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Archive for August, 2011

During primary PCI , when you encounter severe multivessel disease what will you do ?

Posted in cardiac surgery, Cardiology - Clinical, cardiology -ECG, Cardiology -Interventional -PCI, cardiology -Therapeutics, cardiology- coronary care, Cardiology-Coronary artery disese, tagged , , , , , on August 15, 2011| Leave a Comment »

Surprisingly it is common !

A .Abandon the procedure call the surgeon for an emergency CABG

B. Open the most critical lesion.*

C.Attempt to open and stent all possible lesions.

D.Send the patient back to CCU for a conventional  thrombolysis or attempt a intracoronary thrombolysis.

Answer : All  can be a right response depending upon the available expertise ,  time window, associated complication and hemodynamic stability etc .

* Please note ,the most tight lesion may not be the culprit artery. Though there is high chance for that  being the culprit , it  can be very deceiving   especially when  there is multi-vessel  CAD with  chaotic collaterals.

The site of lesion and site of infarct can unimaginably remote.  (A traffic snarl at remote flyover  can have its impact  right on the busy commercial street due to diversions ! ).

What will happen if you open  a non culprit artery first mistaking it for a culprit ?

This could lead to  dangerous turn of events as whatever little perfusion the patient was getting through the ill-fated  IRA will be challenged by the fresh diversion  facilitated by non IRA angioplasty. Extreme caution is required.

Emergency CABG  within 3 hours  of MI even though advocated  by few ,  is still considered a risky  way to reperfuse  the heart.(In India  there  is  nothing called primary CABG!)

An energetic interventional  cardiologist would vouch for opening all lesions . Only thing  , he has  to  make sure is  , the patient also has enough energy to withstand  his  onslaught. Never   non culprit lesion if a patient is stable . 0ur aim is not that.If the patient  is in shock or impending LVF one can justify opening  few more lesions  that improve total muscle function which can be vital.

What about fall back on thrombolysis?

This may be seen a defeatist attitude ,  but  when the aim is  in the  well being of patient ,  there is no defeat or success. If severe  CAD is encountered and both  CABG / PCI  or not an option,  the cardiologist need not feel guilty or  humiliated to refer him back for thrombolysis. (Of course , Intracoronary thrombolysis  is  an option !)

Final message

Primary  PCI  is often made  to  appear ” As  a  kids play”  by many modern  day cardiologists . It is not so.  It requires a team effort. It is  race against time.   Feasibility depends largely on the coronary anatomy. The failure rate of  primary  PCI is often camouflaged .(Currently Success of pPCI is boasted at 95%)   Logically it should include pPCI ineligible anatomy as well . Many still do not understand the real purpose of pPCI.   The aim is to salvage the myocardium  at risk , sure and fast. Never attempt for total revascularisation in an emergency situation however tempting it is !

In young persons with discrete single vessel disease  the procedure is simple and outcome is straight forward. In elderly , diabetic , STEMI on  preexisting CAD,  diffuse  multivessel disease  ,   complex main left,  bifurcation lesions , one requires  lot of brain sense  to provide optimal outcome . Many times that sense includes abandoning the procedure !

Please read a related article in this site  Primary CABG

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A classical ECG of “Dead sinus node” and a “Sick AV node” !

Posted in Cardiology - Clinical, cardiology -ECG, cardiology -Therapeutics, Cardiology-Arrhythmias, tagged , , , , on August 14, 2011| Leave a Comment »

A man  in his 40s presented with an episode of syncope and followed by recurrent episodes of near syncope.

His ECG showed (See image)

  • ECG shows absolutely no evidence of sinus activity . That is  sinus arrest.
  • He lives by the mercy of his AV node.(“Great  escape” junctional rhythm  ! ) . Please note ,  It  fires at less than its intrinsic rate indicating AV nodal sickness as well.
  • The Heart rate is around 18/mt.

SA node is dead(Sinus arrest ) as evidenced by absent p waves. AV node is sick(Depressed) because the junctional rate is less than 20 /mt.

At what  heart rate a person  would develop syncope and near syncope ?

There is no fixed cut off rate for  syncope. It all depends upon the baseline LV function, his exercise capacity, vascular tone etc.

Most will develop some symptoms at  a heart rate less than  40/mt .

Dizziness occur and 30, syncope is sure  when hear rate  dwindles  less than 20 /mt.

A heart rate of 10-15 circulation tends to stall. But still few men are found alive at this rate.

What is the  risk of this patient dying suddenly ?

Contrary to the expectation SCD is not common in  isolated sinus node dysfunction .

It is more common with AV block. The reason being as long as the AV node is fine it will support the rhythm at least at about 30 or s0.

The cause of death in SND is extreme bradycardia induced phase dependent VT /VF.

Will you do a  EP study for him  ?

No. He  does not require it. He is symptomatic ,  and his  ECG shows  tell- tale evidence for SND with AV node depression.

So the there is not even the  necessity to assess  AV nodal status. But .one should  be aware  , there is a battery of tests for SND evaluation (SNRT, cSNRT SACT, etc*) .These are  done only when diagnosis is in doubt or for an academic purpose in teaching hospital.

What pacemaker will you use ?

  • DDDR
  • AAIR
  • VVIR

AAIR can not be used as we have evidence for AV nodal  slowing .

DDDR may be ideal.  In India we still  use VVI mode extensively . Ventricular pacing always safe when you have no EP facilities.  It makes EP study to assess AV nodal function  redundant.

