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Archive for October, 2010

The following  questions  are asked frequently  in clinical cardiology classes on congenital heart disease.

What are the chambers that dilate in ASD ?

Right atrium and  right ventricle .

What are the chambers that dilate in VSD ?

LA, LV , ± RV,

* Image courtesy Wikipedia

While there is no controversy about ASD, The chambers that enlarge in VSD ,   is  by and large  poorly (or rather wrongly ) understood .  Whenever we  diagnose  VSD , our brain is tuned  to think  this way : Blood  will be  shunted form LV to RV.  RV  would  handle more blood and it  should   enlarge . In reality it does not happen.

The VSD  shunts  the  blood from  LV to RV outflow*   or even directly into  pulmonary artery  .  Hence , VSD even if it is large  , does not dilate  the RV until the onset of  pulmonary hypertension and RV dysfunction sets in . It is surprising to note , even the RVOT ( The entry point of most VSD jets) does not significantly  enlarge

Importance of diastolic shunting in determining RV size in VSD

It is also important to recognise, the VSD shunt predominately occur in systole .(90% ?) In systole , the RV is also contracting along with LV  , so it’s size is diminutive  and hence RV can not be volume overloaded in  most of the VSDs however large it may be. Instead in ASD , there is diastolic overloading   involving  all regions(Inflow, Body, Outflow) of  RV   .This enlarges the RV   in a classical  fashion.

Significance of  anatomical location of VSD and RV enlargement

When VSD shunts blo0d into RA as in Gerbode defect it is bound to enlarge RV (like ASD) as there is diastolic volume over load of RV.

In some large muscular VSD , RV body can be  volume  overloaded. This is because the VSD and RVOT are well separated geographically .The  blood that is coming in from LV can enter the pulmonary artery , only in the next cardiac cycle  . So , RV needs to accommodate the shunted  blood till the next beat. Hence RV enlarges.

What are the situations RV can enlarge significantly in VSD ?

  • Rare VSDs of inflow or large muscular VSDs.
  • Eisenmenger syndrome.
  • Tricuspid regurgitation
  • Pulmonary regurgitation
  • Associated RSOV.

Final message

Right ventricle   does not enlarge  significantly in uncomplicated  VSD .This is in contrary to the  traditional teaching and understanding  for  many years. It enlarges only in specific sub types of VSD  or  after the onset of PAH and cardiac failure .

Coming soon

Katz-Wachtel phenomenon is not  due to  bi -ventricular hypertrophy !

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 Cardiologists  often  think heart is the supreme organ.  As medical  science  advances at a rapid pace we fail  to notice the development  in other  specialities .It is getting more and more difficult  for a  physician  in one field ,  to  understand the  advances  in other  . Often it becomes a  struggle to  decode  non cardiac  case sheets and prescription  filled with latest  generation treatemnt  modalities .

Here is a stunner  at least for  me  !   to find  , artificial  valves  being used   in the human bronchus ,  to regulate the air flow  in patients  with emphysema.

So,  cardiologists be ready  to prescribe  ” lung valves ” for  managing severe cases of cor pulmonale  secondary to emphysema !

 

Reference

http://www.sciencedaily.com/releases/2007/10/071022120150.htm

http://en.wikipedia.org/wiki/Endobronchial_valve

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  • Second heart sound is widely split because the pulmonary hangout interval* is wideFixed because , the RV stroke volume does not show the normal respiratory changes.This is due to dynamic phasic shunting across the IAS ( For example : During inspiration , if RA,RV volume gets augmented by 50ml from IVC inflow , in expiration this IVC augumentation is removed but a 50 ml augmentation from left atrium takes place , this keeps the RV diastolic , as well as systolic volume relatively constant.) This makes the 2nd heart sound fixed .

    * Hangout interval is the gap ( in time ) between the arterial pressure curve and the respective pumping chamber pressure curve (RV, LV) at the level of incisura.

