is a perfect example . We need to learn a lot still !

This I  call as  Para cardiology : Heart  facts without  evidence !

Counter point

One may argue this   is an  exceptional case  in STEMI  intervention. Don’t  hype   exceptions  and undermine the importance of a great concept ! Exceptions  and rules  are directly related to our  experience  we have accrued.  Exceptions are the great  knowledge substrates  and help  crack  medical  mysteries !

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Ventricular septal rupture is a major mechanical complication of STEMI . Excruciating  chest pain ,  is the sine qua non of  any myocardial tear , dissection and rupture . It is surprising ,   VSR  following STEMI  is rarely a painful event . I can recall number of  such events  , when a  stable   patient with persistent ST elevation  in the  coronary care unit ,   wakes up next morning  with a systolic murmur.And echo reveals a septal defect promptly.

Three  reasons  can be  proposed  for relatively  pain free rupture of IVS in STEMI.

  1. Typically  VSR  occurs in 3rd or 4 th day of infarct . By this time myocardium  can be as  soft as an ice cream ! . There is not much stress and strain at the site. The necrotic  debri just gives way to spikes of   LV systolic pressure .
  2. For rupture to occur there   must be  transmural infarct  .The pain nerve terminals also die in the process .
  3. Further , it is a cavity to cavity rupture  (LV to RV ) . Direct pericardial  stretch  does not occur .

* Ventricular free wall tear   is a near fatal event is extremely painful .This  often occurs  in the first 24 hours when  the nerve terminals are  alive . The free wall rupture is more of  a  tear in the plane of  myocardium . The  pericardial  (epicardium)  layer has  rich   somatic  nerve supply .

In summary

Early  myocardial  tear   involving the epicardial  surface can be severely  painful  .  Late giving way  of softened  , necrotic  often  hemorrhagic muscle ( especially in the IVS ) is less painful or totally painless.

Coming soon   . . .

By the    . . .  what happens  to  pieces of  septal myocardium as it  gives way  and enter the right ventricle   ?

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A pulse wave is generated  with each heart beat  when  the potential energy is converted into kinetic energy.

  • For the pulse wave  to travel from the heart to periphery  Aortic integrity is vital.
  • The pulse wave travels through the walls of arterial tree  , in the process the wall itself is set into oscillations .
  • Whether the  moving blood imparts the  pulse  on the walls or the walls itself  vibrate  independently is not clear .

The following   M -Mode  echocardiogram  of  aorta from young man   stunningly  documents  the  morphology  of  central aortic  pulse  wave . Note how closely it resembles the  Intra- aortic  pressure curve recorded with a catheter.

The anterior aortic wall motion was sliced from the above motion image  to create a non invasive recording of aortic   pulse wave

This simple observation was made in  a crowded  echo lab our hospital. Cardiology fellows can explore  further  ,  the link between aortic pulse transduction (From mechano -hemodynamics)

Further studies are warranted regarding the  rate of raise (Slope)  of aortic  wall motion  , and the quantum of motion ,its correlation with central aortic pressure etc. This would unravel the the mechanisms  of Isolated systolic  hypertension  , where a stiff aorta amplifies  the systolic pressure due to loss of elasticity .

Read also

Rail roading of  Aorta in Severe  LV dysfunction

Wind Kessel effect

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Caution: This is a fairly lengthy article . Optimal Reading time  15  minutes

Cardiac failure is a progressive systemic disease  ,  even though the primary problem originates in the heart .Most of the symptoms and clinical features are related to Neuro-Endocrine activation instigated by poor pumping function.When the diminishing cardiac function exceeds the compensatory mechanisms , full blown cardiac failure sets in and get into a vicious downward spiral unless  intervened.

The conventional treatment model involves  on three targets.

  • Reduction in pre -load(Diuretics)
  • Improving  contractility (Inotropics)
  • Reduction in afterload  (Vaso- dilators)

Though the concept looked attractive  there are many missing links . Medical treatment   lags far  behind  the desired goals. Still , it  can stabilize most of the patients with cardiac failure till they reach very late stages.


Inadequately  treated  CHF is not  synonymous  with refractory failure  . But  ,  practically it is the commonest cause for refractionaries . Hence  , every patient must be scrutinised meticulously for adequacy of treatment.

Primary mitral  , aortic valve  lesions causing cardiac failure need  not be considered as refractory  cardiac failure . In the strict sense myocardial disease /damage  either  idiopathic or secondary to CAD  would form  bulk of refractory failure .

(For example a patient with critical aortic stenosis with severe LV dysfunction is   technically  refractory cardiac failure but functionally it could be a  simple  expression of  after load mis- match )

COPD -Cor pulmonale /Primary pulmonary  hypertension  / End  stage congenital  heart disease  and   Eisenmenger syndromes   form separate  group of  CHF and would not be discussed  here.

