Feeds:
Posts
Comments

Archive for the ‘cardiology -Therapeutics’ Category

How to manage complete heart block during pregnancy ?

Posted in Cardiology - Clinical, cardiology -Therapeutics, Uncategorized, tagged , , , , , , on September 19, 2010| 1 Comment »

For the lay public   the term complete heart block (CHB) often convey a sinister message . When  encountered in   pregnancy,  it is   frightening    for the  physicians as well .  One need not  say  . . .the anxiety to the Obstetrician !

Congenital complete heart block is the usual etiology. Though there are other important causes of CHB in general population , it is very rare to  get an  ischemic or  degenerative heart  blocks  in the reproductive age group.

There are  many  ways it can present .

How does it present ?

  • Symptomatic CHB detected  first time during ante natal screening
  • Asymptomatic CHB detected incidentally during ante natal screen
  • CHB first time recognised during active  labor. Either symptomatic /Asymptomatic
  • A more familiar  situation  is  CHB  diagnosed in child hood . Women in question can undergo an  elective marriage and a managed  pregnancy.

* The success of modern medicine  lies in the  mantra  of  “early  diagnosis ” .Ironically , early detection  of CHB in  pregnancy adds  considerable anxiety  to mother , family  and the treating physician  . So ignorance  can be a  bliss here ,  as 99/100 with CHB  would not require any intervention during pregnancy  .But , in this hyped up scientific world  one  needs  lot  of courage to  simply watch a pregnant mother with a heart rate of 45  !   .You are tempted to do something . We have seen CHB presenting  in labor room as emergency and delivering successfully  by vaginalis .

Where is the pathology in congenital complete heart block ?

It is  usually due to anatomical discontinuity between AV node and the bundle of his. The most fortunate thing  here is ,  these patients  develop a junctional escape rhythm at around 40-45/mt .This is enough for most basal activities. Further this junctional rhythm can increase   up to 100 in many, or  even up to 120 at times of stress.(Accelerated junctional  rhythm )* .An ECG which shows a narrow qrs  complex is nearly  100 %  specific  for a stable junctional escape rhythm.

What is the hemodynamic stress of pregnancy ? Will a heart rate of 50 /mt enough , to support the labor or cesarean section ?

Nature  is a wonderful equalizer. What the pregnant mother requires is a good cardiac output to nourish the baby as well as herself. A heart rate of 50 is often able to sustain and support the entire pregnancy with ease.

How it is done  ?  . . . is  it not simply  amazing ?

In pregnancy there is less of  systemic vascular resistance due to various reasons (Low impedance  placental circulation, reduced sensitivity to Angiotensin 2  ) . The heart can always increase it’s out put by increasing  the heart rate or stroke volume.  In  patients with CHB , as the  rate can not be increased much , the heart  accepts  the  alternate option quite easily without  any protest  . The low SVR also facilitates  increase in stroke volume. This  is the reason pregnancy  is  often well tolerted  even with the heart rate < 50 /mt.

But , at the time of delivery increase in heart rate may be important in some.We do not know , who will require this HR support .This makes it mandatory to have a  temporary pacer standby.

What are the ominous signs and symptoms of CHB in pregnancy ?

Having discussed a lot about the benign nature of congenital CHB ,  one need to realise it is also a potentially dangerous heart rhythm . Syncope, symptomatic hypotension  (BP<90) and some times  signs of PIH ,  all possibly indicate a pacemaker support .

Can we do an exercise test  to  assess  the chronotropic competence in pregnancy ?

Tread mill test is generally not done  in pregnancy. It is a good option ,  to test the adequacy of heart rate increase during activity . If the heart rate increases up to 100 -120 it is a good response .

What about holter ?

A less predictive , but more acceptable investigation is the 24 hour holter monitoring  that gives a rough idea about lowest and highest heart rate. If there is a  long pause > 5 sec ,  she will be a technical candidate for permanent pacing !  once you have documented this ,  we will be sued if not paced however asymptomatic the patient is ! So beware of this investigation !

Atropine stress test ?

This again is a simple test , that will measure the chronotropic reserve. A concern for fetal tachycardia is genuine !

Pre-conceptional  counseling

A patient with congenital complete heart block should never be adviced against pregnancy.

“Pace and become pregnant ” strategy is also not warranted.This is based more on the perceived  scientific approach the and  litigation  fear  than reality !

Only issue is we have to make sure ,  the women in question has  adequate hemodynamic reserve. This  can be easily accomplished  by asking some basic questions about exercise capacity .Or , she can be put on a  tread mill (or atropine stress test). If the heart rate increases up to 100/mt  there is absolutely , no need to put  permanent pacemaker.