    Incisura is the notch on the descending limb of arterial pressure curve , when the pulmonary or aortic valve closure occurs . When we analyse the simultaneous pressure recordings of RV ,LV/Pulmonary artery/Aorta , the arterial pressure curves faithfully accompanies the chamber pressure curve along the dome of the chamber pressure curve till it descends , where it dissociates , from the chamber pressure curve and hangs out for a certain milliseconds. This time interval is called as hang out interval (Named by Shaver et all )

    What is the normal pulmonary hangout interval and systemic hangout interval /

    Pulmonary hangout interval is 60-80ms

    Aortic hang out interval is 20 ms

    Why does it happen ? What does it signify

    It happens because , even as the chamber pressure falls below the arterial pressure ( Note: Semi lunar valves close at this cross over point ) blood continues to rush forward , with momentum in to the pulmonary and systemic circulation, in spite of the pressure cross over has happened, the semilunar valve doesn’t get closed exactly at the cross over point .It gets closed little later than true cross over point.This gap in time is the hangout interval. This Interval keeps the arterial pressure not only to be sustained little longer but also slightly higher .

    This interval is an indirect( inverse) marker for vascular impedance of the distal draining circulation .The impedance is same as vascular resistance for all practical purposes.Since pulmonary circulation is a low impedance circulation , it has a wide hangout interval and the systemic circulation vice versa.

    How much of S2 widening is contributed by RBBB in ASD ?

    This is not known .But it has a minor role in prolonging S2 split. This is because , the RBBB in ASD is most often incomplete and peripheral one .( Pesudo RBBB due to RVOT dilatation )

    What happens to S2 when pulmonary arterial hypertension develops in ASD ?
    It is often narrow and fixed . Pulmonary arterial hypertension makes the pulmonary circulation to behave like systemic , hence the impedance becomes high and the hang out interval is significantly lost and second sound is narrowly split. (But fixity may be maintained.)It also depend upon the RV function and associated RBBB. RV dysfunction and RBBB both tend to widen the split.*Mild PAH usually does not alter the S 2 splitting

    Is there any other cause for wide and fixed splitting of second heart sound ?

    Having known the reasons for widening and fixity it is easy to understand , a patient with right heart failure and RBBB can have a wide and fixed split .

    Widening is due to RBBB (Delayed activation of RV ) . Fixity is due to severe right heart failure makes the RV out put relatively constant .(As RV inotropism is not good enough to handle the inspiratory augmentation of RV end diastolic volume.)

    Why in VSD the second heart sound is not wide and fixed split even though hemo- dynamically it fulfills the same hemodynamic scenario ?

  • This is due to dynamic phasic shunting across the IAS ( For example : During inspiration , if RA,RV volume gets augmented by 50ml from IVC inflow , in expiration this IVC augumentation is removed but a 50 ml augmentation from left atrium takes place , this keeps the RV diastolic , as well as systolic volume relatively constant.) This makes the 2nd heart sound fixed .

    * Hangout interval is the gap ( in time ) between the arterial pressure curve and the respective pumping chamber pressure curve (RV, LV) at the level of incisura.

    Incisura is the notch on the descending limb of arterial pressure curve , when the pulmonary or aortic valve closure occurs . When we analyse the simultaneous pressure recordings of RV ,LV/Pulmonary artery/Aorta , the arterial pressure curves faithfully accompanies the chamber pressure curve along the dome of the chamber pressure curve till it descends , where it dissociates , from the chamber pressure curve and hangs out for a certain milliseconds. This time interval is called as hang out interval (Named by Shaver et all )

    What is the normal pulmonary hangout interval and systemic hangout interval /

    Pulmonary hangout interval is 60-80ms

    Aortic hang out interval is 20 ms

    Why does it happen ? What does it signify

    It happens because , even as the chamber pressure falls below the arterial pressure ( Note: Semi lunar valves close at this cross over point ) blood continues to rush forward , with momentum in to the pulmonary and systemic circulation, in spite of the pressure cross over has happened, the semilunar valve doesn’t get closed exactly at the cross over point .It gets closed little later than true cross over point.This gap in time is the hangout interval. This Interval keeps the arterial pressure not only to be sustained little longer but also slightly higher .

    This interval is an indirect( inverse) marker for vascular impedance of the distal draining circulation .The impedance is same as vascular resistance for all practical purposes.Since pulmonary circulation is a low impedance circulation , it has a wide hangout interval and the systemic circulation vice versa.

    How much of S2 widening is contributed by RBBB in ASD ?

