Archive for the ‘myocardial disease’ Category

The right ventricle  is considered as a docile cardiac chamber with passive filling and  emptying  properties .

This belief  was reinforced when Fontan  in early 1970s suggested a principle in the management of  cyanotic heart disease  when  the right side of the heart is underdeveloped. He  proved  RV can be by-passed safely , with  great veins  (IVC/SVC)  by  themselves  take care of filling the pulmonary circulation  without the need of RV pumping function.

While it is true for few complex cyanotic heart disease, largely this a misleading  concept. In clinical cardiology practice  ,sudden or non sudden  RV deaths happen every day in the form of . . .

  • RV Infarction
  • Acute RV dysfunction in massive pulmonary embolism
  • COPD with RV dysfunction
  • Most cases dilated cardiomypathy  the terminal event is due to RV  failure.

So , RV function can never be dispensable in day to day cardiac hemodynamics.

RV has some unique properties in terms of shape , size and  hemodynamics . We are getting more insights from  modern blood pool imaging by MRI , about  how the RV handles the blood volume .

We know RV has a unique shape  triangular ( partially  pyramidal ) . It can be inferred the RV cavity is formed by fusion of  many  eccentric spacial planes. We have always believed  RV handles the blood it receives from right atrium in a unique way .Now we are beginning to understand it .It is now documented the RV segregates the blood it receives into 4 components.


right ventricle physiology anatomy hemodynamics

It is curious  to know  RV inflow is connected to the outflow by an invisible   physiologic Bridge . About 44% of  blood traverse the RV in this fashion.


RVOT blood flow right ventricle

Note : RV blood flow preferentially enters the RVOT with out transiting RV body and apex.Image courtesy http://ajpheart.physiology.org/


Which is the most important part in RV ? (Among Inflow, Body, Apex, Out flow)

After reading this article it seems to me , the mechanical  function of RVOT could be most  vital. If it fails to handle the first increment  which  comes directly from  RV inflow, stasis  is likely in RV body and apex , elevating RVEDP and later promoting stasis leading to clinical events.

Clinical implication of this study

  • Differential dilatation RV chambers to pressure or volume  overload is observed .
  • We need to analyse why RV dilates in some   but   goes for hypertrophy in others when confronted with pressure overload (VPS vs PAH)
  • RV apical clot in restrictive cardiomyopathy  is a direct consequence of stasis  of blood  in RV apical zone .
  • RVOT pacing  may have a hemodynamic advantage  over RV apical pacing  . However , for anatomical reasons RV apical pacing  is  far safer than RVOT pacing where the lead  is subjected to constant life long strain due to this busy RV inflow to outflow express  high way !

Final message

Traditionally we have labeled  RV  as a  passive venous chamber .It is clearly a misnomer.It  has to handle both the venous and pumping function beat to beat with precision  without  back log .Obviously ,  RV has to think and work  more than it’s  big brother !


I wonder , if  there is  any other site other than APS . . . to  find crucial  answers in cardiac physiology  !


Right ventricle physiology blood flow  3d 4d analysisAfter thought

  • There is huge gap between physiologists  who work in research labs and the physicians at bed side .
  • I appeal all young cardiologists  to visit  APS  once in a while ,between your busy cath lab schedule and help narrow this gap.
  • Without understanding the physiology properly how are we going to intervene the pathology ?


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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

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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.
myocardial scarring mri

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Takotsubo cardiomyopathy is an  unusual response  of the left ventricle to extreme emotional stress .The catecholamine  surge  has  a profound stunning  effect of LV apex  and  a paradoxical hypercontractility of basal LV.

The exact mechanism is not clear , Following factors may contribute.

  1. Multi-vessel coronary artery spasm,
  2. Cardiac microvascular dysfunction.
  3. Abnormal myocardial fatty acid metabolism,
  4. Reperfusion injury  after an ACS *

However , the most accepted mechanism is Endogenous catecholamine-induced myocardial stunning and microinfarction

Why is LV apex alone affected  ?

