Archive for May, 2011

LVH is traditionally believed to be adverse marker for both coronary events and cardiac failure. . (Framingham ) While  this may be  true most of  time  we  also  have evidence to  suggest  patients with LVH  tolerate ischemic injury better.The area of MI is less.  In fact , the coronary drug project was not able to identify LVH as a major risk factor  for MI.  But many other studies continued to portray  LVH  dangerous parameter in ACS.

This paper from Sheba medical center Israel   tries  to answer this  question succinctly !


LVH  indeed  is an  adverse  predictor  for cardiac outcome  in the  long term.Meanwhile , since the   7 day mortality of STEMI  is well below  3% if  associated with LVH    keeps the controversy alive  ( 5-7% in non LVH group ) .This piece of statistics     gives credibility to the belief   LVH  may  really prevent  early deaths  in STEMI.

This phenomenon about LVH is  consistent with our observation  in  one of the Asia’s oldest coronary  care units (Started in 1972)   .None of the  STEMI patients with LVH  had a cardiogenic shock  in the recent past   !

* It is important to realise not all LVH are same. Inherited LVH, Diabetic LVH and  uremic(  or sub uremic ) LVH  behave differently. Since  the concept  of LVH is  carried  by physicians   in  a single basket ,  we tend to miss the  true benefits of LVH that occur purely due to good exercise training or a mild HT !

In other words , LVH that do not involve interstitial proliferation  is  probably  good for the heart !

Final message

With due regards to Framingam study  , presence of LVH in ECG in any form of acute coronary  syndrome  should  bring a sense of comfort  in the coronary care units .I agree  , it may increase risk of sudden death in some of the population but still it has some unique and definite  advantages at times of  ACS.


1 Levy D, Garrison RJ, Savage DD, Kannel WB, Castelli WP. Prognostic
implications of echocardiographically determined left ventricular mass in the
Framingham Heart Study. N Engl J Med 1990;322:1561–1566

2.The Coronary Drug Project Research Group. Left ventricular hypertrophy patterns and prognosis. Experienced post infarction in the Coronary Drug Project.Circulation 1974;49:862–869.

3.Behar S, Reicher-Reiss H, Abinadar E, Agmon J, Barzilai J, Friedman Y, Kaplinsky E, Kauli N, Kishon Y, Palant A. Long-term prognosis after acute myocardial infarction in patients with left ventricular hypertrophy on the
electrocardiogrm. Am J Cardiol 1992;69:985–990.

*Coronary drug project (A old study done in early 1970s has more credibility when LVH was not considered as pharma target !)

Read Full Post »

We presume  ECG  fails miserably against echocardiography for assessing hemodynamics , while  echocardiogram  has  little value  when it comes to studying   electrophysiology .  Ironically ,  we often  ignore  the fact  ,   ECG can  provide  important long-term   hemodynamic  data . The pattern of  chamber enlargement  give us  vital clues to the prevailing hemodynamic  stress and loading conditions. While echo  can be termed as an  anatomical and  physiologic   modality  , ECG  apart from  its unique capacity to record cardiac  electrical finger prints ,  it  provides  useful ,  anatomical ,  hemodynamic information too !

While Doppler is a  fascinating modality to measure hemodynamic data in a moment to moment fashion it can never ever tell us  , what has been going around in the preceding months or years. This  is were chamber size helps which  give us chronic physiological information (Chronic  Doppler ?)

A simple E:A reversal  in  mitral inflow doppler can be a  innocuous  finding in isolation  . If it is associated with even   minimal grades of  LAE  it gains huge importance. That is why left atrial size is  funnily referred to as HB A1C of diastolic dysfunction ( A marker of chronicity  of  diastolic dysfunction)

If LAE is so important to diagnose diastolic dysfunction , why  we are so  obsessed  with doppler filling profiles  of mitral valve ,pulmonary veins, mitral annular tissue Doppler and what not ! .Many of these sophisticated doppler methods are extremely operator dependent  and are  subjected  to technical and mathematical errors. Especially , with  tissue doppler where we  magnify the errors as we  filter  extremely  slow tissue motion .

For  many  decades  we  have failed  to impress ourselves  , about the importance of subtle P wave abnormalities in the  ECGs   of  hypertensive patients.

