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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.

Ventricular tachycardia is a regular wide qrs tachycardia.It can be monomorphic or polymorphic.

General diagnostic  rules In VT  (Gross though, with considerable overlap)

  • Polymorphic VT is more often Ischemic , drug induced, electrolytic, and includes many inherited VTs .Most primary  ischemic VT are polymorphic.
  • Monomorphic VT occurs  more common with structurally abnormal heart.(DCM, HOCM, ARVD etc .Please note late scar induced  VT are often monomorphic , which is also being referred to as Ischemic VT in literature )

*Its important to realise any  VT will transform to polymorphic just prior to degenerating into VF.

Management Issues.

The management of VT in acute setting is same irrespective of morphology of QRS complex.Either you DC shock or administer Amiodarone, Lignocaine , and other reserve drugs.

The issue comes only in stable VTs.In stable VT or if VT recurrence it’s advisable to bother about the ethology and choose a drug.Its believed , Amiodarone is contraindicated in true polymorphic VT that was precipitated by prolonged QT interval or Brugada syndrome.

In Ischemic  VT , lignocaine may be preferable over Amiodarone as the later may prolong the QT interval and VT could recur if the index VT was triggered by ischemia induced prolonged QT and subsequently  gets worsened by the drug Amiodarone.(please note, Lignocaine has neutral or even shorten the QT)

Let me conclude with a controversial observation, many of VT storms  we are witnessing only in the era of Amiodarone.Most episodes of VT Storm are polymorphic and often precipitated after blouses of Amiodarone punctuated with DC shock. With an explicit pro arrhythmic potential of this drug, I strongly believe some of the episodes of VT Storm  is iatrogenic and it tends to disappear as the drug effect of Amiodarone weans off.

Final message

In  monomorphic VTs, drug choice and selection may not be that important , polymorphic it could make a big difference !

Always ask a query  whether the VT you are tackling  (in any setting )is likely to have precipitated by prolonged  Action potential duration (Read as QT Interval ) ? Of course  ,one  can’t get a clear answer to this in bed side .But,  if you have strong reasons to suspect , better to avoid drugs that prolong action potential duration ( Amiodarone comes top in this list, though it can terminate VT of any ethology  with any morphology because it has all 4 group action of Waghaun williams !)

Comments welcome from EP experts ,  still to understand things in perspective.

Brugada syndrome is  probably the most fascinating discovery  in  Inherited cardiac  Ion channel dysfunction that linked the basic sciences to bedside . Its due to genetic defect in SCN gene that results in sodium channel blockade of phase  of action potential  to cause troublesome ventricular tachycardia (Phase 2 reentry ) . Now we realise, there are some phenotypic expressions to this gene defect . RV epicardial anatomical substrates are found to responsible for these Arrhythmias.

So ,does Brugada turn out to be a structural heart disease (At least histological ) ? Where is the evidence coming from ?

Now, we realise  RF ablation of epicardial aspect  of  RVOT / Adjacent anterior RV wall can eliminate Brugada pattern confirming anatomical defect  at cellular level. Our changing perception of Brugada from pure functional to anatomical cause is exciting and  intriguing as well !  ICDs were  the specific therapy so far.This discovery make it RF ablation an option.

The recent data from Brugada himself  was presented in World congress of electrophysiology / European Heart Rhythm Association (EHRA) EUROPACE-CARDIOSTIM 2016 confirming the therapeutic benefit of targeting  the epicardial structural phenotypic substrares (Ref 3 )

Final message

We have been taught  Brugada syndrome is  a primary electrical disease .It was  never considered as structural heart disease. Knowledge evolves slowly, so we shouldn’t conclude prematurely .Shall we conclude , Brugada syndrome is truly a  structural heart disease at least in some ?*. This  makes RF ablation  a new  cure for Brugada ,  making it a useful alternate modality to ICD , Of course there can be an overlap between ARVD and Brugada  syndrome. Mind you RF ablation scores over ICD on any  given day as its potential  cure , while ICD is  just a back up device and it simply wait & watch for the VT to occur.We also know  ICDs are still learning human EP data, and are  not intelligent enough to differentiate true VT from false ones with acceptable error** margin.

* Let the experts decide

**Acceptable ? What  do you mean by that ?

Reference

Questions queued

1.Is Brugada VT monomorphic , polymorphic or both ?

2.Is Amiodarone Indicated in Brugada syndrome ?

.

lv apex radiological clinical anatomicallv apex radiological clinical anatomical 002

 

Read a related article

How do you define apical impulse ?

How do you define apical impulse ?

Its a funny world out there in medical science, more so in the field of cardiology ! A new treatment comes as a revolutionary breakthrough , lives merrily for a while . . . only to blink , few years down the lane . . . and  make a sheepish exit !

