Archive for the ‘Uncategorized’ Category

Rules of the PCI game 

  • Mind the physiology. It is the new norm in selecting the lesions for stenting.
  • Now, If physiology is ok, you have to mind the Anatomy and vice versa.
  • If Anatomical (severity of block )is ok, then, you have to mind the morphology and vulnerability.
  • Finally. and most importantly mind the patient’s symptoms and clinical scenario.

So what should we do in a case of 70 % LAD with  .9 FFR ? (Still shabby looking, eccentric plaque, looks vulnerable  with a thin cap on OCT)

  1. I will stent, no doubt.
  2. I shall wait, and treat with Intensive optimal medical management (OMT).High dose statins will surely seal the cap.
  3. I will defer and watch.
  4. I will teach the patient and their family the basics of coronary hemodynamics and accept their decision.
  5. I simply leave the LAD for God to heal.

Which is correct?

All can be fair depending upon the clinical scenario.

In the ACS setting, one can’t afford to ignore these lessons.

Many would argue even in CCS setting it need to be tackled with PCI.

But isn’t also a fact, (maybe, we have been taught wrong as well ) non-flow-limiting lesions are more at risk in terms of ACS risk.

Hmm . . . then why we Insist to celebrate the concept of FFR  and its magic cut off of .75?

Do we practice coronary care at its height of confusing times ? or Am I make it appear so? 

Watch this, (https://rutherfordmedicine.com/videos )It might help you to get a better answer. Its called FORZA study. freshly delivered at TCT 2019, San Francisco.It compares FFR vs OCT guided PCI



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The term Ischemic cardiomyopathy(ICM) was originally coined by Dr. Burch from Tulane University, New Orleans, USA in 1970. For many decades there was skepticism regarding the existence of such entity. WHO classification over the years never included this term. ESC working group of 2008 (Elliott P, European Heart 29(2):270–276) decided not to include CAD as a cause for cardiomyopathy. Even the current MOGES system doesn’t invoke CAD as a cause for cardiomyopathy. But, I am sure, most of practicing cardiologists would agree, there is a need for such an entity.

Why there is much reluctance to diagnose Ischemic cardiomyopathy as a distinct entity?

It is because of the basic principle, that cardiomyopathy should be a primary disease of cardiac muscle. (or at least secondary ).The presumption is, Ischemia per se doesn’t lead to muscle disease as such. It is just nutrition deprival.

Does this justify?

No, not at all. When a cardiac muscle is chronically deprived of nutrients it goes for necrosis, dilatation, scarring and dilatation, and progressive LV dysfunction. At some stage, it becomes true muscle disease or its equivalent (Secondary cardiomyopathy).In fact, adverse remodeling, Infarct expansion, extension lead to myocyte disarray, slippage and apoptosis, and cellular and interstitial fibrosis. All these changes are similar to Idiopathic (Postmyocarditis)cardiomyopathy.

What happens in the real world?

Even though there was some hesitation to diagnose ICM in the past, gradually the term shrugged of its taboo in academic circles. In heart failure clinics the only question seems to matter for everyone is, Is it Ischemic or non-ischemic DCM? Surgeons and EP guys also actively pursued the term Ischemic cardiomyopathy while they are selecting patients for CABG or CRT/ICD etc.

Further, in the research world involving community-based heart failure cohort, they required a basic distinction between the group of Ischemic from Non-Ischemic cardiac failures.

DUKE university definition (By Felker et al)

I think DUKE ended the controversy in the Nomenclature of Ischemic cardiomyopathy. It suggested the following to diagnose ICM (Read REF 2)

  1. LV dysfunction < 40% EF
  2. >Atleast one significant proximal coronary lesion (Usually 2 or more)
  3. With the history of MI or Revascularisation

* We are analyzing our data (Madras medical college, Chennai India) and propose to write WHO/WHF to include the following additional criteria to diagnose ICM.

4. At least 6 months should be elapsed between the MI and diagnosing Ischemic cardiomyopathy,

5. Must have significant LV dilatation & global Hypokinesia(With or without regional variation).

6. At least one episode of clinical heart failure is required before labeling it as Ischemic cardiomyopathy.

Other definitions that endorsed Duke

STITCH criteria *Surgical therapy in ischemic DCM study ICM was defined CAD with cut off EF < 35% with triple or double vessel disease.

iFAQs in Ischemic cardiomyopathy

1. Can we diagnose ICM without a history of MI?

This is tricky. As we all aware its very much possible as in silent MI of diabetes. One more possibility is even chronic coronary syndrome with microvascular dysfunction can lead to ICM.