In fact those  innocuous looking  slurs and notches   in P waves ,  suggest the left atrial  stress and a definite marker of underlying LV diastolic dysfunction .

P wave is the only electrical wave that occur in diastole .Hence there is no surprise  ,i  gives us enormous information about this phase of cardiac cycle .

If only we look  at them carefully, zoom it (Now it is made easy with so many softwares)  analyse critically we can find a wealth of information about the atrial behavior in hypertension.

Experience from our hypertension clinic  with periodic echocardiograms suggest ,  the following  ECG  findings   can be   good markers  of significant  diastolic dysfunction .

  1. Notched P wave
  2. Wide  P waves
  3. Slurred  P wave
  4. Bi-phasic P waves

* Surprisingly  , these abnormalities correlated with at least grade 1 diastolic dysfunction even in the absence of  for LAE or LVH by echocardiogram.

** In an  occasional patient  P waves  can widen due to inter atrial block or conduction delay. This a rare exception for wide P waves without LAE.

Final message

A well recorded and   analysed   ECG can  predict diastolic dysfunction  with fair  degree of accuracy .This fact need to be emphasized  by every one  .  Next to ECG ,  LA size and volume  by 2d echo are excellent parameters  to assess diastolic function in a long term fashion. Sophisticated  but  error prone ,  momentary doppler parameters are getting too much attention  at the cost of simple ,  shrewd ECG and 2D echo  !

Read Full Post »

LVH can be diagnosed with fair degree of  accuracy  by surface ECG . We have a set criteria .The Estes  scoring is  the most popular. Very rarely we have all  the classical features of LVH in a given ECG .

With the advent of echocardiography ECG diagnosis of LVH has become redundant . Still , it is essential to  build the  foundations  in cardiology  for the current generation cardiologists.

The following are the  magnified views from the above   ECG

High Voltage

High voltage QRS is a hall mark of LVH .It increases in both chest  and  limb leads .In chest leads , both R and S wave gets amplified , while in limb leads only the R wave  is taller . We have to sum up R  from lead  V 5 and S from V2  (Practically any deep S and tall R can be added . LVH is diagnosed  if  sum qrs voltage  is  >35 mm . Voltage criterias in limb leads do not require these  addition business . An  R wave amplitude > 11mm  in limb leads by itself  would indicate an LVH (In the absence of bundle blocks )

Pit falls in voltage  criteria

It is our belief    qRS voltage  would faithfully   reflect the   quantum of cardiac muscle mass ,  but in general  to equate qRS voltage  to myocardial  mass  is   a  huge error we make ! (Of course  It  may be true in  some cases  following MI )  .

The qRS  voltage is determined by   numerous  factors (Important ones are :  chest wall thickness , age , LV cavity size ,  amount of blood inside LV cavity,  heart rate , conduction delays  etc ) This is the reason a 10-year-old boy’s   ECG will  satisfy the criteria of LVH  by 100 % .Do not ever report a ECG without knowing the age of the patient .

At high heart rates R wave amplitude increases(Broddy effect) due to high conductance of blood

Chest lead always balances RV and LV forces .One can mask the other .So be ready for surprises when you find a perfectly normal ECH in bi-ventricular  hypertrophies ) A balancing act !

Mini summary : Never diagnose LVH with high voltage alone

Left axis deviation

The axis deviation is again non specific  . The LV mass shifts the mean axis to left (Beyond -15 degrees) .The axis shift would also be contributed by mild forms of LAFB . This  fascicle  which criss crosses the LVOT  easily gets injured to hemodynamic stress ( or rather insulted ) and  lose its function . So its job is  transferred to  the posterior fascicle  which  shoots  towards  anterior and superior and left , hence the  left axis deviation) .The LAFB is generally a benign defect unless it occurs in an acute fashion as a response to ischemia.

Mini summary : Never diagnose LVH on the basis of left axis alone

Left Atrial  abnormality

This need not be present in every one with LVH . It happens only  if  LVH  is associated with relaxation defect , when   it calls for  LA’s  assistance .(In other words , presence  of LAE in hypertensive  patients is  a  sure and simple way to confirm diastolic dysfunction ) . Similarly absence of  LAE (  with a   significant LVH )  is a good sign as the LV is able to tackle the hypertensive stress in solo fashion in all likely hood free from significant diastolic dysfunction.