    This is not known .But it has a minor role in prolonging S2 split. This is because , the RBBB in ASD is most often incomplete and peripheral one .( Pesudo RBBB due to RVOT dilatation )

    What happens to S2 when pulmonary arterial hypertension develops in ASD ?
    It is often narrow and fixed . Pulmonary arterial hypertension makes the pulmonary circulation to behave like systemic , hence the impedance becomes high and the hang out interval is significantly lost and second sound is narrowly split. (But fixity may be maintained.)It also depend upon the RV function and associated RBBB. RV dysfunction and RBBB both tend to widen the split.*Mild PAH usually does not alter the S 2 splitting

    Is there any other cause for wide and fixed splitting of second heart sound ?

    Having known the reasons for widening and fixity it is easy to understand , a patient with right heart failure and RBBB can have a wide and fixed split .

    Widening is due to RBBB (Delayed activation of RV ) . Fixity is due to severe right heart failure makes the RV out put relatively constant .(As RV inotropism is not good enough to handle the inspiratory augmentation of RV end diastolic volume.)

    Why in VSD the second heart sound is not wide and fixed split even though hemo- dynamically it fulfills the same hemodynamic scenario ?

  • Guess the answer .It will be posted soon.

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    Acute massive  pulmonary embolism is a dreaded medical  emergency  . In the past,  surgical embolectomy was the main option . Now , we have thrombolysis as a viable option.But , it does not work in all cases.* (90% success ?). It is critical to evaluate the success of thrombolyis , before embarking upon rescue embolectomy.

    As it is often in critical care  medicine , this decision making is not easy .

    The key question is how long , we shall wait before labeling  thrombolysis a failure !

    In-fact , premature  assessment is the commonest cause for failed thrombolysis. True failure is different from deemed to be a  failure . This  is often related  to  , lack of patience  among  the   members of  treating team . Unlike acute MI ,there is not a  strict time window to  follow .The issue hear is ,  not lung salvage but  restoring VP/VQ and  dead space ventilation . The assessment is made , by clinical ,   MDCT ,Echo  parameters.

    When there is difficulty in judging success , clinical parameters will prevail over medical images !

     

    Key clinical parameters for monitoring

    • Heart rate
    • Saturation
    • Blood pressure

    There are  four  options  available to manage in  failed pulmonary thrombolysis.

    1.Emergency embolectomy in an unstable patient *

    2.Elective , planned embolectomy  in a sable patient **

    3.Repeat thrombolysis ***

    4.Continue Intensive heparin regimen  for up to a minimum of   72hours  and up to a week .

    *  Dismal outcome .

    ** Best option (Ironically,  these are the  patients , who improve  with medical  management , as well !)

    ***This is especially useful  when  partial success  is noted in a stable patient . ( For rescue thrombolysis it is  logical tom use TPA if SK was used initially and vice versa.) The logic here is the initial dose was  either insufficient or ineffective  to lyse the thrombus completely. If TPA is not available /or not affordable,  repeat SK can still be considered .It can be  safely administered within the 5 days of initial dose.

    **** Least popular and considered inferior but has worked wonders in many .

    How to manage a relatively  stable patient with a large thrombus load  in his pulmonary artery ?

    Option number 3 could be tried. Prolonged  monitored heparin

    What  are the surgeons concern about  management in failed pulmonary thromolysis ?

    Every  surgeon( Especially  the  cardiac  surgeons)  loves  to operate in a stable patient . If you hand over  a case  for pulmonary  embolectomy  ,  with  sinking  O2 saturation  and  falling  blood pressure  ,the outcome can be  easily predicted !

    Further, RV dysfunction  is notoriously known    for pump dependency  .  CT surgeons are vastly experienced   in  the intra operative tips and tricks of  managing  LV dysfunction (They may not be  in  so  in RV dysfunction !)

    Bleeding risk  is also high especially  in the milieu of   intensive anticoagualtion and thrombolysis .

    The mortality could be as high  as 30 % in many centers.