2. Can Ischemic cardiomyopathy present as HFpEF or RCM?

While most Ischemic Cardiomyopathy present as DCMs with HFrEF, It is currently not clear how much of Ischemic heart failure present as HFpEF and if so they can’t be included technically as Ischemic cardiomyopathy in spite of the fact they present as HF.(as EF would be >50%)

3.When does a Post MI failure become Ischemic cardiomyopathy?

If the definition of STITCH or DUKE is applied, any acute STEMI can fulfill criteria of ICM. Hence it advisable to have a time limit say 6 months following MI to be referred to as Ischemic DCM. Pathologically to call it true cardiomyopathy, scarring, dilatation is required. Myocytes should be in independent self-destruction mode irrespective if hemodynamic conditions.

Response to treatment

The only purpose to diagnose ICM is to try to remove the I from ICM( ie Ischemia) Unfortunately, it is not an easy task. (While correcting Ischemia in ACS seems to be such an easy job.)

Following principles apply.

  • Medical management of HF/Ischemia is the key.
  • It is advisable every patient with cardiomyopathy should undergo coronary angiogram to rule out ICM.
  • Effect of revascularisation remains equivocal.
  • Viability of remaining muscle mass must be documented. (At least one-third of total cardiac mass should be viable.(Not very easy to prove though)One may use Doubutamine /Nuclear stress/PET etc) .It’s very important to realize even if the viability is demonstrated, the area that shows viability must be supplied by an artery that has a revascularisation eligible lesion.
  • STITCH can be called as a negative study (meaning positive outcome for patients if the patient doesn’t receive CABG in mulitvessel CAD and LV dysfunction ).However , STICHES (Extension of stich showed some long term benefits) The probable reason for CABG not helping much in ICM is the muscles didn’t get further useful life, either because it’s fully dead or extremely viable, that revascularisation made no impact.
  • CRT/ICD is known to prevent SCD and improve the functional class.
  • Heart transplantation is a life-modifying specific strategy.

Final message

I agree, many times our valuable time is wasted in renaming /Altering /relabeling a disease /process or pathology without any useful purpose. Medical nomenclature and classifications are done to make diagnosis simpler, choose an appropriate therapeutic modality and make a positive impact on the outcome.

In that sense, segregating ICM from other causes of cardiac failure do help in choosing a specific management strategy.

Let us welcome MOGES, It is the most comprehensive cardiomyopathy classification system (Like TNM classification for cancer). Still, I am not clear why it hasn’t included CAD in that system. Thanks to Dr. Burch who thought of this 50years ago.


1.Burch, G. E., Giles, T. D., & Colcolough, H. L. (1970). Ischemic cardiomyopathy. American Heart Journal, 79(3), 291–292.

2.Felker G.M, Shaw L.K, O’Connor C.M (2002) A standardized definition of ischemic cardiomyopathy for use in clinical research. J Am Coll Cardiol 39:210218

History of cardiomyopathy classification

The landmark thoughts originated in 1972 .When Goodwin and Oakley defined cardiomyopathies as the heart muscle diseases of unknown cause and described them as dilated (DCM), hypertrophic (HCM), and restrictive (or obliterative) (RCM) cardiomyopathy types.

WHO adopted it mostly and suggested Primary and Secondary cardiomyopathy in 1980. In 1995 WHO revised it.

The current MOGES classification doesn’t mention about Ischemic etiology

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Master health checks* , superficially look like a perfect modality to practice the greatest medical concept ie “Prevention is better then cure” .Let us detect all human diseases early , prevent its progression, regress it or completely cure it . Absolute bliss is it not?

Why then articles such as this one should ever get published, that too in one of the prestigious journal of medicine?

*Master health check .( Also referred to as annual General health checks.)

Master health check up geenral cochrane bmj editorial

While the title itself is provocative, it adds a tag line which is still more a shocker.

There are specific well-researched reasons for this preventive health check fiasco.The masters, who were originally the guardians of health soon became disease mongers.In the process, the primary aim of propagating the doctrine of “prevention is better than cure”, could not reach its desired goals. Instead of ignoring and reassuring the minor deviation of biological data and Imagery generated, they became a perfect feed for the hunters who are after the trivial and non-existing illness.

Final message

Good intentioned health checks are always welcome in selected high-risk population say pregnant women/children of developing a world (As in endemic countries of rheumatic fever) Also cancer , CAD , screening in people with a positive family history can be critical.

