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Mitral valve strands : Hey . . , What’s that moving object over AML ?

October 9, 2016 by dr s venkatesan

Hey , What’s that moving object over  AML ?  It looks odd,  it doesn’t look like a thrombus or a vegetation.

Yes, I agree , its moving  independently  but  I think , Its benign threads of fibrin attached to the valve .They are called as valvular strands.

Is it ?, I haven’t heard about it !  Can you please  tell me something about it.

Strands are  highly mobile, fine, filiform  threadlike excrescences that is seen arising from valvular structures. Synonym : Its same as Lambl’s excresceneces , the Czech physician who described  it over Aortic valve in 1860.

The following TEE clip shows strands attached to Aortic valve

Incidence

Reported Incidence of valvular strands  varies .Some reports suggested it may be up to 5-10 % .( SPARC study Mayo clinic 1999 its staggering 46 % !)The reason for  such high incidence  is,   many of us are still not clear what we refer to as strand.The imaging modality also has a say. With improving resolution of TTE and liberal TEE use more  strands are detected .A recent large study from Israel , suggest a good news , in large population based study (21,000) true strands are  observed in  just around  1 %.(Marina Leitman 2014 )

Is it Physiological or Pathological ?

The valve closure lines are physiologically stressed , some amount of denudation of endothelium is expected .This leads to a thrombus formation along with the exposed mucopolysacchride  layers of the valve form a filiform ,filamentous structure. .To call it physiological or pathological is left to our wisdom and  perception. The size however matters. It could be  the reason behind many  unexplained strokes.

What is the natural history of these strands ?

Its difficult to believe It may persist for lifetime.If its truely fibrinous strands it may have a life cycle and disappear.

Size

Should be less than 1 mm.

Length varies between  3 mm to 5 mm

Location 

Can be seen in any valve or even in aortic root.

Attachment : Atrial side of mitral valve and ventricular side of Aortic valve.

Strands over prosthetic valve is also reported.

Clinical significance 

It has three common issues.

One: Getting confused with other more pathological entities.

Two : Risk of stroke.

Three: Nidus for normal native valve endocarditis ?

Strands may closely mimic 

  • Vegetations
  • Bland thrombus
  • Redundant leaflet /Chrodae (Marfan and variants)
  • Disrupted chordae (After MVR)
  • Flail leaflet
  • Fibroelastomas

Risk of dislodgement and  stroke 

These strands are minute. It seems plausible dislodgement need not necessarily result in stroke or other organ ischemia.We don’t know whether it gets dissolved on transit.However the risk of stroke is increased in most reports except few studies(Roldan).

Management

First question to ask is , Should we inform our patients about  these ubiquitous accessory valve  tissues if detected incidentally ?

Largely benign and can be ignored in most.A follow up echo may be adviced once in a year or 2. (I have one anxious patient  after I reported such strands in Marfan syndrome )

In patients who has h/o stroke presence of these strands gains importance and  is an indication for anticoagulation.

Surgical excision of large strand is a dramatic option and is rarely performed.

Queries with no answers 

Is it accessory valvular (mesenchymal) tissue ?

Does Atheromatous plaque contribute to these strands in Aortic valve ?

Strands , if  disappears  by natural means , do they regrow from the same spot of raw surface  ?

Final message 

Fibrous strands detected  over the valves by routine echo are uncommon .However , It may give considerable  anxiety if  documented and reported to our patients and physicians .Though these have negligible clinical significance , the risk of stroke is increased in those with large strands.

Reference

1. Leitman M, Tyomkin V, Peleg  Clinical significance and prevalence of valvular strands during routine echo examinations. E  Eur Heart J Cardiovasc Imaging. 2014 Nov;15(11):1226-30

2.Aziz F1, Baciewicz FA Jr Lambl’s excrescences: review and recommendations.Tex Heart Inst J. 2007;34(3):366-8.

3.Cohen A1, Tzourio C, Chauvel C, Stroke.  Mitral valve strands and the risk of ischemic stroke in elderly patients. The French Study of Aortic Plaques in Stroke (FAPS) Investigators.1997 Aug;28(8):1574-8.
4. Roldan CA1, Schevchuck O, Tolstrup K Lambl’s Excrescences: Association with Cerebrovascular Disease and Pathogenesis., Cerebrovasc Dis. 2015;40(1-2):18-27.
5.Faisal Aziz, Frank A. Baciewicz, Jr.Lambl’s Excrescences .,Tex Heart Inst J. 2007; 34(3): 366–368
Links
Video clip of Lambl’s excrescence link to British society of Echocardiography 

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Cardiology classics : Bernard Lown . . . The cardiologist who won Nobel “peace” prize !

