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Break through in Brugada syndrome ! . . . always carry this vital data in FINGER tips !

Posted in cardaic physiology, Cardiology - Clinical, Cardiology - Electrophysiology -Pacemaker, cardiology -ECG, cardiology -Therapeutics, Cardiology -unresolved questions, Cardiology-Arrhythmias, tagged , , , , , , , , , , , on June 10, 2012| 2 Comments »

Brugada syndrome continues to fascinate  us for two reasons.

One , it deals with mysterious sudden  deaths of young  men and women

Two , it is one of the  fine  examples  of how  advances in molecular biology , links  physical defects in ionic channels to  sudden electrical  death (Most of them  are due to inherited defects  sodium channels  of myocyte cell membrane )

While high risk subsets of Brugada are easily managed , it is  the asymptomatic  ones  that bother us.

The following are some of the  difficult  questions ,   a  cardiologist faces when dealing with   patients , who exhibit  only Brugada pattern in ECG .

  1. Should I go for an EP study Doctor  ?
  2. Will  I  require an ICD  Doc ?
  3. Do I carry a significant risk of  dying  suddenly  ?
  4. Do  I need a genetic test for sodium channel mutation ?

Fortunately,  we can answer  all these questions with much  courage than before.

(Thanks  to the European Finger registry published in 2010  !)

“No” is the  clear  answer for all of them !

Summary from the FINGER registry. 

(France  , Italy, Netherlands, GERmany)

The registry included 1029 consecutive individuals

(1) Aborted SCD (6%);

(2) Syncope otherwise unexplained (30%);

(3) Asymptomatic patients (64%).

In the  follow-up of 31.9 (14 to 54.4) months . A total of  7 death occurred .

The cardiac event rates per  year was 

  • 7.7% in patients with Aborted SCD,

  • 1.9% in patients with syncope

  • 0.5% in Asymptomatic patients.

Predictors of cardiac  event

  1. Previous syncope
  2. Spontaneous type 1 ECG

Non predictors ( Surprisingly there were more non predictors ! )

  1. Gender has no predictive role
  2. Familial history of SCD,
  3. Inducibility of ventricular  tachy-arrhythmias during  EP study,
  4. Presence of an SCN5A mutation

 

Follow up

PRELUDE study  almost reaffirms  Finger data

(PRogrammed ELectrical stimUlation preDictive valuE)

Just publicized in JACC 2012 from the pioneer of   Brugada Silvia  Priori of   university of Pavia  Italy

Reference

http://circ.ahajournals.org/content/121/5/635.full.pdf+html

http://content.onlinejacc.org/cgi/content/abstract/59/1/37

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Tough calls in cardiology : Refractory hypotension in septic shock and the role of Hydrocortisone in Septic shock ?

Posted in Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, tagged , , on June 5, 2012| 1 Comment »

Time and again cardiologists are called to opine  in critically ill ICU patients with  hypotension.  The circulatory shock of septic shock  is often refractory  . Many  times it  degenerates  into multi -organ failure . The mortality remains high in- spite modern treatment .Even in those patients who recover , they require prolonged  inotropic support  (for days or even weeks)

Here is a  recent call I attended to .

A 44 year old   febrile   , ventilated patient  (With a pneumonitic patch , PEEP of  6 , near ARDS )  ,  precarious renal function and altered sensorium , maintaining a blood pressure of 100/70mmhg with high dose dopamine and nor- adrenaline  , monitor showing a heart rate of 125 /mt sinus  .This status -quo  has continued for more than 72 hours. To my surprise,  the ICU physician told  me there is  in-fact a  minor improvement in general condition than before  . After blinking  at the patient’s  file for few  minutes  , I did a customary bed side echocardiogram .The only positive finding  I  found was  his  heart was  structurally normal  and EF was  64 %  , still the right heart chambers were struggling  to do it’s job   fighting with the PEEP.

The physician had  a very  specific query  from the cardiologist . How to wean the inotropic support and shift him off  ICU ?

(The poor patient  has no  insurance  , and has to shell  Rs 10000 everyday  which is equal to his monthly income ! )

A very  valid question indeed   !   After all  , cardiologists  claim to  have special  knowledge  and wisdom about disorders of  vascular system .

