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Archive for the ‘cardiology -Therapeutics’ Category

Cardiologists are  closing in ,  trying to capture the final frontiers. The  trans-cutaneous Aortic valve Implantation now has  a two year follow up. (NEJM March 2012  Issue) . The results are encouraging .

While two companies are fighting for the supremacy in TAVI ,   the real  threat is for the cardiac surgeons. Currently Edward  Sapiens  has an edge over Medtronic core valve as it  has a provision to redeploy or fine-tune the  final geo- position.

Reference

PARTNER 1

PARTNER 2

Medtronic core valve

Open access  article  by Martin Leon

http://www.rmmj.org.il/userimages/22/1/PublishFiles/25Article.pdf

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We owe a lot to our past genius minds for our current understanding of  cardiology.Youngsters   should  know how the filed of cardiology  evolved .Few  great  brains  taught us how to think   hemodynamically  in the setting of  STEMI.

The Diamond and Forrester classification is  an  undisputed achievement of  modern cardiac  hemodynamics.They gently converted the  clinical classification of  Killip into more scientific  hemodynamic  one .Both these classification continue to fascinate  us even in the era of instant PCI for STEMI .

And youngsters  should read this again and again and critically evaluate their patients  within this system.The two key parameters he used was PCWP of  18mmhg /And cardiac Index 2.2liters . He also suggested a simplified version where  intra- arterial monitoring is not feasible.  The   cardiac Index could be replaced by systemic blood pressure  lung congestion   represents PCWP >18mmhg .

The DF classification would become

An important inference from DF classification !

The class 3  of   DF   grading  has no pulmonary congestion  but persistent hypotension . What does it mean ?

It is a stunning proof of a great concept.  As the patient moves (Worsens)  from  DF  two  to   DF three  , the lung congestion tends  to regress . This sub-set  actually  means   development of  bi-ventricular failure or isolated RV failure  . This is an ominous sign and indicate a bad prognosis . ( One may call it a paradox  , according to conventional thinking   “The more the lung crackles  , dismal  is the outcome”   DF  grading clearly proves this is  not  always true ,  as long as  the systemic pressure is maintained  crackles can be managed effectively  . In  DF 3  the right ventricle  as a pump is  becoming so weak it is not able to congest the lungs  at the same  process leads to  systemic hypotension.

James Forrester

http://www.cedars-sinai.edu/Bios—Physician/A-G/James-Forrester-MD.aspx

Forrester is also a pioneer in how we evaluate chest pain in the emergency rooms and cardiology OPDs .  His thoughts on utilization of Besean theorem revolutionized   the interpretation of exercise stress testing.

* Killip is a genius of different caliber would be discussed later .

Reference

Forrester, J, Diamond, G, Chatterjie, K, et al Medical therapy of acute myocardial infarction by application of hemodynamic subsets (first of two parts). N Engl J Med 1976;295,1356-1362


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Magnesium   is a powerful anti-arrhythmic drug . It has a well  established role in controlling VT when administered  Intravenously   especially in polymorphic VT .

Mechanism of action

  • It acts at the cell membrane.
  • It has a unique action of blocking calcium channels  that reduces the number of oscillations of  both  early and late  after potentials

Link for more  on mechanism  of action

https://drsvenkatesan.wordpress.com/2010/01/13/how-does-magnesium-acts-as-an-antiarrhythmic-drug/

How often cardiologists administer oral magnesium for long-term control of VT ?

As for as I know ,  no one uses it ! but dietary  supplements are used for general well  being .

Why ? Is it because

  1. Magnesium does not get absorbed in the gut
  2. Magnesium levels are un- predictable in plasma if administered orally

Answer : No one has really tried  it as a  chronic therapy in VT  yet  !

Final Message

Tablet Magnesium can give a tough fight to Amiodarone and Flecanaide in refractory VT at a fraction of the cost !

Who has the audacity  to  compare Magnesium  with Amiodarone head on ?

Reference

Magnesium as health supplement . 

Magnesium is available  in tablet form as  Malate , Stearate, Taurate and Aspartate  along with calcium and Zinc etc .