Apart from LAE , note also the p wave encroaches good part of PR interval .

Mini summary : LAE can be very useful parameter to diagnose LVH . (Is it not ironical  to note   LAE is more reliable to diagnose LVH ! . This is because qrs morphology is unreliable as it influenced by many factors  while p wave  changes are  not subjected to such influence )

Secondary repolarization changes

We know ventricular depolarization and repolarization are interlinked phenomenon .Both  occur in  opposite directions still  , able to  record   ECG deflection  in same direction  (positive QRS/positive T)  . This is due to the fact  the epicardium and endocardium has  action potential with different velocities . At times of   LVH this epicardial  , endocardial heterogeneity in repolarization becomes void. (Note : This is a simplified statement of a complex repolarization process)

Because of this the repolarization is recorded opposite to that of depolarization .Hence we get all sorts of secondary ST /T changes. (The  term secondary is used to denote secondary to alteration  in depolarisation ).

Many times  all of the following  could   mean the same  in the bed side clinical parlance !

  • Secondary ST/T changes
  • Non specific ST/T ,
  • LV strain
  • LV systolic over load etc .

Note : Primary ST depression occurs in true ischemia without any alteration in LV Mass or conduction defect.

*** For advanced readers  only : Some of the ST depression that occur in ischemia could again be secondary changes. This  needs further reading.


Echo is the gold standard for diagnosing LVH .There are two definitions .

  1. Based on septal thickness
  2. Based on LV mass*

LV mass > 200mg in men and 175mg in women is considered LVH . LVH based on LV mass is  ideal . But can be misleading in a dilated heart where the mass may be increased with a  relatively   thinned  out IVS .

Final message

There are numerous  ways to miss    LVH in ECG,  But the definite way  for not missing  is by echocardiogram !

Read Full Post »

Mechanical complications are not rare  following acute MI .In fact , it closely competes with electrical deaths . Many times it is not recognised  and get wrongly labeled as  simple pump  failure .

Echocardiography has revolutionised the way , we approach these deadly complication.(Of course , many  deaths  could  not be prevented still !)

The early days of STEMI is critical . This is the time the infarcted muscle softens and invaded by blood components like  neutrophils etc. The biochemical events  in the infarct zone is a least studied aspect by  current generation  cardiologists. Some ,  especially women tend to lyse their interstitial collagen faster. This minute break ups  coalesce to form a tear , When this tear is subjected to hemodynamic stress and mechanical stretch a rupture is  all too likely.

The rupture site is predetermined by the patients fate !. If the tear occur in free wall of LV  , in all likely-hood ,we are going to lose the patient. If he is blessed  , the rupture take place in the interventricular  septum .Here , the issue is less disastrous as the  blood is  simply shunted to a different chamber .In fact , some consider VSR puts an ailing ventricle at  a slight hemodynamic advantage which is referred to as decompression .   The LVEDP has  a biphasic response to VSR  .An  initial raise bfollowed by a flat response.This has a clinical correlation too  with a temporary deterioration and subsequent stabilisation.

The issue of thrombolysis and ventricular rupture  was controversial for decades  .It never got a correct answer and finally we have our own conclusions  .

Thrombolysis as such reduces  the net incidence of ventricular rupture even though  late thrombolysis do  increase the risk of rupture. What does the above statement mean to you ?  confusing is isn’t ?

For population based approach  thrombolysis  has a  no negative impact ,  but in a given individual  one has to weigh  the risk vs benefit .

An irregular tear in the mid ventricular septum

This patient did well with initial medical support and referred for surgery electively

How to manage ?

Unstable patients (Real shock or impending shock  . . .please note every one with  90mmhg  pressure   is not  unstable !)

  • Emergency coronary angiogram  , VSR closure , CABG
  • VSR closure only , without  angio /CABG  (An useful option if your surgeon )

Stable patients

Four approaches available

  • Treat as emergency as above
  • Wait still instability  begins (Yeh . . .I really mean it !)
  • Sort out a  elective  plan.
  • Send the patient home with VSR * ( we have two patients attending our OPDs for >5 years )

* Exceptional case not to be taken as a model for management.

