Feeds:
Posts
Comments

Archive for the ‘Uncategorized’ Category

Medical profession has  evolved over centuries with humble discoveries by genuine researchers in the past . As we  pursued  science vigorously  , we  looked  for innovations , when innovation  work ( or many times shown to work !) we jump to sky , even as  some of these  innovations fail and crash down  to earth , many times  we continue to be in the clouds . This is the fundamental problem of modern medical science . When  our expectations reached  unrealistic proportions ,   we tend to lose the common sense . Prolonging life and reducing human suffering may be the ultimate aim of the medical  profession , but  If we try to fight the death with science and money without application of mind , our current  life may become  miserable ! Thats what is happening for the majority of the population of this planet . After all ,  death is an essential and final  component of life !

Coming to the issue of CAD ,  in our country , a  rich gets a 4th generation drug eluting stent for a insignificant  asymptomatic PDA lesion , and poor fellow with left main dies without any intervention .This is  fairly acceptable   to this uneven world  , where a rich westerner  dies due to obesity related disease and a  poor African dies to malnutrition .

This article is in   response to  my  recent  experience  when  . . . I advised

Simple life style modification &   few drugs   for a patient with chronic multivessel   CAD  , I was  made to look   ordinary , inferior  and funny   by  many of the current generation cardiologists .

Further , the term optimal medical therapy(OMT)  for chronic stable angina has evoked laughter in one of the interventional cardiology  conferences  I  attended !

It is a sorry state of affairs  for the whole cardiology community , a  genuine scientific  fact , proven by  real life experience  as well,   is  being  ridiculed.

Richard  Conti tells in this excellent editorial in his journal   Clinical cardiology about the issue of medical management of CAD

“Respect in clinical trials”

Chronic stable angina pci vs cabg vs medical courage trial oat trial ethics in cardiology

Click here to reach the article  http://www3.interscience.wiley.com/cgi-bin/fulltext/122512853/PDFSTART

A similar study which  suggested  exercise  could be  better than PCI in the recent 2009 ESC is suffering the same fate !

What if regular exercise were as good as a stent for stable angina?

http://www.theheart.org/article/1000047.do

Read Full Post »

Internet has revolutionised  in sharing our knowledge . But  , the  freedom it gives  has a trade off .Identifying   genuine  knowledge  in the  vast cyberspace is like searching for lost treasure in the ocean bed.

Have a look at this site which innovates medical teaching

great medical videos top cardiology web site drsvenkatesan

Read Full Post »

Pharmacology is a major discipline in medicine where we learn how a drug acts in our body for various ailments . Now  in this era ,  doctors need not only how a drug acts but also how a drug company acts ! This has become vitally important   for the welfare of the mankind .

In this context one of the best books on medical pharmacology is from the

Famous Editor of New England  journal of medicine

A must read for all genuine medical professionals

ethics hippocrates ebm

Watch Marcia Angell  talk http://www.youtube.com/watch?v=ouF3ISihHLM

Full lecture of Mercia Angell  http://videos.med.wisc.edu/videoInfo.php?videoid=940

Click to buy/read the book  http://www.amazon.com/Truth-About-Drug-Companies-Deceive/dp/0375508465#reader

A Review  about the book  http://calitreview.com/176

Read Full Post »

Wide qrs tachycardia has a unique place in clinical electrocardiography .It is  a much fancied and glamorous entity for the simple reason , it continues to be the  cardiologist ever solved puzzle .For over three decades of research, clinical debates , symposiums , seminars have effectively failed to take away the uncertainties in decoding the wide  QRS  tachycardia . (Specifically ,  VT vs SVT with aberrancy)

Some wondered , should we really waste our efforts in differentiating the two . In emergencies it never matters , in fact one need  not attempt to do this often futile exercise !

Few dedicated criterias like Brugada etc have helped us .

While the difficulties in differentiating between VT and SVT with aberrancy remain over the decades .A less reported  , but more common issue is  confronting  us .

