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critical decision making cardiology cath lab tricks coronary  angiogram primary angioplasty ptca vs cabg acc aha guidelines esc guidelines

Answer

While our brain perceives  whatever option  we  choose is the best for the patient  , in reality it is rarely true !

The only comment I wish to make,  there is nothing called standard guidelines for complex and unusual problems .We need not be obsessed with protocols  !

Please remember , If you apply standard guidelines  in  non-standard situations  9/10 times we  are going to err !

So my  choice  would be, to  go with your gut feeling , of course  your gut should  be alive ,  up to date and periodically maintained !

If you don’t have the guts  . . . don’t worry  you have plenty of other options !

 

Here is a  video recipe  !

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

Human atria is a rough terrain infested with peaks and  troughs like the  Himalayan range . The two atria together has a minimum of ten entry or exit points . Cardiac arrhythmias are   something similar to the  uneven  earth plates  triggering an  earth quake.  Like the earth surface there are  areas in the atria  with high seismic activity !

It is now discovered there are nine vulnerable points in human atria that can initiate focal electrical activity at times of hemodynamic/ischemic/metabolic stress .

The common causes for Focal /Ectopic atrial tachycardia are

  • Hypoxic AT -COPD ( Probably the most common cause .If persistent it will degenerate to MAT- AF )
  • Structural atrial disease
  • Hypertensive heart
  • CAD
  • Valvular heart disease
  • Drug induced

Note ,  all these  vulnerable points are located either in the  junction of  an anastomosis  with a venous structure or valve or septum.

Further, these sites are often the  embryological fusion points making it still more vulnerable due to tissue defects.

Why free wall of atrium  is  a less common  focus ?

They are relatively smooth, lack ridges and joints. Unless the walls of atria are diseased  focal tachycardias are less common from these sites .

Other forms of Focal atrial tachycardias

Indian perspective  and Rheumatic atrial tachycardia.

In developing  countries  focal atrial tachycardia in rheumatic heart  differ very much from the tachycardia described above. In fact many of the rheumatic atria present straight away  to atrial flutter or fibrillation.

Pulmonary vein focus should rarely be considered in atrial tachycardia that occur in RHD.

Post operative tachycardias

Surgical scars can result in what  is called  Incisional tachycardia.(Especially after complex atrial  surgeries like Sennings, Glean/TCPC  etc )

Multi focal atrial tachycardia .

This is nothing but a focal tachycardia which tend to fire from different angles towards different targets  often lead to a chaotic atrial rhythm .  Digoxin and DC shock paradoxically aggravate this arrhytmia.

Atrial epicardium/pericardium interface as a focus

When pericarditis is the predisposing  event  then it can emanate from anywhere from  epicardial surface .

Since left atrium is only  partially covered by pericardium it is not logical to assume pericarditis related AT arise from RA epicardium.

Atrial tachycardias in congenital heart disease.

Complex atrial anomalies, SVC type ASDs, PAPVCs can  give raise to abnormal  electrical focus

Reference

An excellent original work from  Royal Melbourne Hospital, Melbourne  Australia.

A must read  . . . http://content.onlinejacc.org/cgi/reprint/48/5/1010.pdf

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Is reciprocal ST  segment changes  occur  only in STEMI ? Can it occur in UA/NSTEMI ?   

                           

