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Patent foramen ovale (PFO) is the new generation hole in the heart for  21st century  cardiologist. Present in about 20% of population  , would correspond to 140 crore  “man holes”  as  on  2012   in this planet. PFOs are embryological remnants across the inter atrial septum.

These minute  holes measuring few mm  are largely a  benign finding .In the recent  decades , it is being increasingly debated these holes  may  not  be innocent after all .Extensive  use of echocardiography in recent times   has contributed to  the awareness  as well as anxiety.

Evidence  is mounting  linking PFO to

  • Migraine,
  • Stroke and
  • Peripheral embolism.

While the above   observation may be true  ,  the  fact that >100 crore people have this entity   , raises  a serious question ,  as labeling  all of  them as heart disease will create chaos among the already health obsessed   population .

So , the main purpose should be ,  to identify the high risk subsets* of PFO population .(This will be a <5 %  at the most). People with PFO may  carry  a mental  stigma because it is referred to as a hole in  the heart by the  general  public .For many  the sense of living with a hole in heart is often more damaging than the hole itself ! (Incidentally , many develop  migraine only after reporting about this hole !)In a strict sense  PFO  is not a hole , rather  it is a communication it may be tunnel  or  slit like .It is argued physician should avoid calling PFO as a hole .

*What is a significant PFO ?

  • Large PFOs >5mm
  • PFOs that shunt blood
  • PFOs with septal aneurysms
  • PFOs with documented stroke or embolism
  • PFOs with atrial chiary network
  • PFO in  persons with systemic pro-coagulant states (Except probably in  pregnancy )

Final message 

PFO is a common residual congenital  atrial septal  anomaly . Usually  benign  . One can  live with it perfect harmony. Only occasional patients  are  at risk.

So the prime job of cardiologists is to not diagnose and create panic about  this entity. rather reassure  them (Is it better do not reveal to them if it is found incidentally ? Patient empowerment group would call  this a  foul !  I do not support blind empowerment  )

At the same time our main  aim is to identify the  high  risk subsets who are prone for events.

Closure of   PFO with device is required in a fraction . (*By the way ,  if   PFO is really dangerous ,  why It is never an indication for surgical closure ?  )

Reference

Your  search for best information  on PFO  would end here .  Here is  land mark   article  in JACC  by  Hara   also contributed by  Renu Virmani . A US  Japan  combines initiative  : A must read by every cardiologists

http://content.onlinejacc.org/cgi/reprint/46/9/1768.pdf

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

Hypertrophic cardiomyopathy(HOCM)  is a relatively common inherited myocardial disease.Since it predominately involves  LV myocardium and we know LV muscle mass is an integral part of  mitral valve apparatus , it is natural HOCM  has a major  impact on   mitral valve function .

The mechanism  of MR in HOCM is attributed to the following .

  • Asymmetric septal hypertrophy (ASH ) related abnormal pap muscle alignment (Geometric distortion  )
  • Exaggerated SAM(AML  is attracted towards LVOT with every systole that tend to  keep the mitral  valve  unguarded and MR results)*
  • Intrinsic abnormalities of mitral valve.
  • Associated MVPS
  • VPDs and Non-sustained VT can result in transient MR
  •  Pacemaker mediated MR (DDD pacemaker was used to induce desynchrony of LVOT vs LV free wall .This  concept  is almost a failed  one now !)
  • End stage HOCM -Left ventricular dilatation

* This mechanism is considered less important ,  as SAM is almost universal in HOCM  but MR occurs in less than 20%  patients with HOCM.

Eccentric MR vs central MR

In HOCM the MR is more often eccentric .This is understandable as the primary mechanism is related to faulty angle of pap ,muscle vs leaflet attachment.

If SAM is primary mechanism jet is directed posterior.

Murmur of MR in  HOCM

Is rarely pansytolic as the mechanism of MR begins to operate well after the systole starts .

Many times it is difficult to differentiate LVOT murmur from MR murmur . Th ever confusing and tentative  maneuvers might help in few shrewd cardiologists.

Issues  during echocardiogram

Very often MR jets are mistaken for LVOT gradient.Ideally two gradients in isolation (or  overlapping each other)  one bell shaped other dagger shaped must be documented.

