Archive for the ‘cardiomyopathy’ Category

Check out these two posters* for are a quick reference on HOCM with current updated evidence. The first one details about  Echo evaluation. The second one illustrates the genetic screening flow chart of the HOCM families.

Some of the queries, you will find the answers from these posters are,

1. How to recognize Intrinsic mitral valve defect by MR jet morphology?

2. How to cross-check the true LVOT gradient from MR jet?

3. When to do a provocative test to document the LVOT gradient?

4. What are the standard pre-myectomy measurements by Echo?

5. How to screen a family member of HCM?  Pros and cons of  Phenotypic vs Genotyping screening 


The poster is created by: Karan Kapoor, MD; Allison G Hays, MD, FASE. Design and illustration by medmovie.com.


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Even though cardiologists consider themselves master of ischemic heart disease , their collective clinical acumen is  put into  acute stress test   when they  confront  a patient with dilated LV and severe  LV dysfunction.This is not  a  rare situation  in clinical cardiology we stumble upon such instances often .Most of them are conferred a  tag  of DCM .

The differentiation from ischemic  vs idiopathic or primary muscular is not a  wasted academic exercise  , since   ischemic  DCM  may get reversed with revascularisation .We have  various  tests to differentiate  ischemic from idiopathic like CAG,MRI, 3D RTE, etc . Still common sense would tell us   95 % of times we can  differentiate ischemic DCM from non ischemic by asking  two critical questions  in the  bed side  echocardiogram

  1. Is there a regional wall motion defect ?
  2. Does all 4 chambers of the heart is enlarged ?

Idiopathic DCM is primary disease of muscle hence  the cardiac   muscle as a  whole  fails  ( We know they are a single  folded  muscle sheet )

Since  Ischemic DCM  primarily affect left ventricle and left atrium  RV,RA enlargement  are terminal events.

* Please note the traditional dependence on CAG to  diagnose  ischemic DCM is fraught with a risk of missing small vessels  induced  DCM,

*** If atrial fibrillation is present longstanding it can dilate both atrium but still RV will be normal  in sized in  ischemic DCM until very late stages

Here is a  20  second flow  chart  to differentiate ischemic  DCM  from idiopathic

ischemic verses idiopathic dcm

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The principles of pre-discharge EST  

This concept came about 20 years ago (1980s) to risk stratify patients following  ACS to triage early coronary angiogram and revascualrisation. Generally patients are discharged by 5-7 days after an MI  (May be  3-5 days in some hospitals)  . Doing an exercise stress test  early within  2 weeks has not been very popular with many cardiologist even though it was recommended by many guidelines.The type of stress recommended  here  , is heart rate limited sub maximal 70% of  THR (Usually around  140 /mt )  is performed . This is due fear of precipitation another ACS.

Still,  there are definite  advantages for  pre-discharge EST .It help us  identify  high risk  subsets of  STEMI and reduce the  intermediate term mortality .More importantly it  gives  us an opportunity  to  exclude  inappropriate  revascualriations  even without an angiogram . (The well known coronary dogma  ie  if a post STEMI patient performs > 10  METS ,  his  heart carries little  risk  for  future events  still holds good  !)

With the advent of liberal usage of CAG and improved techniques of revascularistion ,  most  patients  directly undergo pre-discharge CAG rather than EST !

Further reading

Does any cardiologist have guts to do a pre- discharge EST after  a successful primary PCI ?

Read a related article in this blog .

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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.


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.


Apical ballooning , Broken heart syndrome ,  Stress cardiomyopathy.


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


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 )


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


  • 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 !



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