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Archive for July, 2011

Often general practitioners refer  ECGs  with abnormal resting  ST/T wave patterns  to cardiologists .

Following are few of them

  • ST elevation
  • ST depression
  • T wave inversion
  • Tall T waves
  • A relatively uncommon  finding is  a flat ST segment  , which  is discussed here.

The commonest( benign) abnormality   is  T wave inversion  in women and tall ST /T waves   reflecting  early repolarisation  pattern in men. A flat ST segment is an occasional finding in general population.

ST segment is inscribed  during the most important  time  of  cardiac cycle.This is the period the ventricle is doing its prime function , namely ejecting the blood in systole .Hence it is subjected to maximum stress . During times of ischemia  ST segment  gets elevated or depressed depending upon the severity of ischemia. For the same reason , even  subtle changes in this segment is  frowned upon by cardiologists. Most of them would receive a EST.

It is ironical to note  , few normal people  show almost silent electrical activity during this  crucial  phase of   their  ECG .ST segment is often  a flat line  in them . This is a ECG of a women referred as CAD. She was asymptomatic . Echocardiogram  was normal . She was asked to do  a EST.

This asymptomatic women was refered for ECG opinion

The peculiar thing about T waves  are ,   a 10 mm upright  as well as  5 mm inverted T wave ,  both can be normal. So .  there is no element of surprise  to note absent  T waves  or a flat  T wave  to be called as normal .

The curious case of lost ST segment !

* T waves are recorded when K+ efflux occur rapidly out of cells . Hypokalemia  can be an important cause of flat T waves.

It is still a  mystery to me  why some people inscribe a tall T when  potassium comes out  of cell and  an equal number (Esp women)  record a down ward T wave  for the same event !  I wish  I get an answer  to this  lingering  question from  any of the readers !

Is a flat T wave represent  a T wave in  transition  to become inverted T wave  later ?

Possible .But we  are not sure ! A static T wave is safer than a dynamic T wave .

Final message

Flat ST segment and absent T waves  represent a same spectrum of ECG  findings  which  are  referred to as  non specific ST segment changes in  clinical practice .Generally , they have  little clinical significance.* In our experience we have found , female patients, Anemia  hypothyroidism  are  often associated with flat ST segments  . If CAD is suspected exercise stress test  should be done. Some believe a flat ST segment  is more likely to  result in EST positivity (Not necessarily true positive !)

* Non specific ST/T changes by itself is a  huge topic.  Ideally the term non specific ST /T changes should be avoided , as it  primarily came into vogue  to denote non ischemic ST segment (Still , other pathologies are very much  possible) It is estimated there are about  50 causes for non specific ST/T changes , right from a  benign situation  like deep   respirations , to significant  myocardial disorders. However , it still makes   good clinical sense for a  general practitioner  , to refer to a cardiologist , whenever ST  segment deviates  without any reason .

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Landing an aircraft is a high precision job. A pilot and co pilot with the help of air traffic control  must  do this job meticulously every time .They   are not  afford to make any mistake .Number of lives are at stake.

In cath lab something similar happens every day  although a single life is at stake !   We call this coronary stent landing  . If  it lands  wrongly  it is referred to as  geographical miss ,  a descriptive  terminology for a poorly deployed coronary stent !  ( In strict terms it  should be called as  failed PCI !)

But there are few vital differences   between the two . . .

If an aircraft overshoots  the  runway   it is visible to every body and it becomes a national news next day !

If you deploy a stent away from a lesion it is usually a  silent  event  . Only a few alert fellows and staffs know it ! Patient  often gets discharged  next day (of course after paying the bills )  and  the consequence is often delayed  by weeks  or months  when he comes back knocking  the  ER doors with an ACS !

Final message

The stent -plaque  dissociation is  much more common than we perceive ,  for the simple reason cardiologists have  learnt  to accept   luminal shadows  as surrogate markers for plaques . ( Coronary blindness !)