                      Even   after   100 years of electro cardiology   the electrophysiological mechanism of ST elevation in STEMI  and ST depression in Unstable  angina is   still in the hypothetical stages. One popular theory   says that the   current of injury   as we see   as  ST  segment elevation  in surface ECG  is  actually   an illusion. It’s   apparently due to   constant negative current    pushing down the   rest of ECG segments. Ironically   the concept   of  reciprocal ST depression in patients who have  ST elevation is well debated  for over 3 decades and  is considered  a  settled issue. It   probably   represents , a  purely electrical phenomenon where the  tail end  of the  lead   picks up the opposite vector. Even   as   conflicts   continue to confront the basic electro physiological   concepts management    strategies   of   acute coronary syndromes is witnessing   great strides.
Aim
                                     We   hypothesized   if   ST depression occurs as response to ST elevation it’s logic to expect strong ST depressive forces should  possibly elevate The ST segments in the reciprocal leads .
In fact  we have seen this phenomenon in three distinct  clinical situations. 
1) ST   elevation   in posterior leads: Patients who present   with isolated   ST depression in V1,  V2 , V3  and  ST elevation in posterior chest leads V7, V8 .These patients were initially thought to have isolated posterior MI. But later the cardiac enzymes were found to be normal   indicating no myocardial necrosis   echo evaluation revealed wall motion defects in anterior segments rather than in posterior segments. CAG revealed critical   LAD disease .  This we believe a pure reciprocal ST elevation in the posterior leads to  a  ST depressive forces in anterior leads.
 2) Inferior  ST   elevation   with ST depression   in   V4- V6 : Few  patients who present with  infero    lateral STEMI   later  do not  evolve into  Q  MI but as a NSTEMI .The initial ST elevation  was found  be transient and  disappeared  much earlier,  while the  ST depression  lateral leads persisted.
 3) ST elevation in AVR   in high risk unstable angina :As   already reported in the literature,  we have seen  ST  elevation in AVR  in patients with  high risk unstable angina. This was   more often observed when there is > 3mm ST depression in V4-V6. The AVR  ST elevation  possibly   represents   the  reciprocal  vector.
    Conclusion
                                            ST elevation in certain   specific leads in   some of the patients with ACS,   could   be   a pure reciprocal   electrical phenomenon   to   dominant ST depressive forces in Opposite leads .  And hence   ST elevation in the surface ECG during early hours of ACS   should be interpreted more cautiously. The   sanctity   assocociated with ST segment   elevation   could  be  opened   for debate. 
 
                                     To down load full PPT  click on  the slide

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The right ventricle  is considered as a docile cardiac chamber with passive filling and  emptying  properties .

This belief  was reinforced when Fontan  in early 1970s suggested a principle in the management of  cyanotic heart disease  when  the right side of the heart is underdeveloped. He  proved  RV can be by-passed safely , with  great veins  (IVC/SVC)  by  themselves  take care of filling the pulmonary circulation  without the need of RV pumping function.

While it is true for few complex cyanotic heart disease, largely this a misleading  concept. In clinical cardiology practice  ,sudden or non sudden  RV deaths happen every day in the form of . . .

  • RV Infarction
  • Acute RV dysfunction in massive pulmonary embolism
  • COPD with RV dysfunction
  • Most cases dilated cardiomypathy  the terminal event is due to RV  failure.

So , RV function can never be dispensable in day to day cardiac hemodynamics.

RV has some unique properties in terms of shape , size and  hemodynamics . We are getting more insights from  modern blood pool imaging by MRI , about  how the RV handles the blood volume .

We know RV has a unique shape  triangular ( partially  pyramidal ) . It can be inferred the RV cavity is formed by fusion of  many  eccentric spacial planes. We have always believed  RV handles the blood it receives from right atrium in a unique way .Now we are beginning to understand it .It is now documented the RV segregates the blood it receives into 4 components.

 

right ventricle physiology anatomy hemodynamics

It is curious  to know  RV inflow is connected to the outflow by an invisible   physiologic Bridge . About 44% of  blood traverse the RV in this fashion.

 

RVOT blood flow right ventricle

Note : RV blood flow preferentially enters the RVOT with out transiting RV body and apex.Image courtesy http://ajpheart.physiology.org/

 

Which is the most important part in RV ? (Among Inflow, Body, Apex, Out flow)

After reading this article it seems to me , the mechanical  function of RVOT could be most  vital. If it fails to handle the first increment  which  comes directly from  RV inflow, stasis  is likely in RV body and apex , elevating RVEDP and later promoting stasis leading to clinical events.