It is  the big question of  differentiating a  wide  QRS tachycardia from a narrow QRS  tachycardia

wide qrs tachycardia vt svt aberrancy

This  occurs  more often than we realise  ,because we define wide  QRS  tachycardia in a vague manner

  • Normal qrs width between Up to 80 / up to 100 ms acceptable  ?*
  • Narrow qrs tachycardia 80 ms?
  • Wide qrs tachycardia i> 120ms  ?
  • Definitely wide qrs >140msec

* The confusion is mainly because 20ms difference between limb leads and chest leads .

In reality one may not be able to all  tachycardia into narrow or wide .

There is big  overlap zone that need to be labeled a intermediate qrs tachycardia

If we can  triage the tachycardias into three instead of two it may help us arrive  fast  ,  to the  correct diagnosis

Narrow QRS tachycardia ( qrs 80ms)

  • Sinus
  • All svtS (avnrt etc)

Intermediate QRS tachycardia 90-120

  • Most of the SVT with  aberrancy  ( Except antidromic SVTs which are really to wide !)
  • Septal VTs*
  • Fascicular VTs*
  • VT in PPM and ICD /CRT patients **

*  Any VT that arise near the major conducting system of ventricle conduct  fast and hence qrs are relatively narrow.

**These are rare entities where  base line wide QRS getting narrower with the onset of VT . (Ref : http://europace.oxfordjournals.org/cgi/content/full/eun254v1)

Wide qrs tachycardia >120ms

  • Most of the genuine VT (Ischemic , myocardial origin)
  • Post MI VTs
  • SVT aberrancy especially AVRT
  • Any SVT with preexisting BBB
  • Marked electrolytic disorders

Unresolved questions

  • Which lead we should look for measuring the width of qrs ?
  • Should we take the narrowest qrs or widest qrs or should we take the average ?
  • Should we calculate how much the tachycardia has widened the qrs from the baseline  width of a given patient ?  Is it not possible , what is wide for some may be normal for another !
  • If  there is no isoelectric line  and ST segment  blends with qrs complex  how to mark end of qrs ?
  • If  limb leads show a narrow qrs and chest leads shows  wide qrs what is the significance  ?
  • In precardial leads  if one lead alone shows a narrow qrs , what is the significance ?
  • Can a narrow qrs VT conduct  with aberrancy and making it  really  wide ?

Final message

When we are  able to solve   complex electrophysiological  problems  , we must also realise  even   simple  tasks can be demanding in medicne ! It is proposed to create a  new  group “Intermediate QRS tachycardia “that can help solve the issue where we have difficulty in labeling these  tachycardias which fall  in the  greyzone .We can try &  apply the modern EP based VT criterias  to this group and find out the hidden truths !

Read Full Post »

Left main disease  is an important subset of CAD , and it has special interest for the interventionist. Traditionally cardiologist have   a fear to touch this lesion , as they thought a sudden occlusion within this vessel is life threatening   . Later on as  they gained experience  it was thought  we could intervene safely at least in protected left main . Subsequently  it was realised this fear was largely unfounded  , after all  the proximal LAD is equally  dangerous and we spend hours together inside an LAD ! .Now we have technology and expertise to do successful PCI any where in LM. And  unfortunately , the same expertise is not applied in selecting the ideal patients who will benefit the most . LMD has become a glorified indication for PCI.

The terminology of protected and unprotected LMD is in vogue for many years . Unfortunately it do not convey a uniform meaning . In next few minutes ,  I shall share  my views on the nuances of protected and unprotected LMD .

The term   protected was  not  coined by  cardiovascular physiologists   but by   interventional  cardiologists . Hence it connotes a  anatomical  meaning rather than physiological.  Protected LMD  meant there must be a at least one  graft to either LAD or circumflex . And this graft should be functional . The presence of this graft is supposed to increase the comfort levels of the interventionist as well as  the patient.

A left main coronary artery disease angiographically  can be  classified  as

Common types of Left main lesion

  • Asymptomatic , non flow limiting , angiographically insignificant disease(< than50%)
  • Ostial
  • Ostio proximal
  • Shaft : Mid, distal or diffuse Left main
  • Bifurcation

Unprotected left main

  • All the above lesions
  • Non functional GABG grafts ( eg: LIMA occlusion makes LAD unprotected)

Protected left main

  • Post CABG  with atleast one functional graft to LAD /LCX
  • ? Left main   with total  LAD and very good LAD collaterals from RCA /LCX

Partially protected Leftmain

It could mean any of the following,     Left main Plus  .  . .

