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Unlearning cardiology :Diabetes is not CAD equivalent

April 30, 2016 by dr s venkatesan

There can be no debate to call diabetes as major cardiac risk factor . But , how about calling all diabetics to be deemed (Rather doomed ) to suffer from CAD and label them  with a fanciful terminology as CAD equivalent ?

This is what happened few years ago.From the beginging it was a controversial concept. The argument in favour of it was , many diabetics will have micro or macro vascular disease  process in coronary or peripheral disease which are sub-clinical .One major   study from Fiinish population  in (NEJM 1998 ;Ref 1 ) suggested this possibility and was dissiminated without proper scrutinty . The same Finnish group ( I need to confirm this as few authors are same in both studies !)  has comeout with 18 year old data (1998-2016 ) and conclude their earlier conclusion could be wrong after all (Reference 3 )

Premature conceptualisation can be rampant and crucial time is wasted in unlearning. This emphasizes an important aspect of medical learning what I call as “discontinuing medical education” (DME) that would make sense in the future for sure !

Reference

1. Haffner SM, Lehto S, Rönnemaa T, Pyörälä K, Laakso M. Mortality from coronary heart disease in subjects with type 2 diabetes and in nondiabetic subjects with and without prior myocardial infarction. N Engl J Med. 1998;339:229–34

2.Type 2 Diabetes as a “Coronary Heart Disease Equivalent”An 18-year prospective population-based study in Finnish subjectsdoi:  Diabetes Care  2005 vol. 28 no. 12 2901-2907

3.Auni Juutilainen, Seppo Lehto, Tapani Rönnemaa  Jamal S. Rana , Jennifer Y. Liu, Howard H. Moffet Diabetes and Prior Coronary Heart Disease are Not Necessarily Risk Equivalent for Future Coronary Heart Disease Events  Journal of General Internal Medicine April 2016, Volume 31, Issue 4, pp 387-393

 

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Comical concepts in cardiology : Prehospital thrombolysis is great , but its “no good” inside the hospital !

April 26, 2016 by dr s venkatesan

This happened  recently in one of my private ER visits. When I asked my fellow to lyse a patient with STEMI who arrived within 20 minutes after the onset of chest pain to our CCU.

He was reluctant and surprised, seemed to suggest  thrombolysis is a banished indication.

I asked him , whether he is aware of any study  that showed early , fast pre-hospital thrombolysis is as good as primary PCI ?

Yes sir. . but these studies clearly say it is useful only if its done prehospitally sir, not inside the hospital or coronary care units. 

I told him to think CCU as an ambualnce ,consider the patient is  in transit and  lyse him.

He was amused , as it looked  a comical concept and an unscientific uttering from a professor !

Still, he was courteous enough to follow my advice.The  patient stabilised within 6 hours and the ST segment  resoluted to near 100 % , No LV dysfunction.Discharged in 48 hours.

Final message

I realised in a harsh way , modern day scientists driven by evidence would struggle to regain the lost common sense ! There is a real risk for  irreversible damage to our faculty of wisdom !

STREAM trial nejm

 

http://www.nejm.org/doi/full/10.1056/NEJMoa1301092

 

 

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When STEMI dressup like NSTEMI. . .Cardiologists can easily be fooled !

April 22, 2016 by dr s venkatesan

The ECG changes in ACS can be  “as dynamic as”  an occluding thrombus. The initial events include sudden total occlusion, early lysis, a trickle of flow, partial re-occlusion, reflow, no-flow, etc. The extent of transmural vs sub-endocardial ischemia, the competing force of re-perfusing vs necrotic wavefront, would define  ECG findings. This makes the ST segment labile in the 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,

 

img-20160423-wa0012_1.jpg

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, one of them could find one more ECG available taken a few hours ago in another hospital.