The valves , the fibrous skeleton, the  pericardium are integral parts  of the heart . Individual disease process can affect these compartments in a differential pattern .

When we  refer to  refractory heart failure   it amounts only two  large disease groups.Ischemic and idiopathic  cardiomyopathy.The whole myocardium is a single unit. If it is destined to fail  it will fail in toto.  There can be reversible factors that can be addressed.

The coronary artery   though not a part of heart has a major say in the outcome of cardiac failure as they determine the cardiac muscle  integrity.In every patient with refractory cardiac  failure , an attempt must be made to rule out  any  re-vascularisible  lesions.

The primary difference between ischemic and Idiopathic DCM   is ,  in ischemic DCM left ventricular  segments  are predominantly involved . RV function  is relatively   preserved until very late stages.

Patient factors

Age , gender, body weight , systemic illness that increase metabolic demands have an adverse impact . Diabetic patients fare poorly .

Fluid management  and  diuretics

In refractory cardiac failure the renal blood flow is reduced .Diuretics usage will further worsen this if ECF is depleted .

So it is obvious we have to use it very judiciously .

Why only  certain patients with cardiac  failure   develop significant edema while others do not ?

This lies in the response of neuro -humoral  activation of secondary RASS system.

Both inadequate  and excess diuretic can perpetuate the  status.

Intra vascular hypovolemia and effective renal blood flow reduced

Diuretic strategies

  • Increasing the dose
  • Adding another ( Switching over to another loop diuretic like Bumetanide, or Toresemide  can be tried )
  • Sequential nephron blockade ( Add  metalazone a powerful thiazide acting in proximal tubule  to be used with caution risk of hypokalemia)
  • Continuous IV infusion  is an option

Ultra filtration  can be  used  in severely volume over loaded  patients.

Refractory diastolic failure .  How common is that ?

The incidence of significant LV filling defect are more commonly observed.There is no specific  drugs  available to tackle this .It may be argued digoxin and other positive inotropes worsen diastolic dysfunction.This  may not be true in the bed side.Unless severe  LV restriction feature are present  digoxin can be continued.

The simple and effective way to improve LV filling in the presence of diastolic filling defect ,  is to slow down the heart rate. At low heart rates  diastolic filling period prolongs and dysfunction tend to vanish.Beta blockers usefulness  in   DCMs  is attributed to this phenomenon

Specific  therapeutic targets

RV dysfunction

RV dysfunction is responsible for systemic congestion .RV function improvement alone can improve the functional class in  many .Controlling and targeting pulmonary hypertension is beneficial . There can be a role for off  label use for chronic pulmonary hypertension associated with DCM.

Importance of  weight reduction :

We can comprehend  complex equations  in  cardiac failure  , still we often  forget a simple logic  . Body wieght is an  indirect but powerful determinant of aortic after load.  A 80kg body needs more heart power than a  body with a 40 kg  mass. If a  patient with EF of  25 %  loses 50 % of his body mass,   his heart can serve  his body  for   100 % longer duration.   (Of course ,  this happens  in certain patients  by a mechanism  called  cardiac  cachexia !  shall we call  it as  natural adaptation ?  )

 Inflammation   control

Tumor necrosis factors and Interleukins are responsible for systemic reaction . These levels are high in CHF. Anti -Inflammatory drugs and diet would help. Statin usage is shown to be beneficial.

Metabolic modulation

ATPs ,fatty acid are fuels for the  heart .Ailing hearts  require  it in plenty. Certain drugs like Trimetazidine, L carnitine has been shown to be useful .

Cardio-Renal syndrome

This is nothing but raising renal parameters  as heart failure worsen .This  essentially  involves fluid and electrolyte management.

Natural course of refractory cardiac failure

It is sort of a  delayed near death sentence . 5 year survival is comparable to many cancer inflicted patients.Basic medical care  remain the corner stone. CRT /ICD*  , LV  assist devices are slightly more effective with substantial  risks and cost involved. Indicated only for  rich  and  insurance infested  population who can tolerate both scientific and  financial excesses.

ICDs* do prevent sudden electrical deaths.

 There is a  fundamental flaw  of  electrical and mechanical device concepts  in refractory heart failure .It  forgets  ,  CHF is a  systemic disease .A  cardio centric approach rarely works to perfection .

Cardiac transplantation  is the ultimate . It works well beyond any doubt. In best centers  like  Stanford 85 %   for 5 year survival is expected. Heart transplantation is limited by donor  availability and  surgical infra structure.Total artificial heart is a distant dream , but will be definitely accomplished

Role of surgery

CABG ( Strictly Indicated only in absolutely deserving .The habit of  revascularising scarred, akinetic DCMs to be abandoned )

Ventricular reduction( Batisda -seems to work only in Brazil!)