  1. Incomplete occlusion of single  LIMA graft
  2. Occlusion of  SVG-LCX and patent LAD-LIMA
  3. Occlusion of LIMA-  LAD graft but patent SVG-LCX  graft
  4. Patent LIMA-LAD  but a  critical  LM / LCX  bifurcation lesion with no grafts for LCX*

The above 3  situations may demand a  PCI .But logic would  suggest one would try to open up the partially occluded graft rather than open the left main . Of course the decision involves status of RCA .

*The only indication for a  PCI  in protected  LMD could be 4

Unusual ( Crazy !) questions  about  left main disease

Can left main be protected by collateral circulation ?

It is very common to find Left main   bifurcation  lesion   with LAD having  very good collaterals from RCA sometimes filling up to proximal  LAD .This can be considered   “protected left main equivalent”

As on today , cardiologists would rather   believe  a surgeon’s graft  rather than a naturally grown  collateral from RCA however extensive it may be !

But logics and real case experience would indicate in a patient  with LMD and an  extensively collateralised LAD can in fact be  considered a protected left main.

If a  left main is well protected by a functional LAD graft , why should we do a PCI for left main at all ?

This question was risen in one of our cath conferences , a patient   who had functioning  LIMA to  LAD graft.His   RCA had a functioning  venous graft  and his circumflex had a partially functioning  graft.The left main had a near total  obstruction and the proximal  LAD was  faintly visible .

Since the  patient  had class  2 angina Options were discussed .He  satisfied  the  current criteria of protected LMD .Just because he fulfils the criteria of protected left main , he  does not  become eligible for  left main    PCI .  After all he is having this LMD for many years. Protecting again the left main which is already protected is not a big deal in terms  of outcome .  Double protection is waste of resource at additional risk. It was decided to attempt a PCI to SVG graft to LCX. If it does n’t work leave him with medical management.

Does  every patient  after a CABG   has a high chances of developing LMD ?

What is accelerated atherosclerosis of Left main following LAD /LCX  grafts ? It is  true  left main  has high risk of  accelerated atherosclerosis and it   undergoes  gradual obstruction once the LAD and LCX is grafted.This is due to low flow across the native left main as distal grafts maintain the flow . This is all the more likely in good bulk of patients who had undergone  CABG  where   LMD  was the indication .

A typical scenario

A left main patient   who undergoes a CABG  a follow up for a suspected  angina  angio after 5 years show the  totally  or near totally occluded native left main . Sudden   Visualisation of worsened leftmain disease    makes this patient eligible for  a  PCI as he fulfills the criteria for  protected leftmain .

Final message

A well protected left main  with a good  functioning graft especially to LAD   most often do not require a fresh revascularisation  procedure  irrespective of the tightness of left main disease . Most of such patients will be candidates for medical therapy .Contrary   to the popular belief ,   left main  intervention   could  be    confined  to   ” unprotected LMD   rather than well protected LMD” as the  potential benefits are more .Further interventional resources need not be wasted in giving second alternate protective channel  for an already protected vessel !

Of  course it should be remembered  in any given patient  with  protected or unprotected  LMD  the indication for  revascualrisation  is based on  the severity of lesion , symptoms,  LV function ,  residual ischemia, viability  etc .

Suggestions  , comments  and  corrections  welcome

Read Full Post »

Atrial fibrillation and CHF are close companions. Either it   precipitates  CHF  or  follows it.In advanced heart failure of any etiology  the incidence of AF can be up to 40% .Medical therapy of AF is fairly effective in patients with normal LV function  .But when associated with refractory cardiac failure  it becomes  too complex to control .

Currently CRT with ICD  is becoming the standard OF care for advanced CHF. The efficacy of CRT is being rigorously being assessed . Even as the controversy  about  the wideness of QRS is being settled , the issue of optimal  timing of CRT has risen  . Now ,  the MADIT-CRT has answered this issue “Earlier it  is better , it can be  indicated even for  class 1 patients”

While MADIT -CRT will increase the number of CRT implants , we  have no clear cut answer for the  efficacy of CRT in patients with AF .( Of course , the MUSTIC and CARE HF sub group analysis suggested AF has no significant impact on CRT efficacy )

atrial fibrillation crt cardiac resynchronisation therapy icd madit crt care chf

Why is AF important in CRT ?

