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  • CRT -Cardiac resynchronisation is done  by putting multiple wires and electrically organizing the contraction  sequence and improving mechanical function.
  • ICD-Implantable cardiovertor defibrillator shocks whenever VT or VF occur and suden death is prevented.
  • CRT-D (Combo device which functions as both )

CRT is done for advanced heart failure to improve exercise capacity and hence the quality of life .It does not do any thing significant in prolonging life .ICD is again implanted  in advanced LV dysfunction with either documented VT/VF or patients who are at  propensity for VT .It has dramatic benefit in preventing  sudden cardiac death.

Both CRT and ICD has some overlapping indication in cardiac failure. Attention young cardiologists,   please realise among these two the value of ICD is many  many  fold higher than CRT.This fact is rarely discussed and disseminated.

 True benefits of CRT is realised only when it is combined with ICD.

Summary

  • Ideally all advanced cardiac failure patients should receive both ICD and CRT (CRT-D)
  • ICD as stand alone therapy has a  distinct role in patients with severe LV dysfunction (LV EF<30%) without  wide QRS in ECG
  • There is no role for  CRT  as a standalone procedure in cardiac failure  .it should  always  be combined with ICD (ie CRT-D) *

*Except  in patient with  degenerative complete heart block , both ventricles are paced  the term Bi-Vi pacing is used  instead of CRT.Since LV function is normal here , there is no de-synchrony in the first place .The synchronised  BIVI pacing is meant to prevent future heart failure

Final message

Always use a combo device in advanced symptomatic heart failure which  is refractory to medical therapy.

After all , there need to be a life in the first place  so that we can improve it . ICD ensures life while  CRT tries to improve it.

http://europace.oxfordjournals.org/content/14/9/1236.long

The correct  answer could be any of the above , depending  upon the level of your knowledge.

Ever since Herrick reported coronary thrombosis as a cause for MI and Davies documented it by angiogram many decades later (1980) ,the fate of thrombus  and the mechanism of its dissolution is the key to our understanding of ACS.

Even though we are now able to take on this thrombus in a direct fight  by aspiration techniques ,still the hematological  aftermath  and the aberrant coronary behavior  can fool us at any time ! The major lesson learnt  in recent times  is the  success of pPCI  is not in clearing the thrombus but ensure it never accumulates again  at the site  in the future .This is why there is whole big industry working on post PCI anti coagulation and anti platelet strategies .

Clinical correlates of poor  perfusion in micro circulation.

Plugging of micro circulation is the most under-recognised  issue.This results in no reflow in acute fashion or LV  dysfunction and micro-vascular angina in long term . Late recovery of LV function is attributed to late clearance of thrombotic debri.

RCA vs LCA thrombus load.

*One interesting observation is RCA thrombus clears more slowly as it has no well formed venous circuits .most RCA blood drains through thebesian veins which traverses  RV  myocardium .this can be hemodynamic hurdle unlike the LCA venous drainage

As the medical care advances  human care  has taken the back seat. It is said super specialists  read more and more about less and less ! In the  process they  fail to see the  patients  as a single biological unit  instead as collection of organs .

While  organs in turn are looked as  pile of data.Hence the  treatment they provide lack the soul !

In the prevailing circumstances , how do we ensure  modern medicine  does not interfere with  these vulnerable souls,either to live in peace or leave in peace ?

Medical Ethics

Image : Source and Courtesy of http://illuminationstudios.com

It appears doctors are not at fault . The system is  biased towards raw science .Highly trained  doctors are tied down by  both  true and pseudo  scientific Intellect .Often  times they are compelled to do some procedure or interventions  just to  justify  the  premier status of the hospital  .While few do it  to show off  their expertise or  to impress  their peers   others are simply bound by rigid and obsessive  protocols and guidelines . Few others do it  for the burning  desire  of  scientific accomplishment .

One can offer hundred reasons for doing a procedure . . . but we always struggle to justify  with a valid reason for not doing a investigation or  procedure !

In fact , the  concept of appropriateness  criteria came out with good intention .But , it had failed miserably.

The irony is  . . . we need to indulge in something to avoid something.

Example 1 If homocystiene and  hsCRP vanish from the CAD screening industry   Adiponectin and Vitamin D3 comes in with a thunderous applause like a new Hollywood movie  !

Example 2: In cath lab  for leaving alone an insignificant  coronary stenosis , we have to do  another procedure  called FFR to satisfy  scientific ego ! (I know one senior doctor , who left a 80% LAD  lesion for medical management without FFR ( with all his clinical acumen )  was ridiculed for being unscientific !)

Here is a recent perspective article NEJM has discussed  this  important issue that plague us

Why should big  Tertiary  teaching hospital  are  flooded  with super specialists  which by default shun basic human care ?

Read this article*

Super specialist tertiary care hospital NEJM

*The article I have quoted  may  not  be completely relevant here  . . . It  answers  few of the queries raised!

The diastolic mitral filling pattern has been  named and  graded  umpteen times in the last  decade. We believe it has  reached some semblance of clarity.I beg to differ.

pseudo abnormal relaxation grade 1 003

Image template taken  from  http://www.learntheheart.com

There need to be one more  grade between Grade 1 and grade 2 .Grade 1  is defined as A velocity > E velocity . This is the  commonest abnormal pattern and is often  man made.We can’t help it . We have to report it  anyway. Significant number of elderly show this pattern  without any pathology. It simply represents augmented atrial contribution  at times of apparent ventricular stress .

