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Pre-stenotic dilatation : Why do the coronary artery dilate proximal to an occlusion ? What is the clinical significance ?

July 10, 2011 by dr s venkatesan

Laws of fluid dynamics dictate there is a pressure drop across   a point of narrowing  and recovery  thereafter  . At  recovery point if the vessel wall is weak it tends to balloon out .This is called post- stenotic dilatation .This is  the anatomical equivalent of Bernoulli or venturi  effect. This theoretically  occur only distal to obstruction .

How do you explain the common observation of pre- stenotic dilatation?

  • Intimal weakening due to disease process is the prime  suspect.
  • Pre stenotic  increment in mean pressure  also play a role .
  • Mechanical distention due to stagnated blood  proximal to  critical obstruction  is  a  logical explanation.
  • Finally and most importantly ,contagious , sub – angiographic  atherosclerosis.

How is  dilatation  different from ectasia ?

May be they are all related phenomenon. The definitions  of ectasia ,  dilatation, aneurysm are  more to do  with semantics than with academics.

Clinical and hemodynamic implication in cath lab

  • Sluggish  flow prone for thrombus
  • Stent selection errors likely
  • Stent dislodgment  and migration

Long term effects

  • In stent re-stenosis is more common if adjacent segment show dilatation.

Finale

Enlargement of vessel wall in both pre and post stenotic segments are possible . In small vessels pre- stenotic dilatation is  more common , while in large vessels post stenotic dilatation is  more prevalent .(Aorta, Pulmonary artery)  The mechanisms are slightly different. Apart from the lesion tightness ,  hemodynamic  and genetic factors are also responsible These dilatations are  often labeled as ectasia in coronary artery  and  most cardiologists  tend to   ignore this finding especially if  the margins are smooth.

But , newer imaging modalities like IVUS, OCT have given   better  insight about these dilatations.These   are  actually an  expression  of the  contagious  atherosclerosis .  Pre-  stenotic segments are prone for extensive disease  than even the diseased segment due to  more hemodynamic turbulence. There is some evidence atherosclerosis progresses  proximally more than distally.Smooth margins within the  pre -stenotic dilatation  does  not guarantee  disease free status.

During PCI  there could be  an  argument for covering the dilated  pre- and post stenotic segments  as well* . (We vouch for endovascular stenting when aorta is dilated why  do we hesitate  in coronary  ?)  .Careful selection of  coronary stent size  is  recommended  and  allowance should be given  for these two (Pre and post coronary dilatation ) patho -anatomic phenomenon.

* Stent missing a lesion is stylishly called geographical  miss ! This should logically include dilated segments also.

Posted in Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, cardiology- coronary care, Cardiology-Coronary artery disese | Tagged , , , , , , , | Leave a Comment »

How to rule out critical left main or proximal LAD disease with near 100% specificity without coronary angiogram ?

July 10, 2011 by dr s venkatesan

Very often in clinical  practice  cardiologists are asked to R/O significant coronary artery disease in asymptomatic persons .This population includes  people with multiple risk factors like diabetes, HT dyslipidemia  and non specific ST/T changes in ECG.

Many of us have lost the confidence of   ruling out CAD   in these population without looking at their  coronary angiogram.

Is it a right way of practicing cardiology ?

What we need to realise is,  we are asked  to rule out any critical lesions that are going to make a impact on these  other wise comfortable patients.  Nothing wrong if you miss a 30% lesion in PDA or OMs or diagonals !

Can we do this without doing coronary angiogram ?

Yes ,  we can .

Step by step  Ask these questions

  1. Ask the patient , if  he /she   can climb three  flight of  stairs  without any difficulty or
  2. Walk briskly for  20 minutes (5km/hr)

If yes , give  a   certificate   that he  has no critical  left main or proximal LAD  disease.

If you do not believe in his words , put him on a tread mill ,  if he crosses   stage  3   Bruce in TMT ( 9 mts)

give the above certificate  “with a frame”  now .

For still suspicious  physicians ,  We have  one more  investigation called  echocardiography !

Echo : The forgotten tool  for screening left main lesion.