Peculiar  issues in   pregnant  women with permanent pacemaker

The paradox of modern medicine  felt at it’s  best here !

We think ,  we are  implanting   a  pacemaker in CHB of  to provide good hemodynamic support  during the stress of labor. But a  fixed rate VVI pacemaker will not do this job . The real reason  to put a pacemaker is to avoid a dangerous bradycardia during the labor .

Hence ,   patients  with CHB carry equal  concern (if not more !)   during labor as the pacemaker fires at a  fixed  rate of 70/mt and  the native rhythm is often suppressed due to long-term pacing . Hence their heart rate often fail to increase   beyond the pacemaker rate of  70  . Paradoxically , patients with untreated  CHB (with their native rate ) , can increase their  heart  rate often up to 100-120  at times  of stress .This is possible because  their AV node is still under the control of autonomic system , while artificial  pacemakers* are not !

*Some of the current pacemakers have overcome this problem with rate adaptive pacing .

Mode of delivery ?

  • Natural , expected
  • Induction  of labor
  • Elective cesarean
  • Emergency Cesarean

Can complete heart block per se , become an  indication for cesarean section ?

No. It is always an obstetrical indication .It  is better to avoid GA / Regional anesthesia  in cardiac disease. The stress of  second stage of labor is always less than   that of   surgery provided it is not unduly prolonged .

Assisted /accelerated vaginal delivery is the  best option .However , one should be ready for any intervention. Some obstetricians  feel  that, elective cesarean section  could  be less stressful than  labor( which could be prolonged for some unpredictable reasons  ) while a ,  Cesarean section  can not  be a  prolonged one  !

Cardiologist’s role in the labor room

The role of cardiologist is to provide support to the obstetrical and anesthetic team   prevent   extreme bradycardia. Inserting a temporary pacemaker with back up pacing of 50/mt is preferred.Trans-jugular approach is ideal .In difficult cases fluroscopy guided temporary pacing in cath lab is advised.

Role of temporary trans cutaneous pacing  as stand by ?

This method of pacing with two sticky electrodes in the chest wall  with external pacing .It is proven , efficient useful modality of pacing in coronary care units  .However this can be a substitute for  only few hours of support . May have patient discomfort .In places from expertise for temporary  pacing is not immediately available  this can be used .However presence of such a machine increase the comfort level of physicians.

Is there a rate adaptive temporary pacing available ?

Currently available temporary pacemakers  are not rate adaptive , and hence we have to pace  roughly at  about 90 or 100 give  allowance  for labor related demand  (We would not know, how much  the mother is compensating with increasing with  stroke volume ) in this case pacing rapidly may  reduce the net cardiac output as the mother’s heart is  used to operate  at different  point in the  frank staling curve right  through the 10 months

 

Anesthetic issues in complete heart block  during cesarean section

Anesthetists have a concern here.(Genuine one of course)  A cardiologist  with a standby temporary pacemaker is  to be arranged. Cardiologist  will decide whether to have sheath or sheath plus lead  in standby mode .

Many anesthetic drugs have an adverse effect on heart rate. Drugs to be avoided are  Fentanyl ,suxamethonium, neostigmine  Induction with propofol has risk of worsening bradycardia . Controlled epidural anesthesia is preferred .This ensures slow onset anesthesia and limits hemodynamic instability.Bupivacaine is known to cause depression of heart rate .(Even with epidural route )

Miscellaneous questions

A often debated  query among obstetricians : Should I refer a CHB patient  to a cardiologist or electro-physiologist ?

There  is no  academic answer  to this question.Logic demands conservative (without compromising patient/baby  safety ) management .Electrophysiologists are rarely conservative

Radiologically how safe it  is ( for the fetus ) to undergo permanent  pacemaker implantation ?

For implanting a permanent pacemaker, about   15 minutes of  fluro time is required which could be significant .So it should be used in  exceptional situations only.

What is the effect of maternal  complete heart block on the fetal hemodynamics?

Nil or almost nil (Surprise ! surprise)

 

 

Issues during  weaning of pacing  in postpartum

Post partum period can be troublesome in few as fresh  blood volume  injected from contracting uterus.If temporary pacing has been done , it is usually possible to wean by 48 hours. Permanent pacing  is rarely required

 


Final message

  1. Congenital complete heart block* during pregnancy is  a well tolerated rhythm.
  2. The panic  this   entity creates is  largely unwarranted. This conclusion is derived from decades of observation by eminent clinical cardiologists.
  3. The heart  rate reserve can be estimated by a  minimal exercise test .(Atropine test with caution )
  4. Insertion of either permanent  pacemaker is not necessary* in most .
  5. If there is symptomatic hypotension /syncope during any time during pregnancy  pacemaker becomes mandatory .
  6. During labor /or cesarean section  insertion of temporary pacemaker  “may be” needed. Hence a cardiologist stand by with a temporary pacemaker  is advised to tackle any  emergency(Which is anyway  highly unlikely  !)

