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Archive for the ‘acute coronary syndrome’ Category

DAPT -Dual anti-platelet therapy has become  a standard in many clinical situations of CAD.There has been significant confusion about ,Indications, best combination, duration of DAPT, withholding of DAPT, conversion to MAPT (mono) etc.The  JACC september 2016 issue  brings much needed clarity  on this issue.

Link to key summary from NEJM journal watch.

http://www.jwatch.org/na42407/2016/09/28/update-dual-antiplatelet-therapy-patients-with-coronary?

Full text guideline

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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)

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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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Less than a century ago an easy chair  was enough to manage this most important medical emergency of mankind. Of course, at that time mortality of STEMI was estimated to be around 30%.We have since pushed the in-hospital death rate down to less than 10 %  and its around 5-8% currently.(*The lifeless chairs were able to save 70 lives is a different story!)

Heparin , thrombolytic agents, critical coronary care has helped us to achieve this , of course It must be admitted primary PCI also played a small role (at best 1 % ) in our fight against this number one killer.

Now, why not combine  both lysis and PCI ?

The concept of PIA (Pharmaco Invasive approach) came into vogue  primarily for two reasons.

1.If thrombolysis and  pPCI are powerful strategies by individual merits why not combine both and achieve double the benefit ?

2. Since pPCI is going to be a logistical nightmare in most points of care and we can’t afford to lose time . So, let us lyse first and consider PCI later !

Unfortunately medical science is not math .One plus one in medicine is rarely two !

Though , it looks attractive , Pharmaco invasive approach  has its own troubles.Fortunately , most of them are man-made, few are beyond our knowledge though.

Following general rules  may help us

  • STEMI  should ideally managed by early thrombolysis (or PCI) in all deserving patients.
  • Don’t wait for PCI if you think , there will be delay or reduced expertise and poor track record of the center in this modality.
  • Pharmaco invasive  therapy is not a default in all STEMI .Do good quality , monitored  lysis , (Not necessarily new generation thrombolytic .(I prefer one hour sustained thrombolytic regimen , not the hit or miss bolus) .As a learned cardiologist we need to assess individual patients according to the type and risk of MI.Its not wise to blindly follow the guidelines ,because these guidelines , though based on evidence never answers a query in a single patient perspective !

The key “branch points”  in decision making  after lysis

  • Invasive strategy  should begin within one hour if the patient has failed  thrombolysis and has developed any mechanical issues.( Mind you, LVF requires good medical stabilization .Rushing  such patients to cath lab without application of mind can be disastrous )
  • If the Initial  lysis is excellent and the patient is asymptomatic  one need not proceed with invasive limb at all.(A significant chunk of apparently failed lysis by ECG are asymptomatic and comfortable , these are patients require delicate assessment regarding further intervention. )
  • If the MI is large and the clinical  stability is “not confirmed” one may  proceed urgently within 24 h.
  • In any case there is no role for invasive approach after 24 hours* Unless fresh ischemia  suspected to come from IRA or  non IRA.
  • Having  said that, there are many centers that do a diagnostic  angiogram alone just prior to discharge  (48-72h) for risk stratification and then take a genuine call for a possible PCI or  CABG. In my opinion it appears a sensible strategy , though a non invasive stress  test pre/post discharge can even avoid that  coronary angiogram !

One issue with Rescue PIA

Though by current definition  PIA is to be done  3-24 hours , don’t wait for the 4th hour if you have recognized a failed thrombolysis earlier than three hours.( Ofcourse , as the gap between P and I gets too narrowed it may  carry some adverse  effects witnessed in routine facilitated PCI -Refer FINESSE study ) Similarly,there need not be a blanket ban on PCI beyond 24 hours if residual ischemia is active.

Final message

PIA is a dynamic  coronary  re -perfusion strategy . Nothing is fixed in science. . The optimal gap between Pharmaco and invasive strategy  can be anywhere between  1 hour to “Infinitely deferred” depending upon individual risk perception and wisdom of the treating cardiologist.

 

 

 

I

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Scientific cardiology has forced us to believe ACS management must be catheter based and all others are inferior  and  those who pursue the later , carry a risk of  being labelled as unethical in near future. However ,experienced cardiologists will know  where the truth lies.

Now,in the interventional cardiology board rooms  there is a big  debate going on regarding the value of early total revascualrisation in STEMI with multivessel CAD.Suddenly , every lesion looks suspect ( Ex,current or future culprit ! ) and all stentable lesion are stented  either in an emergency or semi emergency fashion (The new age post PCI dialogue goes something like this “I have tackled one culprit , other one seems to hide in LAD ,  we will arrest it  next 48 hours or so* ? ( This is the concept of  deferred or staged  non-IRA stenting )

*Ironically it brings   one more dubious therapeutic time window in ACS !

ptca ira non ira multivesssel pci

The recent  studies like  PRAMI, PRIMULTY ,CvLPRIT are trying to find out an answer to this issue  and suggest acute multivessel PCI may be  good strategy. Some of them advocate a FFR guided non IRA intervention , knowing fully well micro-circulatory bed is completely altered by the index acute thrombotic event.( Mind you , for FFR,  we need to induce maximum hyperemia with Adenosine in a highly varying local autonomic milleu within the thrombus clogged capillary network)

Final message ( Intentionally biased !)

Till we learn or unlearn  it is vital to go with conventional wisdom.Don’t pursue a random hunt for coronary culprits in acute phase of  STEMI.Many of them are innocents and likely to suffer in cross fire.Tender coronary arteries need some rest,peace and time to heal thyself  . Just keep away , they will definitely say big  thanks with folded hands !