It is imperative to  apply all our senses properly  in the cath lab ,  like  our  pilots  do while they land  . Be prepared  for  turbulent weather which  is common in cath lab as well !

http://www.sciencedirect.com/science/article/pii/S0735109701011123

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This  article is from the journal JAMA July 2011 , and  “The  Telegraph”  breaks  the News in general media because of   the immense  importance it has  for the public.

http://www.telegraph.co.uk/health/8589168/High-dose-statins-increase-Type-2-diabetes-risk.html

http://jama.ama-assn.org/content/305/24/2556.abstract

HMG COA reductase has a new side effect  when used in high doses. It is  now official ,  it is confirmed by this meta analysis.

According to this study the risk is mainly  with  80mg of Atrovastatin . But  the dose at which the diabetic risk develops is highly variable.

In simple terms  . . . It all depends upon how a  person’s liver responds to ingested statins.

Statins are not  divine molecules  that can heal atherosceloris. It mercilessly  blocks the vital  cholesterol synthesizing   enzyme HMG COA* located in every cell ,  especially  it has a  virulent action in the hepatocytes . We know liver  is the major metabolic hub  which co ordinates glucose and Lipid  metabolism and to certain extent amino acids as well . These statin infested   hepatocytes  can  interfere  with   glycolysis  ,  neo-glucogenesis   and  lipolysis in a complex fashion  . It  would  not require great brains to understand how diabetes can  be induced  by statins !

* Which also has a  indirect cell/  lipid servicing action.

Final message

It is becoming increasingly clear , statins should be used judiciously in whatever dose . We need to be in constant vigil even as   the  human lipid  is under siege  from the   corporate  board  rooms ,  who are  primarily  worried  about  the decline in the per capita consumption of these ubiquitous molecule !

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Can you diagnose inferior MI with poor R waves ?

No , you need  a “Q ” that’s  for sure !   Do not diagnose inferior MI without a  q wave  . ( The luxury of diagnosing MI without q waves  is available  only for LAD region )

Any axis deviation ( even 30 degrees) from  base line  can alter the inferior lead qrs morphology to a great extent. R wave amplitude is  primarily determined by the  initial septal depolarisation .  So if the  inferior septum is intact  it will never allow to inscribe a q wave  . Further ,  limb leads are bi polar leads and they are   sum-mated  potential  reflected along the entire  bottom half of the  torso . Hence it is not  reliable to attribute  significance  to presence or absence of  r wave (Unlike  chest leads).

The lung and diaphragm  exert  not only electrical insulation but   also mechanical  alteration of septal profile with phases  of respiration.

Counter point

Not really  . . .  you do not need a  Q   waves  to diagnose inferior MI  ,  electrically  diminutive R  is same as  “Q”

There is  an alternate way of  reasoning  too  . R wave is muscle , We diagnose LVH with tall  R waves so muscle loss should be equivalent to R wave loss .We have innumerable examples where  low voltage R waves are  recorded in inferior leads after a well documented inferior MI.

How do you diagnose old inferior MI by ECG ?

  1. Near normal ECG with degeneration of q waves and regeneration* of  R waves
  2. Residual T wave inversion
  3. Simple low voltage inferior leads
  4. Slurred or notched qrs  complex in 2 3 AVF
  5. Rarely with atrial abnormalities and AV nodal prolongations

The concept of regenerated R is well established . And it brings to the age-old debate of R with live muscle Q is dead muscle

Regeneration is salvaged muscle (Natural salvage , awakening from hibernation etc)

How good is Echocardiogram in diagnosing old Inferior MIs ?

Surprisingly , echocardiography do not help much either .Technically inferior transmural MI  is expected to  leave  a residual wall motion defect.  But many times it do not. Many non q inferior MI (Is there such an entity ?)  do look perfectly normal by echo .

The primary reason  for this is ,  infero-posterior surface is anatomically remote and it makes  wall motion analysis difficult .Newer tissue motion analysis (Velocity vector imaging)  could aid us better.

Some times a trivial or mild  mitral regurgitation is the only sign of   old inferior MI  as  the pap  muscle  lags behind in it’s  functional recovery  while  free posterior wall is  fully salvaged and contracting well .

Final message

It needs  that extra bit of   of  knowledge to  expose  our ignorance.