.

* This rule is applicable only in  isolated congenital CHB.  Ischemic CHB  or CHB  with associated LTGV,AV canal defects etc  need special attention.

References

Books

Elkayam

Journal articles

The famous paper which first described safe outcome four patients with CHB in preganancy without pacemaker

http://www.jpgmonline.com/article.asp?issn=0022-3859;year=2003;volume=49;issue=1;spage=98;epage=98;aulast=Mehta#ref3

http://medind.nic.in/iad/t06/i1/iadt06i1p43.pdf

http://www.joacp.org/index.php?option=com_journal&task=check_subscription&id=1077

anesthetic issues in pregnancy and CHB

http://www.ispub.com/journal/the_internet_journal_of_anesthesiology/volume_12_number_2_1/article/labour_analgesia_in_a_patient_with_complete_heart_block.html


Read Full Post »

Which is the best vasoconstrictor in shock ? Dopamine or Norepinephrine ?

Posted in cardiac drugs, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, Uncategorized, tagged , , , on September 6, 2010| Leave a Comment »

Belgium SOAP  wants a  knock out punch to  Dopamine in shock !

Vaso constrictors are  the mainstay  drugs  in the management of shock  syndrome. While ,the ultimate outcome depends on the primary  cause for shock, these vaso- constrictors  have  a critical role in sustaining life , till the organ function is recovered.

The physicians world  over,  differ  in their choice of  vasoconstrictor support .They  are almost divided   equally in their usage between  dopamine and norepinephrine  .

Surprisingly,  there  has been no one to one comparison trial till  this study   in 2010 .This trial  is called SOAP 2 published from  Brussels , BELGIUM .It  compared the usage of these two drugs in variety of shock  syndromes. It favors norepinephrine use ,  that includes  cardiogenic shock as well.

The disadvantages of dopamine noted in this trial was

  • Increased  risk of arrhythmias
  • Increased rate of death  in cardiogenic shock

The implication of this trial may force the ACC/AHA guidelines , which  advices  dopamine as the first choice in shock syndromes especially in cardiogenic cause.

Read Full Post »

How common it is , for an “Acute STEMI” to present with stable ventricular tachycardia ?

Posted in cardiology -Therapeutics, Cardiology -unresolved questions, cardiology- coronary care, Cardiology-Arrhythmias, Uncategorized, tagged , , , , , , , , on August 31, 2010| 2 Comments »

Acute MI and ventricular tachycardia are closely related entities.In fact ,  the earliest response to ischemia could be a VT .But what  is peculiar about this VT is,  it  almost always degenerates into VF  within a minute or so.(Unlike idiopathic VTs /RVOT/LVOT VTs)

This arrhythmia in  every sense  can be called as  “primary VT“ which is the cause for “primary VF”

It is strongly  believed VF cannot occur without  a  brief episode of VT preceding it .Logic would also suggest  the ischemic myocardium  can not suddenly  become chaotic  “with the first  beat  “. There is little documentation available to unprove this presumption.

In spite of  this intimate relationship between VT and STEMI ,  it is very rare for a STEMI patient   to enter  ER with a sustained stable  ventricular tachycardia .  While  many VTs are known for it is hemodyanmic stability and immunity against degeneration   into  VF  , it is extremely rare  for  VT to remain as VT  in acute STEMI.

*Note : NSVT can be common   in  hospitalised patient in the coronary care unit . In our experience a sustained  VT in STEMI  will enter the VF mode within 60 seconds .If not , it is a highly  unusual phenomenon .

“But surprise is the other name of medicine ”

Here is  case report, a patient walked into coronary care unit with sustained( relatively stable) VT with LBBB morphology .We thought  it was   a  non- ischemic VT  (cardiomyopathy  , RVOT etc) .As we were examining him,  he became  unstable  and  was shocked 50 J biphasic .To our surprise a classical STEMI was unmasked and he was immediately  thrombolysed.

* It is possible ,  the patient had  suffered a  old MI  which got infarcted again and the VT  was scar mediated .

But it is still uncommon  for  it  not to degenerate into VF  with fresh  STEMI

Final message

Nearly all episodes of  ventricular tachycardia , that occur in the early minutes/ hours of  STEMI would degenerate into VF.This includes  VTs  that  occur within the CCU . Most  of the times , the CCU physicians and staffs  revert this VT  promptly and deny the  ventricles  from performing the dance of death !

It is extremely rare for an acute ischemic VT associated with STEMI to walk in to the hospital,  which our patient did !