There are two issues that need analysis

  1. A patient who  has chronic AF at the time of CRT
  2. Development of  new onset AF after CRT implantation.

Impact of AF during CRT

  • Inter atrial synchrony is lost. ( Significance not clear . . . makes AF permanent)
  • AV synchrony is lost
  • Rapid AV conduction : May trigger   too much of Bivi pacing if sensed by LV lead

Presence of AF at the time of CRT gives us an opportunity to tackle this issue.

How to tackle  sudden AF induced CRT response ?

There are variety of algorithms available to

  • Ventricular sense response
  • Conducted AF response
  • Atrial tracking recovery

In dual chamber pacing mode switching converts DDD into VVI  .This happens  at the cost of loss of AV synchrony .This may have profound implication in CRT .

Then the big question comes  . What is the use  of  having Intraventricular  and interventricular  synchrony without AV synchrony ?

When nothing works .The best strategy is ( Rather deemed to be best ! )

  • To ablate the  AV node  pace  the atrium and ventricle  (RV & LV)  .

Note : Ablation of AV node and putting a dual chamber pacing can never guarantee a physiological pacing as the atrium continues to fibrillate and AV synchrony is rarely there .

Final message

For CRT is to be successful , there should be maximal Bi-Vi capturing , of course this capture has to optimally timed , and must reverse the three pathological asynchronies , namely intraventricular , Interventricular  and  atrio  ventricular  asynchronies.

It is obvious , presence of AF complicates the issue as it demands  constant monitoring and programming of the device (Of course  now most  of them are automated) . It may   require  knocking down of AV node , which  not only carries a risk of SCD *  ,  it also make these  patients   permanently  dependent   on the RV pacing  . This  adds on ,  another  risk ,  for an  acute complication   if the RV lead fails for some reason.

Reference :

*Sudden death after radiofrequency ablation of the atrioventricular node in patients with atrial fibrillation
Journal of the American College of Cardiology, Volume 40, Issue 1, Pages 105-110
C.Ozcan

EP experts generally take  too much liberty in adopting this  strategy for the simple reason it solves the nuisance of atrial impulses  interfering with   ventricular  leads  function that result in  inappropriate ventricular capture fusion or ultimately poor BiVi pacing . But it is not an easy decision  atleast for the patient ! This article , emphasises the dangers involved in ablate and pace strategy for uncontrolled AF.

Further reading

  • Fung, J. W H, Yip, G. W K, Yu, C.-M. (2008). Does atrial fibrillation preclude biventricular pacing?. Heart 94: 826-827 [Full Text]
  • Khadjooi, K, Foley, P W, Chalil, S, Anthony, J, Smith, R E A, Frenneaux, M P, Leyva, F (2008). Long-term effects of cardiac resynchronisation therapy in patients with atrial fibrillation. Heart 94: 879-883 [Abstract]
  • Buck, S., Rienstra, M., Maass, A. H., Nieuwland, W., Van Veldhuisen, D. J., Van Gelder, I. C. (2008). Cardiac resynchronization therapy in patients with heart failure and atrial fibrillation: importance of new-onset atrial fibrillation and total atrial conduction time. Europace 10: 558-565 [Abstract] [Full Text]

Read Full Post »

AV dissociation is the specific marker for diagnosing VT. Evidence for AV dissociation manifest in many ways in ECG. *Random p waves unrelated to qrs complexes , fusion beats , capture beats are  the common features that help us diagnose AV dissociation. Unfortunately these  occur only in about  40 % of patients  with VT.(Fusion beats in VT are also  called as Dressler’s beat)

For clinical features of AV dissociation follow this link

What is the normal AV association ?

In  normal physiology ,  even though atria are passive , powerless chambers  in terms of mechanical activity  ,  it reigns  supreme control over ventricle and   dominates   electrically  . In fact , the atrium  and the AV node together ,    dictates when the ventricle has to contract and at what rate  .  So,  in normal human  beings in  sinus rhythm ,  there is a complete AV  association   where both chambers live in a perfect harmony.

