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Unusual tips in PTMC : How to cross a critically narrowed mitral orifice ?

October 12, 2013 by dr s venkatesan

Click over the Image  for animation

ptca balloon for PTMC inoue 002

Posted in Cardiology - Animations, Cardiology -Non coronary Interventions -PTMC, cath lab tips and tricks, PTMC -Tips and tricks | Tagged , , , , , , , , , | Leave a Comment »

Why we take LV end-systolic diameter(LVESD) in mitral regurgitation assesement ?

October 11, 2013 by dr s venkatesan

Regurgitant  lesions of cardiac valves  are often tricky for the heart . Myocardium shows “love- hate” relationship with these  leaky valves.  Some of them are  “sort of”  stress relievers for  LV . A mild MR will make the LV comfortable in terms of wall stress. When the wall stress is reduced the contractility increases and LV EF may raise a little.Hence EF is never going to help us to assess true LV function in MR .

LV end diastolic dimension(LVEDD) is  a preload dependent  parameter .A patient with 6.5cm LV EDD  may still  have good contractility  and he may reach even a  40mm LV ESD, implying an intact LV function.

LV function should be best  assessed  in systole .(After all ,  systole is the prime function of heart) .Further , it should be assessed when the LV is  free from  influence of the all  loading  conditions of heart .  (Note : The initial part of systole  depends on after load. As the systole progresses the influence  of after-load lessens .In the pressure volume loop* , the point at which loading conditions are least operative is end systole.)

* Please realise , heart is a dynamic organ there is no true load independent point in cardiac cycle  as pressure and volume are eternally coupled.

What happens in AR ?

The same rule applies for Aortic regurgitation, but the parameters worsen little later than that of MR. For same degree of regurgitant fraction MR will require early surgery than AR.The reason for better  tolerablity of  AR  is due to largely  intact LA function and compliance till very late stages of AR.(In AR- it’s single chamber volume overload , while in MR  it’s two chambers !)

Final message

LVEDD is not used in assessing MR  as it is a pre-load dependent parameter that will not reflect true myocardial  function /dysfunction. LV ESD is fairly accurate  measure of LV systolic function minus all loading factors .

Watch out  for next topic

Vasodilator therapy in MR and AR : How is it different ?

Posted in Cardiology -unresolved questions, Infrequently asked questions in cardiology (iFAQs), Mitral regurgitation, rheumatic heart disease, valvular heart disease | Tagged , , , , , | Leave a Comment »

Future directions in cardiology : A land mark review by Valentine Fuster

October 4, 2013 by dr s venkatesan

Medical research   often ventures into a directionless and meaningless  exercise with or without intention .The reason is simple , unlike  other fields,  scientists enjoy  the ultimate freedom of expression.

How to find genuine treasures from this chaos ?

We need people like Valentine Fuster ,

valentine fuster global cardiology what is the future

Here is link to the article in   circulation 2011  which I consider a must read for all cardiologists !

global cardiovascular health valentine fuster circulation 2011

Posted in cardiology journals, Cardiology research topics, Cardiology Risk assesment, Great Men in cardiology, Great websites in cardiology, history of cardiology, Land mark articles in cardiology, Top ten in cardiology | Tagged , , , , , , , | Leave a Comment »

What do you mean by adequate LV function . . .Doctor ? !

October 1, 2013 by dr s venkatesan

Many modern  day cardiologists  consider  doing echo ,  a mean job and leave it to  technicians and fellows . Final report  often ends up with a cursory glance. The culture of reporting an  important aspect of LV  function is reaching a new low. It is common  to find the following terminologies  in  the  echo reports in many  parts of the country*     (Guess it is not used elsewhere ! )

  • LV function good
  • LV function adequate
  • Good bi-ventricular  function
  • LV function fair

what is adequate LV function

Among these , the term adequate LV function has caught  the  imagination  of young cardiologists ! Especially , this description  often appear in pre- operative  screening echo for non cardiac surgeries .

Recently ,one of my patient asked me what do we mean by adequate  LV function . I told  him it means nothing . . . it’s all  fancy words  !  but , generally  it is used to imply  normal LV function . . . I  clarified .

Think over for few minutes   . . . what do we  want to convey  by calling LV function  as adequate ?

