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Archive for 2010

Extramarital sex : A coronary risk factor ?

Posted in Uncategorized, tagged , , , , on April 22, 2010| Leave a Comment »

It is well-known sexual arousal and activity is a powerful hemodynamic stress .In the healthy persons it is never an issue .In fact there is data to suggest sexually active men and women live longer.

But , in patients with cardiac risk factors or an established coronary event unrestricted  sex can be a risk factor for CAD.

There needs to be a distinction  between a coronary risk factor and a coronary  trigger .Trigger is an  immediate switch  for a coronary event in a  patient with  baseline risk profile .It is highly unlikely triggers alone can  cause an ACS .There need to be risky substrate.

Extra marital sex could be such a trigger in some .(Both male and female)

  • The sexual activity performed with guilt  has  more powerful risk.
  • First time offenders
  • New  partners
  • New environment

All of the above are  supposed to increase  the risk .

The mechanism  attributable is  a   sudden adrenergic  surge  which inappropriately high when compared to marital sex . In conservative societies , the effort taken to hide the illicit relationship   is much more stressful than the event itself. And hence these men and women carry on their new-found coronary risk for longer periods.

Reference

http://www.ncbi.nlm.nih.gov/pubmed/20382352

http://drwes.blogspot.com/2010/04/extramarital-affairs-and-heart.html

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An unusual form of constrictive pericarditis : Annular constriction

Posted in cardiology-Anatomy, echocardiography, Uncategorized, tagged , , , on April 22, 2010| Leave a Comment »

Constrictive pericarditis(CP)  has been a fascinating disease   for the cardiologists  for many decades .  (Of course , not  so fascinating for  our  patients!) The reason why clinicians were thrilled to diagnose this entity is due to the unique clinical and echocardiographic and hemodynamic features. Further , it is  one of the few  curable forms of cardiac failure.
It is also about the  philosophy  , pericardium an inert  membrane  which is supposed to protect the heart , becomes a  villain  . When this innocuous layer  is insulted by  chronic   infection (Tuberculosis most common) , radiation injury or post cardiac surgery  it takes a dangerous avatar and  start invading   the organ which  it  guards .
The pericardium becomes thickened , (often > 5mm -2cm) calcified , behaves like a “shell of tortoise‘ and begin to constrict the heart . Once the process of constriction sets in it becomes relentless . It only   requires   , a 10 -15mmhg of constrictive  pressure to make  the poor heart  struggle to relax .(The maximum intracardiac  diastolic pressure ,12mmhg(LV)   .For the right side of the heart it is very low (0-5mmhg) .
So it is obvious the right side of the heart RA, RV gets compressed first .This is why the classical features of constriction with edema , ascites elevated JVP occur.The associated hepatomegaly some times mimic a chronic liver disease.  Of course  relying only  on the  classical findings to diagnose CP would be a crime now .
There are many atypical varieties of CP
  • Localised constriction
  • LV>RV constriction
  • RV>LV constriction
  • Transient constriction
  • Effusive constrictive

* Rarely  constriction is confined to AV groove .  This article  is about this entity.

It is difficult to imagine how a pericardium constrict a rigid fibrous skeleton of the heart namely the AV groove.
But what happens is ,  there  are some gaps in the ring  . The  posterior mitral annulus which  has a deficient  rim  and forms  the most vulnerable  zone for pericardial constriction
Further , AV groove  is located  in a relatively  gravity dependant portion  of the heart  . It facilitates  stasis of inflammatory exudate  in this groove .This may be  the reason  why the  AV groove  shows high incidence of   calcification.
Clinical features of AV groove constriction
It mimics  a presentation of valvular heart disease.
A mid diastolic murmur across mitral valve may occur mimicking valvular MS.
Synonym : Mounsey’s pericarditis
This type of pericarditis should ideally  be called as Mounsey’s constrictive pericarditis   for his
elegant description of this entity 5o yearts ago  even before    Echocardiography was invented.
(These are the days , we struggle to diagnose Mitral stenosis without echo is a different story !)

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Caged heart within a pericardial shell !

Posted in Cardiology - Clinical, pericardial disease, tagged , , , , on April 22, 2010| Leave a Comment »

The LV angiogram that stunned me  !

See how a heart is encased within the pericardial shell , still fighting hard

Thanks to circulation for it’s greatness  to offer such great video free

http://circ.ahajournals.org/content/vol118/issue16/images/data/1685/DC1/CI191060.DSmovie2.AVI

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Indian journal for cardiothoracic surgery : A unique data base

Posted in cardiac surgery, cardiology journals, tagged , , , , , on April 19, 2010| 1 Comment »

The one and only journal for cardiovascular surgery from the subcontinent. Great to  know   full text articles are available from year 2003  , free of cost .Every cardiologists from India must read this journal regularly to update  about what our surgical colleagues are doing  in our country.

Thanks to the  National Informatic centre  for hosting this journal in their server .

http://medind.nic.in/ibq/ibqai.shtml

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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.