Please note : LVOT jet is different from MR jet in size, shape, timing and site of maximum signal . Still it is often be confused with one other. Most common reason for this is technical .A careful apical 4 chamber view with well opened LVOT will reduce the error . Never record a HOCM echo without ECG gating . The MR jet may be very trivial in color flow but doppler will still pick the signal well . Realise ,for hemodyanmic reasons MR jet must be always more than LVOT jet.Finally if you get a report a LVOT gradient > 100mmhg in HOCM suspect it to be MR ! More often your suspicion will prove to be right !

Can mitral regurgitation occur in non obstructive HCM ?

Yes , in few . This is due to intrinsic abnormalities of mitral valve .

What happens to MR with surgical correction ? Can medical management  regress the MR ?

It is expected to regress.But many patients don’t. Effect of beta blockers   on MR severity is not studied well.

Management

  • Most cases of MR  do not require specific intervention.Just reassure them.
  • Correction of LVOT obstruction is expected to relieve MR considerably.
  • Intensive beta blocker or calcium blocker can regress the MR.(Negative inotropy)
  • Mitral valve repair may be necessary in few  with re-engineering of pap and chordae .
  • Mitral valve replacement should be a last resort. It  may be highly tempting  .But restraint is warranted. Much  damage has been done by showing undue haste in replacing mitral valve in HOCM

Final message

It needs to be realized whatever we do  for the HOCM patients , the ultimate outcome is determined by the quantum myocardial disarray  the patient has inherited from their parents.The myectomy , the alcohol ablation, mitral valve repair,  DDD pacing , beta blockers all are palliative. Except a few  , most HOCM patients generally live their natural history .

Atherosclerosis is an  inflammatory and degenerative disease of blood vessel.The common  belief is  (Of course , it is a fact ) it  mainly causes vascular obstruction and compromise vital organ function(heart, Brain, Kidney etc)

Here is a different facet of atherosclerosis , A middle aged man  surprised us with this  coronary angiogram .   Instead of obstructing the flow the  coronary vessel begins to dilate. This is due to a medial weakness .(The media for some reason begins to give way rather than proliferate to the atherogenic  stimuli.)

Same patient's RCA

One may wonder why he underwent CAG when obstruction is least expected in such a vessel   !  It was paradox of sorts , this man  in spite of his  wide bore coronary artery ,   was prone for coronary thrombus and one such episode landed him in our CCU . ( Please note both faces of atherosclerosis “obstructive and dilatory” can manifest in the same  vessel in different combination.)

This angiogram may be reported  as any one of the following

  • Diffuse atherosclerosis
  • Diffuse atherosclerosis with focal dilatation  and aneurysm formation
  • Coronary  ectasia

These patients should get life long  medium  intensity  (INR 2-2.5) oral  anti coagulants  for preventing coronary thrombosis.

Watch out for similar aneurysmal changes elsewhere (Renal, Cerebral, Aorta etc )

Counter point

How are so sure it is is due to atherosclerosis ?  Can it be a  congenital coronary medial weakness ?

Your guess is not my guess . . . My vote is for atherosclerosis .

In this politically and scientifically  uncertain world nothing is  in black and white. How can you  expect  EST to behave differently ?

Even as  we  are fully  aware of the  limitations  of EST  ,  it  does not make sense   to categorize  EST result into either positive or negative .

In fact , our  estimate suggests  a significant bulk of the patient would fall in the grey zone  .

It is referred  in various terms by  the reporters of EST .

  • Borderline positive
  • Mildly positive
  • Equivocal
  • Inconclusive

What does all these terms mean to the patient ?

It mans only one thing . . .

Physician  who reports  the  EST    is unable to  conclude whether  his patient has  significant  CAD  or not . It is a dignified way of  expressing  the  limitations .

Many factors may play a role. (See the illustration above )

  • Patient factors : Poor exercise stress levels and conditioning
  • Lesion factors:  Collateralised CAD, treated CAD  can result in partial or mild  changes.
  • Machine factors :Caliberation errors.
  • Interpreter : (Physician ) factors

Error in measurement of ST segment . What is borderline  for  one doctor may indeed be true positive  for the other and vice versa .

How will be the  EST in  a  revascularised  or  medically treated CAD ?

If revascularization is a complete success ,  stress test  would  revert back to normal or it can be a borderline as we have just mentioned.

To our  surprise ,  it may  remain  positive in spite of apparently successful procedure.(Residual wall motion defects , scar mediated  ?)