Does it mean normal ?  or  Just less than normal  ?

If adequate LV function  is accepted ,  what is inadequate ?

Adequate for whom ?  For the patient ?  or  for the physician ?

Adequate  for daily activity  ?  or  Adequate to  with-stand  the proposed  surgery ?

Final message

Even  learned cardiologists indulge in this  term  frequently . This is  rather a fancy and unprofessional  way reporting LV function . They pass this  style to their residents  as well para medics .Adjectives  in medical science are not banished . . . but should be   judiciously used . In my opinion  the term adequate LV function should be removed from all echo labs .   Youngsters please  watch out.

Related links in this site .

LV ejection fraction fallacies

What is LV dysfunction ?

Posted in Cardiology -unresolved questions, echocardiography, LV function | Tagged , , | Leave a Comment »

What are the patterns of RV enlargement in various clinical entities ?

September 30, 2013 by dr s venkatesan

Right ventricle is a passive venous component of the heart .It simply acts a  transit pump for blood to reach the lungs.

It  is true  , RV is dispensable in many complex congenital heart disease as we  can connect the great veins directly into the pulmonary artery  by  Fontan , Glean and it’s clones  bye passing this chamber . Still , by no means the importance of this chamber is to be underestimated.  RV dysfunction and failure  is the key to survival  many  disorders.RV shock is is cause of sudden cardiac death in acute pulmonary embolism and RV infarction .

RV is an unique muscular chamber .It is more of a triangular shape. It has  three different parts connected by three different angle .There is no true  apex  for RV , it is   connected  to Inflow and outflow in peculiar fashion .

In the  following table I have  tired to  describe  of how different parts of RV  behave in various disorders.

what is the morphology of RV enlargement RV inflow outflow body sinus portion of RV

Posted in cardiology congenital heart disese, Clinical cardiology, myocardial disease, Right ventricle | Tagged , , , , , , , , , , , , | Leave a Comment »

Clark’s classification of congenital heart disease

September 30, 2013 by dr s venkatesan

Congenital heart disease (CHD) still constitute an significant  subset in cardiology practice.The moment you ask how do you classify CHD  to any cardiologist , the answer  would come promptly as “cyanotic and acyanotic CHD “. Such is the power traditional clinical teaching .
 
There is a fundamental embryological and functional classification available put forth by Clark.It lifts  our understanding about congenital heart disease to a  different perspective. I wish,every cardiology fellow should know this.
 
 Link to embryological classification of congenital heart disease .
 
 A subset for cono-truncal anomalies is also available.
cono truncal anomalies embryology of heartReference
Clark EB. Mechanisms in the pathogenesis of congenital heart defects. In: Pierpont ME, Moller J, editors. The Genetics of Cardiovascular Disease. Boston, MA: Martinus-Nijoff; 1986. pp. 3–11.

Posted in cardiology -congenital heart disease | Tagged , | Leave a Comment »

Enigmatic relation between LA blood volume and LV stroke volume ?

September 30, 2013 by dr s venkatesan

Normal  left atrial  (LA) volume is about  22ml/sq.meter body surfacearea  at all ages.Maximum LA volume in physiology is  about 46ml in  females and 56 ml  in males( Average 35 ml)

LV stroke  volume  for each beat is  about  70  ml . . . so where does  the remaining 35ml come from ?

Answer .

  • Pulmonary veins ?
  • Residual LV end systolic volume ?
  • Mix of the two ?

It is logical to assume about 35 ml of fresh  blood  from 4 pulmonary vein*  rushes into LV with every diastolic cycle  .It  never stays in LA  .It just uses LA as a transit  route ,

*In diastole the four PVs,LA  and LV all act like one single chamber .

 

Is this reasoning correct ?.

If we believe the continuity equation this explanation is correct . However still what  we need to know the fate of residual  LV volume (End systolic LV  volume which is also  about 35 ml that would be  in queue for ejection into Aorta  for the next beat !)

Further , we know the LV end systolic volume is not constant .During exertion it  can reach  negligible levels (<10 ml) .At times of vigorous contractions  it can touch near zero as well . Then , It become vital for the  pulmonary venous reservoir  to be act as a  major donor for  LV blood volume for  every ensuing beat.