Heart being normal , the crux of the problem is loss of vascular tone. (Autonomic dysfunction ) .How to improve it ? I  discussed the following suggestions.

  • Early passive muscle exercise (Augmenting  muscle tone and transforming it to  into arteriolar and venous tone )
  • Venous support ,stockings etc.
  • Ensure adequate intra-vascular  fluids
  • Sodium supplements
  • Corticosteroids.
  • Fludro-cortisone , the mineralo-corticoid may have a specific advantage as it could retain sodium in vessel wall that can be exchanged with smooth muscle calcium and improve vascular tone .
  • ECMO is  often a pre terminal intervention .
  • Will power . We know vascular  tone is in fact neurogenic in origin .The tone flows from brain stem .Administering  will power could be a useful intervention . (parental infusion of fighting spirit !)It can be done through pep talks from  close family  members   in   conscious patients .(One controversial advice is to allow  near and dear  into bedside , ICU phobia may delay recovery of vascular tone !)
  • Finally  I suggested , a  vascular consult from the GOD  . Organised prayer .  There is some evidence ,  even  proxy prayers do exert benefits in unconscious patients .

After a 15 minutes stay in the ICU , for doing nothing  I  received a significant consultation fee  , and I left the  place  sheepishly  with a  definite dose of guilt !

Reference for role of Hydrocortisone in septic shock

The CORTICUS study

It has no overall impact but hastens recovery from septic shock . Even though the study appears to denote a negative connotation

it has the role in selected individuals .http://www.nejm.org/doi/full/10.1056/NEJMoa071366

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If you are not aware of this classification . . . propably . . . you are unfit to treat Infarct patients !

Posted in Cardiology -Interventional -PCI, cardiology -Therapeutics, cardiology- coronary care, Cardiology-Land mark studies, Clinical cardiology, tagged , , , , on May 31, 2012| Leave a Comment »

We owe a lot to our past genius minds for our current understanding of  cardiology.Youngsters   should  know how the filed of cardiology  evolved .Few  great  brains  taught us how to think   hemodynamically  in the setting of  STEMI.

The Diamond and Forrester classification is  an  undisputed achievement of  modern cardiac  hemodynamics.They gently converted the  clinical classification of  Killip into more scientific  hemodynamic  one .Both these classification continue to fascinate  us even in the era of instant PCI for STEMI .

And youngsters  should read this again and again and critically evaluate their patients  within this system.The two key parameters he used was PCWP of  18mmhg /And cardiac Index 2.2liters . He also suggested a simplified version where  intra- arterial monitoring is not feasible.  The   cardiac Index could be replaced by systemic blood pressure  lung congestion   represents PCWP >18mmhg .

The DF classification would become

An important inference from DF classification !

The class 3  of   DF   grading  has no pulmonary congestion  but persistent hypotension . What does it mean ?

It is a stunning proof of a great concept.  As the patient moves (Worsens)  from  DF  two  to   DF three  , the lung congestion tends  to regress . This sub-set  actually  means   development of  bi-ventricular failure or isolated RV failure  . This is an ominous sign and indicate a bad prognosis . ( One may call it a paradox  , according to conventional thinking   “The more the lung crackles  , dismal  is the outcome”   DF  grading clearly proves this is  not  always true ,  as long as  the systemic pressure is maintained  crackles can be managed effectively  . In  DF 3  the right ventricle  as a pump is  becoming so weak it is not able to congest the lungs  at the same  process leads to  systemic hypotension.

James Forrester

http://www.cedars-sinai.edu/Bios—Physician/A-G/James-Forrester-MD.aspx

Forrester is also a pioneer in how we evaluate chest pain in the emergency rooms and cardiology OPDs .  His thoughts on utilization of Besean theorem revolutionized   the interpretation of exercise stress testing.

* Killip is a genius of different caliber would be discussed later .

Reference

Forrester, J, Diamond, G, Chatterjie, K, et al Medical therapy of acute myocardial infarction by application of hemodynamic subsets (first of two parts). N Engl J Med 1976;295,1356-1362


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Takotsubo cardiomyopathy : In extreme mental stress . . . Left ventricle takes a shape of banana !