It had something on it ,

img-20160423-wa0009_1_1.jpg

This ECG taken a few hours ago, shows ST elevation in 1 and AVL, and few VPDS in the 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!

img-20160423-wa0011_1.jpg

How to manage a patient who presents as NSTEMI but had STEMI a 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, . . . don’t live in the primitive era of managing ACS in CCU . Forget the ECG take him to the 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 that ) 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 later, for further evaluation. This is a typical example of a patient with ACS managed successfully without entering the cath lab.(A forbidden practice and a potential coronary blasphemy )

Final message

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

 

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When a left main decides to drain this way . . . left ventricle has every reason to rejoice !

April 21, 2016 by dr s venkatesan

It is believed coronary artery branching pattern is as unique as our finger prints.Left main coronary artery usually bifurcates .Uncommonly it may trifurcate or rarely quadrificates.

When it gives a cluster of branches like in this patient , the left ventricle is richly supplied with multiple pathways .

p_20160421_181013_1.jpg

These are the patients who are protected well during a coronary event as any one of these branches can back up.However, if leftmain is involved one can guess the consequences !

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Sutureless AVR : Surgeons shed the needle . . . to take on TAVR !

April 16, 2016 by dr s venkatesan

With TAVR (Transcutaneous aortic valve replacement ) threatening to take away the Aortic valve surgery atleast in high risk subsets from surgical domain ,a new development is taking place in aortic valve surgery. Minimally Invasive aortic valve replacement and implantation of low profile , bio prosthetic valve placed in aortic root without active suturing .This type of AVR  can be done without traditional  sternotomy  with minimal bypass time , less surgical morbidity and mortality.

It has some specific advantages over TAVR, as the native valve is removed , calcium is debrided and hence less stroke and para-valvular leak .In TAVR cardiologists are blinded ,do lot of guess work to place the valve in right position ,  struggle to handle the deformed and distorted native valve tissue .My belief is,surgery does a more precision job , since the valve is placed in  optimal position .One more issue is, complication of complete heart block and subsequent requirement of pacemaker , its prohibitively high for TAVR as on 2016.(up to 25% )

These new generation valve  are expected to  narrow the gap between AVR and  TAVR. Still. avoiding a surgery is the biggest advantage which drags most patients to TAVR. However, one should ensure quality shouldn’t be compromised for simplicity.

There are two valves available for suture less AVR  , both from Bovine pericardium.

1.Perceval (Psorin)

2.Intuity (Edwards)

p_20160415_174424_1.jpg

Evidence

CAVALIER and TRITON  (PERSIST -AVR forthcoming)

Message for the  patients

TAVR is a revolutionary  treatment modality, agreed .However , one need not blindly accept the  TAVR if offered especially in low and medium risk* situations just because it avoids a surgery.(*Of-course technology may evolve further ) Discuss with surgeons .Be well informed about all the intricacies.Currently  surgical risks seem to  overstated and TAVR risks are underplayed in spite of huge cost advantage in favor of surgical AVR.

A note of caution , for suture less AVR must be made .Basically , surgeons  tried to imitate the cardiologists, .Ironically , it has the same issues of TAVR for possible migration of valve.Conventional AVR  with active permanent fixation sutures will remain the 24 carrot gold standard for AVR and all others may  just glitter !

Please realise, medical decision making and consent forms are increasingly looking  similar to signing a  house mortgage loan which comes with  lots of known and unknown “conditions apply”!

Reference

tavr tavi avr surture less future of avr metaanalysis phan

 

 

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Why we may “never-ever” understand the seriousness of NSVT in HOCM ?

April 3, 2016 by dr s venkatesan

Hypertrophic cardiomyopathy (HCM) is the most common primary cardiac muscle disorder.It is one of the  extensively studied medical  entity in terms of pathology, genetics, electrophysiology and treatment.Though it has dramatic myocardial  phenotypic expression , longevity  can be near normal  except in a minority who are prone for LV dysfunction and SCD due to the indirect electrical instability.These arrhythmia arise due to myocardial disarray , micro vascular disease or fibrosis.

NSVT  by definition is runs of VT at a rate of > 100 /mt occurring less than 30 seconds.

How common is NSVT in HCM ?