What is VA association ?

The atrium and ventricles are  not only related   antegradelyy it  also  has a concealed  retrograde  relationship , (which is often pure electrical ! ) called VA conduction .The conduction velocity and the refractory period of VA  junction is  variable .The AV junctional refractory period is determined by the penetrating power of both atrial and ventricular impulses .

What is complete AV dissociation ?

For complete AV dissociation to occur there should be no physiologically or electrically  linked relationship between the atria and ventricle.For it  to occur the atrial impulse has to get  blocked  in AV junction .

This block can   either be functional  or organic,   partial or total , persistent  or intermittent

This occurs in   primarily in   AV junctional pathology like CHB  etc, that result  in complete AV dissociation . The next major cause for AV dissociation , is   by an  interference from  an accelerated lower pacemaker as in ventricular tachycardia or accelerated idioventricular rhythm .

What does the atria do when the ventricle  starts  contracting rapidly and  independently as in ventricular tachycardia ?

When the ventricle , starts firing independently at a rate of > 200 each of the impulse and  tries to  traverse  the AV junction retrograde . At the same time , the sinus impulse which does it’s normal routine job  by beating around 70/beat ,   faces an  unusual interference on its normal downward journey by  the pathological bombardment  from  the upcoming  ventricular impulse .What happens when both these wave fronts  meet head on . (The hither to perfect harmonical  relationship becomes  a rivalry for the electrical control of heart.)

Sadly , the ventricle mostly succeeds  in the race and  most of the   ventricular impulses    retrogradely  enter  the AV  junction and colludes with  the incoming atrial impulses. When this happens , the AV dissociation is said  to occur. The important point here is,  many times if the retrograde VA conduction is fast and optimally timed , it can cross the AV node without difficulty  and reach the atria  and  subsequently  even    depolarise  the SA node   and  reset  it  . If the VT is persistently conducting  retrograde  it can suppress the SA node as long as the VT is there. This makes a P wave becoming totally absent.  (Note of caution : If you say VT as one of the causes of absent P wave you may be failed in your cardiology board , but this remains a fact !)

So the atrial  depolarisation  and contraction During VT is a complex one. It depends  mainly on the  intensity of the  upcoming    electrical wave front   from the ventricle  . The distance traveled by this wave front  determines  the location of  p waves .It may be in one of the following ways .

  • P waves can be totally absent
  • P wave may occur antegrade
  • On the QRS
  • Over the T wave

In effect the P wave can  literally be any where   in the given strip of  VT

When does a fusion  beat occur ?  When does a capture occur ?

This again is determined by the AV  junctional refractory period. If it permits ,  an   occasional atrial impulse may sneak through the AV junction and capture the ventricle . This is capture beat. Capture beats   are usually narrow qrs  . So in a wide qrs tachycardia  if we note  an occasional narrow or relatively narrow  qrs complex it could denote a VT.

If the atrial impulse after crossing the AV junction   collides with the   upcoming ventricular  impulse  the surface ECG inscribes  a fusion beat. An incomplete capture beat is a fusion beat. It is a combination of two qrs complex one activated from above , one from below .The width of the fusion beat may be wide , narrow or intermediate.

So the evidence for AV dissociation  in surface ECG  is rarely  manifested  if the VT is successfully  traverse  the AV junction and   reset  the SA node  or keep it in a semi depolarised state  .This could be clinically important  some times , the SA node takes time to recover following  A DC shock especially in elderly

An episode of VT can unmask  a hidden sinus node dysfunction , as VT is technically similar to an atrial override pacing   of course  from  below .

Final message

During VT , electrophysiologically  there must be a dissociation between  the atrial  and ventricular contraction.But the evidence  for which is not manifested in surface ECG in the majorty.The primary reason for this,  due to  the  intact  VA  conduction  that    result in  retrograde VA  association.This  makes the  classical findings of   AV dissociation a redundant or invisible  one .

Read Full Post »

The   failing heart  enlarges progressively and  attain a globular shape . What  looks  for the  naked eye  as a simple global hypokinesia of LV  , when  analysed  ,  reveal multiple  forms regional desynchronisation .This is especially true if the QRS complex is wide.