Even in this  maddening   scientific  era  we have valid  reasons to  go back to fundamentals  of  R wave and Q  wave genesis in MI ,  where clarity  is lacking .

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Cardiac myxoma  is  an  infrequent cause of  stroke in young . LA myxoma is the commonest  tumor  that can partially dislodge to cause a stroke.

It is not necessarily a  tumor emboli that causes the stroke  , super added thrombus is   common in cerebral artery histological  studies. ( In fact , some have advocated successful thrombolysis for myxoma and stroke !)

When do intervene in stroke due to myxoma ?

Image  courtesy: http://www.medicalscale1.com

As soon as cardiac  myxoma is diagnosed by echocardiography  it is customary to call the cardiac surgeons for their  opinion and feasibility of removing the tumor  at the earliest.

Myxomas need not be removed in an emergency surgery even if it has caused a stroke!

What is the optimal timing of cardiac  surgery in patients  with a cardiac cause of stroke ?

  • Stroke is a major vascular  event .Immediate cardiac  surgery is another major vascular  insult .
  • Extra corporeal circulation is known to affect cerebral perfusion  even in normal persons. In  patients with  acute stroke  this   can  have vital impact.
  • Anticoagulants used  peri -operatively  increase the risk of   converting  a simple stroke into hemorrhagic  one.

Hence , it is advisable to wait for 4 weeks after a stroke before removing the myxoma . One can not expect a controlled studyon this issue .  It  is to be  based on collective  experience of many.

Who should decide ?

A cardiologist, a cardiac surgeon and neurologist should  collectively decide along with patient’s input ( or his proxy)

When there is  a dispute in timing of surgery  Neurologists opinion shall prevail over others as the immediate concern is brain function.

Is there any  indication  at all for doing early surgery ?

High risk mobile tumors demand early removal as further strokes can be avoided. Individual discretion and institutional preferences apply.

Reference :

1 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2627525/pdf/TOCMJ-2-115.pdf

2.http://asianannals.ctsnetjournals.org/cgi/reprint/8/2/130

3.http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3064861/pdf/crn0003-0021.pdf

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It was  the year 1812 ,  exactly 100 years before the Titanic sank  over the Atlantic  , a  small bulletin from  Massachusetts General Hospital was  released .  It  later on became  the  single most  important  journal  for the medical community.  The appearance of  an article about  angina pectoris in the inaugural issue ,   reiterates the  importance of cardiology  even in those   days of primitive  medical care .

The volume. 1  : No. 1  issue of NEJM egan with a classical and critical observation of angina pectoris written  by Jhon Warren .

http://www.nejm.org/doi/pdf/10.1056/NEJM181201010010101

The first issue of NEJM . . . Witness to 200 years of medical excellence

Those were the days  when angina  was treated with tincture  opium and Fowler solution (Arsenic  potash ) .They  can be  termed as  height  of  inappropriateness  and  also  condemnable acts  . . .  is it not  ? 

200 years  later   . . .  in 2012  what  do you think has changed ,  in terms   of  appropriateness  of management   of angina pectoris  ?

What a surprise ,  two centuries  later ,  even as we are  treating  angina  in hi-tech cath labs  with bio-degradable stents and metabolic modulators   ,   bulk of our  population is  grappling with inappropriate therapy for angina pectoris .

Today ,patients are subjected to  questionable modalities  in the management of CAD ,  which the following paper   tries to expose !

Keeping the inappropriate flag high . . .200 years later in 2012


What a way to progress in Medicine !  The reason for this  “200 year  old ailment”  is  attributed to  extreme scarcity of common sense !

( A study , which says regular exercise  can be  as good as PTCA in multivessel CAD ,  would  sound  as a  “nonsense article”  for most  cardiologists  of  current  generation  !)

Finale

When we look  at human history , where billions  lived ( and continue to live ) in this  age old planet , it  would appear  a trivial matter  whether you treat angina pectoris with Tincture opium / Arsenical potash or  Prasugrel  / Rosuvsatin . . .

Whatever be the scientific advancement  the ultimate outcome on human health will depend on how we apply it. So, all young  medical fellows beware of this   !

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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.

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