* In all patients with severe bradycardia , a complete workup for systemic diseases like hypothyroidism and other chronic inflammatory pathology must be ruled out. Drug induced bradycardias can exactly mimic pathological  SND. Recognizing these entities could avoid  inappropriate pace maker implantation for  transient reversible bradycardias.

* SNRT – Sinus node recovery time. cSNRT -Corrected sinus node recovery time .SACT-Sino atrial conduction time.

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Can edema legs occur in diastolic heart failure ?

Posted in cardiac physiology, Cardiology - Clinical, cardiology -Therapeutics, Cardiology -unresolved questions, tagged , , , , , on August 14, 2011| Leave a Comment »

How common is edema legs in diastolic heart failure ?

  1. Can not occur.
  2. As common as systolic failure
  3. Can occur in significant number.
  4. Rare.

Answer : 4

Response  3  may be  correct as well .

When cardiac failure was originally defined by Framingham criteria many decades ago , the entity of diastolic heart failure was non existent .The classical  triad of edema legs, raised JVP, basal rales invariably meant systolic ,  congestive hart failure. We will , never ever know how many of the Framingham cohort had isolated diastolic  heart failure .

Mechanism

For edema to occur there need to be water and sodium retention .For  sodium and water to accumulate either of the two things should happen (Hypoprotienemia, Lymphatic dysfunction excluded)

  • Increased venous pressure
  • Reduced renal clearing of water and salt.

When both join together edema is classical and full blown.

In isolated LV diastolic  heart failure the raise in systemic venous pressure is less pronounced .So ,  edema legs is less conspicuous. but in any type of failure  the net cardiac index tend to decline at least marginally . Kidneys are the first organ to sense this , and the nephrons  goes for  a huddle and begin to retain sodium and water as if body is going to face severe water and salt scarcity .(It is a false alarm actually ! )

Neuro humoral mechanism is   “Alive and well”   in any heart failure whether it is  systolic diastolic , forward ,backward  etc. so  , edema  can indeed occur  in isolated diastolic heart failure

Please note ,  the classical edema  that occur in restrictive cardiomyopathy , constrictive  pericarditis  are due to severe  impediment  to right sided filling and  elevated the lower limb venous  pressure .

Other important determinants of edema legs.

  1. The baseline renal function.
  2. Intra vascular volume status.
  3. The associated  HT induced vascular  changes.
  4. Serum protein  levels.
  5. Venous tone.(A good venous pump   in conditioned  legs develop edema late )
  6. Integrity of lymphatic circulation.
  7. Subcutaneous fat  density and interstitial tissue resistance.

All can modify the local hydro static pressure .These factors operate in various quantum’s  and for this  reason only selcted few develop  significant  edema in cardiac failure .

Also  read  . Why some patients  with cardiac failure never develops edema legs ?

* Please note , the terms diastolic dysfunction and failure can not be used interchangeably. Dysfunction is often a  echo parameter while   failure is its  clinical counterpart .Both can be dissociated in time ,   failure may never follow dysfunction .Most episodes of diastolic dysfunction is transitory   in nature.

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What does CRPs, Apo-lipoprotein B, and homocysteine do in coronary care units ?

Posted in bio ethics, cardiology-ethics, tagged , , , , , , on August 14, 2011| Leave a Comment »


In one of the corporate hospitals  which I visited in my city(Chennai*)  ,  happened  to see a nurse taking blood sample from a patient  who has been  just admitted  in a Hi-tech coronary care unit for UA-NSTEMI.

It included blood tests for CRPs,homocysteine,Apo-lioprpitein B etc . She was  being supervised   by  a capitation fee fed  , just delivered  , neo- medical graduate from a country side medical college.

I asked  her  what for you’r doing these  tests.

                        She said ,  it is  to detect risk of developing CAD.

     . . .I  reminded her , the patient  had already developed full blown CAD .

She was too innocent  to say  ” I do not know all those  things sir ,  my consultant asked  me to do it !

This is how  some corporate coronary unit* functions and   handle their  prized  possession . And every one enjoys it , as science  prevails over common sense !

* Shall  I  name the hospital  ?   . . . No , it would invite trouble  . . . oh ,  what  a  freedom of expression we enjoy  !

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Land mark reviews in cardiology :Patent foramen ovale.

Posted in cardaic physiology, cardiac surgery, Cardiology - Clinical, cardiology -congenital heart disease, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, tagged , , , , , on August 12, 2011| Leave a Comment »

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  a  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

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What are the mechanisms of mitral regurgitation in HOCM ?

Posted in Uncategorized, tagged , , , , , , , , , , , on August 12, 2011| Leave a Comment »

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 .

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Beware , there is one more dangerous face for atherosclerosis !

Posted in Cardiology - Clinical, Cardiology -Interventional -PCI, Cardiology-Coronary artery disese, tagged , , , on August 11, 2011| Leave a Comment »

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 .

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Is there an entity called borderline positive exercise stress test ?

Posted in cardaic physiology, cardiac physiology, Cardiology - Clinical, cardiology -ECG, Cardiology -Interventional -PCI, tagged , , , , , , , , , , , , on August 7, 2011|

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 ?

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CAD is . . . coronary artery disease or Confusing artery disease ?

Posted in cardiac drugs, Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology -Therapeutics, tagged , , , , , , , , on August 5, 2011| 2 Comments »

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 ?

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Squat Echo : Poor man’s stress echocardiography !

Posted in cardiac physiology, cardiology innovation, echocardiography, tagged , , , , , , , , , on August 4, 2011| 1 Comment »

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

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