I wish a good chunk  of  grade 1  pattern ,  especially  in elderly or during tachycardia should be labelled  as physiological  grade 1 pattern  (or simply as  normal variant ) . However I would prefer it to be named as  pseudo abnormal pattern* !

* In my experience , currently medicine is taught in a complex manner .Facts that are told  in simple terms are rejected  straightaway . It would seem,too much clarity is not good for  science So,let us get confused one more  time  for the sake of our patients !

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

 

 

 

 

 

 

The news that wasn’t . It is January 1 st 2016 .

NBC reports from Karolinska ,Sweden , Heparin  the wonder drug  has been reclassified as a thrombolytic agent and Jay Maclean  who doscovered this drug in 1916  is awarded the Nobel prize in Medicine posthumously on the 100th  anniversary of  discovery  of  the glorius drug ! The entire Hopkins  campus at Baltimore has erupted into a  non stop party tonight !

Hopkins_hospital

The Majestic Hopkins at Baltimore  : This  monumental hospital is home to 18 Nobel Laureates in Medicine and Jay Maclean is the most famous for missing it !

 

And now to the True story

Heparin   the wonder  drug  was discovered by Medical student Jay Maclean in 1916 at the Jhon Hopkins when the rest of the world was   fighting the  world war 1 . It was separated from the cannine liver and the name Heparin was coined by Maclean’s Guide at Hopkins  William Henry Howell . Even though it was invented early  it was available for human use only in 1936  when Swedish company Vitrum AB produced it .Since then   It has a very distinguished career and still going strong after 100 years.

The only regret is Dr Maclean  narrowly missed  the  Noble prize for this great invention .I still believe he should  get it on its 100th   anniversary  in 2016.

A partial  “curriculum vitae”  of Heparin.

Heparin is an  Anti-thrombin 3 agonist .It blocks the pro thrombotic cascade and hence a powerful anticoagulant. Further ,it completely tilts the balance towards fibrinolytic  system.Hence the natural forces take over and  start dissolving the thrombus  in due course.

So Heparin is an indirect thrombolytic agent .No second thoughts on this.

But a century old teaching  goes like this  . . .

Heparin prevents fresh clot formation . . . but it do not have any action on already formed clots “

What do you infer from this statement . Do you agree ?

Role of Heparin in real clinical scenario

Heparin is the key drug in all acute coronary syndromes when the  coronary artery goes for sudden thrombosis . An un estimated one  million prescriptions are done every day world wide for this indication alone.

(*And mind you it does have a  significant  impact  on already formed thrombus as well ! Ref : HEAP Pilot  study  )

Apart from this.

1. Heparin dissolves post MI LV  apical clot over a period of  few  weeks.
2.Heparin is very effective in most cases of sub-massive pulmonary embolism
3.Heparin infusion has opened up many near total coronary occlusion
4.Heparin clears the micro vascular from thrombotic debri in lungs in CTEPH.
5.Heparin dissolves  deep vein thrombosis
6.Heparin almost result in complete cure and clears cortical venous thrombosis

7.Heparin is exceedingly successful in clearing   thrombosis in placental micro-circulation (APLS) which  threatens the  fetus with IUGR.

Al these clinical events are well documented and well appreciated.

Still we feel awkward to call the heparin as thrombolytic agent

Why ?
It is almost a  scientific non- sense .We think a thrombolytic should  show it’s action in vivo in the lab and it should shrink the clot on a petri dish !  What a wrong  mind set ! We have  tell-tale evidence  for heparin’s  magic act of vanishing clots   inside the human vascular tree (However organized  it may be ! ) .

I struggle to understand  , why  our scientific  mind does not want to give credit to a drug  which does a neat job of  dissolving  clots  through its  indirect action . Is it a curious bias  ?  or is it an act of  ignorance  or  just a nomenclature  error  in the  foundations of therapeutic  pharmacology ?

At this point one should  realise  streptokinase  too does not act directly on the clot.It acts indirectly through a TPA-enzyme complex.So can we call it an  non thrombolytic agent ?

Final message

  • Heparin is indeed a thrombolytic agent , through  a chain  of action and reaction  which  it confers to the naturally occurring lytic system.
  • In vivo ,this  indirect  lytic action can be  powerful than some of the direct acting thrombolytic agents .Not only that, it lacks the side effects  vested with direct  lytics.
  • The only issue is  , heparin is a slowly acting indirect thrombolytic it has to be given long-term or on an infusion .
  • It is right time the pharmacologists  and nomenclature authorities  include heparin as indirect thrombolytic drugs.

Read further

Heparin a forgotten Hero

 

Reference

1.High Dose Bolus Heparin as Initial Therapy Before Primary Angioplasty for Acute Myocardial Infarction: Results of the Heparin in Early Patency (HEAP) Pilot Study Freek W.A Verheugt,  Aylee Liem, Felix Zijlstra,J Am Coll Cardiol. 1998;31(2):289-293.

3.Esteves  FP, Braga  JC, Latado  A; Confirmation that heparin is an alternative to promote early reperfusion in acute myocardial infarction. the CHEAPER study [abstract]. Circulation. 94 (Suppl I) 1996:I-553

 

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