Clinical implication of this study

  • Differential dilatation RV chambers to pressure or volume  overload is observed .
  • We need to analyse why RV dilates in some   but   goes for hypertrophy in others when confronted with pressure overload (VPS vs PAH)
  • RV apical clot in restrictive cardiomyopathy  is a direct consequence of stasis  of blood  in RV apical zone .
  • RVOT pacing  may have a hemodynamic advantage  over RV apical pacing  . However , for anatomical reasons RV apical pacing  is  far safer than RVOT pacing where the lead  is subjected to constant life long strain due to this busy RV inflow to outflow express  high way !

Final message

Traditionally we have labeled  RV  as a  passive venous chamber .It is clearly a misnomer.It  has to handle both the venous and pumping function beat to beat with precision  without  back log .Obviously ,  RV has to think and work  more than it’s  big brother !

Reference

I wonder , if  there is  any other site other than APS . . . to  find crucial  answers in cardiac physiology  !

 

Right ventricle physiology blood flow  3d 4d analysisAfter thought

  • There is huge gap between physiologists  who work in research labs and the physicians at bed side .
  • I appeal all young cardiologists  to visit  APS  once in a while ,between your busy cath lab schedule and help narrow this gap.
  • Without understanding the physiology properly how are we going to intervene the pathology ?

 

I frequently  refer to one of the most famous  medical quotes made in last century by a Harvard professor Dr Herbert Lay  in 1969.

 

medical quote herbert lay fda modern medicine Five  decades have gone since this observation was made by Dr Ley .Mind you ,Dr Ley is not a lay person , he was heading the same FDA  which  he targeted ! I guess when Dr Ley made this  statement  there was  little commercialization in  pharma Industry . Now along with it  an entirely  new field of medical device industry has grown to gargantuan proportions !

I  wonder what Dr Herbert Ley would have to say as on 2014 !

Many modern  medical  professionals would   shrug these views  as controversial , pessimistic and negative forces of science !

Here I borrow my own quote from venkat@thoughts

medical quotes venkatesan ethics

 

We  traditionally believe  LV enlargement  results in dilatation of mitral annulus  from below  and  result in functional MR.
A lesser known  concept is , LA enlargement dilating the  mitral annulus from above and cause MR   !
Can atrial enlargement per se dilate mitral annulus ?

We often find  some degree of MR   associated with chronic  atrial fibrillation.What is the mechanism ?We also know MR begets MR.Is it because of progressive LV or LA enlargement ?

When the literature is searched  we have convincing proof that  LA enlargement can lead to significant  mitral annular dilatation and MR as well .
left atrial enlargement and mitral annuluseffect of la enlargement on mitral annulus
Reference

Spontaneous closure of VSD is  a well recognised  phenomenon, than ASD  though both happen in equal frequency.The simple reason being VSD is a noisy disease , ironically the smaller the size of VSD  more noisy it is . Hence  it is rarely  missed  while ASD is largely silent in children. For this reason  it is  possible ASD may be the most common congenital disease .

Natural history of ASD(OS) closure

  • ASDs of size 3-4 mm 100 % will close by 3  years
  • Bulk of the ASD < 8  mm close spontaneously by 5 years.
  • ASD> 10mm is unlikely to close

Factors that determine spontaneous closure

  • Apart from size and location
  • Closure  is accelerated by remnant of flap of foramen  ovale
  • Fenestrations and  Septal  aneurysms also  favor spontaneous closure.
  • Margins  of the defect if rough  triggers fibrotic reactions

spontaneous closure of asd

Why SVC and primum defect do not close easily ?

Plane of ASD  secundum is single and  bridging of tissue is possible .

Sinus venous and  primum defects exhibit  holes which run in multiple planes hence approximation not possible . They also do not  have a valve mechanism.

Un-natural history of ASD

In the current era, one more  force interferes  with spontaneous closure of ASD . It  comes from the  hyper trained aggressive Interventional cardiologists who compete with the nature and easily prevail over it !

Reference

asd spontaneous closure

IVC filter usage has increased many fold in recent years.Please note , it is not indicated in every case of recurrent DVT/or PE. There are specific indications.