     

    Final message

    • The incidence  of failed pulmonary thrombolysis  is  often subjected to the whims and fancies of treating physician  and the imaging modalities used.
    • Timing of assessment is critical .One need to give a long rope for medical management  , in spite of the urge , to do something more. .
    • Clinical improvement should be the main guiding force.
    • Normalisation of tachycardia   ,  improving  trend  of  o2 saturation(  >90-95%)  , regressing  RV size are useful parameters.
    • Thrombus load  detected by a repeat  CT scan  ,  need not be  the   sole guiding parameter.In -fact , mobilising these patients for CT scan by itself is fraught with a risk of  worsening the hypoxia.
    • The issue of  tackling the source of thrombus should  be addressed separately .Luckily, the same anticoagulant protocol takes care of this issue also. It is rarely a emergent issue.
    • Deploying an  IVC filter as an emergency procedure is a bigger controversy .At best , it is useful in few high risk individuals with high risk mobile ileo-femoral clots .
    • Finally, not every one can handle this  situation .Ideally such  patients  should be  to be  shifted to a well established cardiac surgical  set up .

    From Chest journal

    http://chestjournal.chestpubs.org/content/129/4/1043.full.pdf+html

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    There were days when acute pulmonary embolism(APE) was almost always  diagnosed  post-mortem. We are in the era , where we can recognise most of  the  pulmonary  embolism  without any difficulty.

    Experience has taught us ,  when to suspect this dreaded  syndrome . Any  unexplained, dyspnea, hypoxia, tachycardia , syncope* with  vague chest discomfort  and  a predisposing condition (DVT , post operative  state ,etc) will make  acute PE highly likely .

    *Postural dyspnea and syncope is a classical finding in many.

    Pulmonary Echogram

    We have  advanced  multi detector CT scans  and MR angiogram , V/P scans and pulmonary angiograms  to diagnose and confirm Acute PE .What we fail  to realise  is we also  have a simple bed side tool  called echocardiography   to  rapidly detect,  assess the pulmonary  anatomy and its hemodynamic  status.  In fact ,  we can visualize  the entire  MPA, and its  bifurcation and to  certain extent RPA,LPA. It is strange  physicians  always  ask for pulmonary  angiogram to diagnose APE , when we have a totally non invasive  pulmonary echogram available at the bedside .It can  rule out almost all cases of  massive pulmonary embolism with a good festivity and specificity .

    How often Echo miss a Acute PE ?

    Echo may fail to image a thrombus if it is distal but it is very rare to miss a thrombus in MPA, and its bifurcation. Most of the patients with  massive pulmonary embolism , are likely  have a thrombus in the bifurcation.

    Even if  echo  fails  to image a thrombus , the effects of  acute  pulmonary arterial  hypertension on the tender walled  right ventricle  is conspicuous. In fact, the  effect of Acute PE on the RV morphology and function  is  the  single most important feature to suspect APE . This is also  considered as an indication for thrombolysis.

    The following  Echo features  suggest Acute Massive Pulmonary embolism.Imaging these patients may be difficult especially if they are acutely  dyspneic   .Luckily , pulmonary  artery short axis view can be obtained even in supine position  in most of the patients.

    • RV dilatation ( One popular criteria is End diastolic RV dimension > LV end diastolic dimension .It should be remembered ,  strict criterias  can not be followed in this high risk medical  emergency . Visual estimation of RV size is equally important.If in the para sternal long axis , RV is > 3cm it is significant . The only issue is, in patients with preexisting  COPD  RV size will not be useful to diagnose APE.
    • RA dilatation (this is also a usual accompaniment )
    • RV wall motion defect(Considered , as  RV SOS calls !)
    • Paradoxical septal motion
    • D shaped septum is  an absolute sign of distressed RV.
    • Tricuspid regurgitation(This depends upon the leaflet length and orientation, some may not develop in spite severe PAH )

    Less common features

    • Pulmonary  regurgitation
    • RA , RA appendage , IVC ,  RV clots

    Diagnosing  RV hypertension

    TR jet

    MPA  acceleration  time (Not useful in an emergency situation )

    Other thinks to look in Echo

    • LV function (Hypoxic  dysfunction  or associated CAD )
    • IVC for  thrombus source .
    • IAS anatomy : PFO may increase the chance for stroke as these patients carry the risk of further  embolus. When the RVEDP, RA mean pressure raise to APE, the PFO becomes hemodynamcially patent and may develop propensity to shunt the incoming thrombus to left atrium rather than right ventricle  as LA pressure is considerably  less than RV

    Unanswered questions

    At what  pressure RV begins to dilate ?