It is generally divided into three groups

  • Intraventricular desynchrony (IV)
  • Ventriculo-Ventriculo desynchrony(VV)
  • Atrio ventriculo  desynchrony(AV)

In our search for improving CHF mortality and morbidity  ,  we have  stumbled upon this concept of restoring the lost synchrony of the heart. Cardiac resynchronisation therapy  has become ( Rather projected to become !)  a  great modality for patients  with cardiac failure.It was   initially advocated only   for severe forms of cardiac failure  , now  advised even for class 1 CHF. (CRT-MADIT 2009)

Restoring  the lost  synchrony  by rewiring the cardiac conducting system with multiple leads and optimally timed pacing increases the effectiveness of cardiac contractility.It can improve EF, and also regress mitral regurgitation.

The above concept was perfect on paper , but was very difficult to replicate on real patients. CRT was ineffective in 30% of patients.   Many had partial  effect. Few had adverse effect .

The reason for the poor efficacy  is  technical in many .  Identifying the optimal  sites for  positioning  the leads  and the futility of such an  exercise as the LV epicardial  lead is pre- selected by the patients coronary venous anatomy are the major issues.An electrically ideal site for pacing  can  contain a  mechanically dysfunctional scar.   While these  technical issues may  be addressed  in due course  what worries us is the conceptual flaws.

Emerging  facts indicate timing of asynchrony could be vitally important.

  • Systolic   synchrony
  • Diastolic synchrony

What is the incidence desynchrony with reference to the cardiac cycle ?

CRT resynchronisation

One major reason that was overlooked totally was the presumption cardiac dysynchrony occur only during systole. It is a less recognised fact is the ventricular relaxation is not uniform and synchronous.A  failing ventricle can not be expected to relax  systematically and coherently  for the simple reason the myocytic calcium reuptake into the sarcoplasmic reticulum  is grossly impaired. This  is directly responsible for the diastolic dysfunction observed in dilated cardiomyopathy . If this impairment occur uniformly throughout the  left ventricle it can be termed global diastolic dysfunction which is little easier to correct .But what really happens is  the  defect in calcium reuptake occurs in a random fashion with lot of regional variation. This is called regional diastolic wall motion defect or regional diastolic dysfunction.The above mechanisms result in the typical restrictive filling pattern of many of the advanced  patients with DCM . CRT as a concept should need to address this issue.

How to diagnose Diastolic WMD?

The  fact  is  ,we have not  mastered the quantification of systolic WMD as yet. It may take years before decoding the  nuances  of diastolic wall motion defects. At least we need to know such a thing exists.Tissue  doppler strain rates ,  velocity vector imaging could be useful tools. As such they are not clinical tools.

Final message

crt cardiac resynchronisation asynchrony echocardiography

Cardiac resynchronisation as a concept is good on paper . Heart need to be synchronous both during systole and diastole .This becomes especially important in an advanced stages of  heart failure. Without proper follow up  and potential adverse effects of CRT on diastolic WMD ,   CRT concept    has  miles to travel !  . Some  pessimistic thinking   cardiologists ( Me . . . !)   would even argue  it as a case of prematurely released device into the  patient domain. Of course there is  lot of  scientifc data that  will vouch for its beneficial effects .(The latest being from the prestigious NEJM ,  CRT-MADIT) but it has to prove it’s worth in individual patients. Physicians must exercise caution  before embarking on heroic  attempts to provide resynchrony of failing hearts .

Reference

This study from France published in JACC 2005  by Iris Schuster,

http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109705021005/fulltext

Coming soon

ICDs are better bet than CRT

Read Full Post »

ST segment depression is the classical response to stress during  excercise stress testing. (EST)Not all types of ST segment are  pathological.The ST segment should depress  atleast 1 mm below the  isoelectric segment and it should be depressed for 80msec from the  J point.

It must  satisfy   two criteria .

  1. The quantum of ST depression should be >   1mm at 80msec from  J point.
  2. Slope of ST segment

Always pathological slopes

  • Horizontal
  • Down sloping

Most often pathological

  • Slow up sloping

Non pathological slope

  • Rapid up sloping with ST depression
  • Rapid Up sloping  depression of  only the J point( The classical  normal physiological response to excercise )

Horizontal or down sloping ST segment is easily recognised .When there is  junctional ST depression with a ST segment that is  climbing upwards , it is some times difficult to interpret.