On Holter study with  178  patients  with HOCM (Adabag  JACC 2005 ) 90 % showed VPDs

  • 12%  > 500 VPDs/24 h
  • 40% had couplets,
  • 30% had non-sustained ventricular tachycardia (NSVT).
  • Over a follow-up of 5.5  6% patients died suddenly (annual mortality rate, 1.1%)

For sudden death, NSVT on Holter ECG had negative and positive predictive values of 95% and 9%, and sensitivity and specificity of 45% and 69%, respectively.

nsvt incidence hocm

In this series from StGeorge hospital London from 630 patient incidence of NSVT was 19% and 4 episodes were observed in 48 hr in most .Monserrat L, JACC 2003

What is the duration , How fast  and  how frequent is the NSVT ?

It is expected the total burden of NSVT would have a definite impact on outcome.  Curiously the duration, fastness and frequency of NSVT  was  not related to prognosis in atleast one study (Monserrat L, JACC 2003)

Relationship between age and burden of NSVT ?

Aging has a sobering effect on these ventricular ectopic activity by probable conditioning and fibrotic interruption of electrical activity.

How often a episode of NSVT  convert to VT ?

Considering the day to day even it should be termed extremely rare . Even among person who survived an SCD the next episode of VT can be very rare.

What is the current Indication for ICD in HOCM ?

Secondary  prevention (Consensus > Controversy )

Primary prevention (Controversy > Consensus – Still evolving )

Questions galore  . . . answers struggle !

Does NSVT arising from single focus or multiple focus ?

What is the relationship between NSVT and degree of obstruction ?

What is the relationship between NSVT and MRI detected myocardial scars ?

How effective is beta blocker suppress NSVT ?

Can we implant ICD for only NSVT ?

Is it true  ICDs add more anxiety , distress and harm  than the index disease ?

How to program ICD to ignore  NSVT and fire only for VT ?

For further information , refer this most authentic knowledge base. esc guidelines hocm

Final message

Predicting which NSVT will go for SCD  in HOCM can be as difficult as predicting the next major earth quake  that would strike the pacific rim that  experiences unrecognized tremors  on everyday basis .We have learned to live with that right ? So it appears NSVT is more of a nuisance arrhythmia for both the patient and physician .

Still , science demands identification  individuals  with highest risk for arrhythmia . How to do it ?  Is it the  morphological features  , degree of obstruction  or  genetic finger prints. It is still not resolved . One thing is clear we can’t advice ICD for all those with runs of NSVT  for perceived fear or pressure from peers or industry !

 Referene
2.Occurrence and frequency of arrhythmias in hypertrophic cardiomyopathy in relation to delayed enhancement on cardiovascular magnetic resonance.Adabag AS1, Maron BJ, Appelbaum E,J Am Coll Cardiol. 2008 Apr 8;51(14):1369-74
3. O’Mahony C, Jichi F, Pavlou M, et al. A novel clinical risk prediction model for sudden cardiac death in hypertrophic cardiomyopathy (HCM risk-SCD). Eur Heart J 2014;35:2010–20.
4. Monserrat L, Elliott PM, Gimeno JR, et al. Non-sustained ventricular tachycardia in hypertrophic cardiomyopathy: an independent marker of sudden death risk in young patients. J Am Coll Cardiol 2003;42:873–9.
5. Elliott PM, Anastasakis A, Borger MA, et al. 2014 ESC Guidelines on diagnosis and management of hypertrophic cardiomyopathy: the Task Force for the Diagnosis and Management of Hypertrophic Cardiomyopathy of the European Society of Cardiology (ESC). Eur Heart J 2014;35:2733–79.
6. O’Mahony C, Lambiase PD, Rahman SM, et al. The relation of ventricular arrhythmia electrophysiological characteristics to cardiac phenotype and circadian patterns in hypertrophic cardiomyopathy. Europace 2012;14:724–33.
7.O’Mahony C1, Lambiase PD, Quarta.The long-term survival and the risks and benefits of implantable cardioverter defibrillators in patients with hypertrophic cardiomyopathy. Heart. 2012 Jan;98(2):116-25

 

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Critical management issues in CAD : OMG ! . . where is OMT ?