Further reading and unanswered questions

  • What determines a VT to degenerate into VF ?
  • Why macro-reentrant , scar dependent VTs  often  are well tolerated ? ( In spite of LV dysfunction !)

Read Full Post »

Let us welcome this . . . A forum for cardiac safety !

Posted in bio ethics, cardiology -Therapeutics, cardiology-ethics, Uncategorized, tagged , , , , , , , on June 20, 2010| Leave a Comment »

There are thousands of forums for medical science.

Most are aimed at research.  Few are available  to scrutinize  research.

“Cardiac safety research consortium “

This one from Duke university ,  is a great beginning in collaboration with FDA .

Let us welcome , this whole heartedly and wish all success in it’s motto !

Namely , exposing all safety issues in the modern cardiac therapeutics .

Read Full Post »

The time less windows of STEMI and a curious debate on primary PCI !

Posted in Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, Uncategorized, tagged , , , , , , , , , , , , on June 18, 2010| 1 Comment »

This article is in response to the prevalent belief  about  primary PCI for STEMI   endorsed by world cardiology forums. (Caution: A highly personalized version)

Time window in STEMI

  • Is the window half-opened  or half closed ?
  • Is it open at all ?
  • Or ,does it open only for primary PCI  ,and tend to close down  bluntly for thrombolysis

Modern medicine   grew faster than our thoughts .We have witnessed the audacity of advising  arm-chair treatment  for MI  till later half of   last century . Now we are talking about  air dropping of patients   over the  cath lab  roofs  for primary PCI.

Still ,we have not conquered the STEMI. While ,  we have learnt to “defy  death” in many patients  with cardiogenic shock , we continue to lose patients(“Invite death “)  in  some innocuous forms  of ACS due to procedural  complications  and inappropriate ( rather ignorant !) case selection.

Note : The ignorance  is not in   individual physician mind ,   it is prevalent in the whole cardiology knowledge pool.

The  crux of the issue for modern medicine is ,  how to reduce risk  in patients who are at  high risk and how not to convert a low risk patient into a high risk patient by the frightening medical gadgets.

In other  words ,  arm chair treatment for STEMI was  not (Still it is not !) a dustbin management . It has a potential to save  70 lives  out of 100. What many would  consider it as  ,  nothing but  the natural history of MI .

Medical management of STEMI is ridiculous !

That’s what a section of  cardiologists try to project by distorting the already flawed evidence base in cardiology. Some think it is equal  to no treatment. Here we fail to realise, even doing none has potential to save 70 lifes out of 100 in STEMI who reach the hospital.

Out of the  remaining , 10 lives   are saved by aspirin heparin (ISIS 2) and the concept of coronary  care . Another  7  lives are saved by thrombolysis (GUSTO,GISSI) . PCI  is shown to save saves one more life (PAMI).The remaining 6-7 % will die in CCU  irrespective of what we do .

Of course , now medical management has vastly improved since those days  .  A  thrombolysed ,  heparinsed ,  aspirinised ,  stanised  with adequately antagonized   adrenergic ,  angiotensin system   and   a proper coronary care ( That takes care electrical  short-circuiting  of heart)   will score  over interventional approach in vast majority of STEMI patients.

Now comes the real challenge . . .

When those 70 patients who are likely to survive  , “even a arm-chair treatment“, and the 20 other patients  who will  do a wonderful recovery with CCU care ,  enter  the cath lab  some times in wee hours of morning  . . .what happens  ?

What are the chances  of   a patient  who would otherwise be saved by an arm-chair treatment be  killed by vagaries of  cath lab  violence  ?(With due apologies ,statistics reveal  for every competent cath-lab   there are at least  10  incompetent  ones  world over !)

In the parlance of criminology , a hard core criminal may escape from  legal or illegal shoot out  but an innocent should  not die in cross fire , similarly ,  a cardiogenic shock patient with recurrent  VF  is  afford to lose his  life , but it is  a major medical crime to  lose a simple branch vessel  STEMI (PDA,OM,RCA )  to die in the cath lab,  whom in all probability  would have survived  the arm chair treatment.

Why this pessimistic view against primary PCI  ?

Yes, because  it  has potential to save  many lives  !

Time and again ,  we have  witnessed  lose of   many lifes  in many  popular hospitals in  India ,  where a   low risk MI  was  immediately  converted  to a high risk MI  after an primary  PCI with number of complications .

I strongly believe I have saved 100s of patients  with  low risk MIs by not  doing  for primary  PCI in the last  two decades.

*The argument that PCI confers better LV function and longterm  beneficial effect is also not very convincing for low risk MIs .This will be addressed separately

The demise of comparative efficacy research.

Primary PCI is superior to thrombolysis  : It is agreed , it may be  fact in academic sense .