Modern day echo machines have a  3mm resolution power (Many have 2mm ) .While ,  we are expected to look for 3mm vegetation to R/O Infective endocarditis , rarely is  a  cardiologist ,  tuned to  look for the left main ostium  in routine echocardiography  which averages 4-5mm is size. (Left main by echo link to another article)

In short axis  view just tilt at the level of pulmonary valves  (Atrio- pulmonary sulcus) one can visualise the left main ostium and the proximal left main emerging from the 4 o clock position. If you are lucky you can see the entire left main.

If nothing satisfies the physician (Or the patient)  ,Refer him for sliced CT scan , catheter coronary angiogram , or a  nuclear Imaging .Be ready for the attendant anxiety, interpretation errors, corporate  pressures , urge to  balloon ,  kick backs etc etc

By the way , how can  one  be happy by ruling out only left main disease ?  Is it not other lesions possible ?

Experience (Not science) has taught us  no  critical coronary obstruction is  possible ,  if  a patient walks for  9 minutes  in treadmill (10METS).

Even if it is there (A remote chance)  there is little documented benefit of any revascularisation procedure.

Counter point ?

Is it not a “crazy idea“  to rely on patients history in ruling out  CAD   in these era , where   angiograms relayed  live  into   cardiologists  ipad  ?

Science has no value if it is not applied  for the patients welfare. Meticulous clinical  examination (And application of mind)  is the foundation stone on which  any medical investigation and therapy  should be based  upon. Most of the inappropriate coronary revascularisation are due to  neglect   of  this vital  component of clinical examination.

(I wonder ,  is it  really possible  these ” acts of omission”   be  deliberate some times  ! )

Final message

Clinical interrogation  may  miss an insignificant  CAD  ,  but it can never miss a critical CAD* .

 

Do not do coronary angiogram routinely to R/O  CAD.

It is not the way cardiology is to be practiced !

If only we apply  those  simple,  time tested concepts in every day practice we not only  save millions of  Rupees ,   but also thousands of futile   diagnostic tests and associated untoward effects can be avoided.

* Senstivity of  ruling out any CAD is about 70% , but it’s capcity to R/O critical CAD approaches 100%.

Reference:

Please refer your own Brain.

Posted in Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions | Tagged , , , , , , , , , , , , | 4 Comments »

How useful is balloon atrial septostomy in refractory pulmonary hypertension ?

July 6, 2011 by dr s venkatesan

Management of  severe  pulmonary hypertension continues to be a difficult task .Medical therapy is not definitive, in-spite of the new prostocyclins, endothelin antagonists and  sildenafil analogues.Natural history  depends mainly on  the presence of  any treatable cause ( Especially ,connective tissue disorders)  ,  supportive management along with anticoagulation.

Ultimate  strategy  would involve a   plan  for a “Lung “or  “Heart -Lung”transplantation  , if feasible. Last decade saw an innovative modality of creating an  artificial inter atrial  shunt to decompress the right heart .This had varied response in the  real world  , still  most  showed some benefit .In fact , in 1998 the world symposium on PHT ,  formulated guidelines for BAS (Balloon atrial septostomy)

Principle of  Balloon atrial septostomy (BAS)  and mechanism of benefit

The symptomatology  of  pulmonary HT  is largely  determined by mean RA pressure .

Puncturing  the  IAS and diverting blood  flow into left atrium would decompress the RA ( or even the RV )  and reduce the Mean RAP.

The resultant  right to left to shunt  can   increase the cardiac output  only  slightly ,  still  good enough to  provide   relief from the fatigue.(Though at the cost of  desaturation.)

What is the risk involved in the BAS.

Procedural risk of  a cath study in a sick  patient with hypertensive lungs (Can be really high !)

In some patients  even a small  fall in systemic  oxygen saturation can be counter productive.

What is the balloon used ?

Mansfield or Tyshak balloons are good choices .

Balloon diameters are between 5 -14 mm

Technique

Involves standard Brockenborough needle /Mullin sheath /Guide wire in pulmonary vein.

Atrial anatomy to  be well  analysed prior to BAS  . (Please note even though it is similar to PTMC , anatomically we encounter a large right atrium rather than left atrium .)

Fluroscopy with  TEE guide optimal

Pulmonary angiogram might help.

Intra-cardiac  Echo may be  ideal.