If the hemodynamics of pulmonary vein LA interface is tricky even in physiology ,  one can imagine the complexities  if the LV diastolic function and left atrial compliance  is affected

Debit and credits of  LV end -diastolic volume .

Let us assume LVEDV is about  1o5  ml .LA blood volume is  roughly one third of LV volume .For every beat equal amounts of fresh blood  from pulmonary vein . These two (LA+PV)  adds to the  residual  blood in LV  to make LVEDV 105   ml . From this 70 ml is ejected as stroke volume leaving behind 35 ml.


lvedv lvesv stroke volume wiggers cycle left atrial volume pressure volume loop residual diastasis

Image template from http://www.cvphysiology.com

 Further questions

LA Chamber volume and blood volume need not be same .What  I struggle to understand is , total anatomical  LA volume  measures  35ml , while the amount of blood it is supposed to hold is also about the same .Does  it mean the LA is completely filled with blood . . . air tight !

Will the LA compliance make it accommodate twice or thrice the blood volume during exercise ?

What is quantum of residual end diastolic  LA volume ?

 

Reference.(Normal LV and LA volumes )

echopedia

 

 

 

Posted in cardiac cycle, cardiac physiology, cardiac volume, Cardiology -Hemodynamics, Cardiology -unresolved questions | Tagged , , , , | Leave a Comment »

Obesity paradox in CAD and CHF

September 30, 2013 by dr s venkatesan

Obesity is a major cardio vascular risk factor.We earnestly  believe  this  by  evidence from Framingham and other studies.However , epidemiological  truths   can be dissociated from individuals .

We now understand  some  of the obese  patients fare better in CHF outcomes  apparently because of the obesity ! Even patients who undergo PCI show some benefits.This concept  is being proved in large data base of  > 200,00 patients.

Possible mechanisms

The lay man’s logic may apply (Science hidden somewhere !) Obese persons  have basically a  large heart with better cardiac reserve and  muscle mass .These hearts are  pre-conditioned to extra burden of MVO2  in it’s life time . So it  is able to tackle  hypoxia better, takes more time  to get fully exhausted .After all heart can consume fatty acids for it’s energy requirement.

Adipose tissue may also  secrete favorable anti-inflammatory  chemicals , though majority of adipocytokines are detrimental  except adiponectin .Paradoxically  the tumor necrosis factor TNF  (Same as cachectin or Interleukin 6)  is less  in obese patients .

 

Reference

obesity paradox

obesity paradox 3

obesity paradox 4

obesity paradox 3 jama archives of internal medicine

Reference

The landmark Lancet article that first raised the question of obesity paradox

Association of bodyweight with total mortality and with cardiovascular events in coronary artery disease: a systematic review of cohort studies.Romero-Corral A, Montori VM, Somers VK, Lancet. 2006 Aug 19;368(9536):666-78

http://www.ncbi.nlm.nih.gov/pubmed/16920472

http://care.diabetesjournals.org/content/36/Supplement_2/S282.full.pdf+html

Counter to the  concept

obesity pardox does it exist

http://science.howstuffworks.com/life/human-biology/obesity-paradox.htm/printable

Obesity   paradox applies in stroke too ! This study (TEMPIS) from Berlin  Germany  suggest controversially though

Overweight and obesity are associated with improved survival, functional outcome, and stroke recurrence after acute stroke or transient ischaemic attack: observations from the TEMPIS trial. Doehner W, Schenkel J, Anker SD, Springer J, Audebert HJ.Eur Heart J. 2013 Jan;34(4):268-77

 

Posted in cardiac failure, cardiac physiology | Tagged , , , , , , , | Leave a Comment »

Sexual dysfunction as a marker for CAD !

September 30, 2013 by dr s venkatesan

Cardiologists are  not  single organ  specialists . They are supposed to  be sincere guardians of the  the entire vascular system .Sexual dysfunction in  males  is almost synonymous with erectile dysfunction(ED) .The male sex organ is equally  dynamic organ like the heart . It demands a sudden gush of blood  to the tune of  500 ml  during complete  erection  .This  conveys an important  message . The penile macro and micro vasculature is as important  as coronary mIcrovascular bed. Atherosclerois of  LAD  can be as common as atherosclerosis  of pudendal artery .It can precede or follow the coronary lesion. Penile insufficiency is a early marker of endothelial dysfunction. All patients with CAD should be screened for  ED and vice versa.