Mitral valve  interventions

Some  exotic interventions in cardiac failure

Mitral splinting to  reduce secondary mitral regurgitation in DCM


Newer drugs  and experimental drugs

Nesiritide, (Synthetic Brain naturetic peptide )  Tolvapton ( Vasopressin antagonist) are used with varying  success .

20  point bed side prescription tips  for refractory failure.

  1. Correct the  underlying causes  and triggers.Try to correct any  critical coronary lesion if any by PCI /CABG ( Not a major game changer ! )
  2. Restrict activities (Better to remain in class 3)
  3. Admit  only if  persistent  class 4 .(Intermittent class 4 does not require admission )
  4. Do not try vigorously to move up to class 2  with inotropes  you may  end up in class 4 !
  5. Advice mild passive and active movements. (6 minutes walk > 300 -400meters)
  6. Educate the entire  family / Ask them to shun Internet  (Internet acquired half baked medical knowledge is more injurious to health )
  7. Restrict salt intake
  8. Continue  Digoxin till toxicity develop  or maximum  dose  is reached  (Milrinone /Amrinone make  no major difference )
  9. Optimse diuretics.  Add Metalazone to Frusemide.
  10. Maintain good hemoglobin level (Erythropoitin does not work !)
  11. Add beta blockers  in every one including many of the  class 4 (Not necessarily Carvidilol)
  12. ACEI remain a key drug . Titrate to maximum tolerated dose. (Additional ARBs not much useful)
  13. Aldosterone antagonist has  unique role (Anti-fibrotic ? )  Caution required in diabetic patients  in monitoring renal function .
  14. At-least One metabolic modulator like  Trimetazide  could be tried (ATP utilisation amplified)
  15. Fatty acid metabolism enhancer  L carnitine  may be useful (Recall 1st year medical school basics  . . . Heart thrives on fat energy more  !)
  16. Nephrologist consult  is recommended if electrolyte / ECF status fluctuations are more.
  17. Avoid dobutamine infusions unless patient  insist.
  18. Narcotics like morphine can be used liberally in terminal heart failure  (Both for hemo-dynamic  and  neural benefits )
  19. As far as possible do not send these  patients  to big tertiary hospital unless heart transplantation is planned.
  20. Don’t  be a party  in  exhausting the  personal finance resources of the patient by ordering exotic investigations . Let him not suffer from additional worry ! (By the way . . .  having a hefty health insurance limit  is not an excuse  . Depleting  it  for futile purposes   would make the national economy weaker ! )

Final message

 Three  principles of  management in  refractory  cardiac failure  

  1.   Systemic approach  is the key .
  2.   De-mystifying   cardio centric  interventions  is essential.
  3.   Psychological support is vital .

Functional capacity   has a  poor correlation with LV contractile function . The skeletal  muscle  integrity , blood flow , and its  metabolism has critical say in this. Optimal medications  , properly regulated  locomotion  , weight reduction   can have a major impact.

The secrets of living a good quality of life    in  cardiac failure   ,  lies  not in modern technology  but in the  rare commodities  called  common sense and compassion.

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Angina is the classical clinical counterpart   of  myocardial Ischemia.

True  Ischemia , by electro- physiological rules  must elicit some sort of  ST segment shift .(Usually  ST depression rarely Elevation  )

But  . . .  we know Ischemia and ST depression do not always go together !  Dissociation can occur in both ways.

ST depression without angina is more prevalent  (often referred to as silent ischemia)  , while angina without ST depression is  less common but by no means rare .

We observe both these  phenomenon  during EST.  The  critical issue  here is ,  any pain without ST depression during a EST , the physician is likely to reject it as  non cardiac.

How wise  it is ,  to ignore such chest pain  ?

If a patient  complaints  true  compressive , squeezing  pain  it should be taken as angina  and EST should be  stopped and labelled as positive   even without  ECG changes .

According to the much   famed (De ) theory on ischemic cascade chest pain is supposed to come last. Time and again the rule of ischemic cascade  goes awry in the bed side. Clandestine angina without any ECG evidence be more important clinical entity than we realize.

                                      The argument against this ,  “If you start believing  patient’s  word  more than  ST depression  then the very purpose of EST documentation is lost  !

According to the now  de-famed theory on ischemic cascade ,  chest pain is supposed to come last. Time and again the rule of ischemic cascade  is found to go awry in the bed side .Clandestine angina without any ECG evidence be more important clinical entity than we realize.

Another clinical situation where we  encounter  ST segment  : Angina dissociation is ,  during balloon inflation of PTCA.

Two  explanations can be offered  for Angina in the absence of ECG changes .

1 .Cancellation of ST vectors  due to ischemia of two diagonally opposite areas of ischemia.

2. Electrical  blind spots  in 12 lead ECG. This  is especially common with LCX ischemia  where most of the electrical events are directed to back of the chest.Conventional leads can easily miss .

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