Blade septostomy may be preferred if hardware is available

The endpoint of procedure

  • Size of ASD > 5mm
  • Fall of arterial saturation < 80 %
  • Sustained atrial fibrillation with hypotension
  • Any  disabling complication

Hemodynamic impact

  • Cardiac output increase by 750 ml to 1 liter
  • It is expected ,  RA  mean pressure  would fall at least 5mmhg from  the baseline value.
  • PA pressure , no significant impact expected.
  • Tricuspid regurgitation regresses.
  • RA,RV size marginal reduction observed.

Follow up and outcome

  1. Greatest  relief is from syncope.
  2. Functional class improvement  in >50% .
  3. One year survival benefit is substantial (75-90%)  .Beats the  natural history (40%) convincingly.
  4. Late deterioration  can occur as ASD gets closed in few.

When  BAS is contraindicated ?

  1. Critical RV failure
  2. Patient in class 4
  3. Mean RA pressure > 20mmhg
  4. Pulmonary vascular resistance index> 55 Wood units / sq.meter

* BAV should not be considered as a  live saving  procedure  in any dying patient with PAH.  It needs to be  selected early and carefully .In fact,  the very high procedural complication  rate is related to late selection of patients.

Natural foramen  PFO better than BAV ?

We do not know yet.It is highly possible  natural opening up of PFO is good thing to happen for patients with severe pulmonary hypertension.

Reference

1 . SS Kothari  et all  Indian heart journal 2002

2. http://content.onlinejacc.org/cgi/reprint/32/2/297.pdf

3. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC484602/pdf/heart00028-0066.pdf

  4. http://erj.ersjournals.com/content/early/2011/02/24/09031936.00072210.abstract

Posted in Cardiology - Clinical, cardiology -congenital heart disease, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology-Land mark studies | Tagged , , , , , , | Leave a Comment »

Why this article is vitally important for all Indian cardiologists?

July 5, 2011 by dr s venkatesan

Tuberculosis is rampant in our country ( of course in any developing country ). Many of the patients who are referred  for cardiac  failure has history of pulmonary  tuberculosis.

In our echo lab we handle  100s of  patients every month from the regional TB sanatorium  . While the clinical presentation  mimics  COPD ,  many of them  have be severe bi-ventricular dysfunction  in echocardiography   and  bulk  of them satisfy the criteria for dilated cardiomyopathy . So what are we missing ? or guessing ?

The following paper  which  finds a  strikingly similar observation  . . .   is important for many reasons

  • It  comes for a prestigious Institute from India (PGIMS Chandigarh)
  • It strongly  suggest the link between DCM and tuberculosis
  • It also tells us both can be completely curable.

We know cardiac failure is a relentlessly progressive disease . We also know ,  certain forms  of DCM are reversible  especially infectious and toxic ones .Whenever we ask  our residents (Bitten by the western bug !)   for causes of reversible cardiomyoapthy  they promptly rattle out exotic conditions  like selenium deficiency and cobalt cardiomyopathy etc ,

  we tend to forget  “a big possibility  of   tuberculosis”  as cause for reversible cardiomyopathy.

  Students are not be blamed ,we have never taught them to think  in Indian  perspective !

Finale

DCM is a biggest  cardiac problem in our country next only to CAD. While our country men suffer , we are perennially happy to  label  them    as  idiopathic DCM   ,  even as   we  continue to  loose our  precious time  every day ,   in  ballooning dubious lesions  in  hi -tech cath labs  and help  fill the corporates coffers !

I entirely agree with the authors ,   DCM due to Tuberculosis  is  a hugely under-recognised entity  in a country with over  12o0 million people. So , youngsters  are  argued to find  answers to this   burning  issue . (* I am afraid how many of us are aware of such  an important  article published from India. )

We propose to under take a study from from Chennai  tuberculosis research center about this. Any body wishing to fund this project ?

How does tuberculosis affect heart muscle ?

Will be posted  soon .

Posted in Cardiology - Clinical, Cardiology-Land mark studies, myocardial disease | Tagged , , , , | 1 Comment »

Can epicardial fat constrict the heart ? . . .An authentic “yes” from Ulsan , Korea !

