Oh , it’s a well recannalised IRA  and its flowing TIMI 3  as well.  Now, what shall we do sir” ?, An apparently worried senior resident queried after a second look at the images from a 8 hour old STMEI .Why you sound unhappy  man ?  As if recanalisation is an untoward event” ! I teased my resident !
and went on to ask . . .

What we mean by recannalised  IRA ? (Recan-IRA)

  • It is akin to natural or pharmacological angioplasty (or combination of the two )
  • It can be complete or incomplete from the IRA perspective.
  • It can either result in partial or fully salvaged myocardium.
  • It should be understood even a 30% recanlisation can result in TIMI 3 flow and result in near complete salvage
  • Even a 90% recannalisation may not accrue the same benefit if it has happened late. So its all in timing
  • Spontaneous recannalisation can some times even be  superior  to thrombus aspiration . However , some degree of residual thrombus would be present in most
  • Residual plaque burden is also an important factor that will decide the extent of angiographic recannalisation.
  • Some times the recannalisation  will make the vessel near normal with only luminal  irregularity
  • IVUS/OCT may provide accurate assessment of Recan-IRA , it’s is not logistically acceptable in STEMI setting.
  • After listening to my briefing on recannalised IRA , the fellow looked more confused than before. He bothered to ask again , what am I supposed to do once a well recannlised IRA is detected ?  Should I intervene or not ?

The term recanlised IRA generally convey a hemodynamic  meaning for a successful  early (natural plus or minus pharmacological ) reperfusion .If every parameter is fine , and the lesion is not significantly obstructing better to pause any further procedure ,  as consequences of deploying  stent in a well recannalised segment is not yet clear with a stro ng trend towards harm .The decision is to be taken on individual basis with reference to  symptoms, stability ,  residual ischemia and quantum of incomplete salvage and lesion morphology .

If you believe ,a spontaneously recannalised  IRA has provided a TIMI 3 flow , it is equivalent to well done job of natural thrombus aspiration by  a hidden hand and catheter . Consciously respect that .Most cardiologists would have  realised atleaset once ,  that any aggression on a God handled IRA can be counterproductive !

Is there a non academic angle to this issue ?

Undoubtedly yes , strangely  inspite of a positive phenomenon for the patient , recannalised IRA leads to a difficult debate  in cath lab .Suddenly , the  entire collective scientific wisdom of the cardiologist is put into a stress test. There is direct fight between reality , expectations .True patient benefits , obligations to hospitals , the parasitic  relations with device industry , do have a big say !

Final message

Practicing cardiology is simple , but when scientific and non scientific realities of life are in direct confrontation with patient welfare it becomes a huge struggle and only a determined few can win over this infinite fight against conscience !

Mohandas Karam Chand Gandhi ,  father of my country , India , made these observations in year 1925  about the  fundamental constituents of  violence in society . These words of monumental wisdom came when he was  addressing young Indians in a country- side rally .

mahatma gandhi quotes medical science humanity

Note, his finger points to , what  exactly is relevant to our profession ! He emphasized this  nearly  100 years ago, when medical science was at its infancy .One can only guess what would be Mahatma’s comment about our profession in it’s  current form !

Should we include moral, behavioral and ethical classes  right from the first year of medical  school along with Anatomy , physiology and bio chemistry.Medical council of India obviously need to burn more mid night oil , I wish it happens in my life time. !


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




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 the 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  look back in time and “constantly scrutinize”  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 . . .

NSTEMI  constitutes a  very heterogeneous population .The cardiac   risk   can vary  between very low to very high .  In contrast ,  STEMI patients  carry  a high risk for  electro mechanical complication including   sudden death .They all need immediate treatment  either with  thrombolysis or PCI to open up the blood vessel  and salvage the myocardium.

The above concept , may  be true in   many situations  ,  but what we fail to recognize   is  that ,   STEMI   also  is  a heterogeneous clinico pathological  with varying risks and outcome !

Let us see briefly ,  why this  is very important  in the management of STEMI

Management of STEMI  has undergone great  change  over the past 50 years and  it is the standing example of evidence based coronary care in the modern era ! The mortality  ,  in the early era was around 30-40% . The advent of coronary care units, defibrillators, reduced the mortality to around 10-15%  in 1960 /70s . Early use of heparin , aspirin   further improved the outcome .The inhospital mortality  was greatly  reduced to a level of  7-8% in the thrombolytic  era. And ,  then  came the interventional approach, namely primary PCI ,  which is now considered the best form of reperfusion when done early by an experienced team.