There is rarely an  agreement between surgeon and cardiologist in timing intervention in VSR  patients. Treatment protocols vastly differ in various institutions with the common theme being early  surgery .

Cath based therapy for VSR closure is still  considered a cardiology  adventure sport .

Some  observations about VSR

  • The doppler  VSR jet if  reaches 4-5 m/sec (65-100 mmhg) the prognosis is often good , as it indirectly  reflects the native LV function .A ventricle which could generate 100mmhg pressure head,  even after a supposedly large MI  is great by any standards.These are the ventricles  that fight till the end and patients do well in the  adverse circumstances.
  • In the  other end of the spectrum we have a VSR with a faint murmur and 3m/sec jet .They will be  hypotensive and end up in shock soon.
  • Infero posterior VSRs  do badly due the complexities of tears.
  • Medical management do have an important role in stabilising  these  patients.
  • LVH if present is again a favorable sign
  • Tissue friability could be an important issue why many surgeons fear early surgery.(Some deny this and some say it is never an issue .I am yet to get clarity on this aspect .I expect an answer from cardio thoracic surgeons .)

Read Full Post »

Pulmonary circulation  is a  low pressure  , low impedance  but  a high capacitance  system  . The job  of  pulmonary circulation  is  not only  to  ferry  the  blood from  right ventricle to  left atrium  ,   it should also ensure smooth gas exchange as it traverses the circuit . (How vital  it’s job is  . . . but we tend to be  obsessed with heart !)

The paradox is ,  for  the  flow of blood to occur you need a pressure head . (Note :  the pressure head is 120mmhg in systemic circulation.) The pulmonary  pressure head  is  only about 5-10mmhg it has to push the entire blood .(Pulmonary   pressure head  = Mean pulmonary artery pressure -mean LA pressure )

In  healthy persons

  • Pulmonary artery pressure (PAP)  is not supposed to increase beyond few mmhg.
  • The diastolic pulmonary artery pressure can not  afford to increase  even  those  few mm.

If it does , it  can cause serious hemodynamic and oxygenation issues. Both these statements are  based on  strong scientific  beliefs But now we realise the margin of these elevation has been revised a little higher  in normal persons .

  • In health ,  athletes can reach a systolic PAP  up to 40mmhg .
  • Diastolic PAP still largely remain a mystery . You can’t measure it when the patient is running you know !

Here is a recent article from chest  (2011) which documents pulmonary artery systolic pressure in trained athletes .

Relationship between exertional dyspnea and PA pressure.

The mechanism of  exertional dyspnea in any  individual is largely attributable  to  exercise induced pulmonary vascular  stretch .(J receptors etc ) . Many still believe  human functional  capacity is limited primarily by  the  lung function and the cross sectional areas of  pulmonary microvascular  bed .( Is this the  reason  two  patients with 25% EF  has vastly different functional capacity ?)

* Note : Exercise induced  pulmonary artery pressure  elevation are well-recognized in pathological states.

  • Mitral valve disease
  • In established COPD
  • In patients  with LV dysfunction


Read Full Post »

Can the LV  ejection fraction change with every  heart beat  ?

EF % is one of  the  glamorous  cardiac functional indices that has  caught  the  imagination of both patients and physicians. How accurate it is ? How reproducible it is ? How many methods are available  to arrive at EF % ?

Picture courtesey http://rachel.worldpossible.org/ocw.tufts.edu Munther Homoud, M.D

 How many of us  realise  it can  potentially   change  with  every  heart beat ? *

Apart from the heart rate dependency ,  the echocardiographic error can be amplified  by

  • Difficulty in identifying  the  leading and trialling edges  of endocardium
  • Patient posture errors
  • Edge detection errors in 2D
  • Pap muscle shadowing .
  • Angle errors
  • Sub optimal echo windows  when EF is measured  in the  bed side  in critical care units
  • Mental status of performing sonographer/cardiologist  (One who chops  2D shells hurriedly and obliquely !  )

All these make this index a highly  variable parameter(  next only   to your  city temperature ! ) This happens whether you measure EF  with M Mode, 2D Simpson , 3D volumetric etc .