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Why hypotension is more common in infero posterior STEMI ?

Posted in cardiology- coronary care, Uncategorized, tagged , , , on April 14, 2010| Leave a Comment »

Human heart is a vital bundle of muscle  weighing  about 300-400 grams. The blood  supply of this muscle  mass  is highly variable . Some areas are abundantly  vascularised(  eg -IVS.) Some areas have a balanced blood supply with  twin blood supply (Often the  LCX and RCA in the  crux of the heart ). Certain areas have a precarious blood supply . They are  some time called as water shed areas or  vulnerable   Bermuda triangle of the heart – the  overlapping zone of   LV apex,  free wall and  the anterior surface.

When the blood supply is so  heterogeneous , it is  not surprising  to find  the neural innervation of the heart to have a  unique pattern as well .The cardiac  autonomic nervous system   is  mediated by the  cardiac plexus  . It  has a  dominant adrenergic  innervation in the anterior   aspect of the heart   that is  rich in catecholamines , while the infero posterior  aspect  of heart has a high density of  vagal fibres .

So , it becomes easy to understand , why  ischemia of inferoposterior regions often trigger  a vagal response and an adrenergic response  in  anterior ischemia  .Of course , overlap can occur especially in multivessel CAD with collateral dependent circulation.

The inferoposterior MI ,  generally  have  a better outcome as it imitates  naturally beta blocked heart . (Less heart  rate , less MVO2  more salvage ) Still  hypotension  can be  a worrisome complication in inferoposterior MI .

The following  factors contribute to hypotension in infero posterior STEMI

  • Heightened  vagal tone  due to Bezold  jarish reflex
  • Involvement of RV is known to occur up to 40% of all  inferoposterior MI. Loss of RV pumping action is the classical explanation of hypotension
  • Recently recognised  fact  : Infero posterior MI often have subclinical and subelectrical atrial involvement. This is a powerful trigger for  the atrial  naturetic peptide secretion. ANP  a water losing hormone explains much of hypotension in this situation. .It should also be noted atrial necrosis is not necessary for ANP release. Simple atrial stretch  or even RV stretch can be a stimulus for ANP .
  • Variable degree of LV involvement is  common in infero posterior  MI .This can have detrimental effect on LV pump function . It  can  be a independent  factor for  the hypotension.
  • Excess sedation with morphine may aggravate or precipitate hypotension.(Vagal  action of morphine )
  • Finally , and most importantly a common cause  is  hypovolemic  hypotension (Applicable for any STEMI – Severe sweating  and sometimes vomiting can  loose  up to  10 liters of body water )

How to manage ?

  • Correct hypovolemia
  • Water challenge in RVMI is a popular (Often abused) concept . Rule of thumb is , if 1000ml  of  rapid infusion  fails to correct the hypo it is  highly unlikely  it will  do it at 5 liters  ! Cases of fluid overload and dilutional hyponatremia have been reported.
  • Atropine (This is one of the rare situations  where vagal blockade increases the BP ) .Dopamine may be useful but logically we need to  reduce the high vagal tone  and bring autonomic parity  . (Increasing adrenergic tone to that of high vagal levels  for autonomic parity  is  a lesser logic !)
  • Temporary pacing may be needed if  blood pressure fail to raise because of  troublesome bradycardia.
  • And  of course  , rapid PCI and revascularisation  when Indicated

Final message

Hypotension in inferoposterior MI is often  considered innocuous. But , it can be dangerous in some , especially in the  elderly and comorbid individuals . It has  varied mechanisms  , that are distinctly different from anterior STEMI.  Recognising the underlying mechanism  hypotension  will aid us to correct it  rapidly.

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Can elevated JVP and edema legs occur in isolated diastolic heart failure ?

Posted in Cardiology - Clinical, Cardiology -unresolved questions, Uncategorized, tagged , on April 10, 2010| Leave a Comment »

It is  over a century old dictum , that  edema legs and elevated JVP is the hallmark of cardiac failure.In fact , these two  constitute  major criteria of Framingham  cardiac failure score.When these criterias were formulated the concept of diastolic heart failure was not in vogue. So we  do not know whether the same would apply for diastolic heart failure also.

In all probability these  conventional criteria may not apply to diastolic heart failure  .

But why not ?

We know diastolic heart failure  of the left ventricle  is less likely raise the  systemic  venous pressure  to cause the edema and raised JVP. But still ,  isolated LV diastolic dysfunction can increase the PCWP and PAP and RVP . Remember diastolic  septal dysfunction , may compromise RV relaxation also.(Reverend Bernheim like  effect)

We should  also realise , raised  venous pressure is not the only mechanism for edema legs.

Diastolic dysfunction can trigger  ACE genes  .IT can get activated and hence renal conservation of sodium.This neurohormonal activation can be dominant  mechanism of edema in few. This  prevails over  the hydrostatic forces. And  hence edema can result in isolated diastolic dysfunction.

What about RV diastolic dysfunction as a cause for right sided failure ?