March 31, 2016 by dr s venkatesan

One of my fellows gave a discharge summary  for a 62 year old patient with stable diabetic  CAD  who had Triple vessel disease with a final advice reading as CABG / PCI/or OMT .

There was a near fury over his angiogram report in the cath meet. How can be  eligible for all the three Intervention at the same time ?.(PCI -Percutaneous coroanry Inervention ,CABG-Coroanry artery by-pass graft, OMT-Optimal medical therapy )

The lesion in question was , Triple vessel disease(Non critical LAD) and significant LCX and again a non critical RCA .Syntax was less than 22 for sure , however the patient  had class 2 angina (now reducing ) .When asked to explain  , the fellow  argued since the patient  is symptomatic , has DM with TVD  he is eligible for CABG , since  LCX lesion was discrete and PCI was distinctly possible , of course as all three  lesions would be  eligible for OMT on any given day  ! he inferred .

How can  a cardiologist be so casual and non-commital in an important medical decision where a life of a heart is at stake.There was a unanimous condemnation about the report. As a consultant he has to be specific , one can’t leave the decision to  your patient’s whims  . . . rather it’s our scientific whims  that should prevail  !

 

MEDICAL VS PCI VS CABG OMT COURAGE BARI 2D FREEDOM FAME STUDY MASS 2 CASS OPTOMAL MEDICAL MANAGEMENT SYNTAX ACC AHA ESC GUIDELINES PTCA STS EUROSCORE NEJM

The curiosity continued and looked amusing for many. I was the only one supporting  his argument ! After all , he is being frank and understood the futility of  applying  evolving knowledge base in critical decision making. But, I  asked him to grade the choices .In my opinion  OMT should be the first choice if it can be administered , but reality tells me  true OMT is rare as a modality  at-least in  this  part of world . However every one should insist for it.

Apart from poor  compliance for OMT , pressure  mounts for a procedure from peers and non peers . I am  sure  many  patients  will end up with an  invasive modality sooner or later  backed by a  second or  third opinion  driven by that elusive googled intellect !

Final message

When clinical decision making is debatable with available knowledge (Especially with futile and evolving knowledge base !) , please include your patient into the debate and you may even consider giving him the veto power.If Hippocrates is alive today , I am sure he will argue for medical  knowledge and ignorance should be equally shared with their  patients.

Counter thoughts

Don’t give the choice to your patient  . . . that would mean you lack  clarity, wisdom and confidence !

No, I don’t agree , I know there are  some  patients who are  well informed , rational , more focused than even a professional  !

 

 

Posted in cardiology -Therapeutics, Cardiology -unresolved questions, Infrequently asked questions in cardiology (iFAQs) | Tagged , , , , |

Finally , Junctional tachycardia gets a proper definition

March 31, 2016 by dr s venkatesan

Junctional tachycardia(JT) is often a misunderstood arrhythmia. Technically,  any tachycardia arising from the AV junction could be termed as JT.Even AVNRT was considered as a form of Junctional tachycardia till recently.The crux of the issue is , true anatomical extent and borders of  so called AV junction is  yet to be clearly demarcated .The common perception that  AV node is a discrete  structure is  an anatomical illusion  , rather its collection of  condensed fibers with proximal  nodal approach and distal fanning .

Now , we have a  proper definition by the apex scientific bodies  ACC/AHA/HRS 2015)

definition of junctional tachycardia

Source :2015 ACC/AHA/HRS guideline for the management of adult patients with supraventricular tachycardia: Executive summary A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society April 2016Volume 13, Issue 4, Pages e92–e135

Please note :The key point is , JT by definition  should  be a focal  /automatic tachycardia either due to triggered activity or after depolarisation and the boundaries of  junctional tissue is liberally extended up to  His bundle.