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Irregular  wide qrs tachycardia is a fairly common clinical entity in any cardiac emergency room. The moment you ask about  such tachycardia ,  9/10  fellows will  come out with a  prompt answer   ” AF with WPW syndrome” even before you complete the question !  It is not that common  as we perceive .The problem is with  our traditional teaching methods and the attraction of human brains to  rare and exotic disorders.

traditionally   SVT with aberrancy  is   diagnosed  mainly  in the setting of regular tachycardia .

We often  forget  “AF with aberrancy”  is equally common  , and  it presents   with a  irregular  wide qrs tachycardia . 

I  wonder whether  this phenomenon  can be termed as  orthodromic aberrancy .This can directly compete  in the differential diagnosis  of  antidromic AF  with  WPW !

It should also be mentioned antidromic  AF can run into very high rates  as accessory pathways do not check the incoming signals while orthodromic aberrancy the ventricular rates can not exceed 220 or so at least theoretically . (This simple clue can clinch the issue in favor of  WPW )

There is no proper  published data available for the true  incidence of AF with orthodromic aberrancy in general population

In fact , there are  many  electrical  environments for AF  to  become a  wide qrs AF

1. AF  with  Antidromic conduction through accessory WPW pathway.

2. AF with Orthodromic aberrancy ( Non WPW – Similar to  any SVT with aberrancy )

3. AF with pre existing LBBB

4. AF  with Amiodarone effect. (Especially with DCM and cumulative load of Amiodarone )

5. AF with electrolytic /  especially excess  intra-cellualr  potassium

6. Finally , even  Atrial based pacing (DDD)  can cause wide qrs irregular tachycardia when  mode switching  fails .Here the  ventricles  may track the  atrial irregularity  and respond with a  wide qrs  bizarre tachycardia .

Final message

There are many causes for  wide qrs tachycardias  in  Atrial fibrillation . WPW with anti-dromic conduction is just  one of them .We need to approach the issue with an open mind .Please  be reminded , once contemplated  WPW syndrome  can be a powerful thought blocker  !

Note : *We are not including   polymorphic ventricular tachycardia here .It is an  important subset of  wide qrs irregular  tachycardia.

** VT can co-exist with AF .This is not   surprising  as  many of the diffuse cardiomyopathies  involve  both atria and ventricle  with extensive scarring and fibrosis  a perfect trigger for  both atrial and ventricular arrhythmias .

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We know prompt reperfusion of infarct related artery( IRA) by any means  constitute the specific management of  STEMI .However, It needs  to be emphasized ,  treatment process of STEMI  is not over after  primary  PCI or thrombolysis .Early hours after a PCI or thrombolysis  is vital as well .The ill-fated coronary arteries are as  vulnerable as before.  In the setting of multi-vessel CAD  (Which usually is the case) the unpredictability is still more.

Image courtesy New york times , January 5 , 2009

When a patient complaints of chest pain  24 hours after a STEMI . Think about any of the possibilities and act accordingly.

  1. Infarct related pain ( Dull aching pain from residual neural signals from infarct zone,  till type C  un-medullated  nerve endings  die of hypoxia )
  2. Post infarct angina –From IRA zone (Residual ischemia)
  3. Post infarct angina-From Non IRA zone(New Remote ischemia)
  4. Re-Infarction
  5. Infarct expansion/ Extension /mechanical stretch
  6. Pericarditis
  7. Intra coronary dissection adjoining  a plaque (Plaque fissures  are same as dissections if they extend into media ! But plaque fissures are painless since they lack nerve endings  )
  8. Myocardial tear /Rupture (Generates  severe pain , usually transmit to back , patient often become violent and poorly respond  even to narcotics)
  9. Post resuscitation/DC shock / chest wall contusion . ( I know at least one patient  who was rushed to cath lab for a  suspected  acute stent thrombosis  ,  it was indeed   a rib fracture during an  earlier resuscitation at ER  on his arrival !)
  10. Finally ,when the  pain is refractory and atypical   non cardiac chest pain which might have been pre existing to be considered as remote possibility .

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International Astronomical Union  in the year 2006  removed Pluto from the solar system for a simple reason ,  the so-called Pluto never revolved around  Sun , hence it ceased to be a planet of the solar system , it was more of an asteroid !