The adrenergic receptor distribution is high in LV apex .They are exposed to high concentration  and gets stunned easily . Basal LV has less adrenergic innervation  , so it shows less of catecholamine toxicity , instead  it exhibits.  hyper-contractile mode. However, this rule is not absolute.

One more suggestion was apical balloons correlated with wrap around LAD.(Báñez B et all 2004)

what is the mechanism of apical ballooning syndrome 2 takotsubo cardiomyopathy

Image courtesy Circulation December 16/23, 2008 vol. 118 no. 25 2754-2762

*Some consider ACS should never be  linked to  Takotsubo.But it is not easy to differentiate.(Carrillo JACC 2009(Kosuge JACC 2010)

Reference from this site

A link to related article -Ischemic Takosubo  from this site .


Reference from other journals
what is the mechanism of apical ballooning syndrome takotsubo cardiomyopathy

1.Báñez B, Navarro F, Farré J et al. (2004). Tako-tsubo syndrome associated with a long course of the left anterior descending coronary artery along the apical diaphragmatic surface of the left ventricle.]”. Revista española de cardiología (in Spanish; Castilian) 57 (3): 209–16

2.Carrillo A, Fiol M, Garcia-Niebla J, Bayes de Luna A. Electrocardiographic differential diagnosis between Takotsubo syndrome and distal occlusion of LAD is not easy. J Am Coll Cardiol. Nov 2 2010;56(19

3.Dorfman TA, Iskandrian AE. Takotsubo cardiomyopathy: State-of-the-art review. J Nucl Cardiol. Jan-Feb 2009;16(1):122-34

4.Kosuge M, Ebina T, Hibi K, Morita S, Okuda J, Iwahashi N. Simple and accurate electrocardiographic criteria to differentiate takotsubo cardiomyopathy from anterior acute myocardial infarction. J Am Coll Cardiol. 2010;55(22):2514–6. doi: 10.1016/j.jacc.2009.12.059.

how to differentiate takotsubo cardiomyopathy from anterior stemi


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The other day my fellow got a call  from surgical ward for emergency ECG opinion for a  suspected Inferior MI .It later turned out to be an acute cholecystitis.

One of the important  anatomical mis-perception  among physicians ,  is to consider  inferior, posterior  and diaphragmatic surface  of heart  as separate entities .They are all  closely linked.In fact, they  more often  mean  the same  anatomical zones !

Heart is a dynamic suspended organ within the middle mediastinum .It  can assume a vertical or horizontal position due to number of surrounding anatomical  and physiological factors. (Diaphragm, Lung , being  important ).The ratio of intra thoracic vs Intra abdominal  volume  &  pressure determine whether the posterior surface of the heart is going to face the back of chest  or simply sit and  rest on the diaphragm .We know a horizontal heart is likely to inscribe q waves  in inferior leads .

acute abdomen diaphragm inferior wall mi cholecystitis pacreatitis

Courtesy : Basic image source from digitallab3d

The  diaphragm can be termed as an  anatomical causeway , that isolates   thorax  from the  abdominal  cavity .Close encounters between the organs separated by this delicate biological  membrane is  always possible .This is especially true for electrical signals  which show little  respect for anatomical barriers .

This is the reason there are too  many abdominal conditions that mimic  inferior MI during a painful  emergency (and vice versa  when inferior  MI mimics  acute abdomen .) In  our  department , we   have witnessed  the following conditions mimicking Infero-posterior ACS.

  1. Acute ascites with polyserositis
  2. Gross obesity with APD
  3. Posterior fat pad ( Necrosis ?)
  4. Thickened pericardium
  5. Minimal posterior pericardial effusion
  6. Diaphragmatic pleurits
  7. Esophageal spasm
  8. Fundal air  trapping and ballooning after a heavy meal !
  9. Acute duodenal ulcer perforation ( With gas under diapharam causing q waves)
  10. Acute cholecystits
  11. Diphragmatic hernia
  12. Achalasia cardia
  13. Pancreatitis

Final message

Do not rush to make a diagnosis of inferior wall MI when  you encounter inferior q waves  with  or without ST /T changes , especially  when the symptoms are atypical .