Read  related post  :What does the term junctional tachycardia mean in current era?

Reference

http://www.heartrhythmjournal.com/article/S1547-5271%2815%2901188-1/pdf

 

Posted in Cardiology -Definitions, Cardiology-Arrhythmias, Electro physiology, Infrequently asked questions in cardiology (iFAQs) | Tagged , , , | Leave a Comment »

Does Intentional harm happen in medical profession ?

March 27, 2016 by dr s venkatesan

I don’t know the answer, rather I am afraid to answer that question.

Read this article , that may  help find answer to this forbidden question.

medical ethics inappropriate medical care

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Ignorance based STEMI care : Dynamics of Thrombus in IRA

March 20, 2016 by dr s venkatesan

100% occlusion of a coronary artery result in STEMI.This includes both thrombus and mechanical component .We are very much blinded till we touch , feel and see the lesion with a wire or IVUS to quantify the mechanical component’s  contribution in the genesis of  STEMI.It is generally believed (True as well ) thrombus is the chief culprit .It can even be 100 % thrombotic STEMI with  just a residual endothelial  erosion and hence
zero mechanical component .However , the point of contention that non flow limiting lesion is more likely to cause a thrombotic STEMI than a flow liming
lesion  seems to be biased and misunderstood scientific fact .

What happens once 100 % occlusion take place ?

Sudden occlusion , is expected to evoke a strong fire fighting response within the coronary artery.The immediate reaction is the activation of  tissue plasminogen system. In this aftermath  few succumb . ( Re-perfusion arrhythmia  generated as VF ) .The TPA system activates and tries to lyse the clot.The volume , morphology, attachment, content of thrombus ,  and the elasticity of fibrin mesh , location of  platelet core would determine the life and dissolvablity of thrombus. Even a trickle flow can keep the distal vessel patent .(Please note a timely TIMI 2 flow can be a greater achievement than a delayed TIMI 3  flow !)

thrombus propgation
What happens to the natural history of thrombus in STEMI ?
Thrombus formed over the culprit lesion can follow any of the following course

  •  Can remain static
  •  Get lysed by natural or pharmacological means
  •  Progress distally (By fragmentation or by moving en-mass )
  •  Grow proximal and and involve more serious proximal side branch obstruction
  • Organise and become a CTO

Factors determining thrombus migration

The interaction between the hemodynamic  forces that push a thrombus distally and hemo-rheological factors that promote fresh proximal thrombus formation are poorly understood. The altered intra-coronary milieu with a fissured plaque covered by  platelet vs RBC / fibrin core,  totally of obstruction,  reperfusing forces , re-exposure of raw areas and  the distal vessel integrity all matters.

While, logic would tell us,  thrombus more often migrates  distally  assisted by the direction of blood flow, an  opposite concept also seeks attention , ie since the blood flow is sluggish  in the proximal (to obstruction site )more thrombus forms in segments proximal to obstruction.

(In fact, its presumed  in any acute massive proximal LAD STEMI , it takes hardly few minutes for the thrombus to  queue up proximaly and  clog the bifurcation and spill over to LCX or even reach left main and result in instant mechanical death.)

What is the significance of length and longitudinal resistance of the thrombotic segment in STEMI ?

If thrombus is the culprit let us get rid of it , this concept looks nice on paper , but still  we don’t  know why thrombus aspiration in STEMI is not consistently useful. We also know little about  the length of the thrombotic  segment .When a guide wire is passed over a STEMI ATO it may cross smoothly like  “cutting a slice of  butter” in some , while in few we struggle and  end up with severe no-reflow inspite of great efforts .Why ?

What is the Impact of distal collateral flow in flushing fresh thrombus ?

The efficacy of collateral flow in salvaging myocardium is underestimated. Distal vessel flow if perfused partially by acute collaterals the thrombus load is not only less it’s soft and fail to get organised early that would help cross the lesion easily.

Posted in acute coroanry syndrome, STEMI, STEMI -Managment | Tagged , , , , | Leave a Comment »

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