Inspite of this wealth of evidence   for the   superiority  of PCI  , it is only a fraction of  STEMI patients get  primary PCI   even in some  of the  well equipped centers ( Could be as low as  15 %)

Why ? this paradox

Primary PCI   has   struggled  to establish itself  as a global  therapeutic concept  for STEMI ,   even after   20 years of it’s introduction (PAMI trial)  .  If we  attribute ,  lack of   infrastructure  , expertise are  responsible for this low utility of primary PCI , we are mistaken ! There are so many institutions , at least in developing world ,   reluctant to do primary PCI  for varied reasons.( Affordability , support system , odd hours ,and finally perceived fear of untoward complication !)

Primary PCI may be a great treatment modality , but it comes with a inherent risk related to the procedure.

In fact the early hazard could exceed the potential benefit in many of the low risk STEMI  patients !

All STEMI’s are not  same , so all does not require same treatment !

Common sense and logic would   tell us any medical condition should be risk stratified before applying the management protocol. This will enable  us to avoid applying “high risk  – high benefit”  treatments in low risk patients . It is a great surprise,  the cardiology community has extensively researched to risk stratify NSTEMI/UA   ,  it has  rarely  considered risk stratification of STEMI before  starting the treatment.

In this context , it should  be emphasized  most of the clinical trails on   primary PCI  do not address  the clinical  relevance and the  differential outcomes   in various  subsets of  STEMI .

Consider the following two cases.

Two young men with STEMI  , both present within  3  hours   after  onset of symptoms

  1. ST elevation in V1 -V6 , 1 , AVL   ,  Low blood pressure , with severe  chest pain.
  2. ST elevation in 2 ,3, AVF , hemodynamically stable , with minimal  or no  discomfort .

In the above example,   a  small inferior  MI by a distal RCA occlusion  ,  and a proximal LAD lesion jeopardising entire anterior wall , both  are  categorized as STEMI !

Do you want to advocate same treatment  for both ?  or Will you  risk stratify the STEMI and treat individually ?  (As we do in NSTEMI !)

Current guidelines , would  suggest PCI for both situations. But , logistic ,  and real world experience would clearly favor thrombolysis for the second patient .

Does that mean,  the second patient is getting an inferior modality of treatment ?

Not at all . In fact there is a strong case for PCI being inferior in these patients as the risk of the procedure may far outweigh the benefit especially if it is done on a  random basis  by  not so well experienced cath lab team.

(Note : Streptokinase  or TPA does not  vary it’s action ,  whether given by  an ambulance drive or a staff nurse or even a  cardiologist !  .In contrast ,  the infrastructure and expertise have the  greatest impact on the success and failure  of PCI )

Final message

So , it is argued the world cardiology societies(ACC/ESC etc)  need to risk stratify STEMI (Like we do in NSTEMI ) into low risk, intermediate risk and high risk categories and advice primary PCI only for high risk patients.

Bifurcation  angioplasty is a  newly conquered(Or not yet !)  target  for Interventional cardiologists.We have come a long way  in planning  interventions  for left main  with state of the art  hardware, expertise and  image assistance .However , every  classification , approach, strategy  for BFL talks about tackling the main and  side branches meticulously.

Still . . . one question  is not answered clearly is  . . .

A mini MCQ.

Answer: Open for contribution.

My inference

*It all depends upon the Indication and Individual arterial ischemic burden. In ACS, if  LAD territory is infarcted and beyond 24 hours.LAD becomes a  side kick to the vital LCX which supplies  the remaining life sustaining myocardium which includes the critical basal segments.

Final message 

Since , the risks involved in the interventions of  left main and its bifurcation is inherently linked  with , what exactly we mean (and do ! ) to the side branch .Its mandatory we spare few intellectual moments before our hands invade the coronary battle zone.

Here is an Interaction between  a ER physician  and a cardiologist !


“I should say I am happy for this cartoon cardiologist , It at least thinks , verifies ECG . . . and resists entry for a dubious STEMI to cath lab ”


It has become fashionable for many current generation cardiologists to stent the LAD   with proximal end  liberally extending into left main shaft  in Medina 0, 1, 0 or (1,1,1 )lesions involving distal left main often  jailing the LCX . This concept came into vogue as it helped bail  out few  hemo-dynamically  unstable patients with true left main bifurcation lesions during primary PCI .Of course , it’s potentially useful strategy in  emergency , if  extended into routine situations (like all stable proximal LAD/Bifurcation ) we are bound to create few problems.