    This is not clear.The response of RV ,  to pressure overload is  not constant.  In acute raise of RV pressure ,RV tend to dilate  , while  in chronic PAH RV hypertrophies and dilates .It is  believed   , the first signs of dilation begin , even with a 30mmhg of PA pressure . So ,  even minor dilatation could become important in acute PE.

    Can RV dilatation alone  , be taken  as evidence  for hemodynamic instability ?

    Yes , but realise  ,  clinical , hemodynamic instability  is much more important than degree of RV dilatation  (Hypotension /hypoxia  )

    The curious behavior of RV and TR jet in APE ?

    Normal peak RV pressure is 25-30mmhg .In acute pulmonary  hypertension RV pressure is supposed to raise . But it does not always happen.It all depends upon how the RV respond to the sudden raise in its afterload.

    Some RVs fight vigorously and take on the challenge  imposed by pulmonary  embolus.These are the  patients  who show strong TR jets which may reach 60 mmhg. More  often , the RV  is stunned and overwhelmed  by the unexpected sequence of events and  lose the battle from the beginning  .They become  flabby  and dilated.These  patients  do not  show any significant TR jet ,  in spite of raising PA pressure. This implies,  a  good TR jet > 3.5 could  virtually rule out  severe RV dysfunction.

    (One  popular thought gaining ground is  , the primary determinant of   pulmonary artery  systolic  pressure  in Acute PE is the RV contractile force ,  rather  than pulmonary  impedance .)

    Hypotension is common in APE .What is  the relationship  between PAH and systemic blood pressure ?

    • Inverse relationship is expected . This often result in syncope in these patients.
    • Bernhiem effect
    • Hypoxic LV dysfunction

    Final message

    RV  faces the brunt of the  hemodynamic attack of acute PE. .Differentiating simple RV involvement  from RV dysfunction  is a difficult and subjective  exercise. But ,  it need to be done accurately as  RV dysfunction becomes an indication  for thrombolysis  . RV dilatation  , wall motion defect, mild PAH, all  indicate RV dysfunction . Diagnosing RV dysfunction is  better  done by the  treating physician who has the  overall clinical data.

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    Aortic regurgitation complicating VDS  is an important clinical  entity in congenital heart disease.It is  also  a popular case for the cardiology fellows in their  final clinical examinations . AR is a  late manifestation of VSD (usually in early  adolescent  or adult hood) .This develops due to loss of aortic valvular support provided by the inter ventricular   septum.

    In fact ,   IVS can be termed  as a foundation stone  on which  a  part of  aorta (Mainly its anterior part) rests . So, it is not surprising VSD patients  are prone to develop AR especially,  as they grow when aorta tires to outgrow the septal support . Further,  the hemodynamics of VSD has a crucial impact on the AR progression.(See image below)

    Pulse /Blood pressure

    Large volume pulse,  may be collapsing

    Peripheral signs of Aortic run off usually present

    Apical impulse

    Shifted down and out Hyperdynamic

    Murmur

    To and fro murmur (To -Systolic , Fro -Diastolic )

    It is differentiated from continuous murmur by a distinct reduction  in the intensity of murmur towards the end systole and a different murmur  appear  in diastole  . While , a continuous murmur  is  a single murmur  that peaks  around sound  heart sound , overlaps the second  heart sound and spills well into diastole.

    Other useful diagnostic clues

    • Usually the VSD  is  restrictive  .Left to right shunt is often below  2:1
    • With the onset of AR  ,there is  further reduction in the left to right shunt of VSD
    • Hence,progressive pulmonary arterial hypertension is uncommon and Eisenmenger is reaction is very rare in  VSD with AR.
    • Presence of AR makes  LV dilatation disproportionate to VSD  shunt  (LV size  is not useful to assess the  hemodynamic  significance of VSD)
    • LV dilatation invariably means significant AR rather than VSD.  VSD induced LV enlargement  is  usually less conspicuous as it is  represents  physiological flow across mitral  inflow .  While , AR is a high gradient leak  from a non-physiological chamber (Aorta)
    • ECG volume overload of LV   is  evidenced by  more prominent * q waves in  V5 V6

    *Double dose of volume overload (AR +VSD)

    Management

    • If AR is mild ,only VSD closure is advocated *
    • If AR is moderate  , repair of aortic valve is  considered along with VSD closure.
    • For severe AR , Aortic valve replacement or repair with VSD closure mandatory.
    • Device closure of VSD and percutaneous  aortic valve replacement  not feasible at the moment .May be a future possibility.