Here comes some important knowledge from Rome , European society of cardiology conference 2016 .Its the much expected NORSTENT study from Norway,with a largest number (9013 patients comparing one to one BMS vs DES ) with up to  6 year follow up data ,exposing the limitations and the possible false superiority of DES over bare metal stents .It almost concludes there is no meaningful preference for DES over BMS in obstructive CAD in terms of survival .(ACS included)

medical-ehics-research-inappropriate-interventions-logics-in-medicine-dr-s-venkatesan-einstein-quotes

For over a decade  billions of dollars were drained with a hyped scientific concept of coating the stent with drugs to prevent restenosis . DES , was able to  effectively pull the BMS down and out by statistics. This, in spite of the strong concern of DES, interfering with normal healthy endothelisation of the stented segment which resulted in unexpected sudden DES related thrombosis. The power of commerce is huge , it can  finish of a useful modality,if available cheap.This happens even in a lesser developed country like India.

I guess,the obituary for BMS is already written in most part of the world. (I can vouch for it my city Chennai !) Now that NORSTENT  has come out, though belatedly, I  wonder any company  wants to manufacture BMS in a big way ! Can it infuse a fresh life into BMS which I believe is  surprisingly  sitting alive in it’s  graveyard .

     Baremetal stents where are you ? My patients need you !

Counter  thought and a rebuttal !

Many will say my interpretation of the NORSTENT study is wrong and its a indecent attack on a proven scientific concept of DES which is the only way to reduce restenosis rate.

But , what is the big deal in preventing restenosis,if DES  doesn’t save significant lives ?

The argument that DES reduces repeat revascularisation is largely irrelevant as it amount to only  angiographic gratification and  reduced threshold  for intervention  and ultimately imply inappropriate re-intervention in the BMS group.(Only Clinical restenosis ie symptomatic, flow limiting stenosis   require attention .We need that specific data from  NORSTENT . )

Don’t believe blindly in  whatever is written here .Read for yourself and decide ! The NORSTENT from Norway published in NEJM August 2016 http://www.nejm.org/doi/full/10.1056/NEJMoa1607991

Interventional Cardiologist’s favourite play time is to get rid of of obstructions across any  blood vessel , valve or a conduit . This has been well practiced  for over 2 decades in both coronary and valvular obstruction.Now they wanted more and have since started implanting valves percutaneously. (Aortic valve -TAVR in particular )

Why do balloons work in Mitral stenosis but not in Aortic stenosis ?

It remains a mystery at-least to me ,how  PTMC (Percutaneous mitral commissurotomy ) became a default strategy  for relieving  mitral valve stenosis,  while  BAV (Balloon Aortic valvotomy)  was  never considered good enough for opening  Aortic stenosis.

The reason is,  mitral stenosis(Rheumatic)  primarily involve the commissures, while degenerative aortic stenosis involve leaflets more and calcification is much extensive and hence balloons are less effective .Since the initial reports of BAV had more complication like stroke , AR, the interest has waned (except in children with BCAV ).

The arrival of TAVR in big way has made  things difficult for BAV to prove its real worth   and at best it was considered a bridge therapy.Curiously , BAV is often used as an  integral  part of TAVR as  pre-dilatation with various wires across the valve.Hence , every procedure of TAVR,whether you like it or not carries the  huge risk of BAV (please note,these are the same risk which made it unpopular earlier !)

Now , with accumulating data(Funny we got trained in BAV during TAVR   we have double confirmed BAV is not that risky after all,  even in calcific aortic valve. We also learnt BAV does open up the valve significantly (exact gain contributed by BAV during the TAVR is not quantified as yet).Hence  many believe BAV is grossly underutilized modality .

Final message (As usual , without evidence )

BAV, considered just a  bridge therapy  to TAVR/SVR , (mind you,it may not be flimsy bridge , but a  near permanent  steel bridge that can outsmart the much hyped TAVR!) Let us recall again the mitral valve logic where  you just require dilatation for stenosis .Some  degree of AR during BAV  is acceptable as do we accept MR in PTMC.As I said earlier the perceived complications of BAV has rapidly declined. For those who are interested in health economics , a single patient’s cost of  TAVR  can be shared and  could  confer a fresh bout of life to 20 patients with severe aortic stenosis who can be  tackled well with BAV.

I agree , BAV can not reach the glory of PTMC, but definitely  its going to come back and  expected to give a tough fight to TAVR in atleast high risk patients.BAV has a potential to become a therapy of choice in patients  with critical aortic stenosis with severe LV dysfunction as even a small gain in orifice with a balloon can provide a big  booster effect on LV function.

 A thought and a counter

 BAV is retro technique with  low efficiency and with high complication rate .

