Archive for the ‘cardiology- coronary care’ Category

When a culprit thrombus keep the  myocardium as hostage . . . don’t storm the coronary artery  indiscriminately   !

When a single gun men  keeps 100 innocent people as hostages , threatening their  lives, rescue mission should start .No can can afford to wait. But, without knowing  the  culprit’s true nature the process of rescue mission is always going to be tricky .There are so many instances Newton’s third law  was reversed , when reactions  evoke more chaos  than the index action.

In the recent world terrorist events ,  the  rescue missions  were so delicate and  it was very  unfortunate we  lost  many   innocent hostages !  The reasoning is ,there  is no way we can avoid these. I wonder is it really true ? !

rescue missionNot all culprit lesions  are true ones.They simply threaten  our myocardium with  thrombus and plaques  in various forms .Don’t show aggression to pseudo threats  you may  ultimately end up with more damage.(What I call as crazy culprits!)

(  Read here , why unstable angina even though thrombus is sitting right inside the coronary artery attempting to lyse it causes more  damage !)

After thought

Iam sure ,bulk of  the Interventionists wouldn’t agree with this thought . They would decry , watching a person  silently when the myocardium  is on  fire is a serious crime !

But . . . we  need to  remember the process of extinguishing  the fire  with some more fire arms is a delicate game played in undefined  philosophical turf.

The only way to introspect  such events in life is , to accept any eventuality    arising out of “not pursuing”  a  presumed rescue mission with vigor. No need to be guilty about that,after all , it can be a myth !

Modern human cognition , growing with a staple  scientific  feed  on a 24/7  basis  is  unlikely to realise , restraint can be an effective tool  even in critical moments !

Oh,is all that I have  scribbled so far  is just a repetition  of 1000 year concept of  “Primum non nocere”

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When a patient comes with angina at rest , it could mean two things .Either a  STEMI or an NSTEMI .This , we can diagnose only after seeing the ECG .

Can we differentiate these two by the  character of chest pain alone ?

Very  tough task isn’t  ? But there are some definite clues .

Infarct  pain

  • Is mostly sudden .
  • Likely to be crescendo , lasts more than 20-30 minutes .
  • Fails to get relived by rest or even  Nitrites.
  • Sweating due to sympathetic activation is more pronounced.

Unstable angina

  • Is rarely  sudden .Often has a pro-drome.
  • UA is  mostly precipitated by an increased demand situation or a stress.
  • It has  a typical waxing and waning  pattern . Rarely assume a true  crescendo character  as myocytes  does not necrose (Just threaten to die !)
  • The chest pain radiation   to  shoulder is less  conspicuous , instead it  tends to  reach  the  jaw area .(* An observation,Is it something to do with multi-vessel CAD in UA ?)

Mechanism of the difference : Epicardial vs Endocardial angina

The pain of UA is   due to subtotal occlusion and  endocardial ischemia , while STEMI is  sudden total occlusion  and the resultant  transmural  ischemia . In STEMI  epicardial  surface is always involved (Which lifts the ST segment in ECG .).We know epicardium  is same as  visceral layer of pericardium which is well innervated .Hence  pain  of STEMI   acquires  more of somatic character  than a  predominately visceral type pain  that occurs with  UA/NSTEMI where epicardial ischemia is absent.

Clinical importance

The demarcation between unstable angina and Infarct pain becomes vital when we calculate the time window for thrombolysing STEMI .Many of them have a phase of pre infarction angina which is a type of unstable angina. If we mistake it for Infarct pain then one may falsely calculate a prolonged time window and deny re-perfusion therapy.

Post -amble

It is tricky issue  to differentiate the  chest pain of  STEMI and NSTEMI  .A significant overlap can occur  in  real coronary care scenario . We know   chest pain  that occurs in both   pre and post infarct  phase  is considered  as unstable angina .(With infarct pain sandwiched between them!) Hence differentiating  them may even be termed as futile.

Still,clinical cardiology  can be  made  fascinating by indulging in such exercise !


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We know  streptokinase  is a non fibrin specific   agent that   results in systemic lytic state and hence more chance of bleeding.

TPA is fibrin specific  and it  will act only on fibrin  bound to clot , hence systemic bleeding risk should be less.

However , in real world , it is well  documented  stroke risk with TPA is consistently more than streptokinase .(It varies between .0.3-.5% with streptokinase , 0.7-to 1%  with TPA)

How do you explain this apparent  paradox ?

Possible explanations.

  1. The fibrin selectivity pf TPA is not absolute* .
  2. The lytic power of  TPA is more hence stroke is more likely.
  3. The FDP* released by TPA can trigger a systemic lytic state
  4. In the  post TPA protocol   heparin  is  mandatory and  this  contribute to stroke risk.

*What happens o fibrin degradation products (FDP) levels after TPA ?

FDP levels do increase after TPA  .This peaks at 1 hour after lysis.it Correlates well with risk of stroke.(Ho CH, Wang infarction.Thrombosis Research ).


This is an excellent review with analysis from 14 studies with total of 142 907 patients with thrombolysis

A meta  analysis of thrombolytic agents streptokinase vs tpa tnktpa  stroke risk fibrin slectivity

Ho CH, Wang SP Serial thrombolysis-related changes after thrombolytic therapy with TPA in patients with acute myocardial infarction.Thrombosis Research

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Is “Non-flow limiting coronary  lesions  more prone for ACS ?

