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INTECH : Open Mind . . . Open science . . . what a lovely concept !

June 28, 2013 by dr s venkatesan

I stumbled upon this  web   site . I think this  can be  glorified as the  standing  example  for     “Democracy  of science”

INTECH open science open mind

http://www.intechopen.com/subjects/cardiology-and-cardiovascular-medicine

Posted in cardiology innovation, cardiology journal club, Cardiology journal links, cardiology journals, Cardiology teaching websites, Cardiology-Land mark studies, Great websites in cardiology | Tagged , , , | Leave a Comment »

Gastritis + Cervical spondylosis = Classical Angina

June 27, 2013 by dr s venkatesan

Spinal cord is a busy  neurological  highway to brain .It  runs  24/7  non stop  with unlimited  horizontal and vertical lanes .It is such a compact  structure , it can  easily  get confounded   when multiple signals converge,  diverge, summate , deduct , reflect back,   or cancel out .
A 64 year old women came to me for  second opinion  regarding   chest pain . A  cardiologist  had  just adviced her  an  emergency   coronary  angiogram and also suggested she may require an  urgent  PCI  as well .
I listened to her history in my office  . . .  In  her own words .
Doctor , I am  getting  sudden   compressing  type of  pain which  starts in the centre of the chest and soon transmits to the left shoulder and  gradually reach the inner aspect of the hand up to the little finger . And occasionally it is very severe and some times i feel like sweating as well ! I am unable to predict when it comes doctor !
It was  so convincing  but one  feature was  not fitting In . She said , she used to walk  daily   and do all house hold work with no pain . She also  recalled about the  acid peptic disease , and neck pain periodically due to cervical spine problem.
Her resting ECG was normal .She was  afraid to do a stress test . After thinking  for a minute , I had no  other option  but  to endorse  my colleague’s view and asked her  to go for coronary angiogram .
One  thing I  suggested differently was , I told her it was not an  emergency , I also  conveyed my gut feeling  that it is unlikely to cardiac  pain . One week  later  CAG through radial route  was done . Both of  us were  happy  to find a  normal  coronary  angiogram !

Final message

Pain is a  feeling . It can be  perceived  at  multiple levels  . The site of origin , spill over on transit and at the level of brain .  A patient with multiple  potential source for pain can either summate , deduct , reflect  or cancel out .This can confuse the clinician in a dramatic fashion as it did to us ! . To complicate the matters  further , gastric pain can trigger a cervical  pain and vice versa . (Spill over effect)

Posted in cardaic physiology, cardiac physiology, Cardiology - Clinical, Clinical cardiology | Tagged , , , , | Leave a Comment »

Only fools will manage unstable angina medically !

June 27, 2013 by dr s venkatesan

Only fools will   manage unstable angina  medically !
 
That was exactly the statement ,  one popular Interventional  cardiologist   told a small gathering  in one of the weekly meet .
 
Do you agree ? 
 
 
 
 
 
Answer
 
We can’t  make a blanket  statement like that . We have clear  guidelines (Of course as licensed and certified cardiology  practitioner  you have  every right to violate it !)  .
 
UA is risk stratified in Low , Intermediate and High risk  categories .Only high risk group  require emergency Intervention .Even in high risk group there are some reservation.(ICTUS  study )
 
There are some very mild forms of  UA (High grade stable angina precipitated by an emotional stress will exactly mimic UA. Similarly most  secondary UA due to tachyardia , Anemia  etc should not  cause an alarm .)
 
 
*Please note  , currently coronary angiogram is included in medical  investigation  in most  patients with UA . The  confusion in interpreting  such statements  is partly because many physicians/ cardiologists consider  doing a coronary angiogram by itself an  Interventional  management
 
 
Reference

Posted in Cardiology -Interventional -PCI, cardiology- coronary care | Tagged , , , | Leave a Comment »

“Arrhythmia of life”. . . and . . . “Arrhythmia of death”are one and the same !

June 26, 2013 by dr s venkatesan

This  is the story of a 55 year old  women ,  who was received  in our CCU  with a  dramatic STEMI (ECG looked like an action potential ) ,  LV  S 3  and  hypotension.    It was impending cardiogenic shock.Since we do not have full fledged primary PCI  program  , thrombolysis was planned. She had  cardiac arrest   immediately after  starting streptokinase infusion . She  was  promptly shocked  and  revived .  The ECG changes rapidly  reversed(ECG -3) . Every other  hemodynamic parameter got stabilised as well . To our surprise   ( few hours later ) this patient  was  so comfortable , sat up on her bed ,  demanded a discharge . (Which was refused of course !)  One week  later coronary angiogram was done, a near complete recannalisation of RCA was documented.

ECG 1 on arrival
Inferior MI 2  

ECG -2 Developed cardiac arrest  10 minutes  after  starting the Streptokinase Infusion

primary VF 2

ECG -3 .Taken few minutes following   the VF

inferior MI evolved 2

 

Acute myocardial infarction (STEMI)  kills more than a million life every year . Majority of death  happens within an hour of onset of symptoms. Ventricular fibrillation  is the arrhythmia of death. Why this occurs  only in  few , while  many are  immune to it ?