Rapidly protecting the left main with a long single stent down into LAD is an easy way out for tackling distal left main /LAD combined lesions.  Conceptually it asks you to forget the LCX outright.(Coronary outrage for some to call LCX as  a side branch of left main ! ).Of course, one can reconstruct the LCX  ostium by other means or a second stent if required.

Final message

Conquering  left main disease  with a long stent right from its origin or mid shaft to  LAD (Some times  from Aortic ostium ! ) may be an  interventional pride for the cardiologist. But , in no way it  imply we have crossed the  final frontier in LM disease.In fact,  putting a left main coil is the  easiest task among all  PCI since there is little expertise required to cross the lesion .Maintaining its patency   medium  long run and thus beating the CABG  is  true achievement  ! Achieving  an acute patency  of left main and wheeling out the patient live from cath lab can not  be reason for permanent rejoice ! One should realise his life is at the mercy of DAPT and its pharmakinetics which we know can be unpredictable !

“Protecting the patient is more important than a protecting left main” 

Just because a technique is easy to accomplish it doesn’t confer the right to misuse it .The argument “my patient” is doing fine with this type of stenting  is not an appropriate way of justification.

PCI and coronary stents are revolutionary concepts  but they may not be  great life saving devices  . . . though the collective cardiology wisdom may seem to suggest so !


The ideal way to describe a stent could be “Its a metal coil , if inserted properly in certain population of severely obstructive forms coronary artery disease may save some lives in acute situations  or give relief to pain in non acute situations”

*While the true benefits for the patient population is unsure . . . it’s absolutely certain stents  confer highest  quality of life to the  manufacturers and their chain of associates including the Noble professionals !


I wonder , what would be his comment about ubiquitous stents that rule the current era !

Learnt cardiologist’s  will know the true life saving potential of these stents (In the way its been currently used ) Their conscience will also tell how Inappropriate and Indiscriminate usage of stents has possibly consumed more human lives that may even beat the number of lives saved .(Oh, Its wild, rude statement  friend!)

I sincerely believe the move by Government of India to control the stent price ( to enable all our countrymen to get it)  . . . as if  “stents are the only staple diet” for heart patients is ill-founded and dangerous .

What the Government may not be aware of  is  . . .This 45000 crore omnipresent stent  industry is playing havoc in the life of patients not only financially  but also biologically to harm their blood vessels.

It is near foolish to tackle the scourge of human beings -Atherosclerosis,   a diffuse medical disease with a lesion specific intervention .This is especially true when we want to tackle it in population based approach . Yes, some super rich and elite  get sophisticated stents thinking that they are privileged .Please understand  rich tend to suffer more  with technology. Often times non affordability is also a bliss for the poor .(Rubbish ,won’t agree  . . . Is it , will realise later !)

Who will tell this to our  policy makers ?

Never ape the private sector health care , states must have different priorities.There are Infinite number of studies that  very clearly reveal medical management and life style modification is the sure and successful way to tackle CAD.(I think I need not dwell into this as evidence is explicit .)

Meanwhile, let me give one example of  the futility of innovation and perils of premature release of half baked science .While one section of Industry is coming out with stents made up of exotic new metals , simultaneously other group is innovating and experimenting the exactly opposite , how to get rid of the metal ie bioreabsorable stents. Mind you, one of the latest generation stents was severely reprimanded in a Landmark trial ABSORB 2. Its a comical irony some of the hospitals and cardiologists  feel bad  to miss this red flagged stent that are taken out of their cath lab because of price cap. ( A pat for the Govt for this !)

Its a multi billion dollar Industry (Note : there is no pardon for Indian companies to exploit either !) trying to disseminate a commercially motivated concept intelligently including the stake holder Government in their loop. The move to liberalise stent usage is  most unfortunate thing  as the Govt has  inadvertently increased the risk of abuse .Let the new age Indian not be proud  about “Stent for all ” movement since the  Govt will ultimately  have to shell  out for this imperfect therapeutics through public insurance .