  • If  your  answer  is “No”, you can skip this article.
  • If your  answer is “Yes” , you need to read this article.

ACS is the commonest cardiac emergency .Thousands of patients are treated every day.Millions of dollars are spent.Bulk of the cardiologist’s life revolves around this entity.

Scattered atherosclerotic plaques in coronary artery lead to ACS either in a random fashion or in a predictable manner .

Still, we are  highly  uncertain about  which lesions are likely to result in ACS ! Some time in the beginning of  21st century, the main stream cardiology media were abuzz with the concept, that non obstructive , non-flow limiting lesions are more prone for ACS rather than more tight  stenosis.

atherosclerosis  flow limiting lesion  glagov  plaque rupture vulnerable erosion fissure vs dissection

I fail to understand how a tight lesion is less  prone for ACS. Tighter lesions are  bigger and must be  prone for more complications . Image courtesy :http://upload.wikimedia.org/wikipedia/commons/9/9a/Endo_dysfunction_Athero.PNG

This reasoning was based on few studies, that lacked  solid scientific proof . In fact the initial  observation was  not made in living coronary arteries rather by autopsy observations .(Later live virtual histological studies came ,  but didn’t confirm this !)

Surprisingly the degree of  anatomical narrowing was conferred  vulnerability  , when we know plaque compositions , morphology and hemo-rheological  factors are many fold important in precipitating ACS . (Lipid content , fibrin cap  thickness, eccentricity , etc)

So where is the truth hidden?

Is it really possible, lesser the stenosis more  is the propensity for rupture ?

 We need to introspect .

“In all probability,  it is a meager statistical illusion”

For every tight lesion there are as many minor lesions scattered around in a given a coronary artery. These can progress into ACS  later.

It is basically wrong to assume non-flow limiting lesions are more prone for ACS than non-flow limiting lesions.To believe so , seriously underestimates  the  culpability of big lesions .It appears a coronary mockery to me  !

At best , we can conclude  non-flow limiting lesions  are not benign and can be an important source of ACS.

An unscientific chain reaction !

If we start believing non flow limiting (say  30%  stenosis ) is more prone for ACS , why we are not stenting all  those lesions ?

If the above concept  is  is applied in cath lab  routinely , the principle of  FFR   which relies solely on hemodynamic impact  will  crash into the dustbin !

Some  more truths

However , It is indeed true  when a plaque is hardened by severe sclerotic process or calcification it is less prone for  rupture and clinical ACS  but can be a source for stable angina.

Is it  justified to assume , larger the plaque the harder  would be it’s content  that  resists ACS ?

Meanwhile , we also know there need not be any lesion at all to cause an ACS.( In a young  smoker ,  100 % thrombotic STEMI  is possible  over an area of coronary erosion caused by endothelial dysfunction ! So , where do we go from here !)

Let us be clear

Are you confused more !   . . . after  reading this article, let us clear it by two-line summary !

As on 2014 ,

  • Symptomatic flow limiting lesion   are tackled by stents.
  • All non-flow limiting lesions  are treated by  high dose Statins  and vigorous medical management.

Final message

Contrary to popular  perception, tight lesions are  more complex, eccentric , soft and are at immediate risk of ACS.

Non flow limiting lesions remain static in most,  regress in many , still  carries  distinct  risk of progression into full blown ACS , at any time if conditions are favorable.

Fixed concepts and ideas in medical science do not help us  taking medicine forward. Especially so, when these are based on assumptions and approximations. If only we redo these studies with the currently available technology (FFR/OCT/NIR the conclusions would be dramatically different !

Caution : There is no scientific proof  for the above discussion,  of course . . . we lack evidence against it as well !


2.Glagov S, Weisenberg E, Zarins C, Stankunavicius R, Kolletis G. Compensatory enlargement of human atherosclerotic coronary arteries. N Engl J Med. 1987; 316: 371–375.

3.Fuster V, Lewis A. Conner Memorial Lecture. Mechanisms leading to myocardial infarction: insights from studies of vascular biology. Circulation 1994;90:2126-2146.

4.Ambrose JA, Weinrauch M. Thrombosis in ischemic heart disease. Arch Int Med 1996;156:1382-1394

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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 ? 
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

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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 ”


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  !

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bifurcation angle

  • At any branch point three angles are possible .True bifurcation angle is formed between LAD and LCX .
  • The angle between LM and LAD or LM and LCX can also be important in specific situations ,especially when we encounter short left mains and Medina 1,1,0 lesions .
  • Major bifurcation angle can  occur in mid  segments  as well ,  between LAD / major Diagonal  , LCX and OM.
  • Logic would tell us the  left main  bifurcation  angle is relatively fixed by the anatomical AV and IV grooves. Still early course of LAD and LCX can be out of grooves.
  • Further ,the bifurcation angle is imparted some amount of dynamism by cardiac cycle . It can vary between 80 -120 degrees (LAD/LCX).
  • Most importantly various  angiographic views can alter the true angle (by illusion ) in dramatic fashion . RAO caudal view appear ideal to measure it. (LAO caudal make every bifurcation angle obtuse !)
  • Acute angled bifurcations are prone for stent related mechanical issues both during deployment and in the long term outcome . (When two stent technique is used) This is because ,  acute  angled bifurcations has a tendency to drift the carina , and  encroach  the lumen  which can create new  turbulence . Of course final kissing balloon is expected to reduce this hemodynamic side effect at least on paper !

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