Experience has taught us , academics rarely succeeds in the bed side.

“superiority studies can never be equated  with comparable efficacy”

Only the  questions remain . . .

  • Where  is comparative efficacy  studies in STEMI ?(Read NEJM article )
  • Why we have not developed a risk based model  when formulating guidelines for   primary PCI ?
  • Is primary PCI for a PDA /D1/OM infarct worth same as PCI for left main ?
  • Is high volume center guarantee  best outcomes ?

Who is preventing comparative efficacy studies ?

Primary PCI : Still  struggling !

This study from the archives  of internal medicine tells   us , we are still scratching  the tips  of  iceberg (Iceberg  ? or Is it something else ?)  of  primary  PCI

Even a  pessimistic approach can be  more scientific  than a optimistic  !

When WHO can be influenzed and make a pseudo emergency pandemic  and pharma companies  make a quick 10 billion bucks  ,  Realise how easy  it is  for the   smaller ,  mainstream cardiology literature  to be  hijacked and contaminated .

Final message

Why we reverently follow the time window for thrombolysis,  while  we rarely apply it for PCI ?   This is  triumph of glamor over truth . The open artery hypothesis remains   in a  hypothetical state with no solid proof  for over 2o years since it was proposed.

Apply your mind in every  patient , do a conscious decision  to either thrombolyse  ,  PCI or none . All the three are  equally powerful approaches in tackling a STEMI , depending upon the time they present .Remember , the third modality of therapy comes free of cost !

Never think ,   just because  some one  has  an access to a sophisticated cath lab 24/7   , has a iberty to overlook the  concept of time window  !

Remember  you can’t  resuscitate   dead myocytes , however advanced your enthusiasm and   interventions are !

Realise , common sense is the most uncommon sense in this hyped up human infested planet.

Read Full Post »

What is the importance of recognising slow -slow AVNRT ?

Posted in cardiac surgery, Cardiology - Clinical, cardiology -Therapeutics, tagged , , , , , , , , , , on June 3, 2010| 1 Comment »

AV nodal reentrant tachycadia(AVNRT) is the commonest mechanism of SVT. It is divided into slow-fast, fast-slow, slow-slow , representing the two limbs of he circuit.

Slow -Slow circuit is  the rarest  type of AVNRT.  It should be appreciated  ,  the scientific validity of  slow-slow circuit is  applicable  only in relative terms . A virtually  similar antegrade and retrograde limbs with identical conduction velocity and refractory  properties  , can neither  initiate  nor  sustain an AVNRT.

Caveat in the definition of slow -slow AVNRT.

Even though ,  we call it   a  slow-slow  tachycardia , one of the limbs need to be faster than the other.  So , every slow -Slow AVNRT in reality will have  two types

  • Slow- Slow ( Still , faster than antegrade slow) mimic a slow-fast physiology
  • Slow( Faster than retograde slow )  -Slow closely mimic typical  fast slow .

Implication for electrophysiologists  and   points of contention for the ablationist !

  • In Slow -Slow AVNRT ablation we do not know exactly ,  which of the slow pathway is being ablated , unless we specifically  analyse  the post ablative  data.
  • Very often it is not done.Every one in the lab is happy , for breaking the tachycardia circuit. Only after the procedure is over , we may realise the tachycardia is not really killed as it finds an alternate highway to complete  the short circuiting of heart.
  • We need to  suspect this type of AVNRT   prior to the  procedure .Electrophysiologist  shall  spend little   more time and a wide area ablation done , in the vicinity  of coronary sinus ostium can be attempted. .

It is not a smart practice to advocate  wide area ablation as a routine protocol in all AVNRT

as it directly  increase the rate of complication >

Final message

A   hurriedly  done slow pathway ablation  which  may  temporarily terminate the AVNRT ,only to recur later as  the retrograde  slow pathway may again form  a substrate  .The area of slow conduction  acts as a turnaround gateway and capture  the  retrograde fast  pathway which  could be  available in plenty in the anterior aspects of AV node  .   (Note : The unablated  slow pathway  now  form the antegrade  circuit )

Read Full Post »

Should post prandial angina be classified as unstable angina?

Posted in Cardiology - Clinical, cardiology -ECG, cardiology -Therapeutics, Cardiology-Coronary artery disese, Infrequently asked questions in cardiology (iFAQs), tagged , , on May 25, 2010| Leave a Comment »

Stable angina is graded by Canadian cardiovascular society classification ( CCSC ) by 4 grades. Angina at rest  usually  denotes unstable angina. But,  patients with stable angina  may also experience rest angina according to CCSC ,  still this is   not considered as  unstable angina by many . Post prandial angina is one such  example.