Final message 

Though capping the price of the stent by Government  do carry  some sense  . . . ultimately      I feel its a trap . It’s akin to let loose a dubious  modality in public domain within easy reach . Already the companies want to increase per capita metal consumption. That process will only get accelerated now.

The Government must realise there is an urgent &  broader issue to be addressed by health ministry.Its not only in cardiology but in all walks of health delivery system. How to prevent “contamination of  medical science by pseudo scientific intervention fueled by corporate greed ? They should start  sensitizing the young medical professionals in medical schools that will help the Noble profession remain Noble !

Now , some one wanted to know,  Can we diagnose unstable angina without Chest pain ?

Crazy question isn’t , Angina by definition  should have chest pain .There is nothing called silent angina , only silent Ischemia  .

  • We know Ischemia can occur silently .
  • We also know STEMI can occur silently (About 10 % of MI do occur without any symptoms )
  • If STEMI occurs  silently  why not UA/ NSTEMI combo ? (Collectively called as  NSTE-ACS)

The debate goes like this .If stable angina can present with equivalents ? what prevents  “Unstable angina”  to present with  Anginal  equivalents without chest pain ?

If  a diabetic patient who had a silent MI in the past  . . .  subsequently  experience  severe episodes of resting ischemia  , will he feel the pain , that is supposed to occur  with his  “unstable angina”  or not ?

Hmm , difficult to guess right,   So it seems highly plausible  UA/NSTEMI  do  occur silently ! Literature hasn’t looked into this specifically. Chest pain is built integral  into definition of UA , infact it is a symptom  complex rather than an disease entity by itself, while NSTEMI is ECG and enzyme combo ! Making the term  NSTE-ACS  look  perfect.

Any other technical explanation ?

The concept of Ischemic cascade says angina occurs last, well after biochemistry , wall motion defect and ECG , hence its distinctly possible for UA/NSTEMI present to be painless !

Final message

Anginal pain perception is related to intactness of neurogenic circuits and also probably the severity of Ischemia.If full thickness myocardial necrosis can be painless in few, nothing prevents from an episode of UA/NSTEMI  be truely painless .

Clinical implication of this conundrum

Can we admit a patient as UA/NSTEMI with out chest pain ?

Yes, it would seem so .

No, we can’t .

Indeed we can , if ECG changes are there .

No, we can admit even with normal ECG if its real unstable angina.

This is the crux of the problem in ERs all over the globe. Our knowledge base is simply not good enough. Every one of us has seen Troponin positive silent NSTEMIs ! but . . . to me still something is missing in the link .

Modern day approach 

Pain or no pain,any  fresh ECG changes ( Both T and ST shifts*) should be rushed to cath lab.Whenever you are not sure .Always better to err on the side of over investigation.That’s the mantra ! So ,you do an Angiogram , find an Incidental intermediatroy lesion which may not be responsible for the ECG changes but you are compelled to go after it FFR//iFR , OCT, IVUS and so on !

*There is huge list of non Ischemic ST/T shifts in ECG that can be read elsewhere .


Can’t agree with this article. Foolish to diagnose UA without chest pain. Never  treat ECG  in isolation unless its a convincing  ST elevation or depression with clinical input and thorough scrutiny of  past record . Realise , how important is  the basics principles of medicine taught  by Oslers and Cushings a  century ago.



Artificial pacemaker is one of the major discoveries in cardiology that has given new lease of life to patients suffering from serious bradycardia and heart blocks . Now, the technology has grown beyond pacing , for delivering shock ,defibrillate , resynchronise failing heart etc. For accomplishing  all these tasks we need electrical power . . . non stop on board !

Though , the energy required for sustaining an electric pacemaker is miniscule (About 40 micro watts) still, the lithium ion battery can last only around  10 years with the available technology.Various alternate sources for power* are being  explored. One great innovation is on the horizon .A new “scientific spark”  came from a totally unexpected  quarter.

 If Automatic Swiss watch can run without a battery  life long ?  Why not a cardiac  pacemaker  ?

 How about harvesting mechanical energy from the heart itself  ? (The ultimate biological bundle of energy ! ) .

The concept was  originally suggested by University of Berne Switzerland , researchers from Stanford has successfully used the cardiac  muscle activity as a dynamo to generate and store minute amount of electricity that can sustain heartbeats in an electro  mechanical coil loop model.