Reference

1.Gershlick AH, Khan J, Kelly DJ, et al. Randomized Trial of Complete Versus Lesion-Only Revascularization in Patients Undergoing Primary Percutaneous Coronary Intervention for STEMI and Multivessel Disease: The CvLPRIT Trial. J Am Coll Cardiol. 2015;65(10):963-972.

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The ECG changes in ACS are “as dynamic as”  the occluding thrombus.The initial events include  sudden total occlusion, early lysis , trickle of flow, partial re-occlusion , reflow, no-flow etc. The extent of transmural vs sub-endocardial injury, the competing force of re-perfusing and necrotic  wave front, would define  ECG findings making  the ST segment labile in early hours of ACS.This is also the basis of  some cases of  STEMI evolving into NSTEMI and vice versa.

A 65 year old man  presented to with this ECG,

 

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Does this ECG allow you to go ahead for thrombolysis ? It actually looks like NSEACS with ST elevation in AVr suggesting left main lesion

The initial  diagnosis of  NSTEMI was made , and hence  thrombolysis was not considered. Even as the fellows  were mulling over the diagnosis , we subsequently came to know  there is one more  ECG available taken few hours ago  in  another hospital .

It had something on it ,

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This ECG taken few hours ago , shows ST elevation in 1 and AVL and few VPDS in chest leads unmasks the anterior ST elevation .

The moment we saw this ECG it was decided to go ahead with thrombolysis .The final ECG after thrombolysis with (Streptokinase) showed further stabilization .The question of thrombolysis  in NSTEMI though not indicated in general , in selected  situations we need to Introspect !

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How to mange  a patient who presents as NSTEMI but had STEMI  few hours ago ?

Four  ways to ponder !

  • This patient should not be lysed  as we have to treat the current event not the past.  ,(Its NSTEMI and no need for lysis) Just heparin,dual antiplatelets .That will do.
  • One can go ahead with lysis as there is evidence for STEMI in prior ECG.
  • There is ST elevation  in AVr even in the second ECG and so you have to thrombolyse !
  • “Come on guys , . . . are you still in the primitive era, of managing ACS in CCU , just forget  the ECG take him to cath lab , suck out all thrombus and deploy a stent and come out”.

* The last one , though appear practical (and most of us would love to indulge ) is an unprofessional way of practicing cardiology.Management of ACS requires sound principles of ECG and its correlation  with the Intra-coronary  and myocardial  pathology.

What happened to this patient ?

He did well, free of angina with minimal LV dysfunction. He was discharged .Will be reviewed two weeks later,for further evaluation.This is typical example of a patient with ACS managed without  even entering cath lab.

Final message

ECG changes are as dynamic as the Intra-coronary blood flow in ACS. Various factors  determine  the ST elevation or depression.While ,thrombolysis is reserved for STEMI,  NSTEMI has little or no benefits to accrue with thrombolysis .However this is applicable only for de-novo NSTEMI  and may not apply for a STEMI in transition into NSTEMI as in the above patient .

 

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Every time , patients ask me  what diet he or she  should follow , Iam sort of  amused , as my understanding of diet and cardio vascular disease is at best primitive.I used  go with a standard single phrase  advice “Anything in moderate should be okay  “
What about going for a saturday night party doctor? One of  my shrewd looking  patient who was recently double stented with DES , asked.
Human body is a biological marvel.While medical professional divide it  into various systems  for our convenience. God doesn’t  think that way .He has no systems in mind when the body was designed . There is no wonder , the alimentary system and hematological system has to interact on a daily basis  with the help of circulatory system  to keep the  body alive. Platelets are unique blood cells that exist primarily to plug physiological bleeding if any  or for self-healing at sites of tissue injury.
 platelet lipid ldl tgl triglyceride ineraction 002
With human vascular system increasingly invaded by various metals and wires , platelet are a confused lot since their original biological functions are altered. They simply don’t know whether  fight these foreign body , aggregate over it , flush or simply pass over these .Adding to this  the powerful anti-platelet drugs targeting critical functional pathways .No wonder every other cardiovascular  patient  consumes at least one anti-platelet drug.
It seems diet  can have direct influence of platelet function
With human beings desire to add style to food consumption and eating habits  competing with  top slot of purpose of living , we often forget it is same prevent us from living a good life.
There has been numerous anecdotal and study population and experience  acute coronary events are more common after a heavy meal especially a fatty one .The immediate suspect has been high triglyceride and chilomicrons in blood stream shunted  intestines .
It is logical to expect , these high TGLs some how act a s trigger for pro-coagulant trigger .With the core thrombus  rich platelets it is assumed platelet stickiness is augmented and  maintained  by transient raise in triglyceride formation(Reference 1,4,5)
Glycerol component of  TGL is know for  its sickness and  making the companions wet.
The million dolor question is , at what level of TGL and which forms of TGL make the platelet cry and attract each other ?
Diet, anti platelet drug efficacy  ?
 Now , patients with coronary stents has to live at the mercy of these anti-platelet drugs. The drug resistance(Clopidgrel) is  threatening to be major issue.Like warfarin do we have real issue of dietary binge and acute neutralisation  of anti-platelet drug efficacy that can trigger acute stent thrombosis . This is potentially  important  area of study .
Final message
So does a fatty meal  a new trigger for ACS ? It may sound an alarmist statement .but as of now , its difficult to ignore this.So my advice for that  the that smart young man with soluble stent  was to avoid binge dinners that carries a definite risk of interfering with  stent maintenance .
Reference

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