However, when these masters of health deviated and started making a living out of apparently healthy people. ( The side effects reached monstrous proportions hiking global health cost in a meaningless way).People, especially in counties with poor resources, are the ultimate sufferers, as the cost and efforts are diverted, to fix the health of healthy, while people with true illness continue to struggle.

Will the WHO* wake up and intervene against this skewed practice of routine master health checks in healthy, that are rampant in both rich and poor countries. Ideally, doctors should order preventive health assessment for those who may need it.

There are enough grounds for public Initiated periodic walk-in health checks to be banned (or at least restricted)

*WHO is world health organization

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Hey dudes, will you stent this 76 year old  fragile man’s Aortic valve ?  It looks shaggy and it seems to be leaking as well.Iam not sure its really tricuspid or not .It is so distorted . By the way , he also has a left main lesion with no protection.What shall we do ? Will the Jena valve do the trick ? My experienced collegue threw this question to a flock of freshly hatched senior residents of a upscale cardiac center. 

After rapidly feeding the necessary risk predicting numericals, clinical and hybrid imagery data , they dug deep into the iOS-powered gadget, loaded with latest TAVR app fused with SYNTAX 2 and FAME 2 overlay for few minutes and started responding one by one.

Yes sir , no Issues, we can comfortably stent it , Its class 2 A / with level B evidence according to JACC intervention article, but, I must say , it was class 2B just a month ago. Another fellow interfered, no sir, ESC says it’s still class 3 but the evidence is C so I am  not sure how to interpret it. The third fellow who usually is a quiet guy, came up with this, but sir, It seems TCT and EURO-PCR  has just released an update, the indication is currently upgraded to class 1 backed by level A evidence

Are you talking about TAVR or Left main? the confused consultant quipped… that’s EBM at its best !

Evidence-based errors in cardiology 

Evidence is the most sacred word in current medical practice. How much of our practice is evidence-based ? It is considered as a quality check. But, today we harshly understand, the evidence to which our conviction clings has a very short expiry date. Apart from expiry , the evidence thing comes with serious invisible manufacturing  defects as well. It may become null and void  even before its fully disseminated into the patient domain.(Please mind, your patient’s life is tied to this clueless evidence !)

So, how to tackle this dangerous dissemination of premature wrong evidence from injuring the patient ?

We don’t have a definite answer  . . . except to say, use the available evidence carefully and cautiously. If necessary (it will often be) throw it to the nearest dustbin by your own evaluation assisted by intuition, and a liberal dose of learned empiricism. Mind you, to do this you must be blessed with enough knowledge, wisdom, and courage as you need to overcome strong pressure to do the opposite.

My prediction is, bulk of the future problems in medicine would come from failure to dispose evidence based errors in medicine.

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The most premier course in medicine, DM cardiology just got an entry makeover.

The qualifying mark was lowered to 20% from the current 50th percentile The reason is many private medical college seats went vacant after the Initial counselling in NEET superspeciality exams.

Becoming a cardiologist was a dream come true for those days for us. “You have to read the red covered 3rd edition Brunwald and all clinical chapters from Hurst for two full years” before even to think of writing DM entrance, my senior used to tell me in late 1980s.Yes, life may still be tough in post graduate entrance but, there is an exclusive fast lane for privileged few where the “Goal posts”start coming towards you.Thanks to the explosion of private medical institutes.

Nothing wrong, it’s not a medical calamity. If the entry is made easy. It doesn’t mean all students are below par.Just 80 % below par.

One big consolation

Medicine is an art to be learned. Unfortunately (or fortunately) students of medicine requires more of sincerity, hardwork, motivation, honesty and Intention to learn. Intelligence and knowledge is there in the list but definitely not in the top.

While mediocrity is a menace in medical education, three decades into medical profession, my conscience tells me even merit, expertise, competence end up as double edged swords if they land up in wrong place with a dubious motive. So, ultimately academic guarding of all these so called entry and exit points to DM courses doesn’t really matter much.

Get ready for grand future

Let’s welcome all the new generation cardiologists in whatever form and this country needs more of them to tame the raising cardiovascular disease burden.

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Whenever we have difficulty in accepting our mistakes or unable to forgive other’s mistake,or when we make big fuss about trivial events in life, I was advised to ask these three questions and Introspect.

1. Who you are?

2.From where did you come ?

3.What for, you are present in this world?

It was a really tough ask , until I saw this video. It not only stuns but also humbles us and whatever little knowledge we acquired over the years looks nothing.Yes, whenever my ego tend to bloat up… this 3-minute video never fails to get it deflated.