Few consider post prandial angina as unstable angina . This sort of reasoning can not be faulted .

In  the logical sense ,  we are dealing with varied  categories of unstable angina.  The importance of diagnosing unstable angina is to intervene early ,  so that we can avoid  major adverse outcome .

The problem in CAD is , often , the plaques and angina do not  obey the conventional  rules  !

.The following permutations and combinations could be  observed in any coronary care unit .

  1. Unstable angina –  stable plaques  – stable ECG – stable patient
  2. Unstable angina – unstable plaques  –  unstable patient
  3. Unstable Angina  – unstable plaque  –  stable patient
  4. Stable Angina –  unstable plaque  –  unstable patient
  5. Stable angina  –  stable plaque  –    stable patient
  6. Stable angina –  unstable  plaque  – stable patient

Among the above 6 categories  2nd  is   probably  the most dangerous group and category 5 is most benign.

Post prandial angina is a serious  form of angina.It implies  , even   diversion of  little blood to GI system immediately after a meal can provoke an episode of  ischemia  .This infers a  very tight  lesion somewhere in the coronary tree,  very often it could be the  left main or proximal LAD.

Of course ,  there is  another mechanism for post prandial angina, namely GI neurotransmitters  like gut peptides acting as a coronary vasoconstrictor.

Snippets on  post prandial angina  .

It is also recognised , post prandial angina occurs more often during dinner, followed by lunch and breakfast. Carbohydrate foods are  more likely to precipitate it .

Does PPA cause ST depression ?

Logically it should .In reality It happens in few .

How to manage it ?

It is very important to recognise , even though this article  argues  for including  PPA  as UA, there is no acute thrombotic process during  an   episode of  post prandial angina . In fact , it is  more of a secondary UA due to altered  blood flow pattern.

So , do not admit these patients  in CCU and administer  heparin or 2a 3b blockers.  (Unless of course ,they have other forms of rest angina )

Link to reference

1 PP angina angiographic correlation

2.Effect of carbohydrate diet on postprandail angina

3.Hemodynamics of eating !

Final message

Post prandial angina has all the characters  of a severe form of angina  .There  is every reason to label it as UA .It is suggested , ACC,ESC, AHA  should consider including  post prandial  angina as  UA or at least  UA equivalent .This would help intervene this entity early.

Read Full Post »

How to lose the golden hour in the management of acute myocardial infarction ?

Posted in Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology -Therapeutics, cardiology- coronary care, Uncategorized, tagged on May 22, 2010| Leave a Comment »

“Time is muscle” is  the often quoted “sermon”  in emergency cardiology , implying ,  every patient with STEMI should be taken up for   thrombolysis or primary PCI at the earliest  after the onset of symptoms.

While thrombolysis is the proven method of reperfusion for over 25 years , Primary PCI , a costly , risky but better  alternative is struggling to prove it’s impact in the world of acute coronary syndrome ! (Some may  see non- sense in this statement !  But it still can make sense  !)  In India hardly 3 -5 % of STEMI is taken for primary PCI .This includes the much hyped corporate cardiology centres.

If primary PCI is a revolutionary reperfusion strategy  , why it has not invaded the cardiology field  by strom  ?(A pathetic 5% growth over 15 years will tell the true story !).

We know 6 hours is the acceptable time window before which some form of repefusion must be attempted. A time limit of 90minutes   for the   “door to  balloon”   is  fixed  as optimal for primary PCI .

In other words ,  if primary PCI can be arranged within 60-90 minutes   one  can afford to lose the golden hour !  How does this logic works ?

In fact it does not work ! in many .

The 90 minute criteria is not strictly followed . Common  sense would have it ,  this 90 minute time frame for primary PCI  would  logically be the   “symptom to  balloon time”,

But in reality  the time window of STEMI   is a collection of  following

  1. Symptom recognition  and 911/108 alert
  2. Ambulance arrival time
  3. Ambulance  to ER time (Traffic delays)
  4. ER to Fellow
  5. Fellow to consultant
  6. Consultant decision-making time
  7. Insurance clearance time
  8. ER to Cath lab door time
  9. Cath lab to needle time(Femoral /Radial )
  10. Needle to Balloon time

Where does the   90 minute  rule  for performing primary PCI stand ? It  can  mean many things

After all those hectic  activity  any one of the following is achieved !

Coronary flow – TIMI  3 ?  TIMI  2 ? TIMI 1 ,  Slow flow, Low flow ? No flow , No re-flow ?

* Prehospital thrombolysis avoids atleast   8  (No 3-10)  components  of time delay in our goal to salvage myocardium.

This is the simple reason, why primary PCI is not reaching it”s logical conclusion all over the world.