July 4, 2011 by dr s venkatesan

Constrictive pericarditis is a well known mechanical disorder  of heart that occurs due to the  compression  by thickened pericardium .Constrictive pericarditis is  the classical cause for  severe diastolic dysfunction.

We know , lungs are   prone for restrictive disorders due to chest wall , skeletal  disorders. Does the heart get mechanically restricted in extreme obesity ?

Not really , one may reason out . Chest wall fat can have little effect on cardiac function but when excess fat accumulates within the layers of heart , it is indeed possible for  the  fatty layer to impede mechanical filling of heart. This may be considered rare as of now , but many times it is not recognised ,  as most of the dyspnea in morbid obesity is attributed to some other known factors.

Dyspnea in obestity  can  due to

  • Pulmonary hypoventilation
  • Increased  MVO2 due to elevated cardiac mass
  • Diastolic dysfunction of  LV/RV
  • Increased demand  due to  excess BMI.

Image courtesey : http://www.onlinejacc.org

Now, we have evidence for  altered RV hemodynamics due to compressing effect  of epicardial fat pad. It may be due to   simple mechanical effect  of epicardial  fat over the distensiblity of RV or occasionally  LV. (The distribution of epicardial fat is mainly over the right ventricle or septal areas.)

This   paper  from Korean circulatory journal  succinctly describes this new possibility .

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2771803/pdf/kcj-39-116.pdf

Final message

Bed side cardiology  continues to  bring surprises  , it  never fails to fascinate us   !

Heart  is  a dynamic organ ,  has a potential to get restricted by  any  layer that  surrounds  it. Constriction by pericardium got huge attention so far .We need to realise , the epicardium which is  a part of pericardium has a variable fat depot  . It  can take a different avatar  in an occasional obese individual  and   exert  important hemodynamic impact.

Excess fat is excess load on heart . . .  we have  to unload it

It is possible , sucking out the  epicardial  fat in morbid obesity can bring important relief to  those patients with unexplained dyspnea . We  need to  explore this possibility.

Posted in Cardiology - Clinical, Cardiology-Land mark studies, Hemodynamics, Infrequently asked questions in cardiology (iFAQs), pericardial disease | Tagged , , | Leave a Comment »

Is that a knot in the left internal mamary artey ?

July 3, 2011 by dr s venkatesan

LIMA is a critical conduit for CABG.It  is  the most suitable vessel for  CABG for various reasons.(Radial artery falls far short of expectations  due to anatomical and histological , physiological  reasons !)

Anatomical variations , kinks and bends , loops are more common in LIMA  than we recognise.This may not have major implication but  can be threat to it’s  hemodynamic superiority  .

This man who had a two loops in LIMA and the one above almost tied a knot .(Please note it is an end on view of a loop that mimic a knot )

Can a surgeon un-do the loop before grafting ?

It may be possible in the distal ends where the LIMA is dissected out. I dont think it would be possible high up.

Surgeons should answer this . . .

Posted in cardiac surgery | Tagged , , , , , | Leave a Comment »

Stock market fluctuations as triggers for acute myocardial infarction !

July 3, 2011 by dr s venkatesan

Myocardial infarction is the self-inflicted ,  modern-day death sentence  especially  among the  young generation who are   addicted to the affluent life style .

We know the  cardio vascular events  are  precipitated  due to a  sudden trigger in those  people  who have a base line risk profile. The major  risk factors are ,

  • Diabetes
  • Smoking
  • Hyperlipidemia
  • Hyper tension
  • Obesity

When one or more of the above factors   progress unabated he or she is at high risk for acute coronary event .

Is that a fatal stock market rhythm !

A loaded gun  needs a trigger to fire  , similarly  in a vulnerable patient (Plaque )  any of the following can act as a  trigger to precipitate an MI.

  • Hemodynamic stress (Fall or raise of BP )
  • Any  systemic illness( fever etc)
  • Physical stress
  • Mental stress , any strong surge of  emotion (Negative or positive)*
  • Non cardiac surgery

*Anger, fear , euphoria , guilt , bereavement ,

Now there is evidence pouring in  ,   natural calamities (  perceived fear of death) can  act as trigger  for MI.

We have reports  of  excess cardiac events   following  . . .