How to proceed  after this borderline EST/TMT ?

Few options are available for the physician/patient

Talk  with the patient again  , assess the  baseline risk  of CAD   if it is low ignore the TMT result and reassure.

  • Repeat  stress test after  a month.
  • Stress thallium
  • Doubutamine  stress
  • CT angiogram
  • Regular Cath  angiogram* (May be the best , of course it also carries a  risk of labeling  the condition as  mild  CAD / non critical CAD etc )

For the  patient  the  easiest  option  may be ,   self  referral to a different cardiologist .   (Also called second opinion )

Final message

There is indeed an entity called   borderline  EST  . Do not dare to  ignore it  or else  face the consequences .

Read  related articles in this site .

1.Can medical management convert EST positive to negative ?

2. Should every one with positive EST should undergo CAG ?

Atherosclerosis follows a general hemodynamic  rule.

It has a predilection for medium and small  sized vessels and love to  home in  on the  branch points .

We know coronary  artery disease  mainly involve the proximal tree. We get occasional patient  with mid or distal CAD.

This again ,  in  combination with atleast one  proximal  lesion. Decision making  is easy if there is critical proximal lesion.

Here is a patient who has isolated  critical distal CAD . He created a heated debate in our cath meet

His LV function  was normal , He had TMT  borderline  positive , but no angina ,

What has to be done for him ?

A fellow suggested  a thallium

It was countered by other  ,  we can take it as granted   there is  cold spot in  thallium in a small  posterior segment , then how will you proceed ?

  • PCI, medical , CABG ?
  • CABG definitely  not ,
  • PCI  . . . may be . . .Medical  may be !

When you are confused about  the choice and outcome  . . .confuse the patient* as well ! And , let him decide after a mini  , (but exhaustive ) lecture on coronary blood flow , risk of heart attacks etc .

So in this modern  era of pseudo   empowerment , it is ironical  patients will prevail over doctors after learning   half or quarter  truths  from their android powered smart phones and i pads  !

By the way finally  what  was decided ?

The patient and overwhelming majority voted for a drug eluting stent for  the OM lesion event  as  it appears technically a bifurcation lesion ! This is how cardiology is practiced.

Reference:

Isolated distal coronary artery disease. Presented in cardiological society of  India meet 2005

A clarification .

** One  definition for “confusion” is  being in a  “unclear”  state of mind !

**The aim of this blog is never to confuse the patient. The  above statement is necessary because many patients do believe(or rather want to)  they  understand every thing about their illness even as doctors are baffling with the  great uncertainties and intricacies of  most medical conditions.

Can medical management convert TMT positive into negative ?

There are innumerable  stresses  to human beings in daily life .

Heart  experiences a few  either directly or indirectly.

  1. Physical stress
  2. Pharmacological  stress
  3. Mechanical stress
  4. Hemodynamic stress
  5. Mental stress

Squatting is rarely realised as a form of physical   stress to heart .  Rather , squatting can also  be termed as a  good exercise  ( Western toilets sans it !)

Squatting  raises the afterload at the level of aorta due to  increments  in SVR (exact mechanism not clear ,neural reflex ?)  and temporary reduction in venous return.

After load raise is synonymous with increased  ventricular wall stress  . So,  it is logical to expect wall motion defect in  vulnerable hearts* when confronted with sudden increase in afterload .(*Ischemic hearts with delicate coronary blood flow ) .Hence ,  sudden squatting , a seemingly simple  maneuver   ,  can  unmask  silent CAD .It can be aptly be named as poor man’s stress echo.

Of course , it  doesn’t   mean in any way ,  it should not be used in rich ! The  purpose of science  is  to make things simpler and cheaper . If squatting can replace  dobutamine with fair degree of accuracy  atleast in a few ,  it can help  control the escalating  costs of  cardiology triaging   due to   many futile diagnostics !

http://content.onlinejacc.org/cgi/reprint/46/5/931.pdf

When squatting  is a stress in normal persons , paradoxically it gives relief to patients with cyanotic heart disease

Read the related articles in this  site .

How squatting relieves hypoxia in TOF ?

Squat Echocardiography in TOF

Ventricular  fibrillation is the most dreaded cardiac  arrhythmia  during  STEMI .If  it occurs  outside the hospital , it is usually a  farewell arrhythmia to most  patients . If it occurs within CCU , it is a well tackled arrhythmia  and has  little impact on long term mortality.