How do you measure the slope of ST segment ?

We don’t have the trouble of measuring it as the computer does this job automatically. But a cardiology fellow  need to know how it is measured !


slow upsloping st depression st segment ecg

A slow upsloping ST segment( <1.5mv.sec )can be a significant marker of ischemia.This is especially true in established CAD or individuals at high risk . For  so slow up sloping a .5mm allowance is given to filter out false positive (ie to improve sensitivity) . So for slow up sloping ST segment , to be reported as positive it should depress atleast 1.5mm or some times  2mm.

upsloping st segment tmt st slope ecg

Available evidence suggest a rapidly upsloping ST segment (> 1.5mv /Sec)  is a non ischemic response irrespective of the quantum of ST  depression  at 80msec. However ,  a rapidly upsloping ST  is rarely depressed beyond 2mm .( This is because , the geometric hyperbolic curve  of ST segment does not allow a situation of  3mm ST depression at 80msec with rapid upsloping )

What is the  angiographic correlation of  slow upsloping ST segment depression?

Few studies are availbale  to address the issue. It is believed  slow up sloping  of  ST depression is often associated with CAD but it is very rare to find a critical and proximally located CAD.Left main disease is almost never manifest with slow upsloping ST depression.

What is the significance of slow upsloping  ST in clinical situations like unstable angina ?

It is rare for cardiologist to diagnose or “even look for” slow or  rapid up sloping ECGs in coronary care units. But , a  patient with stable  CAD ,  sinus tachycardia ,  angina can exactly mimic a stress test  situation .

Some of the low risk UA , mainly secondary UA due to increase demand situations manifest with slow upsloping ST depression , while classical thrombotic occlusions produce the typical horizontal or downsloping ST segment depression.

Read Full Post »

Primary ventricular fibrillation is the number one killer in STEMI.It is  believed to occur  ( Rather it occurs really !) in up to 25 % of all patients with STEMI before they reach the hospital and another 4% after reaching the hospital.

What triggers this primary VF  ?

Easily answered : It is the  acute ischemia in majority.

Why it triggers in only in some patients? The  rest reach the ER safely and  some  casually walk in to the  OPD  few days  after a STEMI

This can never be answered with our current knowledge base. Some call this as fate !

Scientists should work hard on this issue, if we know the answer we could  possibly prevent the number one killer of the mankind at bay.

ventricular fibrillation ecg

Many factors are being analysed  to find the reasons for primary VF

  • Extent of infarct
  • Area of infarct
  • Intensity of pain
  • Adrenergic drive
  • Gender
  • Myocardial critical mass
  • Is it the  left main STEMI ?
  • Is it a bifurcation STEMI ?

If nothing  explains the VF it is always safe to blame it on susceptibility and inherited risk for primary VF , which of course is very much likely as the K+ channel  activity and it’s response to ischemia  is largely inherited

Is there any hot spots in the heart that are hypersensitive to ischemia ?

Some studies have clearly documented increased incidence of primary VF in infero posterior MI , and RV MI

than anterior MI .   J Am Coll Cardiol 2001; 37: 37-43

Why  ischemia of a certain location of heart should be more prone for  primary VF ?

The answer is any body’s guess.

Some intriguing possibilities are ,

  • RV is a anterior chamber , when infero posterior MI occur in association with RV MI  the ischemic zone encircles a almost 50% of heart like a band .This could be one explanation for more incidence of VF in infero postero RVMI.
  • Any MI which involves a  antero -posterior axis  of heart is likely to trigger a VF
  • Some of our patients  who survived a primary VF had a short left main  and early bifurcation with a large diagonal branch.The lesion was noted in the bifurcation.This raises a possibility ,  if a STEMI occur at a bifurcation with two divergent areas of  acute ischemia it has a high chance for precipitating a VF.

Related video by the author

Ignorance based cardiology -You tube

Potential research areas

Genetic susceptibility

Environmental Energy flows and primary VF

Some believe  a role for astrological  forces and  VF

Read Full Post »

« Newer Posts - Older Posts »