Posted in Cardiology - Clinical, cardiology -ECG, cardiology- coronary care, Cardiology-Coronary artery disese, cardiomyopathy, tagged , , , , on May 27, 2012| 3 Comments »

The entity of stress cardiomyopathy ,  other wise referred to as  Takotsubo  cardiomyopathy is a popular clinical entity in recent decades.The heart and mind are closely linked entities even though they are  situated apart physically . Extensive neural and hormonal control  mechanisms  exist.

In extreme stress ,the hyper- sympathetic  drive triggers a rush of adrenaline ,  which some how makes the  left ventricle  to bulge out !

The clinical features  are varied .

  • It can exactly mimic an acute coronary syndrome .
  • ECG may  show ST elevation and mimic an anterior STEMI
  • Echo shows a wall motion abnormality  classically  described  as the apex alone dilates /Bulges or elongates
  • LV  may acquire a shape of a  banana. (See below )

A 45 year old man came to the ER with severe chest pain , dyspnea and minimal ST elevation in anterior leads. He  was a smoker and was experiencing  recent major office stress  . Echo showed an elongated LV apex with some thinning .We made a diagnosis of stress cardiomyopathy .( It was disputed by my professor as the LV  apex was contracting well   ! but we  learnt later there are many varieties of Takatsubo )

Echo showed an elongated LV apex with some thinning . Note the LV apex goes  out of plane  with RV apex.

Color  Doppler revealed Trivial Mitral regurgitation

Follow up

He underwent coronary angiogram.  Had  no significant lesions ,   in 48 hours time the wall motion defect disappeared and was discharged with beta blockers.

Incidence

Up to 2 % of ACS could be related to Takatsubo . More common in women especially post menopausal  , with stressful/emotional background like loss of loved ones.

Synonyms

Apical ballooning , Broken heart syndrome ,  Stress cardiomyopathy.

Mechanism

Not clear . Microvascular spasm , excessive catecholamines  ,  are thought to be major culprits.

Echocardiography

Hyperkinetic base and akinetic or dyskinetic LV apex .

Lots of variations are reported .

Shimizu described 4 types

Courtesy : Shimizu et al J Cardiol. 2006 Jan;47(1):31-7.

  1. Apical akinesia and basal hyperkinesia,
  2. Reverse  Takotsubo  (Basal akinesia and apical hyperkinesia)
  3. Mid-ventricular ballooning   with  basal and apical hyperkinesia
  4. Localised  to any one segment

*The Banana type which  is described here (Elongation  of LV apex > Widening )

Histopathology

Focal myocytolysis are described. (Broken heart)   Monocytic infiltrations are common.These are  believed  to be transient .

How to differentiate it between a STEMI ?

  • Enzymes are only mildly elevated.
  • Wall motion defect do not confine to a specific arterial territory.
  • Most importantly coronary angiogram do not reveal any significant obstructions.

Prognosis and outcome

  • Generally good
  • The initial presentation may be turbulent in few with cardiac failure or arrhythmia .Other wise these patients do well

Treatment

  • Mainly supportive
  • Major principle is to avoid inotropic agents as they  are already  heavily expose to it
  • Beta blockers  could be the mainstay therapy .

Final messge

Think about  Takatsubo  whenever an acute coronary syndrome presents atypically . Not surprisingly few of them land in the cath lab !

Reference

http://www.cardiologyrounds.org/crus/cardus1206.pdf

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Atrial fibrillation with wide qrs tachycardia : Don’t get obsessed with WPW syndrome

Posted in Cardiology - Clinical, Cardiology - Electrophysiology -Pacemaker, cardiology -ECG, cardiology -Therapeutics, Cardiology -unresolved questions, Cardiology-Arrhythmias, tagged , , , , , on May 26, 2012| Leave a Comment »

Irregular  wide qrs tachycardia is a fairly common clinical entity in any cardiac emergency room. The moment you ask about  such tachycardia ,  9/10  fellows will  come out with a  prompt answer   ” AF with WPW syndrome” even before you complete the question !  It is not that common  as we perceive .The problem is with  our traditional teaching methods and the attraction of human brains to  rare and exotic disorders.

traditionally   SVT with aberrancy  is   diagnosed  mainly  in the setting of regular tachycardia .

We often  forget  “AF with aberrancy”  is equally common  , and  it presents   with a  irregular  wide qrs tachycardia . 

