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Archive for the ‘acute coronary syndrome’ Category

Evening cardiac clinic is generally a relaxing place until an occasional patient  with vague chest discomfort present with this sort of an ECG .

He was a 68 y old hypertensive and was on Tablet Amlodipine .After a cursory look at his ECG , eyes wandered to look for some specifics. Suddenly ,my  ECG reading skill was stretched . Is it really LVH ? or Ischemia ? I asked for any old ECG which he couldn’t provide. I had to blink  more than a moment , before asking him to describe his chest pain in detail one more time . I got almost convinced it was not ACS  since he was having only localized pain over left side of chest. Still , I didn’t have the courage to send him home. An Echo was done.

Curious to know what the Echo showed ?

 

Yes , you also probably guessed right . It is LVH and there is no wall motion defect either.

How to differentiate between Ischemia and LVH ?

This is a common question asked in the board exams.There are number of ECG clues to differentiate the two .Mostly it will help  fellows  to pass exams. Academics rarely comes to your rescue when patients land with  chest pain  especially at odd hours.

Find the answer in this link

https://drsvenkatesan.com/2009/12/12/how-to-differentiate-lv-strain-pattern-from-primary-lv-ischemia/

 

Now comes the real twister , Does presence of LVH  exclude Ischemia in any way ?

Why can’t be ACS in a patient with LVH ?

When I posed these questions , some one suggested global longitudinal strain  with speckle  tracking to rule out ischemic wall motion defect, my resident suggested  high sensitivity Troponin and Ischemia modified albumin.

Whatever is the technological assistance , one thing  is certain,  we need to finally fall back  on patient’s symptoms . Unstable angina is neither an ECG diagnosis nor biochemical  or Echo diagnosis . (Its all about patient description about his angina , that clinches the  diagnosis !)

It remains a fact normal spot Troponin can never rule out  ACS on time ,( Even patients with unstable angina who  harbor  tight  LAD lesion can be both ECG /Enzyme negative )

When we are not sure ,the traditional coronary care dictum  shall operate .It demands admit, observe, with serial ECGs and enzymes. This protocol cant’t be followed strictly for a variety of reasons . We may have to rely entirely on our clinical Intuition accrued over the years.

A modern-day cardiologist might have a different dictum .The simplest solution in such situations is a diagnostic radial snap shot coronary angiogram .It is an easy way out  . . . , and avoids the trouble of spending wasteful minutes of personal conversation with the patient .The ethics of outsourcing history taking , patient record review or even clinical examination has pushed the definition of professional competence in coronary care into murky grey zone.

One more reason we should hesitate to rush these patient to cath lab is the detection of  incidental insignificant CAD (Which will loom larger than life when they are wheeled in from  ER)  that will  lead on to  further inappropriate chain of events.

How relevant is clinical acumen in modern era ?

Clinical acumen in medicine can never be taught in class rooms or read in text books. It is the innate ability to  combine  knowledge, experience ,skill  and  lastly (and most importantly) courage to ignore conflicting and pervasive data from new generation Investigations. Instead of helping us ,they often directly affect our increasingly vulnerable native medical cognition.

Even if some one is blessed with a good clinical acumen it seems to have little value many times as power of Investigations and fear of missing a event will prevail over it ! I have been victim of this phenomenon many times and not able to follow what my mind preach me !

What happened to this patient ?

I had to admit him against my  wish (Of course I was safe!)  He too got admitted reluctantly and was observed till morning , spent Rs 5000 for pack of investigations and stay , was discharged without any issues with a diagnosis of simple Hypertension and LVH.

The non academic bug  didn’t stop there  . . . again  contrary to my conscience  I had to suggest  optional coronary angiogram to rule out true CAD as a precautionary statutory advisory !

 

Counterpoint 

How do you know this is really not CAD  ? I won’t believe unless and until I see the CAG and its normal.

Ok, Let me post his angiogram if he decides to  undergo it.

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 When half a dozen guidelines from extremely evidence based “Esteemed cardiac societies”  decide to confront an Incomprehensive cardiologist , there is no other way , but to create  a personalised i-Guidelines on STEMI !

*(i-Idiotic)

 

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Some of the noise bites from a busy cath lab after a  mid noon angioplasty

         Oh’  that  looks bad , whats that projecting !

There is some haziness too ,

            Make sure its not a flap,

  Better to do IVUS or should I OCT ?

           Shall I  post dilate with NCB ?

Should we cover with  another stent ?