A person’s heartbeat  moves a magnet and generate electricity for a pacemaker


Trials done on pig’s heart are promising .(Reference 1)

Final message 

The idea may look dramatic , but it works.Hope  it becomes reality in our patients in near future.

Further reading

* Creating gene modified  biological pacemaker cell is .

Sharing this  article from  Via: New Scientist

By Lisa Zyga
Science Blogger

  At first glance, this idea seems somewhat impossible, like using the movement of an engine’s pistons to power a car. However, researchers David Tran and his colleagues from Stanford University explain in a recent patent that the idea is very plausible. For one thing, a heart-powered pacemaker can generate and store more electricity than required to operate, and use the stored energy when needed. Also, a battery could be included in the pacemaker, and power from the heart would extend the life of the battery.

Overall, the researchers hope that the invention could at least double the lifetime of today’s pacemakers. Currently, the batteries in pacemakers can last up to ten years, although they typically last only four to five years. (Originally, batteries lasted for as little as a year.)

The invention also has the potential to reduce the size of the pacemaker by one-half or more. For example, a typical commercial pacemaker with a volume of 16 milliliters may be reduced in overall size to as small as 1-8 milliliters.

An embedded generator could continuously produce power in several ways, such as through electromagnetic induction or the piezoelectric effect (electric energy generated via mechanical stress).

In the Stanford team’s design, the generator is implanted near the heart wall, such as attached to the myocardium or pericardium, which would subject the generator to regular pulsating movements produced by the beating heart.

The generator itself consists of a magnet, a conductor (both micro- or even nano-sized), and electrical leads hooked up to the medical device. Contraction of the heart muscle causes relative motion between the magnet and the conductor (such as a coil of wire). This relative motion between the magnetic and coil induces an electric current in the wire, which is transmitted through the leads to the implanted pacemaker.

Movements produced by the beating heart would have a frequency of between about 0.5 Hz and 2 Hz, which could generate between 40 microwatts and 200 microwatts of power. The pacemaker would only require about 40 microwatts, so the excess power could be stored and used for later use, such as when the heart stops beating.

Besides using the movement generated by the muscular contractions of the heart, other versions of the pacemaker could generate power from heat differentials, physiological pressures, and flows and movements, such as blood flow. And in addition to pacemakers, the researchers suggest that similar systems could be used to power defibrillators, ventricular assist devices, muscle , neurological stimulators, cochlear implants, monitoring devices, and drug pumps.



Knowledge can be a dangerous asset sometimes . A modern day cardiologist reassured a patient  who had an unusual dyspnea after a muti-vessel stenting for a not so complex lesions following an anterior MI.The doctor  was not mystified when the patient uttered this complaint. In fact he was so cool , reassured the patient since he was taking  Ticagrelor ,and it’s well recognised to cause dyspnea in some patients.

Few days later patient  called  again and informed that the  dyspnea is getting more intense  and ultimately he was rushed to hospital only to diagnose  subacute stent occlusion and a fresh ACS.

What do you learn from this story ?

Caution , extreme caution is required when dealing with symptoms following PCI and especially dyspnea.

A brief review about  Ticagrelor dyspnea conundrum

  • Ticagrelor  ,a reversible P2Y12 blocker  has a peculiar side effect of dyspnea (Which happens to be a cardinal symptom of heart disease as well )
  • Its reported by up to 30 % of patients who receive it.
  • It can be either exertional  or even at rest.
  • It seems to be dose dependent
  • Onset within 24 hrs , upto 1 week.
  • Pulmonary function not affected.
  • Cardiac function thought to be unaffected.(No correlation with LVEDP though)

Mechanism of dyspnea with Ticagrelor (Presumed)

  • Its direct cortical effect due  sensory neurone  P2Y12 blockadae.
  • Due to Adenosine


  • Reassurance(Possible in few , but risky unless absolutely confident)
  • Encourage Tea intake (Theophylline might nullify if its Adenoisine induced .
  • Discontinuation is  the specific option (up to 10%)

Final message.

Dyspnea is a  unique side effect of Ticagrelor. Unexplained dyspnea is a delicately dangerous symptom in a post MI patient as it may directly imply a silent ischemia induced LV contractile dysfunction and acute raise in LVEDP.

Don’t ever take it easy and attribute all episodes of  dyspnea to Tiacagrelor .If you are really not convinced consider switching the patient to a different anti-platelet drug. Its simply not worth for both patient and physician to spend anxious moments.