When it occurs in early hours of STEMI it is referred  to as primary VF.

Even though it is a killer arrhythmia ,   primary VF is  often  an  one time re- perfusion arrhythmia. There is no entity called recurrent primary VF  .

If recurrent VF occurs some other mechanism is to be suspected (Drug, hypoxia, scar, ion channel defect etc)

Mechanism

Primary VF is ischemia triggered and secondary  VF is  infarct area triggered .Hypoxia ,  LVF or old  scars  also could  contribute .

How to terminate primary VF ?

Immediate defibrillation  is the only option.

After a successful reversion of VF should we follow it up with anti arrhythmic drugs routinely ?

No . It is not routine.(This is  what  we are debating today !)

What if ,  multiple VPDs  and  non sustained VT  continue to occur in the ensuing hours after an episode of   primary VF ?

It is indeed  appropriate ,   to use an infusion of Amiodarone or lignocaine  in such situation . Following  it with oral Amiodarone is generally not required if the LV function is well-preserved.

Advantage and disadvantages of Amiodarone

  • Pro arrhythmia – A undermined issue.
  • Myocardial depressive action of Amiodarone is a deterrent  for its routine use.
  • Amiodarone induced bradycardia (If it is not a AV block )  may be an  advantage  as MVO2  may be reduced.

By the  way , Lignocaine  how  does it fare vis-a-vis Amiodarone ?

It is equally a good drug  with less side effects .But  the  ALIVE  study delivered a  death knock for this wonder drug. Many (At-least me !)   would still   believe  the unpopularity of    Lignocaine  among the    current generation   cardiologists   is  not due to   academic reasons .

So what is the final message  ?

  • Even though  popular  opinion and ( even some guidelines )  suggest  it may not be  necessary to give anti arrhythmic drugs  after successful reversion of primary  VF . It is prudent  to weigh  the risks. We can’t use it as  a routine .
  • Still , it is always   wiser to prevent further episodes of VF (Rare though ) .
  • If you have a well  performing   CCU , routine  post shock Amiodarone is not advised .
  • If you do not trust your CCU staff  one may  have to rely on  these drugs.
  •  Patients with complicated MI ,  high risk VPDs ( Akin to after shocks after an earth quake ! ) especially in large anterior MIs should receive intensive anti-arrhythmic  therapy (IV followed by oral )

Please note 

**Never plan  for an ICD in patient’s with primary  VF it is an absolute  contraindication.

***Recurrent VT/VF in the setting of STEMI  is  often  termed as electrical storm .It is a rare event which will require immediate CABG/PCI with VT ablation. Again ICDs are  contraindicated  here as the battery depletion will be fast .Further ICDs  it does not cure the VT rather it allows it to emerge from within and then try to tackle it,    while RF ablation eliminates VT focus and prevents it,s origin and provide a potential cure. But , remember only 20%  of VT are amenable for RF ablation ,  while ICD counters all VTs wherever it originates . So there is a role for combination of ablation and then putting an  ICD .

This seemingly straight forward question is often asked in cardiology boards.

The answer to this question is  important in the bedside as well ! Ironically ,  with  sophisticated  diagnostic modalities the complexities  has  also multiplied .

The following table attempts to simplify it. ( Mostly written with a personal knowledge and ignorance !)

Please click on the table to visualise a high resolution  image.

                                                                                 Image courtesey : Jupeter Images

This  is because  . . .

  1. Doctors live in a  false life of pseudo- perfectionism . “I can never err”  attitude .
  2. Ego !  Their  pride at stake !
  3. Accepting a mistake would affect their further client-age
  4. Feels humiliated  among their colleagues and peers
  5. We are ready to accept  our mistakes in public  but the society  is  not  yet ready to forgive  us . So we hide !

Answer

Though  all the above  contributes for this behavior . It is the  response 2   that plays havoc on patient care !

Discussion

It is a well-known fact millions of medical  mistakes happen every  year  across the globe .Most of them are  committed  by  medical professionals and equal number of them result from untoward  effects of   drugs,     complications  of procedures and  surgeries.