This  is not a  sexual  intrusion in academics , but I am sure , a sustained  erection  that  completes  a normal sexual act  may very well  rule out a proximal LAD lesion 99 % of times .

Do you know , > 7  Mets  on a tread mill  will  rule out a  significant left main disease with high degree of accuracy   !  Sexual acts require more than that (One may do a study on this !)

There has been  some interesting guidelines for managing   issue of sexual dysfunction in CAD. .Princeton consensus conference is  the famous one.

References

princeton consensus conference sexual dysfunction in cardiology princeton 3 sexual dysfunction in cardiology

sexual activity in cardiovascular disease circulation 2012
http://onlinelibrary.wiley.com/doi/10.1111/j.1743-6109.2005.00196.x/pdf

Posted in cardiology -Sexual health, Cardiology -unresolved questions, Infrequently asked questions in cardiology (iFAQs) | Tagged , , | Leave a Comment »

How to diagnose DCM with confidence by myocardial scar photography ?

September 30, 2013 by dr s venkatesan

While many of us are preoccupied with wires and balloons ,( coronary  myopia ! )  , our radiology  colleagues are making rapid strides . Let us spend some  time  to understand  how  the myocardial segments  are inflicted the  final insult . We need to realize , there is a pattern  to  this myocardial  end game of scarring and fibrosis.

MRI is the  gold standard to assess the myocardial architecture . It has a role in both assessing the anatomy , function  , perfusion and viability .

how to differentiate ischemic dcm from idiopathic dcm myocardial scar epicardial transmural

  • LV function is assessed  by cine MRI
  • Viability  stud by  delayed enhancement MRI (DEMRI , also called as  LGE- Late Gadolinum enhancement  )
  • Myocardial scar best assessed by DEMRI*
* Why do you require DEMRI to identify scar ?
One can detect scars in plain MRI but contrasts make it better .Hence delayed enhancement in by DEMRI is used  to detect scars.
Is it ischemic  DCM or Non ischemic DCM ?  ( That is the question we commonly ask  
We rely too much on CAG anatomy for this. It can be misleading. Cine MRI with DEMRI  gives the answer straightway with high degree of accuracy  .  CAG is required in all  ,  but if it is normal , or  has insignificant lesions  , the dilemma  of ischemic DCM would continue !)
**Note ,there is one   simple algorithm proposed by the author   to  differentiate  Ischemic DCM from Idiopathic DCM  without MRI – Click here to  Link
Following  scar patterns in DEMRI help us to arrive a diagnosis.
Favors Non ischemic  DCM
  • Mid myocardial scar
  • Epicardial scars
  • Global sub-endocardial scars
  • No scar(Ironically if  no delayed  hyper-enhancement is noted it is likely to be non Ischemic DCM )
Favors ischemic DCM
  1. Regional transmural scars
  2. Localised sub-endocardial  scars
* Ischemic DCM will always involve subendocardium as ischemic wave front goes from sub-endo to epicardium.
examples for Non Ischemic DCM
  • Amyloidosis (Can be restrictive as well )
  • Chagas
  • Fabrys

Why is  scar localisation and Quantification important ?

Apart from differentiating various cardiomyopathies  it has  few clinical implication .

  • Since scar indicates irreversible damage , if extensive  it will  argue  against any re-vascularisation .
  • Scar location becomes vital if we plan CRT .It will be futile  to place a CRT lead over a scar.
  • Scars are often  form a macro re-entrant circuits for VT .Help us localize or zeroing in VT focus.
  • Scar quantification is helpful risk stratification of patients  with HOCM .and their family.
Final message
Myocardial scar location and quantification  is the new mantra in a  patient with dilated heart with cardiac failure.
It may be more important than even a coronary angiogram .MRI  will prevail over   any of the available echocardiogram modalities to assess the scar pattern.
Reference
myocardial scarring mri

Posted in Cardiac MRI, Cardiology -unresolved questions, myocardial disease | Tagged , , , , , , , , , | Leave a Comment »

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