    * If both  VSD and AR are very small ,  simple follow up , and observation (Leaving the patient happy!)  could be a distinct option !

    Pathogenesis of AR in VSD : The landmark article from Japan in 1973 by Tatsuno  and Sakakibara

    http://circ.ahajournals.org/cgi/content/short/48/5/1028

    Thanks to circulation .Such articles are made available .

    http://circ.ahajournals.org/cgi/reprint/48/5/1028

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    Acute pulmonary embolism is a vascular  emergency.Massive pulmonary embolism needs immediate thrombolysis or embolectomy. Success rate  of  thrombolysis  appears good . But , the symptom improvement  is slower .

    Sterptokinase is the commonly used drug to dissolve the pulmonary thrombus  . (Except in USA , where they  prefer the much costlier TPA )

    The sterptokinase  adminstered with the following protocol

    • 2.5 lakh Unit bolus over 30 minutes
    • Follow with 1lakh unit /per hour for the next 48 hours (Up to 72 h)

    When to start Heparin infusion ?

    For TPA ,  there is no confusion .Heparin must be started immediately after the completion of TPA infusion (100mg in 2 hours)

    Cardiology community is divided for heparin protocol with  streptokinase. Because , streptokinase is administered over 48hours it is thought heparin is not required during  this period.But in reality , it  implies , we  deny a role for this  powerful anti thrombin  in the critical hours of ongoing  intra vascular clotting . Hence  logic demands  to start heparin  along with  streptokinase.

    There is further concern that,  the dissolved thrombus generate pro coagulant  debri , that will negate the benefits of thrombolysis. Oral anticoagulants  are supposed to be started  as soon as the diagnosis  of pulmonary embolism is made. In that case , heparin will be required  much earlier as  warfarin has to be overlapped with heparin.

    We would  argue for  , a careful simultaneous infusion of heparin (May be 500units/hour ) .Strict monitoring of APTT is warranted.

    What does the clinical  trials say ?

    There are few studies address this specific issue .I am still searching the data base. Once i get it i will post it. The readers  may also try to find an answer .

    http://ats.ctsnetjournals.org/cgi/content/abstract/62/3/880?ijkey=cdcd223289bd75ffb49a8d1cd1c73d35fe76e08d&keytype2=tf_ipsecsha

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    Planimetery is the age old method to measure the mitral valve  area( MVA) by echocardiography.

    Advantage

    • Simple modality
    • 2D echo  is enough
    • Doppler errors avoided
    • In the presence of MR, planimetery orifice has an edge over other methods

    Disadvantage

    • Optimal gain setting becomes  important .There is  significant inter and intra observer variability.
    • Shape of the orifice is not constant  ( MVO is funnel like) . Narrowest diameter is usually measured.
    • Planimetery is  a purely an anatomical orifice,while blood flows through both primary and secondary mitral orifices .Sub valvular fusion makes secondary MVO the  narrowest point  . Measuring it becomes difficult as it has no defintion of border.
    • Gross errors possible in calcified valve.
    • In post commissurtomy  the  lateral extent of split is often  not tractable

    How to improve the accuracy of planimetery ?

    Color Doppler aided  2D  planimetery . This can improve some of the limitations , as  it provides a hemodynamic MVO(Some what physiological ) Of course  , pressure halftime derived MVO is purely a physiological orifice .

    Other options to measure MVO

    1. Pressure half time
    2. Continuity equation
    3. PISA method

    Advantages and disadvantages  of Pressure half time derived MVO will be posted soon.

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    Bio-chemical diagnosis of cardiac injury or infarction is  well  documented modality for many decades. Now , acute coronary  syndrome is diagnosed  by a battery of tests  that  detects the  proteins leaking from the  injured  myocardium.