October 2, 2016 by dr s venkatesan

Great men dream , but they just do not sit idle. They do what they are passionate about .History just follows them or they create it.Here is a brief story of an ordinary man born in a small European country Lithuania in 1921  ,lived much of his  life in the east coast of USA ,transformed into a brilliant cardiologist  based in Brigham Hospital , Boston.

He is Dr Bernard Lown , best known as a founder of what is used in every coronary care unit and cardiac surgical theaters around the world . Yes, the DC cardioversion was invented by Lown in the year 1961.(Of course,  it was an Improvement  upon the  pioneering work of Zoll’s AC power line  for defibrillating   the heart  which was impractical and caused much injury )

 

drlown_history

Dr.Bernard Lown (Born 1921) ,With his Invention of DC Cardioversion machine Currently  working in  Harvard University

 

He was also the brain behind the  conversion of local anesthetic agent Lignocaine to cardiac anesthetic  which revolutionized the treatment of ventricular arrhythmia.(What a simple  but a path breaking  idea to use membrane stabilising action of local anesthesia to sedate the heart when it behaves erratically !)

We can also credit him for  rediscovering  Digoxin and found the secret that potassium supplementation can largely overcome  toxicity of this drug which was otherwise lifesaving in dilated , failing hearts  running amok with delirium tremors (Surname for Atrial fibillation in those days !)

While the Invention  of DC cardioversion had  a dramatic impact all over  world , he simultaneously popularized the concept of coronary care units along with Julian in London and Dr Day in Kansas city.

Its said great men’s mind  are perennially restless.Accordingly ,he was worried about the impending nuclear war with USSR and other global powers then. He collaborated with Russian cardiologist Dr. Eugene Chazov. It became a hugely popular peace organisation  International Physicians for the Prevention of Nuclear War (IPPN) for which he got ultimately the Noble prize for  in 1985.

 

bernard-lown-dc-cardioversion-lown-institute

During one of his Noble lectures (Linked to video)

 

 

It turned out to be “lovely Irony” for a man who probably should have got a Nobel prize for medicine for inventing DC cardioversion ,  ended up with Nobel peace prize for  his fight against a man made disease called  “Nuclear proliferation”.

Its heartening to note he has visited my country(India)  and was  awarded with Mahatma Gandhi peace prize  as well.He is now 95, active in Harvard   currently turned his vision towards eradicating Inappropriate medical treatment from the noble profession .I wonder , for a man who fought against a  nuclear war, what does this new Initiative mean ? Does he equate the medical profession in its current form and the direction in which travels to something that’s  grossly unacceptable ?

Whatever it is , I humbly endorse his views and has since dragged me to  his Institute.

lown-image

I just joined the institute and signed  a declaration . I wish every physician who take oath on Hippocrates should strengthen Dr Lown’s Doctrine .

Reference 

Link to Wikipedia

nobel-prize-in-medicine-cardiology-drsvenkatesan-venkatesan-madras-medical-college

Posted in history of cardiology, Histroy of medicine | Tagged , , | 4 Comments »

How is management of polymorphic VT differ from monomorphic VT ?

September 22, 2016 by dr s venkatesan

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.

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Is Brugada syndrome, a structural heart disease ?

September 17, 2016 by dr s venkatesan

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

1.Kofune M1, Watanabe I, Ohkubo K,Clarifying the arrhythmogenic substrate for Brugada syndrome.Int Heart J. 2011;52(5):290-4.

2.Nademanee K1, Veerakul G, Chandanamattha P, Prevention of ventricular fibrillation episodes in Brugada syndrome by catheter ablation over the anterior right ventricular outflow tract epicardium.Circulation. 2011 Mar 29;123(12):1270-9.

3.Pappone C, Brugada J, Vicedomini G, et al. Epicardial ablation in Brugada syndrome. Insights from a prospective registry study of 50 consecutive patients. European Heart Rhythm Association EUROPACE-CARDIOSTIM 2016; June 8, 2016; Nice, France.

Questions queued

1.Is Brugada VT monomorphic , polymorphic or both ?

2.Is Amiodarone Indicated in Brugada syndrome ?

.

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Three types of cardiac apical Impulse : An Illustration

September 1, 2016 by dr s venkatesan

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 ?

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Baremetal stents where are you ? , . . we need you desperately !

