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Here is a  video recipe  !

Please click here to  see more videos from my you tube site

It is often said life is a cycle , time machine rolls without rest and reach  the same  point  again and again . This is  applicable for the  knowledge cycle as well .

We  live a life ,  which is infact a  “fraction of a time”(<100years) when we consider the evolution of life in our planet for over 4 million years.

Man has survived and succumbed to various natural and  self inflicted diseases &  disasters. Currently,  in this  brief phase of life  , CAD is the major epidemic , that confronts  modern  man.It determines the ultimate  life expectancy . The fact that ,  CAD is a new age  disease   and  it was  not  this rampant ,   in our ancestors  is well known .The disease has evolved with man’s pursuit for knowledge and wealth.

A simple example of how the management of CAD over 50 years will  help assess the importance of  “Time in medical therapeutics”

  • 1960s: Life style modification and Medical therapy  is  the standard of care in all stable chronic  CAD The fact is medical and lifestyle management remained the only choice in this period as   other options were not available. (Absence of choice was  a blessing as we subsequently realised  ! read further )
  • The medical  world started looking for options to manage CAD.
  • 1970s : CABG was  a major innovation for limiting angina .
  • 1980s: Plain balloon angioplasty a revolution in the management of CAD.
  • 1990s: Stent scaffolding of    the coronaries  was  a great add on .Stent  was too  dangerous  for routine use  was to be used only in bail out situations
  • Mid 1990s : Stents  reduced restenosis. Stents are  the greatest revolution for CAD management.Avoiding stent in a PCI  is unethical , stents  should be liberally used. Every PCI should be followed by stent.
  • Stents have potential complication so a good luminal dilatation with stent like result (SLR)  was  preferred so that we can avoid stent related complications.
  • 2000s: Simple  bare metal stents are not enough .It also has significant restenosis.
  • 2002: BMS are too notorius for restenosis and may be dangerous to use
  • 2004 : Drug eluting stents are god’s gift to mankind.It eliminates restenosis by 100% .
  • 2006:  Drug eluting stents not only eliminates restenosis it eliminates many patients suddenly by subacute stent thrombosis
  • 2007 : The drug is not  the culprit in DES it is tha non bio erodable polymer that causes stent thrombosis. Polymer free DES  or   biodegradable stent , for temporary scaffolding  of the coronary artery  (Poly lactic acid )  are likely to  be the standard of care .
  • All stents  are  potentially dangerous for the simple reason any metal within the coronary artery  has a potential for acute occlusion.In chronic CAD it is not at all necessary to open the occluded coronary arteries , unless  CAD is severely symptomatic in spite of best  medical therapy.
  • 2007: Medical management is superior to PCI  in most of the situations in chronic CAD  .(COURAGE study ) .Avoid PCI whenever possible.
  • 2009 :The fundamental principle of CAD management  remain unaltered. Life style modification,  regular  exercise ,  risk factor reduction, optimal doses of anti anginal drug, statins and aspirin  is the time tested recipe for effective management of CAD .

So the CAD  therapeutic  journey  found  it’s  true  destination  ,  where it started in 1960s.

Final message

Every new option of therapy must be tested  against every past option .There are other reverse cycles  in cardiology  that includes the  role of diuretics  in SHT , beta blockers in CHF etc. It is ironical , we are in the era  of rediscovering common sense with sophisticated research methodology .What our ancestors know centuries ago , is perceived to be great scientific breakthroughs . It takes  a  pan continental , triple  blinded  randomised trial   to prove physical activity is good  for the heart .(INTERHEART , MONICA  studies etc) .

Medical profession is bound to experience hard times in the decades to come ,  unless we constantly look back in time and “constantly scruinise”  the so called  scientific breakthroughs and  look  for genuine treasures for a great future !

Common sense protects more humans than modern science and  it comes free of cost  too . . .

Coronary artery disease (CAD)  is man-kind’s  greatest threat in modern times.CAD ,diabetes ,Hypertension, obesity, mental illness  has become an epidemic  even among the young !

 

Lifestyle diseases cad risk smoking alcohol

There is a simple solution for  lifestyle diseases !