           I think we can manage with Tirofiban or Reopro 

Call the chief ! suggested a first year resident,that seemed to be the most reasonable noise bite among all .Yes, the final command came from the chief cardiologist after a 10 second glance over the workstation ,”Guys,  forget it , . . its acceptable  pinching, DAPT will take care of it , just ensure adequate ACT till night , put the next case . . .on table” !

That’s fairly common chat session in any high volume cath centres (Which ended abruptly  in this case with the chief’s uttering)

Does any body know  what the chief meant by  the term pinching ?

  • Is it the  pinch of Intimal fold ?
  • Is it pinch of plaque ?
  • Is it a flap ?
  • Is it a plaque prolapse within the strut ?
  • Or just a evaginated thrombus
  • A subintimal calcium speck ?
  • A longitudinal stent deformation?

Any one knows the histology ? Is there any natural history  study of such pinching ?

Iam afraid no one knows . But common sense tell us it can be anything  between a totally benign entity to  Imminent nidus  for an acute stent thrombosis , depending upon the patient’s destiny and physician’s luck !

How does one make a decision in such an uncertain situation ?

The decision to leave that pinching is taken by any  cardiologist  based on his past experience or  Inexperience or both. Some do IVUS/OCT , many don’t . Whatever the decision  ( empirical or scientific ) its  going to be tentative  and  outcome is any body’s guess.

Final message

Coronary arterial pinching is a dangerous cath lab slang used exclusively by expert Interventional cardiologists , often after a hurried PCI ! It may sound  innocuous .To label a protruding plaque as a “safe pinch”demands heavy courage that is an essential requirement  for a successful Interventional  cardiologist , which most of them are blessed with !

Reference 

1.No Reference as such :There is no specific study about histology of coronary pinching  .Though , IVUS and OCT data are available for various post PCI shadows , it never addresses the issue of pinching specifically as no one is clear about what they mean by it.  Hence ,we are planning to decode this long pending mystery with our own  PINCH-iVUS  study.

2.This article from Circulation Imaging  new generation IVUS could reveal  histology of pinching

f5-large

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Professional competence is defined as doing things, always in the Interest of patients. It’s generally believed small hospitals are not competent enough to treat cardiac emergencies . . .Do you agree with that ? No, Its largely a myth . Do you know there is a absolute  lack of proficiency  threatening to plague our country’s coronary care system. ? It’s the professional  Incompetence by the space age, star hospitals (mis)managed by masters of the noble business. None (am I right ?) of this hospitals either monitor or publish the outcome of their treatment.

Backed by pseudo scientific data , amplified by unrealistic expectations of ill Informed patients , some  hospitals are avoiding Initial emergency treatment of acute MI  , instead they waste time ( load DAPT ofcourse !) in securing the finance  for the costly Invasive procedures or refer them out of their premises if they can’t afford for it.In the ensuing emotional and financial melee many of the ill-fated patients lose vital  time window of thrombolysis as well ! and carry risk of fatality or damaged myocardium.

Every stake holder in the current  coronary care system simply assume the enforced modality  must be far superior because they administer the most modern and costly treatment suggested by few high intensity cared clinical trials originating from west. The wisemen who run the corporate hospitals  never realise medical competence and outcome is not entirely defined by science. Their primitive cognition wouldn’t allow to think beyond business equations either.

Please believe me, time and again, I have witnessed patients reaching Government hospitals  after being shunned away by  big (Some times even medium sized )  hospitals who boast themself only as PCI enabled care. Even if they want to lyse they stock only the Tenekteplace .

I think tragedy  is a lesser word to describe the scenario , where a distressed family is trying to arrange  for a Rs30,000 shot of Tenekteplace when thirty times cheaper still equally efficacious (Rs 1000 Streptokinase)  is concealed from their visibility .The Govt should urgently look into instances of large private hospitals avoiding Govt insurance scheme patients  even in  cardiac emergencies ! To label our poor patients as unaffordable ones is a outright misnomer, rather its the rich hospitals that are “not affordable” to lose profit and treat our countrymen , in a cost effective manner is the reality !

Who is Poor ? You decide.

Two forbidden things in coronary care

 1.Cajoling  and manoeuvring a distressed  family for a primary PCI as a routine treatment  hyping its beneficial effect and underplaying the true advantages of thrombolysis in largely technical jargons is the current norm in most coronary care units.

2.Another issue is , after confused confabulations with the duty medical officer,  if a rare patient family  choose the option of thrombolysis , comes the next googly*.  Many noble minded hospitals do not stock the low-cost and equally efficacious thrombolytic agent and offering  only the costly option to the anxious families when the myocardium is on fire.