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The popular clinical  entity Idiopathic dilated cardiomyopathy   is often a  dust-bin diagnosis” . The fact is the word   idiopathic simply reflects  our ignorance.

For God nothing is idiopathic . . . he knows how each and every cell  would   behave  .

so , when a patient presents with progressive dilatation and  heart failure refractory to all medical  therapy he is termed as idiopathic and posted for heart transplantation. And only later , we realize the whole thing is due  a  terrible form of reversible  DCM  . That is  pheochromocytoma  induced DCM , which recurred again in the   transplanted  heart.  What a  costly  Ignorance ?

pheochromocytoma and dilated cardiomyopathy reversible dcm tachycardic

Image courtesy and source http://www.dreamstime.com.

Is sub- clinical pheo like situations rampant ?

We know  that  high levels of both epi and nor- epinephrine circulate  in cardiac failure . We presume it  to be a secondary effect .

How can  we  so sure about it ?  There  is a distinct  possibility  of   adrenal gland hyperfunction  and hyperplasia in all DCMs (Idiopathic or ischemic ! )  The dramatic beneficial effects of beta blockers in cardiac failure  will vouch for it .

So , It remains a fertile filed for the youngsters to explore . . . the hyper  adrenergic mediated reversible component of any cardiomyopathy and cardiac failure .

Final message

The default  approach  in any  patient with progressive / refractory cardiac failure   should  be  ,  to consider  whether they fit into  any form of reversible myocardial disease  .  What is idiopathic in remote clinic of   your distant  country side  may be  well recognized secondary cardiomyopathy . The irony is , even sophisticated university hospitals many times miss the true etiology as in the above case report .

                                  So, the term Idiopathic  dilated  cardiomyopathy  (iDCM )  may  aptly be named as  Ignorant  forms  of  DCM  , with an  attractive  abbreviation    . . .   iDCM


1.J Surg Educ. 2009 Mar-Apr;66(2):96-101. doi: 10.1016/j.jsurg.2008.11.004. Pheochromocytoma presenting as acute severe congestive heart failure, dilated cardiomyopathy, and severe mitral valvular regurgitation: a case report and review of the literature.

2.Kelley SR, Goel TK, Smith JM.Prog Cardiovasc Nurs. 2005 Summer;20(3):117-9. Pheochromocytoma presenting as heart failure.

3.Pheochromocytoma   masquerading as a cardiomyopathy. Garcia R, Jennings JM.  Am J Cardiol. 1972 Apr;29(4):568-71.

4.  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1894695/pdf/20070600s00025p244.pdf

pheochromocytoma and dcm dilated cardiomyopathy .catecholamine induced dcm tachycardiac cardiomyopathy

5. http://downloads.hindawi.com/crim/medicine/2011/596354.pdf

pheochromocytoma and dcm dilated cardiomyopathy .catecholamine induced dcm tachycardiac adrenal cardiomyopathy


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Doppler Mitral Inflow velocity profile   is the key to  assess LV diastolic function . The ratio between  E and A has become most popular parameter .

In the absence of atrial contraction what shall we do ?

The answer is simple .  We have 2 D parameters of LV diastolic function.

LA dimension ( > 30 % basal dimension which is  usually >  4 cm  ) is a most specific marker of diastolic dysfunction in the absence of   mitral regurgitation or stenosis.

The only available  velocity E wave profile  can help .A short  E deceleration time in a short cycle  would suggest  significant diastolic dysfunction.High amplitude   E  wave  > 2  M/sec in the absence of MR  will suggest diastolic dysfunction .

Curiously  ,   it can be  assumed    an episode of   lone AF  per-se   ,  be an indicator of diastolic stress for the left atrium .

After all ,  why should a person all of a sudden develop an episode of AF .(Hypoxia, Ischemia ,  excluded )

Other parameters.

Mitral annular velocities / E propagation velocity   / E/E’  are other tissue Doppler parameters  can be used.

Pulmonary venous flow velocity is  largely not useful  (Since A reversal does not occur )

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