Just one requisite , you need to Imagine it’s you lying there instead of that girl.

Post ample

It’s good to realise, how this world suffers by actions and inactions of apparently smart people, who spend some transitory moments in this universe, sharing space with millions of non-human lives and lifeless things (Mind you, the later don’t suffer from death since they have no life!)

Thanks to Google, the technology company for stimulating us to think and find the true meaning of life.

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Identifying the culprit after a criminal event may be easy for the police.For cadiologists investigating the crime scene after a coronary event, it is a different story. (Of course, localization of IRA after a STEMI may not be really difficult.) But , when a patient is having UA  and coronary artery shows multiple lesions, we do have real diagnostic issue. The general dictum could be, tightest lesion or the complex eccentric ones with thrombus is likely to be the culprit. This has important therapeutic Implication,  as we are argued to address the active lesions first. The following study was done in 2009 trying to find the ARA solely by ECG features.

The conclusion was

The following ECG findings were helpful in localizing Angina related artery . ST depression in V3- V5 correlated  with  LAD  angina .Global ST depression was highly correlated with proximal LAD or Left main disease ( 6/6 patients). ST depression in V1 –V3 was associated more commonly with dominant LCX/OM disease. ST depression in 2 ,3 , AVF , or I, AVL  had  no significant correlation with either RCA or LAD  system.However multiple culprit lesions or diffuse inflammatory CAD should always be thought off. One more possibility is , its simply a demand ischemia or micro vascular angina were there is no true epicardial culprit lesion. 

A revisit to my 2009 IHJ article.



S.Venkatesan C.Krishnakumar .G.Gnanavelu .R.Subramanian.Geetha Subramanian B.Ramamurthy.P.Arunachalam.M.Somsundram.V.E.Thandapani.M.A.Rajasekaran.
S.Murugan , Madupraphu doss ,P.Pachiappan.
Madras Medical College. Chennai

Unstable angina( UA /NSTEMI ) constitute a  heterogeneous  group of  patients with  lesions ranging from  normal coronary  artery  to severe multi vessel  disease. Even  though  multiple active plaques are documented ,  one  critical  lesion  would be   responsible  for  the  index  episode  of  angina..  Contrary to STEMI  there is no standard methodology   to identify  the  Angina  related artery.(ARA) in UA .We under took this  analysis  to find  whether  admission  ECG  with the help of echocardiography   could  predict  the ARA  in patients with UA

26  patients with  UA  admitted in  our  CCU  were  the  subjects of  study. Patients with   post  infarction angina,  CABG ,  PCI , old  MI , left ventricular  dysfunction  were  excluded. All patients  were treated  as per institutional protocol. Echocardiogrphic analysis   of  wall motion defects (WMD)  were  documented  between  2hrs  and  24hours of admission  .CAG  was  done  between  24 hrs and  7  days. The  coronary  lesion was considered angina related  if  the  WMD  detected   by  echocardiography matched with  the  myocardial  segments supplied by the  arterial territory  containing the lesion . After locating the ARA , the patient’s  admission ECG   was  compared  retrospectively   with  CAG  finding  to study  whether  it has  any  predictive  value  for identifying  ARA.  6 patients  who  had single vessel disease the ARA  localization  was straight forward. (LAD -4 , LCX -1 RCA-1 ). In 2  patients  there was  obvious  eccentric thrombus containing plaque indicating the culprit lesion . 18 had DVD or TVD with no clearcut culprit lesion.

The following ECG findings were helpful in localizing ARA.ST depression in V3- V5 correlated  with  LAD  angina .Global ST depression was highly correlated with proximal LAD or Left main disease ( 6/6 patients). ST depression in V1 –V3 was associated more commonly with dominant LCX/OM disease. ST depression in 2 ,3 , AVF , or I, AVL  had  no significant correlation with either RCA or LAD  system.

It  is  concluded  ARA  can be  identified  with  fair  degree  of accuracy   by admission  ST segment  profile. This  observation  differs with  the existing literature which  suggest little role for ECG to localize arterial lesion in UA. In patients with multivessel CAD  with  more than one  critical lesion  a  combination of ECG  and echo features  help  us to  fix the angina related artery and possibly the lesion. This has  important  therapeutic implication.

Keywords: Angina Related Artery, Unstable Angina/NSTEMI, ECG, Echocardiography.


I am reposting this abstract again because the same paper has been plagiarised in at least two occasions and got published in predatory journals. Now, we realise Journal article shopping and trading has become a scientific scam .


This paper  from Japan analysed this ARA concept in 1996 itself with SPECT Imaging


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