  • Earth quakes
  • Terrorist attacks
  • Flight scares

Any events which can release  sudden pulse of adrenaline into the plaques can trigger an acute coronary event.

Now,  this study from Shangai ,  documents how the coronary events dance to the tunes of stock market movements in the financial capital of  China .

http://eurheartj.oxfordjournals.org/content/32/8/1006.abstract

Final message

Chaos theory states no two events are isolated in this world  !   When stock market swings it can  pull down your heart too .

be cautious !

Posted in Cardiology - Clinical, cardiology -congenital heart disease, cardiology -Therapeutics, Cardiology -unresolved questions | Tagged , , , , | Leave a Comment »

What is the link between Migraine and PFO ?

June 27, 2011 by dr s venkatesan

The link between migraine and PFO is  . . .

  1. Incidental  & man-made
  2. Almost certain
  3. Definite
  4. A wild imagination

Answer : One of the above  is correct  , but  we do not know  which one is   !

There has been many  patients with TIAs , cryptogenic strokes , who  had  documented PFO  ,complain of prolonged  head aches . This was the beginning of suspicion of PFO as a cause for migraine .Then the device industry foresaw a huge opportunity . Things began to unfold and  the concept is currently as nebulous as it can be .

Mechanism of migraine in PFO

(All are  presumptions )

  • Right to left shunting of  vasoactive amines from venous circulation (Serrotonin)   which bye- passes  the lung where they are supposed to get filtered.
  • Venous micro emboli (Antiplatelet agents reduce migraine as well as TIA ! )
  • Hypoxia transient – cerebro vascular hypersensitivity
  • Atrial naturetic  peptide spills more into systemic circulation through  PFO

Counter arguments

  • If right to left shunting is causing the migraine , why it  is not fully disappearing even after closure of  PFO (MIST data with  starflex  device ,  migraine persisted in a significant chunk !)
  • What is the incidence of migraine in the  prototype  right to left to shunt situations like TOF, Eisenmenger , pulmonary AV fistula ?  if shunting is the mechanism , logically  migraine incidence  should be very high  in this population , but it is not .
  • Migraine occurs in 10 % of population, PFO  is present in 20%  .  What are  the chances of over lap ?  It could be the simple statistics at play !

Where is the evidence  ?  The mystery called MIST study.

This study , done in UK generated more controversy , which  it was supposed to remove  . Still  this  study is considered to be a major evidence for the link between PFO and migraine . Star flex device  was promoted by NMT medical Boston .

http://www.medscape.com/viewarticle/541260

Link to  best review article on PFO

http://chestjournal.chestpubs.org/content/130/3/896.full.pdf+html

Final message

The link between migraine and PFO can be a fact or myth depending upon our belief in current  methods of  research in  science. The issue is  debatable . Of course ,  one issue is probably  closed  forever  , even  if they  are  linked casually (or seriously )  device closure can  never be a  sensible treatment  option for migraine ! *

We  expect a  proof / disproof  in this   mysterious migraine -PFO  hypothesis very  shortly.  Of course , many  cardiologists  already  have their  own conclusions !

 

*Please note , PFO  device closure  for  stroke in young is a different story

Posted in cardiology -congenital heart disease, cardiology -Therapeutics, Cardiology -unresolved questions, cardiology congenital heart disese, cardiology-Anatomy, Infrequently asked questions in cardiology (iFAQs) | Tagged , , , , | 1 Comment »

When HCM involves LV apex exclusively . . . nothing much to worry !

June 26, 2011 by dr s venkatesan

HCM is due to  hereditary mutation of myocyte sarcomere .The molecular defects are  located  in  myosin, tropomyosin, titin .Depending upon the protein  involved the hypertrophy can be regional or localised.

Non obstructive types most often involve tropomyocin mutations. Obstructive types predominate with myosin mutations.

HCM types

Non obstructive

  • Simple ASH
  • Apical HCM

Obstructive

  • LVOT
  • Mid ventricular

When the hypertrophy is in the LV apex there is little hemodynamic consequence

Apical HCM can still be prognostically and practically  important even though there is no  hemodynamic impact.

  • Arrhythmic risk persist(Any focal hypertrophy can be substrate for reentry due to slow conduction)
  • More  importantly  apical HCM is the commonest myocardial condition mistaken  for unstable angina  and they wrongly enter the ACS protocol and might land up in cath lab tables as well !