So, an astronomical fact engraved in our brains for so long  became a fairy tale. It is very hard  to erase  a  myth however solid the new evidence are against it.

The concept of HDL as good cholesterol has been etched deep in physician as well as our  patients.

Now comes the shocker from Lancet

How are we so sure ,  about these  Invisible spheres of  lipids that  move  around  our “Bio-system” in a presumed fashion .  .  .  even huge visible planets  fool us easily !

The Link to lancet study

It is  a wonderfully done study where  thousands of patients  who exhibited  genetically high HDL levels , never showed any advantage in terms of CAD prevention.  A stunning blow to a belief.

Incidentally ,  few years back  the failure of  drug Torcetrapib proved the same point  .  (The drug which elevates  HDL  proved useless in preventing CAD  ) but the  medical world failed to interpret it properly.

I am sure, still sections of physician  community would continue to believe HDL is great molecule for CAD protection !

Science is  often what we presume . . . but the fact usually turns out to be some thing  else !  but the journey towards truth  must continue !

                      When  a  million tonne  Pluto  suddenly disappear from Solar system . . . it is not a  big deal for  a  “miniscule medical myth”   to get shattered !

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An  article , I stumbled upon recently  discusses why American health care is  in deep trouble. There is a huge variation in the health care costs across the country. The article goes on to reveal  ,   a  simple  Appendicectomy can  cost  anywhere between 7500   to 1,70000 $  in different hospitals in USA.  (In India it costs  1000 $  in  any  star hospital !)

The fundamental flaw is   treatment  being the same ,   it is delivered in such a  fashion ,  the cost incurred is  kept ridiculously high.

It is akin to comparing  a 10 dollar  lunch to a 1000 dollar feast , both  ultimately  fulfills a  purpose ,   relive the hunger effectively

while , the later can  damage the country’s economy  in a variety of ways !

https://www.massdevice.com/blogs/massdevice/anatomy-walletectomy

Car makers automate the industry with Robots to   reduce  the  human labor and  cost of a vehicle ,  while medical industry does the opposite   . . .  privileged few get their appendix removed with a help of metal hand  !

Final message

Modern medicine must  aim to improve the quality  of  care  with a   positive impact  at a reasonable cost . In the name of cutting edge technologies ,  it  should not raise  the medical bill in a meaningless  fashion .This is meager exploitation of  human suffering.

It is  hilarious to note  certain medical  Robots* are primarily  made to assist  surgeon  for which  no assistance is required at all !  (I heard a story about a  Robot  which responds  to voice command   and pass on a   knife  for cutting and a gauze for wiping ! What a great medical discovery !)

Disclaimer

*  Of course  Robots (Cyber knifes )   may have a role  in some rare surgeries which require high precision  cutting  especially in  Neuro  ,  Vascular ,  oncological  surgeries.

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Amiodarone acts  by

  1. Correcting the  rhythm  to sinus .
  2. Controls  ventricular rate  alone
  3. Does both ?

Answer is 3

How can it correct the rhythm alone ?  If  the rhythm is corrected ,  rate will automatically be controlled,  unless Amiodarone converts AF into Sinus tachycardia  which is very unlikely !

Of course  Amidarone  is not a  magic drug .The success rate of  Amiodarone  restoring  sinus rhythm is far . . . far less . . . than our expectations ! . It fails to  convert to sinus rhythm in a significant chunk *. Interestingly ,   it may still  control the  ventricular response  by its beta blocking action .

*Our estimate is , the failure rate Amiodarone  is  between  30-40%  or even higher ,  as   bulk of AF we witness   is due to Rheumatic heart disease.

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Ventricular tachycardia is  a major cardiac electrical disorder. Even though it  connotes a deadly meaning the prognosis and outcome vastly vary.It can be a benign arrhythmia in  structurally normal heart that present as occasional fasicular VT  or Exercise  induced RVOT , to dangerous ischemic polymorphic VT which rapidly degenerate to VF and SCD if not reverted . It is ironical we are  trained  to put all VTs in a single basket and  propagate fear psychosis among   physicians and patients .

Management of VT has certain broad principles.