God keeps  this secret  close to his chest ,  how and why  he selects   candidates for this arrhythmia !

Scientists are still  far away  in finding the truth . But , one thing  is obvious .The  moment   coronary artery is totally occluded  , the heart begins a fight  and try  to  get rid of this obstruction . In the process ,  it  goes into convulsion (VF)  with a foolish belief  , it  can shrug of the thrombotic insult . Death often   ensues if  not intervened . (Very rarely  VF can be a non sustained one  and patient survives cardiac arrest !)

VF  as  a electrical  response  to  reperfusion injury .

Often times ,  we witness patients  to  go  for  VF  very early following thrombolysis . The  thrombus in situ is an irritant , it  triggers the inherent fibrinolytic system (Natural TPA included) If it is successful  it opens the occlusion ( atleast partially )  and salvages the myocardium .If the fate is against  the patient , very early reperfusion of IRA triggers  VF  .  If this occurs at home   survival  is  low .If  the VF occur at hospital the probability of survival is near 100 % .

               The  intensity of  natural lytic mechanism  is the major determinant  of   early reperfusion . Ironically  the same  factor   determines  occurrence of the deadly  VF .

I would believe  , the STEMI patients  who die early (even before reaching  the hospital ) are (un) blessed with a  fighting  heart  ! Ironically , the lazy hearts  reach the hospital  alive ! (slow &  steady win the race !) .  Of course , reperfusion  injury is not the only mechanism of VF . Other common suspect is  left main STEMI .

Link to related video “Ignorance based  cardiology ”

https://www.youtube.com/watch?v=J9DH6Vr04es

Final message

While , VF  is  referred  to as arrhythmia  of death , it may  in-fact , represent  a common form  of  reperfusion arrhythmia in  the setting of  STEMI !  .  . .  Hence , it can  Initiate  a new lease of life in  many   lucky ones !  I hope the title of this article  makes sense  !

Posted in cardiology -Therapeutics, Cardiology -unresolved questions, cardiology- coronary care, STEMI-Primary PCI | Tagged , , | Leave a Comment »

Top six reasons why FFR should be renamed as “Futile flow” reserve ?

June 20, 2013 by dr s venkatesan

  1. The concept of  FFR is based on pressure gradient  alone.In any hydraulic model (Both biological and non biological systems ) pressure difference  is the least   important parameter  that determines flow.
  2. FFR  is unphysiological  as hyperemia   is  artificially induced one .(Adenosine  is not the only parameter that determines it !)
  3. Serial obstructions and branch point hemodynamics are  conveniently ignored.
  4. Reproducibility  remains a big question mark .
  5. On safety  issues  FFR  is a suspect.( Often times , it  requires expertise comparable to  that of a  complex  PCI !) .Beware , the FFR unit has stiff catheter system and is an additional health hazard .  I have witnessed   atleast two cases  where  insignificant lesions were  made significant by  FFR related Injury .
  6. And  now the  knock out punch ,  ! Probably the most vital  issue for which FFR should be banished * , it is not taking into account of vulnerabilty of a plaque .( An FFR > .9 with a hanging , eccentric , mid LAD lesion was left alone by one of the  academically up to date ,  evidence  based interventional cardiologist!  )
           (*If perfomed  in isolation without IVUS/OCT  )
I am still wondering how this concept came into cardiologist domain and into the cath lab .It should have  never been let out of theoretical physics labs !
Final message
The best way to assess physiological significance of an anatomical obstruction is  to  do  exercise  stress test .
If  the lesion is  able to sustain good exercise capacity , it  can be deemed physiological unimportant.
While , this is an explicit  proof  in single vessel disease  ,  even  in   multivessel  CAD ,   EST  is   a  collective  measure of  coronary  reserve flow .( Something like instantaneous equivalent of virtual  multivessel  FFR  )
Moderated After thought
FFR is a highly specialized theoretical  tool , that has very limited role in cath lab .
The two major practical (Non academic)  use of FFR   is to shun away  those   internet fed ,  annoying, pseudo  intellectual patients ,  who constantly ask for  angioplasty  for  obliviously insignificant lesions !
FFR comes very handy  to  bail out  cardiologists at  times of distress   ! (To escape  from the wrath of our patients   after a sub optimal &  technically inferior   PCIs   and   in  the  long term confabulations  in   restenosis  after stenting !  )

//

Posted in cardiac physiology, Cardiology -Interventional -PCI, Cardiology -unresolved questions, excercise stress test .EST, Hardware techniques tips, Infrequently asked questions in cardiology (iFAQs), PCI PTCA Hardware | Tagged , , , , | 1 Comment »

Importance of “TIMI 1” flow . . . in pharmaco Invasive strategy of STEMI !

