Archive for April, 2016

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 !

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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 , is there any study that showed early , fast pre-hospital thrombolysis is as good as primary PCI ?

True 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 ST the ST resolute 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





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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,



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 ,


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 !


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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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 .


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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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)




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”!


tavr tavi avr surture less future of avr metaanalysis phan



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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 !



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