  • Identify the cause
  • Whether  specific structural heart diseases present or not
  • Identify the mechanism if possible
  • Rule out transient metabolic cause as a trigger

Therapeutic targets

  • Stabilising the cell of origin
  • Passifying the scars
  • Interrupting bundle branches in  BBR  mediated tachycardia
  • Ischemia related  Focus – Re-perfusion
  • Reversing LV dysfunction

Management

General

  • Correct Cell hypoxia /Acidois
  • Pharmacological ( Class 1A/1B /1C , class 3 and Beta blockers , Magnesium  )
  • Role of  beta blockers for VT management is largely under recognised.It has an important role to play in both acute and chronic  VTs)

Electrical (DC shock ,Ablation and ICD)

  • DC shock is treatment of choice  all emergency VTs
  • Ablation  aims  at preventing episodes of VT .Ablation needs EP study and  expertise of  an electro physiologist.
  • ICDs  revert it only after the VT emanates from the focus . ICD can be implanted without knowing the focus .May not require a EP consult.

Surgical

CABG + Surgical scar excision , Aneurysectomy  might help in certain refractory VT.

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A 55  year old man came with a BP of  1o0/70 with vague symptoms of back  pain to our ER.

Troponin T  was positive

Can we thrombolyse ?

There is a minimal ST elevation in inferior leads  but not amounting to  the required criteria 1 mm

Technically No , Academically yes , scientifically No , logically  yes

*I wont thromolyse but i will take him to cath lab maybe the modern answer

 What we did ?

We did neither !

Just observed in CCU with heparin infusion , Aspirin and clopidogrel .

Note: The ECG becomes almost normal .The initial suggestion of inferior MI is stands questionable

Serial ECGs  were taken .

And now . . . after 24 hours a new complete heart block appear with classical evolved pattern of inferior MI.The most interesting feature is patient has been comfortable all along even as his posterior aspect of heart is experiencing terrible electrical earth quakes.

Is troponin Guided thrombolyis  an accepted  concept  ?

Yes ,  only in few situations like , posterior MI ,   LBBB  , pacemaker rhythm, re infarction .(Note , true posterior MI do not elevate the ST segment but depress it ) .

One may be surprised why we shouldn’t lyse a patient  whenever  troponin is elevated in acute coronary syndrome  (After all it denotes myocardial necrosis and infarct !)  The point here  is ,  troponin can raise in all forms of MI (NSTEMI, even in some cases of chronic stable angina )  Read in this link Why thrombolysis is contrindicated in UA/NSTEMI

The benefits of thrombolysis  is not proven in small and micro infarcts.  ECG  ST  eelvation   remain the  sole criteria for thromolysis for STEMI because  of  high degree of  correlation with total coronary occlusion .

In this era of rapid interventions the treatment concepts has blurred as we tend to do PCI and stenting  most cases of ACS including UA/Unstable angina

OK , what happened to this patient ?

Temporary pacer  was kept stand by with a sheath and catheter in situ.

Next day  morning  AV block disappeared .Patient was comfortable .

To our surprise , in the same  evening his ECG showed a complete heart block with AV dissociation . Still the heart rate was good . The demand temporary pacemaker didn’t take over .

On the third day , every conduction disturbance disappeared and  patient was sent to the wards. He is being discharged in a  stable condition with std drugs .there was  a minimal wall motion defect in infero-posterior segments with an ejection fraction of 50 % . He is  scheduled for coronary angiogram  2 weeks later.

What is the pathology ?

Pathologicallyit could be a small focal area of Infarct  incidenataly invloving the AV node .(This is alss refered to as vital area Infarct”  )It is hard to differentiate whether AV block is due to revrible ischemia or necrosis  , simple tissue edema ,  high vagal tone . or combination of above .If the block recovers it can be concluded necrosis is not the dominant theme.

 

Final message

STEMI presenting  primarily as heart block is less common .  When such a presentation occurs extra caution is required.

Many  of these patients  may not show a classical ST elevation  and hence do not permit us to thrombolyse   as per criteria.

It is  the  individual physician’s discretion to do so ( or not to do  ! ) . No body is going to fault. After  all  5 % of thrombolyis world over is for  benign early  repolarisation syndromes.

The above description is  an example of complicated inferior MI  . . .  still managed effectively by conventional methods.

Further reading

Why inferior MI is considered Inferior ?

 

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