Permanent IVC filters

  1. Patients at risk for DVT /PE  with  absolute contraindication to anti-coagulants.
  2. Recurrent DVT/PE in spite of adequate  anti-coagulation

Temporary /Retrievable filters*

  1. It is used during high risk periods  for DVT following major trauma or Bariatric/Spinal /Neuro surgery (PREPIC 2 study ) .*Some of the retrievable filters can be kept for months ,years or even permanently. (If the risk period extends or it has trapped a huge clot.)

 

indication for IV filter prepic study

Outcome  of IVC filter (PREPIC  -8  year follow up study )

  • Reduces risk of PE
  • Increases risk of DVT
  • No impact on long term  survival
  • Clogging of IVC remain  an important Issue

Reference

Fractional flow reserve(FFR) is an  Intra coronary hemodynamic  parameter  promoted recently to assess the physiological impact of a coronary lesion . Though it sounds logically attractive the concept  is sailing in rough seas  .I am afraid FFR is drowning  a fairly useful tool of IVUS  along with it  !

Read this large study on FFR (JAMA June 2014) .It seems to suggest  FFR is a costly and unnecessary accessory in cath lab

Image

Critical thoughts on FFR

It adds time , money , and procedural risk*  to any given patient .The only possible use is to reduce the proliferating stent usage !But the  irony  is complete as we do our daily business in  modern cath suits .To negate  one indulgence we need to  need to indulge  in  another ! (Junk begets Junk !)

It reflects lack of courage on the part of cardiologists to advice medical management even in obvious low risk lesions !

It is unfortunate ,we need a scientific or  a pseudo scientific tool to lift up our sagging medical intellect !

 

* crossing  delicate and often complex lesions  without any major purpose is bad wisdom !
Continue Reading »

Shall I begin with a provocative quote (My own !)

Inability to think beyond  self , family, private life  reflects a backward and immature  state of human mind

How to eradicate this backwardness  we all suffer from !

I stumbled upon a book which made me wonder , whether  eradication of  backwardness is little to  do with education ! It lies much, much deeper in our cortical thinking influenced by  inheritance , evolution , culture and economy .

The stunning truth was exemplified  by  American political  scientist  Edward C. Banfield  .A must read for every one who have mind for society , community and the humanity !

In this book he introduced a new term to describe this self centered thinking as “Amoral familism”

“Banfield concluded that  human  plight was rooted in the distrust, envy and suspicion displayed by  them in  relations with each other. Fellow citizens would refuse to help one another, except where one’s own personal material gain was at stake. Many attempted to hinder their neighbors from attaining success, believing that others’ good fortune would inevitably harm their own interests”

Banfield theroy  and  “Moral Bankruptcy in Modern medical care

I am afraid  there is a  compelling link between Banfield’s observation in a remote Italian village  to the current  medical  community   mind set who care only for their patients who pay them and keep them happy !

If you  think  education will eradicate social backwardness ,Why ?  one of the most highly educated community that form the noble profession remain backward in their thinking !

How do you explain  innumerable instances of hospitals ,  doctors shutting doors for  lesser humans  even in dire emergencies ! ?

Why do many of them  join hands with powers that can be detrimental to the overall health of the society ?

The stunning irony is , they do it  unashamed (with pleasure  at times!)  in  violation of the oath they take when they join the Noble profession. Shall we call it  as ” Moral Bankruptcy in medical care ?

Read further

Moral Basis of a Backward Society 
 
Moral basis of a backward society banfield

Highlights of this book  (Text from Wikipedia)

The Moral Basis of a Backward Society is a book by Edward C. Banfield, a political scientist who visited Montegrano, Italy . He observed a self-interested, family centric society which sacrificed the public good for the sake of nepotism and the immediate family. Banfield as an American was witnessing what was to become infamous as the “mafia” or families that cared only for its own “members” at the expense of their fellow citizens. Banfield postulated that the backwardness of such a society could be explained ‘largely but not entirely’ by ‘the inability of the villagers to act together for their common good or, indeed, for any end transcending the immediate, material interest of the nuclear family’.

 

Link to this book in PDF

 

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