Always remember  high voltage qrs with deep T wave inversion (90 out of 100 times)  is due to  myocardial pathology not ischemic.

Management

  • Reassurance (First advice is,  not to search for more information from the internet ! It may confuse them !  )
  • Just follow up with yearly echocardiogram .Follow up the siblings too.
  • Marriage counseling . (Not contraindicated )
  • Holter monitoring or  extended loop recording may be done to  detect any sub-clinical of arrhythmias.
  • Beta blockers are generally not indicated  routinely  may be given if family history of sudden death .

Reference

http://emedicine.medscape.com/article/152913-overview

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What is the direction of blood flow across patent foramen ovale(PFO ) in otherwise normal adults ?

June 26, 2011 by dr s venkatesan

  1. Left to right
  2. Right to left
  3. Can be in both directions
  4. No significant flow at all !

Answer :   Every response can be correct

The patent foramen ovale is a physiological orifice , which  becomes  pathological if persist into  adult hood .The incidence is estimated to be about 20 %  of the population (Amounts to 100 crore PFOs roaming  in our planet!). It makes  no sense  to  believe  just spotting  a  PFO  in routine echocardiography be termed  as pathological . But recently  (Adding much to  interventionist’s  delight ! ) the presence of which is being linked with migraine and stroke in young.

The size of the orifice can be from a single millimeter to one centimeter* . The direction of blood flow in PFO   is determined by the mean gradient across the orifice. It has to be  left to right  as the LA pressure is  generally   higher by few mm mercury  ,hence there is a small  tide of flow entering into RA with each left atrial filling or contractile wave .(v and a ). This  quantum is miniscule and has no hemodynamic significance in most life situations.

* Some call( Wrongly ) 1cm PFO  as small ASD.

When can Right to left to flow occur ?

When the right atrial pressure increase more than LA pressure it is obvious  blood can enter LA . It is well-known this occurs  in any pathological situations like RVOT obstruction severe PHT , tricuspid valve obstructions etc.

Physiological  Right to Left flow :

Forced expiration (Valsalva) can cause transient  right to left flow. This  may happen in many real life situations like straining, heavy isometric exercise, blowers, muscians  etc.

Which is clinically  significant ?

Left to right or right to left  ?

Left to right shunting is rarely an issue as there is no systemic  desaturation.

Right to left  shunting  can be  important for two reasons

  1. Arterial desaturation( transient )
  2. Shifting of venous debris into arterial side  can result  in potential paradoxical embolism .(This can be air, clot fat , amniotic fluid etc)  This is the reason stroke in young is closely linked to presence of PFO.

PFOs during positive pressure ventilation

PEEP is a classical example where a right atrial positive pressure ,  shunts the blood in pulsatile manner into left atrium .

Platyponea  hypoxia  syndrome .

This is  postural right to left shunting  across PFO .It  is a less recognised (but a common entity) where -in ,  when the patient  lies down there is a  right to left PFO shunt and transient hypoxia .This is often corrected as the patient sits up. The reason being  the valve of PFO , the   door like flap  which guards  the orifice  ,  is aligned   in such a fashion , it  opens up in a  lying posture(Aided by gravity ?)  , shuts down in  sitting posture .It should be noted  The PFO valve is not a constant feature  . The size  of this valve , the stiffness , the hinge points , ability to  float  are highly variable .Hence the clinical variation in PFO syndrome.

The IAS septal aneurysm is an  important variation where the valve of PFO balloons out into left atrium  may become a nidus for thrombus or a focus for atrial arrhythmias .

Stroke in young  and PFO  :This  topic  deserves a separate article

Reference

Anatomy

Excellent PFO images from Yale university library  ( http://www.yale.edu/imaging/chd/e_pfo/index.html)

 

http://chestjournal.chestpubs.org/content/100/4/1157.full.pdf+html

http://chestjournal.chestpubs.org/content/118/3/871.long

http://www.anesthesia-analgesia.org/content/93/5/1137.full.pdf

Excellent PFO images from Yale university library

Posted in Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology -Therapeutics, cardiology-Anatomy | Tagged , , , , , , , , | 1 Comment »

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