    Nephrologists have long been aiming for  such a  marker for ischemic  renal injury  (Not withstanding the fact , they are already blessed with two age-old molecules  creatinine and BUN !)

    Neutrophil gelatinase associated Lipocalin (NGAL)

    • This is 25 Dalton molecule  richly secreted within renal  cortical cells in response to ischemic injury .
    • It is released without  modification in the  urine  .High urinary levels  of NGAL  reflect  acute renal  injury.
    • Early experience shows it  is a  promising  investigation and could  become a regular biochemical test in the near future.
    • Urine level of  NGAL >250 ng/ml , 2 hours   after cardiac surgery  predicts impending renal failure  in the next 24-48 hours .The advantage is , it NGAL raises well before serum creatinine.

    NGAL After cardiac surgery

    http://cjasn.asnjournals.org/cgi/content/full/3/3/665

    Lipocalin following PCI

    Bachorzewska-Gajewska H et al. Neutrophil-gelatinase-associated lipocalin and renal function after percutaneous coronary interventions. Am J Nephrol 2006; 26: 287-292.

    www.ngal.com

    References for  NGAL

    http://www.ngal.com/literature/popular_reviews_of_the_nature_of_ngal_with_a_focus_on_acute_renal_injury

    Final message

    • Cardiologists  and cardiac surgeons  have started  performing  complex    PCIs and  CABGs in  patients with   delicately  and precariously balanced renal function.
    • While ,  cardiologists   challenge  the kidneys with high  osmolar contrast agents ,  the surgeons stress it with extra corporeal circulation.  Many of these patients also  have co- morbid conditions .
    • Often , the cardiac outcome is directly linked to pre /post procedural  renal function .Nephrologists usually  arrive  late  into the filed (Creatinine SOS calls !).By this time the full-blown ATN sets in many.

    Now , we have a tool to identify impending ARF , it gives us  little more time and  flexibility in managing the issue .

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    Medical science is  not like mathematics or economics .

    • It is about how a  bundle of human cells(organs) behave at times of adversity .
    • It is  about how our mind  takes on the body .
    • It is also   about , how the care takers  Heal/Manipulate /Manhandle  these cells at times of distress !

    We know, two persons with identical injuries , sustained in a car crash one dies within an hour  , while the other with a  many fold serious injury successfully fight the trauma and walk out of hospital with victorious  .That is the fighting spirit .This  is either  inherited  are  nurtured or both.

    This implies , an accidental injury may be an  external , unpredictable  event,  while the  response to  that injury is predetermined or even a predictable response !

    In the name of modern science , we “the human animals” are trying to buy this fighting spirit  with money.We are made to believe ,  survival and well-being is a commodity and  can be  bought with high cost  medicines , and high cost care .

    Remember  , one of the most astonishing medical  fact is , while we  may struggle to induce  swine flu  in  a laboratory on a given  individual ( Even if ,  H1Ni  viral  concentrate is  infused or inhaled  )   , an  other person gets this disease  , while simply  flying over an  infected country  . Such is the complexity  of  the host response  system in medicine .

    So , it is foolish to think health can be bought or maintained  with  money power or modern hi-tech medical care .At best it can save   few lives  with  its   life supporting drugs and devices . Ultimately,    human survival  is determined  by the way we  live  and the way  our  ancestors lived and how we fight the illness.

    Yogi’s  of  Himalayas lived for more than 100 years without the need for drug eluting stents and LV assist devices .

    Having totally misunderstood  the concept of health and illness the world is wondering how on earth , we can reduce the escalating cost of  healthy living  (pseudo health  !)

    An article in the current NEJM ponders over ,  Why in  Grand junction,  Colorado ,USA ,  the health care cost is very much lower ,  without compromising the quality of life and survival.

    The answer is very simple .There is some body in that county , who  dares to think beyond  raw  science  and adds  little  bit of common sense ! Obviously he has to be rewarded and  this  model need to be replicated  elsewhere.

    http://healthpolicyandreform.nejm.org/?p=12706

    This article discusses the phenomenon  of  high quality , low cost medical care , but what it misses out is , the reverse could also be true !

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