Just  . . .  Remove style from your life !

lifestyle diseases coroanry cardiology medical ethics inappropriate stents over treatment excess medical care , bio ethics,

Instead . . . try to live like these  Tibetian villagers

life purpose of living

Final message

One study which researched all lives who crossed 100 Years  concluded something like this !

“To live a longer and healthy life* ,Get up early  , have a purposeful daily chore that must include a physical component , work with conscience ,love every one sync with the nature and  lastly and most importantly remove style from your life !

Choose  your life . . . It is simply there in your hand for grabs !

Post-amble.

* Please note , Doctors  are never listed in the top with relevance to health of mankind  ! They simply cure some illness !

Answer  is question is wrong : RAA clot do occur in AF and severe right heart failure.It is less often recognised , since echo views are difficult and clinical events are silent.

RAA right atrial appendage clot tee echocardiographyBrief account of RAA clot formation

  • RAA is broad flat ,thin ,  chamber comparable to elephant’s ear.The ostium is not that distinct as the body as it  blends  with crista  terminalis .
  • Rough pectinate muscles  should make it prone for thrombus.Further , RAA has more sluggish flow than LAA  increasing the propensity for thrombus.However , the flat nature of the chamber , absence of tortuous tracts , constant  SVC flow which is abutting the  RAA can counteract this.
  • RAA clots are  less recognised as echo views are difficult .TEE is often required.
  • Overall RAA clot is 50% less common than LAA.
  • RAA clot should be specifically looked  for  in chronic AF and any severe right heart failure. (Unlike MR jet TR jet has less efficiency in flushing the  Right atrium )
  • Finally,clinical events from RAA clot are less conspicuous as the emboli reaches the pulmonary  bed silently.Unlike its colleague on the left side it  neither triggers TIA nor a stroke !

Reference

right atrial appendage clot raa clot in af atrial fibrillation

1. Buğan B, Baysan O, Demirkol S, Güngör M, Yokuşoğlu M. Right atrial appendage thrombus in a heart failure patient with sinus rhythm. Gulhane Med J. 2011; 53(3): 214-215.

 

2.Subramaniam B, Riley MF, Panzica PJ, Manning WJ. Transesophageal echocardiographic assessment of right atrial appendage anatomy and function: comparison with the left atrial appendage and implications for local thrombus formation. J Am Soc Echocardiogr.; 2006; 19(4):429-33.

3.Sahin T, Ural D, Kilic T, Bildirici U, Kozdag G, Agacdiken A, Ural E. Right atrial appendage function in different etiologies of permanent atrial fibrillation: a transesophageal echocardiography and tissue Doppler imaging study. Echocardiography;2010; 27(4):384-93

4 .Ozer O, Sari I, Davutoglu V. Right atrial appendage: forgotten part of the heart in atrial fibrillation. Clin Appl Thromb Hemost; 2010; 16(2): 218-20

 

A tense anesthetist  calls for help !

I had an unusual cardiac consult last week .A middle aged man who was to undergo routine ortho surgery wanted  a cardiac clearance.

It was  a through and through fracture of clavicle , why do they need a cardiology opinion , it seemed a  simple  procedure I asked over phone

The anesthetic  fellow who was  in charge of the patient told me ,”There is a wire just going parallel to the clavicle sir .I  believe it is pacemaker lead” I agreed to see the patient immediately

This was the X-ray

pacemaker lead clavicle fracture electro cautery surgery

It was obvious why they got tensed up  as the pacemaker wire criss -crossed surgical field . His ECG showed own rhythm of 80/minute but occasionally VVI pacemaker was capturing his ventricles.

I suggested

General precautions

  1. Strict Intra-operative  ECG monitoring
  2. Keep another temporary pacer ready .
  3. Hold a cardiologist on call and  pacemaker programmer on site.
  4. Surgical field  kept small with  minimal   manipulation .
  5. Issue of cautery : Free to do as long as it’s  bipolar and good earthing plate.
  6. Ensure the cautery is  applied in one or two second pulses with a gap of 10 seconds pause in-between
  7. Wiring the clavicle – Signal interference  are  very rare  as the wires are inert

Use of magnet in such situations  (Link to magnet and Pacemaker)

Keeping a magnet over the pacemaker generator removes the pacemaker sensing function and is an option if  prolonged electrical interference.