I  wonder whether  this phenomenon  can be termed as  orthodromic aberrancy .This can directly compete  in the differential diagnosis  of  antidromic AF  with  WPW !

It should also be mentioned antidromic  AF can run into very high rates  as accessory pathways do not check the incoming signals while orthodromic aberrancy the ventricular rates can not exceed 220 or so at least theoretically . (This simple clue can clinch the issue in favor of  WPW )

There is no proper  published data available for the true  incidence of AF with orthodromic aberrancy in general population

In fact , there are  many  electrical  environments for AF  to  become a  wide qrs AF

1. AF  with  Antidromic conduction through accessory WPW pathway.

2. AF with Orthodromic aberrancy ( Non WPW – Similar to  any SVT with aberrancy )

3. AF with pre existing LBBB

4. AF  with Amiodarone effect. (Especially with DCM and cumulative load of Amiodarone )

5. AF with electrolytic /  especially excess  intra-cellualr  potassium

6. Finally , even  Atrial based pacing (DDD)  can cause wide qrs irregular tachycardia when  mode switching  fails .Here the  ventricles  may track the  atrial irregularity  and respond with a  wide qrs  bizarre tachycardia .

Final message

There are many causes for  wide qrs tachycardias  in  Atrial fibrillation . WPW with anti-dromic conduction is just  one of them .We need to approach the issue with an open mind .Please  be reminded , once contemplated  WPW syndrome  can be a powerful thought blocker  !

Note : *We are not including   polymorphic ventricular tachycardia here .It is an  important subset of  wide qrs irregular  tachycardia.

** VT can co-exist with AF .This is not   surprising  as  many of the diffuse cardiomyopathies  involve  both atria and ventricle  with extensive scarring and fibrosis  a perfect trigger for  both atrial and ventricular arrhythmias .

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A partial list of chest pain in the “Post-Infarction” period

Posted in Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology -Therapeutics, cardiology- coronary care, Cardiology-Coronary artery disese, tagged , , , , , , on May 22, 2012| Leave a Comment »

We know prompt reperfusion of infarct related artery( IRA) by any means  constitute the specific management of  STEMI .However, It needs  to be emphasized ,  treatment process of STEMI  is not over after  primary  PCI or thrombolysis .Early hours after a PCI or thrombolysis  is vital as well .The ill-fated coronary arteries are as  vulnerable as before.  In the setting of multi-vessel CAD  (Which usually is the case) the unpredictability is still more.

Image courtesy New york times , January 5 , 2009

When a patient complaints of chest pain  24 hours after a STEMI . Think about any of the possibilities and act accordingly.

  1. Infarct related pain ( Dull aching pain from residual neural signals from infarct zone,  till type C  un-medullated  nerve endings  die of hypoxia )
  2. Post infarct angina –From IRA zone (Residual ischemia)
  3. Post infarct angina-From Non IRA zone(New Remote ischemia)
  4. Re-Infarction
  5. Infarct expansion/ Extension /mechanical stretch
  6. Pericarditis
  7. Intra coronary dissection adjoining  a plaque (Plaque fissures  are same as dissections if they extend into media ! But plaque fissures are painless since they lack nerve endings  )
  8. Myocardial tear /Rupture (Generates  severe pain , usually transmit to back , patient often become violent and poorly respond  even to narcotics)
  9. Post resuscitation/DC shock / chest wall contusion . ( I know at least one patient  who was rushed to cath lab for a  suspected  acute stent thrombosis  ,  it was indeed   a rib fracture during an  earlier resuscitation at ER  on his arrival !)
  10. Finally ,when the  pain is refractory and atypical   non cardiac chest pain which might have been pre existing to be considered as remote possibility .

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When “Quality of life” fights with “Quantity of life” doctors get confused !

Posted in bio ethics, Cardiology - Clinical, tagged , , , , , on May 19, 2012| Leave a Comment »

A  72 year old man in  terminal heart failure with  three previous admissions in  last one year  comes with severe breathlessness . He was  exhausted with  rigorous  drug regimens  for refractory heart failure in the past few months. Since he  was always feeling better after an infusion of Dobutamine he demanded it . Doctors were very clear  , ” Repeated  Dobutamine infusion will  hasten  the LV dysfunction and longevity is  will shorten”

The family began to think . While they  wished  for him to   live longer , the sick man  insisted  on  early  relief from his  symptoms .