Apart  from  these ,  laboratory errors in   reporting  and interpreting  diagnostic tests   happen  on hour to hour basis in any hospital . Many of them could  have  serious  implication  in patient outcome .   Though doctors  do  periodic auditing the  incidence continue to  galore  and there is very little data  to suggest  the overall  incidence has reduced  in any  significant fashion .

In many sense doctors  do share  some similarities   with  drugs and devices  . Like the ubiquitous  drugs  and devices , diagnostic tests, ,  doctors too cause side effects  by their action or inaction . It  is referred to as ,  undesired  response, complications, error in judgement , negligence , ignorance  etc ( Read a related article in my site)

Like the famous quote of  ( Osler I think )

A drug  which  causes  no side effect will not have the desired effect as well  . . .  a doctor  who has not  caused any injury to their   patients   can  never be  considered as  an  accomplished  doctor !

Drugs like  statin which is supposed to reduce cholesterol  in blood  misbehaves  with  liver and can even result in fatality .We accept it .The matter ends  with a   FDA box   warning .

If a ventilator crashes due to a soft ware problem ,  we accept it . We can boldly admit medical  errors  if it is a  fault of a drug or machine.  But , errors by doctors are rarely pardoned ! So it is natural they are  swept under the carpet.

When  doctors do  delicate  cardiac surgeries ,  it takes only  a  fractional  loss of concentration   to cut  the aorta and that could cause serious after effects .

These can be called as errors, mistakes or  negligence in whichever way you like to call it. The problem is ,  these minor events  (Which   occur in thousands every day ) are not recorded,  logged , or disseminated  to our patients . Even medical law makers and judiciary is blinded to most of thing that happen inside the medical institutions.

So , the world will never  know the reality .When we want transparency in all walks of life ,   we should at least  fight for  a minimum  transparency  from doctors.(Why cant  they conduct the   customary internal auditory meeting in the public domain !)

If only doctors admit their mistakes with courage medical  profession will get more respect .Living behind  veils never  liberates . This  traditional suppression of    facts  make  the  medical  professionals   high risk for guilt when  truths unfolds .There is one  Tamil proverb which says  A half  doctor  is the one who has  killed  at-least   1000 patients . Still ,  a  minuscule of doctors  are ready to accept their mistakes   .(Especially  to their patients and their relatives  , though they admit in private !)

Final message

  • Implementing transparent medical care , right to information , informed  consent  etc all  demand  honesty. To be precise  . . . extreme honesty ! Ego and honesty are rare companions .
  • How many times we blame it on the disease  and  hide behind the technicalities   for our mistakes and errors.
  • Can  any doctor accept  an  error that occurs  during a surgery or a procedure that  causes  death and  request a  pardon  from patient’s relatives .  I  suspect ,  if there is  such a breed among  doctors   . . . I am sure  he will be branded as  a lunatic by their colleagues !

Coming soon

  • Consequence of  doctors  not accepting errors  !
  • Errors in medical data base and literature.
  • Imperfect  science . Another important aspect of medical error is attributible  to the  vagaries of  science itself. What looks as a perfect modality suddenly becomes  , not only  obsolete but also dangerous . If  a surgeon does a  gastro jejenostomy for  acid peptic disease today ,  his  license  is at risk of  being clipped ,   the same  surgery was a  privilege few decades ago. This aspect  deserves  special debate .
  • LVH is classically diagnosed with high qrs voltage either in limb or chest leads or both.
  • High voltage is a specific ECG  sign,   presence  of  which  would strongly suggest LVH  ,   absence of which  is not  useful to rule out true LVH.
  • LVH with   flattish  or  down sloping   ST segment ,  with or without  T inversion  , can be a sole presentation of LVH . This should not be taken as sign of ischemia.  Here is  patient  with such an  ECG

Mechanism for LVH without high voltage

  • Intrinsic muscle  electrophysiological  property – Arrangement of muscle fibre orientation  will determine the voltage .(Parallel vs perpendicular, disarray etc)
  • Pathological LVH with fibrotic process and interstitial hypertrophy may not  record high voltage.
  • Presence of  high voltage LVH  would indicate a dominant physiological muscle mass that lacks interstitial reaction.
  • Finally , technical cause like thick chest wall in obese can dampen the LVH voltage.

Read a related  topic in this blog

https://drsvenkatesan.wordpress.com/2010/07/21/why-lvh-generates-high-voltage-qrs-in-some-and-low-voltage-qrs-or-even-q-waves-in-others/