Summary

In simple terms ,  one  do not require a double blinded multicentred trial  to  show  primary PCI  performed at 2 hour time ( 2 hour  + 90 minute door to balloon time )  window   would be  far inferior to   pharmacological thrombolysis done at   15 -30  minute time window  (An ambulance driver can do it !).

Finally the most important fact , the often ridiculed thromolytic agent does not show  discrimination in it’s  effetiveness whoever  administers  it ! A  lay person or an ambulance driver with 10th grade education can open up the coronary artery 70% times  while  a cardiologist with a 20 year training  does the  slightly  improved version of the same job  costing   nearly 100   times( Rs  25oo for streptokinase vs  2 lakh for a PCI )  more  . In  the process  often  the   golden hour is lost ! Apart from this,  primary PCI is fraught with a risk of  procedure related  hazard  and  it is a hugely expertise driven procedure .

One more message  is ,  poor countries need not  feel dejected for not having those sophisticated country-wide cathlabs  and emergency air dropping of patients.What we  need is good transport systems and quick access to a near by   coronary care units with support staff.

Always remember  at any given time frame  , a well equipped  CCU can save  thousand lives more than a cath lab

Note of caution :

This article is written in the  overall interest of cardiac patient in the developing and non developing and Primary PCI can make merry in all those rich countries for the simple reason they can afford to  do that (Not necessarily  cost-effective !) . Still , primary PCI/surgery  is the only option for patients coming with a electrical or mechanical complication.

Reference

All that glitters is not Gold !

Know , how even high volume centers  struggle to prove he worthiness of primary PCI !

This is not a small study ,  it  is a huge study involving 5 lakh patients with STEMI spread all over the United states.

The conclusion from  his article indirectly supports the view , an early non PCI approach in STEMI can be superior  even if  infra structure and technical expertise are available  for PCI.

Read Full Post »

The most important journal in cardiology !

Posted in bio ethics, cardiology -Therapeutics, cardiology journal club, cardiology journals, tagged , , , , , , , on April 17, 2010| Leave a Comment »

Which you think is the most important journal in cardiology ?

  • JACC ?
  • Circulation ?
  • American journal of cardiology ?
  • American heart journal ?
  • Heart rhythm ?
  • European heart journal ?
  • The Heart  ?
  • Journal of invasive cardiology ?
  • NEJM ?
  • Lancet ?

None of the above  . . . is the right answer !

Probably,  the best journal  that is going to have the  greatest impact in cardiology practice in the future  could be  this  . . .

 Unfortunately  most  cardiologists are unaware of   this journal . The need for this journal , that  too from most respected Circulation family , will vouch for its importance in the current era  of  cardiology  that is driven more by the market forces than by the academics.

Click here  to reach  journal

Journal  Highlights

  • This  journal is 3 year old , and most of the medical colleges   do not subscribe to this.
  • None of the 100  cardiologists  who were questioned , were unaware of such a journal.
  • Even those who read this journal often term as boring  , academic and not practical !

 

The Circulation team which  started this journal  with  only one purpose  . . .that is ,  auditing the uncontrolled  proliferation of  pseudoscientific literature without proper quality assessment and dubious outcomes. Three cheers to the circualtion team for publishing this journal and let us propogate the importance of this publication.

Read Full Post »

The funny logics in cardiology :The dichotomy of thrombolysis in Ischemic stroke and STEMI

Posted in Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, Infrequently asked questions in cardiology (iFAQs), Uncategorized, tagged , , , , , , , , , , , on March 28, 2010| 3 Comments »

Thrombolytic therapy  is the specific  therapy  for Ischemic stroke ,  when administered in less than 3 hours ( Now 6 h ?)  and has proven to  save lives and brain .The only issue is , we need a 100% exclusion of hemorrhagic  stroke by a CT/MRI. The mechanism of action of thrombolytic agent is simple .It lyses cerebral thrombosis and makes way for sustained reperfusion and arrest or even  reverse  the  ischemic damage to  neurones .

And now ,   let us see ,  how we perceive the same therapy in a patient  with a  history of  recent ischemic stroke  with an  acute STEMI .

The issue is two fold.

  • He needs urgent myocardial salvage in the form of thrombolysis or PCI .
  • The thrombolysis or PCI should not worsen the  cerebral infarct.

According to  most standard literature thrombolytic therapy is an absolute contraindication in a patient with STEMI and recent history of ischemic stroke (<3 months )

The  term absolute means ‘it is medical  crime” to give TPA or Streptokinase.

How  is it possible when the same drug  is  projected a savior in acute ischemic   neurological  emergencies  and  be dangerous when administered  few months later in an evolved ischemic stroke ?

The major  reasoning  against thrombolysis in recent stroke is  the  potential concern for  converting an  indolent ischemic  infarct into hemorrhagic  infarct in  a  patient who may start  bleeding  into brain.