*Caution : Response to magnet can be quiet variable .Should be done only with cardiologist supervision.

What happened to this patient during surgery ?

Nothing alarming.When anesthesia was induced he was entirely  on pacemaker rhythm . limited cautery was used with ease. Patient  tolerated well.

Final message.

One need not  panic when a pacemaker patient is taken up for non cardiac  surgery .It is not a major issue .Few precautions are required .

Read a related article in this site .Electrical cautery  in pacemaker patients.

Reference

pacemaker and electrocautery diathermy

 

 

 

 

 

 

Reperfusion arrhythmia was described originally  in the thrombolytic era .

It can be any of the the following .

  • AIVR(Accelerated Idio Ventricular rhythm)
  • Sinus bradycardia (In Infero posterior MI )
  •  VF can occur as  Re-perfusion  arrhythmia.

Does these arrhythmia occur following primary PCI ?

It should  isn’t ? 

In fact it  must be  more pronounced  as we  believe PCI is far superior modality for reperfusion !

Busy Interventional  cardiologists  of the current era  either do not  look for it or fail to document it . These arrhythmias occurs only  with early Primary PCI (Say less than 2-3 hours) .If re-perfusion arrhythmias are  really less common with primary PCI , are we missing some thing ?

 

 

As we practice this Noble  (&  Delicate )  profession ,we often tend to Ignore the  warnings  even from our learnt colleagues , Why ?

Wisdom ego quotes brainy best dr s venkatesan top inspirational

 

 

 

Primary VF is the arrhythmia that occurs within minutes to few hours after acute coronary ischemia .This is most common fatal arrhythmia following STEMI accounting for 90% of all pre hospital deaths.

It  occurs within  4 hours after onset of symptom and the risk rapidly fade as the hours go by.One variant of primary VF is the re-perfusion arrhythmia after thrombolysis  .This  can occur up to 12 hours or so.Primary VF responds  well to prompt defibrillation.Follow  up anti arhythmic drugs are not required in most situations.

What is secondary  VF ?

  • As a rule secondary VF is  not related* to  index event of ischemia but to the anatomical substrates of Infarcted myocardium or pump failure
  • It generally occurs after 24 hours .Response to defibrillation is less favorable .Continued anti- arrhythmic  drug therapy  is required.
  • Few of them may end up with ICD.

(*However,a role for ongoing ischemia can never be disproved ! What about a small re-infarct  trigggering another episode of primary VF ? )

 

A STEMI patient arrives late after 48 hours with chest pain .There is  persistent ST elevation.

What is the likely mechanism of this chest pain ?

  • Index infarct pain continuing . . .
  • Post infarct Angina-IRA territory
  • Re-infarction following intermittent re-perfusion  and re-occlusion
  • Remote  ischemia from a branch of IRA
  • Ischemia from a possible  non IRA lesion in a multivessel CAD

If this patient  comes to a non PCI eligible centre. Will you lyse him  ?

If post infarct angina is  unstable angina  . Isn’t  thrombolysis  contraindicated in UA  ?

How to differentiate Post Infarct Angina from Re-Infarction ?

A very tricky issue indeed.

Unless fresh ST elevation with fresh enzyme peak is documented these entities  cannot be differentiated.

(Even  fresh ST elevation can be related to infarct expansion ,stretch or early acute remodeling.Fresh enzyme  release or new peak  may not represent new infarct always .It can be due to intermittent re-perfusion of IRA .It may  simply represent a  enzyme  flush from the index infarct zone)

What is the practical , realistic , (Unscientific !)  solution  ?

Why break our head ? Never bother to differentiate PIA   from Reinfarction  etc . Let  it  be any thing . Do a emergency CAG .Stent  whichever  lesion looks good  for the same . Of course , make sure he has enough insurance coverage .

 

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