August 30, 2016 by dr s venkatesan

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

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Balloon Aortic valvuloplasty (BAV) will be back with a bang . . . should pose a genuine threat to TAVR !

August 30, 2016 by dr s venkatesan

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

2.Percutaneous Balloon Aortic Valvuloplasty Revisited  Hidehiko Hara, Wesley R. Pedersen, Elena Ladich, Michael Mooney, Renu Virmani, Masato Nakamura, Ted Feldman and Robert S. Schwartz  Circulation. 2007;115:e334-e338

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

August 16, 2016 by dr s venkatesan

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)

Arena R, Lavie CJThe obesity paradox and outcome in heart failure: is excess bodyweight truly protective?. Future Cardiol. 2010 Jan;6(1):1-6.

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 !

 

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A “Right main” coronary artery with a dual RCA

August 16, 2016 by dr s venkatesan

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.

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Primary prevention of CVD with Aspirin : The confusion need to stop here . . . but it may not !

August 2, 2016 by dr s venkatesan

Aspirin for primary prevention of CVD is an ongoing controversy for more than 2 decades. Please note, the controversy is not in the competence of Aspirin to prevent cardiovascular  event, but in the potential risk of GI bleed and whether that risk is worth taking. Secondary prevention has no such issues as the benefits easily outweigh the potential bleeding risk .

Male vs female

There is a “gender” and “age” difference  in the ability of Aspirin to prevent vascular events.Aspirin primarily prevents MI in men(>45)  and stroke in women(>55)  (Funny it may look,  that’s what data says!)

Age

Hence, the target age group  for aspirin is between 45/55  to 80 years. (Up to 45 and beyond 80 it has no role .Beyond 80 ,  risk of hemorrhagic stroke is significant )

Diabetic vs non diabetic

Many believe  all diabetics should straightway  get Aspirin as it was considered  CAD equivalent.Its not acceptable to all. . American diabetic association  has risk stratified DM and advice Aspirin only in high / Intermediate risk.Look for Key word ie “Net benefit“ (Ref 2)

Why so much confusion  ?  and What can be  the conclusion ?

The confusion is because each scientific body like AHA, ESC, ACCP, ADA ,USPSTF have  their own inference and the presence of too many risk assessment tools adds further dizziness .(SCORE /FRAMINGHAM, etc). It tempts me to say ignore all these and use  cortical sense !

Fortunately ,we do have some clarity as there is a common theme in all these advisories .Aspirin is indeed a wonder drug and able to block the platelets to prevent acute thrombus formation in the critical circulations.(FDA doesn’t seem to agree with this , How can a cheap generic do that job so effectively  ? Let the Bayer fight ! ) 

It seems reasonable to conclude

All men and women  between 45/55  to 80 years should get Aspirin (81mg /day or 325mg alternate days ) if there is at least one or two CVD risk factors provided there is no major bleeding risk .

Ongoing  studies on primary prevention with Aspirin 

ASCEND: A Study of Cardiovascular Events in Diabetes; or with diabetes taking a statin 

ENVIS-ion (Aspirin for the Prevention of Cognitive Decline in the Elderly )

ASPREE (Aspirin in Reducing Events in the Elderly) 

These  studies are  expected to  bring more data (and be ready for more confusion!)

Can we use Clopidogrel  for primary prevention if a person is intolerant to Aspirin ?

Logic may say yes.As of now it can not be advised for primary prevention.

Reference

1.A elegant advisory is hosted in Healthcare Research and Quality (AHRQ) website with supportive data from U.S. Preventive Services Task Force.

primary prevention of cad by aspirin

2.Pignone  M., Alberts  M.J., Colwell  J.A., et al; Aspirin for primary prevention of cardiovascular events in people with diabetes: a position statement of the American Diabetes Association, a scientific statement of the American Heart Association, and an expert consensus document of the American College of Cardiology Foundation. Circulation. 2010;121:2694-2701

3.Sigrun Halvorsen,Felicita Andreotti,  Jurriën M., Aspirin Therapy in Primary Cardiovascular Disease PreventionA Position Paper of the European Society of Cardiology Working Group on Thrombosis  J Am Coll Cardiol. 2014;64(3):319-327.

 

2016 Update by USPSTF in Annals of Internal medicine has a Major revision.

It raises concern over bleeding risk, and ask for restricted use of Aspirin

within the age group of 50 -69 for both male and female.(Who are at risk of CAD)

Link to the Annals of Internal Medicine Article  Aspirin primary prevention 2016

 

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