Hospitals that  practice these two coronary protocols  need to be shamed and labeled as  “Coronary Incompetent  ” In spite of having 24/7 cath labs.  (Realise , they are just like  any remote rural hospitals , at least  the later can’t be faulted  as they don’t  withhold  a  reperfusion strategy  !)

Final message

I think , mindless proliferation of cath lab based cardiac care , which follow this theme , ie  “Thrombolysis incapable but PCI capable “ are  biggest threat to coronary care in our country ! For the best coronary care for any country ,what we need is efficient prehospital thrombolysis team .We have conveniently forgotten the great study of CAPTIM wherein the ambulance drivers replicated the same effect of primary PCI performed by highly trained cardiologists in modern labs.

In India,  primary health centers which is within  few km reach of entire population  can be designated as static ambulance equivalents  with basic resuscitation facility . If a multipurpose health worker can be trained to lyse, with remote supervision that will accomplish  90 % of what the cathlab guys can achieve ! Selective shifting is suffice.

Postample :  Ofcourse, not doing  pPCI for high risk or complicated STEMI is unscientific and we need to have proper consenting and referring frame-work for such patients.

Counter point : One of my colleagues asked me ? Why do I enjoy attacking the established scientific practices ?  May be I have a problem , yes, but  I think in a  true medical democracy we have right to debate anything , absolute truth is a ongoing journey !

 

 

*Googly:  An unplayable ball delivered to a batsman in the game of  cricket.

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This paper was presented as a poster (Not good enough for  oral ! ) in the just concluded CSI 2016  (Cardiological society of India ) Annual conference at Kochi, India.

 

What constitutes successful  Primary PCI ?   A proposal to include “ LV dysfunction”  as an  essential  criteria !

A  series of breakthrough technologies  in drugs , devices, techniques has revolutionised the management of STEMI in modern times.This  includes various formats of heparin , antiplatelet agents thrombolytics  and coronary interventions.Of all these, primary PCI is considered to be the greatest thing to happen in STEMI care.

The success of primary PCI is currently defined as diameter stenosis less than 30% and TIMI 3 flow on final angiography without procedural complication. True success of reperfusion essentially lies  in the salvage of myocardium and in the prevention of LV dysfunction. In real world scenario we often find a paradox , ie Inspite of  successful pPCI by current definition a subset of patients suffer from significant  LV dysfunction. Surprisingly, LV dysfunction has  never been included in the definition of successful primary PCI .

success-of-primary-pci

In this context we did a reversed cohort  study  of patients with significant LV dysfunction (<40%) following primary PCI to find out possible factors contributing to LV dysfunction.10 patients who had LV dysfunction inspite of successful primary PCI were the subjects of the study. Patients with late PCI  beyond 12  hours were excluded .Echocardioraphy had been done at discharge and 2 weeks after the procedure to assess LV function.

TIMI  3  flow  has been  documented in all  patients at the time of primary PCI.6 patients had undergone pPCI within 6 hours.4 had it by 12 hours. 7 patients had a smooth , fast  pPCI as described by standard protocol.Of these,  2 patients had LV dysfunction inspite of TIMI 3 flow established early.7 patients 3 had complex angioplasty with no reflow managed subsequently.One had deferred stenting after 4 days for IRA.Non IRA lesion were also  tackled in two.

We also confirmed  there is no linear no correlation  between TIMI flow and  subsequent LV function .This becomes vital as time and again we are seeing PCI reports with successful TIMI 3 flow only to find  weeks later  thinned scarred ventricle. Time to reperfuse with anticipated and unanticipated procedural delay  was also  a critical  factor.

However, its clear the  incidence of significant LV dysfunction inspite of  timely, and apparently smooth  PCI is real .Why this happens is beyond the current reasoning. A scientific basis for  individual myocardial sensitivity to ischemic time is yet to be found. (Dynamic host dependent time window ?)

Meanwhile , It seems prudent , we should awake to a harsh reality of practicing coronary care  with a seemingly incomplete criteria for success of pPCI . Its proposed,  an  acceptable levels of  “LV dysfunction at discharge ” (It could be > 50 %) as an essential criteria  to define the success of pPCI  .Custodians of STEMI care should  immediately rectify this glaring omission. This will dramatically impact the current  outcome analysis of STEMI and help Improve the quality of care.

Conference bulletins

dr-venkatesan-e-poster

E-PosterPresentationSat10thDec csi cohin 2016

Session – Preview 

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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)

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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