How often in medicine ,   there is a trade off  between  symptoms and survival ?

It is a more common situation than we believe , especially in many  chronic  disorders like terminal organ failure and malignancies. .  So we need a simple scale to  asses the quality of life and survival  outcome for our patient. The following table  could help us . I  learnt this from   the great teacher Valentine Fuster’s  lecture  which  I attended in New Delhi recently !

Final message

Let us  attempt to  make a patient’s  life ” feel  good “ ,  if  he is going to live shorter .  Let us avoid  prolonging  a  life ,  if the treatment is making him feel  bad  , when the  life  expected  is  short !

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How to diagnose complete heart block without ECG ?

Posted in Cardiology - Clinical, cardiology -ECG, Cardiology-Arrhythmias, tagged , , , on May 18, 2012| Leave a Comment »

You are asked to see a patient with a pulse rate of 45 /mt .  Is it sinus bradycardia  or  complete heart block  ? 

Only one condition , . . .  you must conclude in the bed side !

  • Heart rate  may give a clue ( HR of  30-40 is common in CHB . Less common in sinus bradycardia.)
  • Pulse volume is large in both (More so in CHB )
  • JVP  shows occasional cannon waves hitting the neck  in CHB. Cannon wave can never occur in sinus rhythm
  • S 1 intensity may vary in CHB (As  Marching through  of  P waves  occur in CHB  ,  when it falls close to QRS  , it results in a  short PR interval  and a  loud S1   . Since marching through is a intermittent phenomenon S 1 intensity also varies.)
  • A short systolic murmur may be  heard intermittently due to   trivial MR/TR in CHB  ( Competitive AV valve movement )
  • A  simple bed side test  . Ask the patient  to exert for a minute -Sinus bradycardia raises  the HR with a fair regularity  to 80-90/mt  or so. CHB doesn’t  (Note :  CHB with  junctional rhythm can  sometimes increase the HR  significantly )
  • Finally response to Atropine   is prompt with sinus bradycardia.

Final message

Bed side skills in recognising cardiac arrhythmias are still relevant even in the current  era of carto and 3d electro anatomic mapping .

After all ,  the 19th century clinical wizard Wenke back recognised the second degree  AV  block at the bed side  well before  the ECG machine  was invented. He meticulously observed progressive prolongation of a-c interval and subsequent drop of c wave in the jugular  vein !

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A shocker of a discovery : HDL cholesterol could after all be a “Good -Old ” Bad cholesterol

Posted in cardiac drugs, cardiology -Therapeutics, Clinical cardiology, dyslipidemia, tagged , , , , , , , , on May 18, 2012| Leave a Comment »

International Astronomical Union  in the year 2006  removed Pluto from the solar system for a simple reason ,  the so-called Pluto never revolved around  Sun , hence it ceased to be a planet of the solar system , it was more of an asteroid !

So, an astronomical fact engraved in our brains for so long  became a fairy tale. It is very hard  to erase  a  myth however solid the new evidence are against it.

The concept of HDL as good cholesterol has been etched deep in physician as well as our  patients.

Now comes the shocker from Lancet

How are we so sure ,  about these  Invisible spheres of  lipids that  move  around  our “Bio-system” in a presumed fashion .  .  .  even huge visible planets  fool us easily !

The Link to lancet study

It is  a wonderfully done study where  thousands of patients  who exhibited  genetically high HDL levels , never showed any advantage in terms of CAD prevention.  A stunning blow to a belief.

Incidentally ,  few years back  the failure of  drug Torcetrapib proved the same point  .  (The drug which elevates  HDL  proved useless in preventing CAD  ) but the  medical world failed to interpret it properly.

I am sure, still sections of physician  community would continue to believe HDL is great molecule for CAD protection !

Science is  often what we presume . . . but the fact usually turns out to be some thing  else !  but the journey towards truth  must continue !

                      When  a  million tonne  Pluto  suddenly disappear from Solar system . . . it is not a  big deal for  a  “miniscule medical myth”   to get shattered !

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Essential Cath lab philosophy !

Posted in bio ethics, Cardiology quotes, Clinical cardiology, Venkat quotes, tagged , , , , , , on April 30, 2012| Leave a Comment »

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