This is a poorly  understood entity.Logic suggests  it may have clinical significance. Since  morphologically and developmentally LV  and RV share a common  sheet of muscle  , LV diastolic dysfunction can have it’s impact t on the RV as well.

Final message

Edema legs and raised JVP is a hall-mark of  isolated  systolic heart failure or combined systolic and diastolic failure   .It is not rare to find an occasional patient isolated diastolic dysfunction*  to present  symptoms of  systemic congestion .

*Of course ,  in this era of hi tech cardiology practice  it may be  inappropriate  to  depend on these  primitive clincal criterias  to diagnose CHF . (These  manifest very late in the course of CHF!)

Read also

Why  some patients with cardiac failure never develop edema ?

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“Incomplete” left bundle branch block

Posted in Cardiology - Clinical, cardiology -ECG, Cardiology -unresolved questions, tagged , , , , , , , , on April 8, 2010| 1 Comment »

LBBB is probably the most important  conduction defect of the heart .When we say LBBB , we visualize a  strikingly  wide bizarre qrs complex .

Left bundle even though is considered  a discrete structure , the fascicles  make it a diffusely spread structure. Many varieties of LBBB with various degrees of involvement occur.

Talking about the basics of  LBBB  electrophysiology  is out of place for the current generation cardiologists,  who  have little spare time as  they sweat it out inside the cathlabs.

In early 1960s and 70s great articles came from pioneers regarding these defects. If we want get a good insight  read  this  articles from  Sodi palleres .Who  says LBBB is a dynamic process, where it can occur from mild functional  delay to a total block .

The conduction  properties of left bundle is very much influenced by heart rate.

Law of statistics would  suggest  for every complete LBBB  at least three to 4 times incidence of incomplete  LBBB

Then . . .

Why we are not diagnosing ILBBB often ?

  • We miss it
  • Mistake it with LVH
  • We know it  is there , but we do not  want  to diagnose it .

How to diagnose ILBBB?

See  Sodi palleres criteria*

What is the relationship between qrs width and completeness of LBBB ?

Surprisingly and contrary to the belief , the width of the qrs has no linear correlation between severity of LBBB. In fact incomplete  LBBB can occur with even 150ms qrs !

Then ,  what  exactly determine the completeness of LBBB ?

What  matters is , whether the down coming impulse gets blocked  and split in the  left side of the IVS or not ? This causes the  the septal vector to  change  it’s direction ( ie  right to left instead of the normal left to right) It  removes the initial small r wave in v1  and q in v6  in complete LBBB. In  incomplete LBBB these  r and q are  often retained .

What is the differential diagnosis of ILBBB ?

Type B WPW may mimic LBBB and vice versa.

LV hypertrophy .

Differences : See table in  the Barold’s article  linked above .

Unanswered questions

  1. How common is ILBBB in STEMI ?
  2. How often ILBBB progress to LBBB ?
  3. ILBBB in dilated cardiomyopathy : Is desynchrony an issue ? (Normal QRS CHF !)
  4. Is functional  rate dependent  LBBB in cornary care units  same as transient  ischemic LBBB ?
  5. Intermittent LBBB and Incomplete LBBB  aren’t they  synonymous ?

Final message

ILBBB is not that uncommon as one would  tend to perceive.

Reference

My humble tributes to  Barold, Sodi -palleres , and Leo  Schamroth . Probably  one of the best  article on ILBBB is linked below. Reviewed    in 1963 !  Not much data has been added  in the next 47 years as on 2010

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Some more “bad news” for people with early repolarisation syndrome

Posted in cardiology -ECG, Infrequently asked questions in cardiology (iFAQs), Uncategorized, tagged , , , on April 4, 2010| Leave a Comment »

ERS -Early repolarisation syndrome  is known as a   benign ECG finding  for  many decades  .Now it  is beginning to look dangerous as evidence is accumulating  it may have a link with ventricular arrhythmias.

ERS represents complex changes in  ionic movements during  cardiac repolarisation . (To be specific , it is due to a functional gain of  K + ionic channels during phase 3 of action potential).Generally this is a very benign condition. But , what concern us is ,  it can predispose to ventricular arrhythmias when these patients are confronted with ischemia .

When repolarisation occur early it indirectly shorts the QT interval .We know QT interval is a notorious period in human ECG as both a short and long (<320ms, > 460ms)  can be dangerous.

Is ERS a marker for potential cause for primary VF ?

Read this article from NEJM 2009

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Annals of pediatric cardiology : An unique journal for the emerging speciality in cardiology from India

Posted in cardiology -congenital heart disease, cardiology journals, tagged , , , , , , , , on April 3, 2010| 2 Comments »

There are thousands of medical journal published worldover. Dozens are available in the field of cardiology .Only a few  are dedicated for pediatric cardiology.  Annals of pediatric cardiology is one .

It is all the more  creditable , as it comes from India , A country which is lesser known for scientific infrastructure  .  Full credit to the  pediatric cardiologist associataion of India and the medknow publishers for  bringing  this  highly specialised scientific content in this part of the world .

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