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Archive for September, 2019

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.

Reference

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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Caution : Non-Academic stuff

Anti hypertensives, lipid-lowering drugs along with antiplatelet drugs always find a proud place in most cardiac prescriptions. The toxic rivalry between various drugs and their creators is a well-known secret. However, the current fight among the antiplatelet agents is reaching comical proportions. The punches and reverse punchs on and off the podium is there for everybody to see.

It all started with clopidogrel two decades ago which was crowned after conquering then-popular Ticlopidine. It was followed by Prasugrel and Ticagrelor. Ticagrelor seems to taste its own medicine from Prasugrel, which brought back memories of the same knock out punches both of them gave to clopidogrel in the past. I guess the ISAR bruised Ticagrelor is just taking a time out, expected to REACT with fresh vigor in the next bout vs Prasugrel.

While these financial heavyweights struggle to keep the bull run, in the multi-billion-dollar stent maintenance market . Aspirin, the aged warrior is enjoying the theatrics silently. While Aspirin is repeatedly shown ( shown literally means shown: Mind you, It is not a synonym for a proven fact ) that it is inferior in stented patients.For stable CAD Aspirin still in the very much in the reckoning. Let the Twilight shine soon. Don’t get a shock of your life, if Aspirin regains the championship one day.

 

Final message

Let us hope the fight gets over till another Grelor  crash lands from nowhere. Meanwhile, we shall strive hard as professional physicians to increase the per-capita antiplatelet drug consumption in  every acute and chronic coronary syndrome (with or without PCI). This will help keep Homosapien’s coronary artery eternally patent.

 

For pure Academics  (Conclusions in science is a misnomer . . . )

 

 

 

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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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William Withering the British Botanist of 18th century now laid to rest in the St Barthomlew Churchyard ,Edgbaston is known for his astonishing isolation of the wonder moelcule Digoxin from Foxglove. (Of course, let us not forget original old lady Ms. Hutton from Shropshire who was treating epidemic dropsy with a concoction of herbal Tea ) He reported this in the seminal paper “An account of Foxglove’ in the year 1750 and subsequently became a fellow of Royal college of science.

(The story of Withering and Digoxin is extensively researched and written by Dr Dennis M, Krikler in a classic review article of 1985 JACC )

Near-death experience of Digoxin

After 250 years , saving millions of life, modern science has killed this warrior (inadvertently ?) by a minuscule study with serious flaws called DIG trial *published in NEJM 1997. It exposed the truth that science in flimsy forms can misrepresent fact. Actually many wouldn’t agree its a bad study. But , everyone realised , the conclusion was misinterpreted and disproportionately given weight to one aspect.The conclusion was worded in such a fashion, which sort of implied a negative bias.

*Yes , flaws were discussed in one of our detailed journal club meeting .

DIG trial

This one study was good enough to smear this drug with a knockout punch as if we are administering poison to a patient with heart failure.Thus a grand old drug became an object of ridicule in academic forums. Subsequent offline real-world scrutiny clearly indicated reduced hospital rate admissions and preventing worsening of HF was directly improving the mortality for which there were no takers. At least occasionally we need to realize there is foolish face for statistics. Now we are beginning to restore some lost sense.

 

What’s happening in 2019

The same scientific methodology finds Digoxin to have great value . JACC.  Awais Malik from Veterans Affairs Medical Center, Washington DC and others try to  dig out a truth.

screenshot_2019-08-24-23-37-54-789_com1423849373.png

Whoever is blaming this as a withdrawal study are requested to go through the basics of how adding a drug doesn’t help but stopping it worsens. Another group has a different issue. There is a tendency among the scientific community, to look down on studies done in VA hospitals as if they have lesser academic value. I strongly object to that if it’s true. Never have preformed opinion about a study by its source.

How does Digoxin act?

Mind you, Digoxin was working all alone in CHF in the past without the help of all-powerful loop diuretics which was discovered 200 years later, This adds more credit to Digoxin since it has a combined the action of diuretic, anti sympathetic and vagal modulating action, and AV nodal regulation. The only issue with Digoxin could be its safety profile, which if carefully taken care can be overcome. (Afterall, we are trained for this job ) One may call it a most comprehensive drug amongst others in cardiac failure.

Final message

Ignore the greatness of old drugs at your own peril. Foxglove blossoms again, after a gap of 30 years. Please don’t crush it this time! Let Willaim Withering smile from deep inside his resting place at Barthomlew Church along with millions of heart failure patients.

 

Reference

1.

2.History of William Withering

3.Ahmed A, Rich MW, Love TE, et al. Digoxin and reduction in mortality and hospitalization in heart failure: A comprehensive post hoc analysis of the DIG trial. Eur Heart J. 2006;27(2):178-186

Postamble 

A funny business Idea

I guess Parke Davis those days had wholesome rights for Digoxin. May I suggest few tips for the industry how to capitalise this newly generated enthusiasm. Please ensure this drug sounds anything other than Digoxin which seems to have a stigma attached for the modern guys.

Try renaming this drug , a sodium-potassium ATPase blocker, as DiNaKatban and patent  it as a unique weekly depot Injection with an attractive  499$ price tag. Another option is to add Digoxin ,Neprilysin and Frusemide,  possibly an ARB  ( Dinephrimab) and project it as polypill for HFrEF . Publish it in NEJM with a huge non Inferiority trial,break it in  ESC or ACC .Consider selling it on all heart failure clinics with a special launch. I am sure, the same guys who ridiculed this drug for so long, will ask their patients to stand first in the queue. Call me, if this new generation Digoxin doesn’t vanish like hot cakes from these pharma malls.

 

 

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Preamble

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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