* The term  “beat to beat” changes may be  a little exaggerated  statement .It is used   to convey the point of   ” huge  variability” of this parameter.  It  means there can be variations of EF %  with varying heat rate.

The heart is not an Independent organ rather, it is a slave to preload and afterload !

How to overcome the limitation  of EF ?

To overcome this  error a new  parameter called myocardial performance index (MPI) which accounts for heart rate came into vogue . (Did it come really ? Ihaven’t seen a single cardiologist  do this in his clinic ) . 3D volumetrics,  velocity vector imaging , and many other innovations has been added.  Nothing  was  able to replace the EF % . Because of complexities in the newer  modalities  most cardiologists (including  the author  )  continue to romance  the  much flawed EF %  .

Simplicity  shall   reign supreme   .  .  . in spite of  inaccuracies ,  in any walk of life  !

 How does  EF  change  beat to beat ?

The answer is simple . The contractility of heart is dependent   upon the previous  diastole ,  during which heart fills. Heart is primarily an elastic organ. Whenever the  filling is  is more   ventricle is stretched  more ( diastolic filling is the stretch ) and the subsequent force of contraction is more . This is the basis of famous frank starling law.

LV filling is dependent on RV filling which in turn depend on venous return ..Venous return is a function of  vascular tone and the persons physical activity .

Apart from this  adrenergic drive make the heart contract vigorously . This is the reason ,  many patients  with  severely compromised  LV function  in ICU  , supported  with  inotropic agents  show vigorous contraction of heart .(Basis of doubutamine  stress test )

** Every one of us is aware about the huge influence  the preload  has ,  on LV contractility .  Surprisingly,  it   can also  swing  with changing  after load . This fact is often  under recognised .This is called Anrep effect .

So , imagine the scenerio . . .the heart is simply  a “squeezing- slave”  of   pre load and  after load  !  . . . And still we are happy with assessing the cardiac function ,  in isolation without giving any respect to the loading conditions.

Final message

EF ,  would rank  first among all  medical  investigations ,  that is  significantly  flawed , still  continue  to  enjoy huge popularity  ! It has little value as a  screening   test for assessing  LV function in  general  population . But ,  it  has an  important role to assess  the damage following   MI and in  the  follow up of patients with   significantly  compromised LV function.

Cardiologist are aware of this fact ,  but most non cardiologists , especially  Anesthetists  and Surgeons  revere  the  EF% with    sanctity  . This is definitely un-called for . It is the duty of the cardiologists to pass on  this  message to their colleagues in other fields.

Read Full Post »

Trans catheter  aortic valve implantation(TAVI )  is gaining acceptance  as an alternative to surgical aortic valve replacement  .It has successfully negotiated the  initial hurdles and entered the clinical domain . More and more patients receive this modality as the expertise and hardware show consistent  improvement.

Although  TAVI  is   limited to patients in high risk category for surgery , it is expected to make in roads into  intermediate  risk patients  as well  and pose a  real threat to cardiac surgeons  in the years to come .

The only  point surgeons  can rejoice is ,  it cannot be  implanted in patients with aortic regurgitation  as of now.

This video is posted  free by NEJM ,  is stunningly clear in conveying concept of TAVI !

Thank you NEJM .

And this one from  Siemens  seems to  beat the NEJM .

And  now a Hybrid  imaging  creates a virtual aorta in the  cath lab

Read Full Post »

Angina and dyspnea are the  two cardinal ( classic ) symptoms of cardiac disease . While dyspnea is a manifestation of raised LV filling pressure ,  angina  implies reduction in blood supply to heart .

In other words dyspnea is related to excess blood in the  lungs and angina is due to less  blood in  the coronaries  !

So , it is obvious  even though these  two  symptoms are closely knit entities , patho- physiologically  they are  distinctly different  in real time , when an actual  cardiac event unfolds in the bed side .

This also partially explains  , why simultaneous  presentation   of  angina and dyspnea is  relatively  uncommon in CCUs  , than one would expect .(In a given patient , one of them will be dominant)

Why and how our patients (and also  physicians !)  get confused  with dyspnea and angina ?