This is  highly conjectural  , as  a previous history of  ischemic   stroke in no way increases the bleeding risk .Conversion of ischemic to hemorrhagic   infarct tend to  occur  in the very early  hours  of acute stroke (not weeks later) .This could be part of calcium induced  reperfusion injury .

Unanswered questions

The issue become further  complicated with our  skewed  thinking pattern.

If thrombolysis  is contraindicated  in STEMI , does  it any way imply a automatic indication for  primary PCI ?

It seems so , for most of us !

How safe is PCI in a patient  with a previous  history of ischemic stroke ?

  • An emergency PCI in a patient  who is expected to have   widespread  cerebral  carotid , and peripheral vascular  disease  is fraught with added hazard.
  • Aortic arch manipulation  and aortic  valve  atherosclerotic  changes  might  increase a risk  of another stroke.
  • The drug we administer  during PCI  are  not innocuous ones  . Aspirin ,  Heparin, clopidogrel (sometimes  even 2b 3a!) will  keep the  risk  of converting the ischemic infarct into  hemorrhagic infarct remain  at  dangerous  levels . This ridicules  the  very  logic  of   PCI being preferred over thrombolysis in such situations .
  • So it is not an  easy decision to do  primary  PCI in an elderly  patient  with STEMI and a recent CVA. It is only a mirage of  medical  intellectualism  and  the blind following  of unscrutinized  scientific  literature   that   determine  many of the decision  making  in cardiology .

The argument here is ,  in a patient  with evolved ,  uncomplicated ischemic  stroke thrombolysis can safely be administered  irrespective of the age of stroke.  .This is contrary to the published literature.Let us not make unethical practice against scientific literature  but let us also understand   it is unethical  not to realise  many of the so-called scientific  evidence  are  merely speculative.I  request  the  neurologists  and cardiologists give their   input on  the issue

As far as  I have searched  the superiority or inferiority  of thrombolysis   vs PCI in  recent  ischemic CVA has never been compared one to one. The fact may be ,  such a study is never possible in the future .But  it seems PCI has won the   trial  without  a trial .

Unanswered  questions

How  many deaths have happened due to worsening of stroke after thrombolysis ?

How safe is a  combination of aspirin, heparin and clopidogrel in a patient with recent stroke ?

How shall we decide about thrombolysis  in these situations  of STEMI and recent CVA) depending upon the

  • Age of  CVA
  • Location of cerebral infarct
  • Size of the infarct
  • Residual neurological deficit

It may be prudent to redefine  the indication for thrombolysis and PCI in a patient  with history of recent or remote stroke.

  • It is logical to assess the potential   risk of   converting the ischemic cerebral infarct   into hemorrhagic infarct.
  • It is expected only large infarct in vital locations need to be feared upon for this complication
  • All small healed cerebral infarct need not be worried about reactivation.

How to asses the healing of cerebral  infarct?

The healing  and gliosis  is highly dependent  on individual response to inflammation. Some heal  within weeks. Neo vascularisation within the necrtoic area may get hyperpermiable .These are very speculative concerns. In all probability   the risk of converting an ischemic necrosis into hemorrhagic  necrosis  is less than a  percentage .The 3 months time for  fixed for infarct healing  is an arbitrary one

How good is MRI to predict a healed infarct from nonhealed infarct ?

As of now,  we have no good tools to identify the  safe infarcts that can withstand intensive  anticoagulation or even thrombolysis .If the imaging techniques improve we may able to predict complete gliosis and the vascularisation  of cerebral scars.

Post blog query

How to manage an elderly man with STEMI in a patient with recent ischemic stroke ?

A.Take him to cath lab and do primary PCI
B.Thrombolyse with TPA or Streptokinase
C.Just observe and  manage  with Heparin*

Answer : Any of the above can be correct answer .

If  we  still think  the answer is only   “A”  great reforms need to be done in  medical science  . . .

*Another important option for STEMI and recent stroke (Perceived  as inferior form of management of STEMI !)


An important option is ,  neither thrombolysis nor PCI just simple heparin for STEMI in these high risk individuals .This simple treatment has saved many lives .

See A Related video  from you tube : Forgotten hero  in cardiology

Final message

In this world of gross approximation  and perceived fears ,  it may be reasonable to  shift  the  indication of   thrombolysis for STEMI( with h/o recent stroke ) from absolute to relative contraindication.

Many of the  junior  physicians  in the learning curve may take it as granted  in the management of STEMI  “If thrombolysis is contraindicated  , then primary PCI must be indicated ” This again  is absolutely not true  !

//

Read Full Post »

« Newer Posts - Older Posts »