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.


Cardiac arrhythmias  are tackled by drugs, devices, electricity etc. How about using the light energy ?

It would be sort of revolution if we could tame dangerous cardiac arrhythmias  by optical energy.Exciting new developments are happening at Jhon Hopkins.The emerging field is optogenetics.Preliminary mouse  and human MRI models suggest  red light has a unique property to interrupt electrical  signals in cardiac tissues.(Tissue level induction of light sensitive protein?).It has been shown to revert ventricular arrhytmias.



A preview

Curious thoughts and a corollary in Hindu mythology


There are anecdotal reports in vedic Indian literature  where super powered sky Gods  equipped with the power of light (Lightening/IR rays ? ) can bring life to dead man on earth  . . . Is it the same  optical defibrillation we are talking about now ?

This paper was presented as a poster (Not good enough for  oral ! ) in the just concluded CSI 2016  (Cardiological society of India ) Annual conference at Kochi, India.


What constitutes successful  Primary PCI ?   A proposal to include “ LV dysfunction”  as an  essential  criteria !

A  series of breakthrough technologies  in drugs , devices, techniques has revolutionised the management of STEMI in modern times.This  includes various formats of heparin , antiplatelet agents thrombolytics  and coronary interventions.Of all these, primary PCI is considered to be the greatest thing to happen in STEMI care.

The success of primary PCI is currently defined as diameter stenosis less than 30% and TIMI 3 flow on final angiography without procedural complication. True success of reperfusion essentially lies  in the salvage of myocardium and in the prevention of LV dysfunction. In real world scenario we often find a paradox , ie Inspite of  successful pPCI by current definition a subset of patients suffer from significant  LV dysfunction. Surprisingly, LV dysfunction has  never been included in the definition of successful primary PCI .


In this context we did a reversed cohort  study  of patients with significant LV dysfunction (<40%) following primary PCI to find out possible factors contributing to LV dysfunction.10 patients who had LV dysfunction inspite of successful primary PCI were the subjects of the study. Patients with late PCI  beyond 12  hours were excluded .Echocardioraphy had been done at discharge and 2 weeks after the procedure to assess LV function.

TIMI  3  flow  has been  documented in all  patients at the time of primary PCI.6 patients had undergone pPCI within 6 hours.4 had it by 12 hours. 7 patients had a smooth , fast  pPCI as described by standard protocol.Of these,  2 patients had LV dysfunction inspite of TIMI 3 flow established early.7 patients 3 had complex angioplasty with no reflow managed subsequently.One had deferred stenting after 4 days for IRA.Non IRA lesion were also  tackled in two.

We also confirmed  there is no linear no correlation  between TIMI flow and  subsequent LV function .This becomes vital as time and again we are seeing PCI reports with successful TIMI 3 flow only to find  weeks later  thinned scarred ventricle. Time to reperfuse with anticipated and unanticipated procedural delay  was also  a critical  factor.

However, its clear the  incidence of significant LV dysfunction inspite of  timely, and apparently smooth  PCI is real .Why this happens is beyond the current reasoning. A scientific basis for  individual myocardial sensitivity to ischemic time is yet to be found. (Dynamic host dependent time window ?)

Meanwhile , It seems prudent , we should awake to a harsh reality of practicing coronary care  with a seemingly incomplete criteria for success of pPCI . Its proposed,  an  acceptable levels of  “LV dysfunction at discharge ” (It could be > 50 %) as an essential criteria  to define the success of pPCI  .Custodians of STEMI care should  immediately rectify this glaring omission. This will dramatically impact the current  outcome analysis of STEMI and help Improve the quality of care.

Medina classification  is the most popular angiographic classification  of bifurcation lesions based on the presence or absence lesions at the three levels  of branching  (0,0,0 ) to (1,1,1). The popularity of this scheme is essentially due to its simplicity.

It can further be subdivided according to angle and size .Though there are three angles possible it is the angle of LM with LCX that matters most.

T shaped  left main. Angle of LM-LCX is around 90 Degrees

Y shaped left main. Angle of LM- LCX is > 120 Degrees

Three types of Y according to size of branch vessel size.

Y1 Large left main divided two equal LAD, LCX.

Y2 Left main and one of its branches are equal

Y3 All three are equal diameter.

Here is a series of  lectures on left main (Probably the best I guess  !)  from Dr.Boris Varshisky ,Hadassah University hospital  Jeruselam.He critically discusses about the   nuances of left main disease from pathology, technical and therapeutic considerations.

Spend some time on these videos , you should be able to learn about

  • Distribution of left main disease
  • The complexities in defining the true shapes of of left main ostia .(Ostial sharing between LCX and LAD ?)
  • Lesion based strategy
  • Carinal shift vs plaque shift
  • Stent sizing in Y 3 left main

and much , much  more !