June 11, 2013 by dr s venkatesan

           Do not ever under estimate  the importance of  TIMI 1 flow .  It can save a  major chunk of myocardium !   A late TIMI 3  flow   . . . is far inferior . . .  to  an early TIMI 1 flow . * Even a trickle  of  flow (Ooze )   can keep the myocardium  alive .  This point we have realised very late. Thus came the   pharmaco Invasive strategy for  all STEMI  who have no immediate access to cath lab ! (please note 90 % of STEMI belong to this group )

pharmaco invasive strategy for stemi002

For a high resolution Image  click below

pharmaco invasive strategy in stemi

* Even a trickle (Ooze )   blood flow can keep the myocardium  alive .

Posted in Cardiology -Interventional -PCI, cardiology -Therapeutics | Tagged , , , , | Leave a Comment »

America’s best hospitals for cardiac care : US news and world report

May 31, 2013 by dr s venkatesan

best hospitals in usa us news and world report

The top 3 cardiac care hospitals for the year 2012-2013 

  1. Cleveland clinic
  2. Mayo clinic
  3. Jhons Hopkins Hospital

america's top cardiology hospitals

//

Posted in Top ten in cardiology | Tagged , , | 1 Comment »

Caring for the Post PCI patient : A presentation

May 31, 2013 by dr s venkatesan

pci powerpoint presentation ptca follow upFile1-PCI 5

Click  on the file   to download  the presentation

Note : The contents are prepared in 2006 .Recent input are to be added .

//

Posted in Cardiology -Interventional -PCI, My presentations | Tagged , , , | 1 Comment »

CCU riders : ST depression + Rest angina is not equal to unstable angina !

May 31, 2013 by dr s venkatesan

Thrombus laden plaque  is sine qua-non of UA/NSTEMI . That’s what we  have been taught  !  right ?  It may be  true in many  situations , but please remember there is another concept  called  demand ischemia , where in there is  no active thrombus ,  still resting  angina may occur due to  increasing heart rate etc.

I just wanted to test how far this concept is understood ,  by the  fellows in our coronary care unit . Following  is  story of a patient who arrived at CCU with  angina  at rest .  I showed  this   ECG asked them the  management .

positive est and unstable angina

History was  purposefully blinded . 5/6 cardiologists wanted to admit the patient either in CCU or rush to cath lab.  Heparin/ Fondaparuinux was prescribed by all. Tirofiabn was suggested by few.It is a  high risk UA with left main disease some one  mumbled .

I silently listened to them and  revealed the history . This patient  has just finished the  exercise stress test , it was terminated as he had angina at peak exercise. and was  reported as  positive . A date was fixed for elective   coronary angiogram. 10 minutes later ECG totally normalised  , and the patient went home (Boarding a crowded Chennai  city bus )

The fellows realised the importance of history . In fact no body asked for it ?  I felt  bad  as  all my fellows failed in this test That reflects bad teaching on my part !

What is the mechanism of ST depression here ?

  • Fresh thrombus ?
  • Mechanical occlusion ?
  • High  heart rate ?
  • Combination of high rate and probable flow limiting lesion .

(Severe forms of  stable angina can occur at rest . So do not equate all rest angina as true  unstable angina !)

Final message

Do not label an ECG straightaway  as acute coronary syndrome when there  is  baseline  tachycardia and ST depression . Spare few minutes and apply your mind !

If  a combination of ST depression  and angina  can be taken  synonyms with UA  every EST positive fellow should be labeled as UA and admitted in CCU. Please remember any tachycardia with a fixed tight lesion will  mimic UA . Further ,  since there is no thrombus here  and there is absolutely  no role for heparin.

Posted in Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions | Tagged , , , , | Leave a Comment »

What is the reference point to measure ST elevation in STEMI ?

May 31, 2013 by dr s venkatesan

ST segment elevation is the key parameter on which the fate of millions of infarct patients are recognised and managed. It is ironical we do not have standardised reference point for measuring the quantum of SR elevation .

This is especially difficult when ST segment blends with forward limb of T waves.

While we have reference point for measuring  ST depression  (Like during EST ). . . why we do not have one for ST elevation ?

Now we have adopted a rough criteria .Read below .

where will you measure st segment

How to measure ST elevation in ECG
How to measure ?
Measure The ST segment 40 ms from J point.
how to measure ST elevation in STEMI 2
                        I lost track the source of this Image .(STEMI hand book 2012 ?)
Final message
ST segment  elevation  is  the key parameter in ACS.  Quantifying  it becomes  important in  assessing  the efficacy of reperfusion strategies and risk stratification. Fresh ST elevation can represent pericarditis, reinfarction or an early dyskinetic  segment . Unless we have  proper reference point there is  a room  for  error in this simple parameter.

Posted in Cardiology - Clinical, cardiology -ECG, Cardiology -Interventional -PCI, Cardiology -unresolved questions, Cardiology-Coronary artery disese, Clinical cardiology | Tagged , | 1 Comment »

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