However,  isn’t  ironical ,  complications with TAVR  ,which includes 25 % of permanent pacemaker assistance  is accepted .(with a pride ?)  while that of  BAV is magnified and made to look unacceptable.Of course , many have mastered BAV and complications has come down recently .I have heard few anecdotal examples where  TAVR was abandonded for some reason after  pre-dilating the aortic valve and patient doing fine with BAV in the long term.Its  being predicted BAV is going to reemerge (already is !) as a useful strategy in critical calcific Aortic stenosis

The  emprical  utterrings in this discussion  are  dangerous and  unethical  and not evidence based !

It would appear  “not doing” a large  randomised trial comparing one to one  (BAV vs TAVR) in  a real “high risk” setting of AS amounts to ” unethical”  act  as complication with BAV has grossly reduced in recent times ! Its our duty to provide  best or near best to our patients.Let us  ensure reasonable inferiority/Non inferiority  is accepted that  can  prevail over a perceived superior modality , if it comes at low cost !

Further reading

1.

balloon aortic valvuloplasty bav

Cardiac failure is defined as a clinical syndrome where the cardiac output is inadequate and fails to fulfill the metabolic demands of body  or its able to do so, only  at a raised filling pressure, causing the classical symptoms of exertional dyspnea.

Consider this simple equation,

A 70 kg normal human requires an EF of 60 %  to supply blood  to his total body mass. If his EF falls to 30 % , certainly he is going to  struggle with reduced cardiac  output by 50 %. Now , theoretically if he loses his weight by 50 % (70 to 35 kg ) in-proportion to the loss in EF, . . . isn’t likely , he goes back to the original ” comfort zone” again as his metabolic demands are  declined by 50 %  and hence easily managed with the severely compromised  EF of 30 % .

Is this a scientific or quixotic logic ?

By all means , it appears the later is right ! but wait . .  nothing is Idiotic in a true scientific democracy ! Human beings can live a near normal life with one kidney, one lung, half the liver function and brain function ! Nothing wrong in wondering  why not , one can live comfortably  with “half heart” function?(ie EF of 30 %)

Having said that ,cardiac failure is not a simple mathematics of EF % .It’s extremely important to understand cardiac failure is systemic disease (often an inflammatory reaction  as well) which progress to a  net catabolic sate  .Numerous named and unnamed counter hormone response(ACE,NEP, BNP etc)  retains salt and water.At some stage the body either adopts or  mal-adopts to it.Countering or mimicking these hormones has been a major therapeutic strategy.(ACEI, ARBs )

The final end point of cardiac cachexia is nothing but extreme response of the body to reduce its weight  (with Tumor necrosis factor /IL6) .Survival occurs with whatever available cardiac output that matches metabolic supply to tissue.

Now ,coming to the title discussion,  If weight-loss is the ultimate compensatory mechanism in chronic HF , what about conditioned and monitored weight reduction  regimen ?

The management of cardiac failure after addressing all specific problems like structural ,functional abnormalities plus or minus  revascularization should include a mandatory  exercise training program that help optimize the weight.Reducing total body mass is directly going to improve the cardiac function, or  at-least make it static and might dramatically  relive symptoms and increase survival.However , the beneficial effect of exercise is  mainly attributed to improving muscle mitochondrial function and augmenting exercise capacity.

Where is the evidence coming  from ?

 

excercise training in heart failure

wieght reduction in cardaca failure

A point of controversy !

There are few reports  that suggest good-weight is essential as a body reserve during the catabolic state of HF.In fact, low fat and cholesterol was unwelcome in some statin and  HF  studies. Some provocative papers even  suggested a paradox  where weight loss could be counterproductive in HF (I strongly dispute this as do many others.)

(T.B Horwich,The relationship between obesity and mortality in patients with heart failure J Am Coll Cardiol, 38 (2001), pp. 789–795)

Final message

Unfortunately , truths without  evidence is worse than plain falsehood !

When heart as a pump is failing , we go for  sophisticated drugs, ICDs CRT devices, variety of surgeries etc . Shall I say , none of them has conquered the inevitable. We know ,HF’s mortality and morbidity is next only to burden of cancer.Applying  all our wisdom , intentional and monitored weight reduction  may be  best bet to unload the heart in many of the HF patients .Mind you, this comes  free of cost ! and that is not the only reason it  should be tested in every such patients .My own experience and interpretation of available data would suggest its going to work in all  and the benefits are going to be  overwhelminng in overweight patients .

Dear heart failure patients . . .Wishing you all a  controlled weight loss  and a happy life !

 

RCA is known for unusual variants.Here is a right main trunk which divides into two major branches, both taking a surprisingly similar course.Shall we refer it to as Dual RCA  or is it an early RV branch ? But how can both run posterior and parallel ?

PS: His LAD and LCX  were  normal.