When William Heberden described  angina over a century ago ,  he was  so meticulous in his description and observation. In fact , it was,  as if  he felt the angina  himself  and wrote it .One can rarely  expect such a  description from any of our patients .  So , it is not at all a surprise  for mistaking  any mid sternal discomfort as dyspnea instead of  angina . (This error in describing angina  is the commonest cause  for dyspnea  playing this  dubious dual role !)

When to suspect  dyspnea  as an Anginal equivalent ?

Here  are some real situations ( and clues )  where  dyspnea  may be  considered as  anginal equivalent.

  • Diabetics
  • In elderly with autonomic dysfunction
  • Patients with chronic beta blocker and other anti anginal drugs.
  • Post PCI/CABG patients (Normal LV function but dyspnea : Denerved heart blocks pain  ?)
  • Exertional dyspnea that stops immediately could be anginal equivalent.
  • Dyspnea with palpitation is  rarely be anginal  equivalent as palpitation indicate good LV /mitral valve function.
  • Dyspnea on  isometric  exercise rather than isotonic exercise .

Mechanism of anginal equivalence

While the trigger for dyspnea is elevated LVEDP  which   stimulates the  stretch receptors in lung .For angina ,  it is the free nerve ending in myocytes that gets irritated and generate pain signals.

When ischemia  presents as dyspnea  two mechanisms are considered. One is myocardial , other is purely neurogenic.

  1. It is  believed critical   ischemia  of myocardium  ( Defective Ca ++ uptake  into sarcoplasmic reticulum) induce  “a wide area  diastolic dysfunction” of LV  that   raises  PCWP  to generate  dyspnea. Further , ischemia induced regional LV dysfunction  that  subtends the pap muscle could  result  in ischemic  MR and severe dyspnea. (Exertional Mitral regurgitation is getting major attention now  )
  2.  In many patients with diabetes or autonomic dysfunction the velocity of  pain signals  become sluggish  or  blocked  en-route  to brain stem . Often they change track to travel in the nerves  meant  for  carrying somatic siganls  ,  J receptors  , intercostal spindle etc . This spill over and cross talk  creates a  false sense of dyspnea , whenever ischemia  occurs. This is attributed to the  wide and complex  neural network of thoracic sympathetic ganglions.

Some of the known  associations with Angina equivalent .

  • Diastolic dysfunction
  • Ischemic MR
  • Small rigid  left atrium
  • Atrial fibrillation

How to  investigate a patient who is  suspected to have  angina equivalent dyspnea ?

  • ECG
  • X ray chest
  • Echocardiogram will settle the issue most times.

Nuclear scan and angiogram in deserving patients

When can  angina and   dyspnea occur together  ?

Angina and dyspnea  if   truely  occur together causes  grave concern for the physician.

This indicates two things .

  1. The myocardium is ischemic  and generates  pain (And possibly ongoing necrosis) .
  2. Simultaneously its  pumping or receiving function is also compromised resulting in  entry block from the lung resulting in acute dyspnea.

Both are ominous signals . This situation occurs  most often in  STEMI with LV failure .

If  dyspnea occur in NSTEMI/UA ,  it is a worst possible complication . GRACE  registry quotes  maximum  mortality for unstable angina with cardiac failure .The reason being the cardiac failure in UA is due to non necrotic global ischemic stunning of LV myocardium with or with out acute  mitral valve failure.(Flash pulmonary edema)

Why angina is rare  in  chronic congestive  cardiac failure ?

The main reason being  , a severely dysfunctional heart  contracts  poorly .In reality , it is never thirsty for blood  . Even if it  is  perfused  well  , there is no good muscle  mass  to burn the ATPs from it .A failed myocardium is  more or less a  sleeping  myocardium .It does not even have the  energy   to cry with pain at times of ischemia ! .However significant the ischemia  is ,   it can often  evoke only  a gasping sensation .

The other explanation  is more imaginative . In cardiac failure heart  dilates .The end diastolic and end systolic  volume is high. The cardiac chamber is always filled with  excess residual blood .This , some how tend to perfuse the myocardium directly and provide a good reserve .This may be  more important in  RV perfusion  .( Trans myocardial laser revascularization is based on this concept – direct myocardial perfusion from the chambers)

While angina is  rare in chronic cardiac failure,   it should also be realised ,dyspnea  is  rare in  uncomplicated acute coronary  syndromes. We know ACS  primarily present with angina.  Exceptions are always there.

In elderly, diabetic , with co morbid   patients ,    ACS  may  present without  angina . Instead  they present with vague dyspnea and shortness of breath . It is here ,  physicians  face a tough task to identify  dyspnea  behaving like   angina  equivalent.  Of course , the  good old  ECG bails us out most of the time.

Therapeutic importance of recognising anginal  equivalents ?

The revascularisation  procedures (CABG/PCI)  are too good  in  relieving  angina , but least effective in providing relief from dyspnea.So  real anginal equivalents if recognised properly can be subjected to early revascularisation .

Can we consider  exertional dyspnea as evidence for ongoing ischemia  in a post MI patient ?

This is tricky question . We do not have answers to it. Readers can try to  answer . The commonest cause of dyspnea following MI is due to physical deconditioning and associated LV dysfunction.

Final message

Coming back to the basic question  , Is  this dyspnea  . . .  an angina equivalent  doctor ?   No simple answer is available .

The first and foremost investigation to do  is ECG .This will settle the issue many times.  Next is the reassessment of  history  clinical  presentation and past history.  Every patient with unexplained dyspnea must undergo a minimum of three investigations (ECG,  X ray chest and Echocardiogram )  If any of these  suggest a cardiac compromise   further evaluation is   indicated.

So, the message here is ,  clinical findings  are insufficient  to rule out ischemic etiology for dyspnea.


Nil . Every thing is my random thoughts !

Read Full Post »

Even as we make rapid strides in  conquering coronary atherosclerosis by all those fancy gadgets , the  fundamental coronary  hemodynamic principle   is poorly understood . Hence  there is no surprise  for the  “perennial ambiguity”  in the indication  and effectiveness of  coronary revascularization .

Why the hell ,   reliving  a  coronary obstruction  may  not provide the   expected hemodynamic benefit  or do not prevent future  heart attack  in many ?    One of my patients  asked ?

I told him . Wait , do not get  excited , we also do not know  . . .We are just beginning to understand mysteries of coronary  circulation.

It is a well documented fact  ( but a  debatable )   that  lesser the  severiity of a  lesion more likely it is prone for an acute coronary  event .( Vulnerability , shearing stress or is it a simply a statistical mirage !) While the  vulnerability aspect is  complex , the hemodynamic  impact of  coronary  lesions  is   relatively better  understood. Here is  an important  documentation from Dr B . K  Koo from  Seoul , South Korea  who has elegantly shown the behavior of  fractional flow reserve (FFR ) in various grades of  stenosis  .This study was done in jailed side branches following PCI.

FFR  shows a surprise   relationship  with severity of coronary stenosis  . Even severe lesions showed equal if not more flow  reserve ?

and mild lesions might have lost all its reserve.

 How is it possible ?  Can it be true ?

Yes , it is indeed a  fact . God generally  keeps a stong link between anatomy and physiology  , structure and function . But he adds a rider and keeps  a reserve in every  human cell   meant for  emergency  back up . FFR is  one aspect of this , we have  partially discovered .  When we fail to understand this we are bound to get confused and make a wrong decision in cath lab.

Simply stated ,  flow across a coronary  artery is much more depedent on the status of microvascualture  than the hurdles they face in the epicardial highways !

Link to this original article from JACC .

How to do the FFR procedure ?


Soon to follow . . .  If less severe lesions are more  dangerous why we are ignoring it in cath lab ?

Read Full Post »

Most important MCQ in clinical cardiology

Many cardiologists  would love to do away with detailed  clinical examination because  . . .

  1. They think it is an inferior job to do  . By skipping  it , they get a false sense of superiority.
  2. It is a time killer  and eat into precious cath-lab  time
  3. They no longer believe in  these “perceived – primitive” medical methods.
  4. Fear of colleagues making  fun of hem if they  indulge  in detailed clinical examination.( At-least in India ! )
  5. To give more job opportunities  to para medics.
  6. They are no longer confident about making a good clinical examination as they  are neither  trained  adequately nor interested in it !

Answer :  All of the above can be true .  The 6th response is  likely to be  more  correct !

While cath labs can prevent few deaths occasionally . . . it is the general wards and OPDs that add life every day

Read Full Post »

Older Posts »