Archive for May, 2013

best hospitals in usa us news and world report

The top 3 cardiac care hospitals for the year 2012-2013 

  1. Cleveland clinic
  2. Mayo clinic
  3. Jhons Hopkins Hospital

america's top cardiology hospitals


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It is believed  T wave alternans  is a marker of impending ventricular fibrillation. Though it is not applicable in every clinical setting it is indeed true if we observe T wave alternans in an acute ischemic setting .Here is a patient with  ACS and inferior MI who developed T wave alternans after temporary pacing.

T waves alternans torades de pointes 3

t wave alternans

T waves alternans torades de pointes

went in  for a chaotic  T wave rhtythm  and ended up in VF that  required s shock.T wave  alternans is other wise known as repolarisation alternans .

Twist dance of Heart

Torsedes is twist around it’s axis.   Any   ECG wave  can twist in it’s axis .If T wave alternans  becomes gross it will twist 180 degrees   .Once this happens the heart can go for  fibrillation any moment !

Final message

Extreme form of T wave alternans would result in  complete twisting of repolarization vector which is a  harbinger of ventricular fibrillation

I wish  this can be referred to as Torsades  “T” pointes instead of  Torseades “de” pointes


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pci  powerpoint presentation ptca follow upFile1-PCI 5

Click  on the file   to download  the presentation

Note : The contents are prepared in 2006 .Recent input are to be added .


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Thrombus laden plaque  is sine qua-non of UA/NSTEMI . That’s what we  have been taught  !  right ?  It may be  true in many  situations , but please remember there is another concept  called  demand ischemia , where in there is  no active thrombus ,  still resting  angina may occur due to  increasing heart rate etc.

I just wanted to test how far this concept is understood ,  by the  fellows in our coronary care unit . Following  is  story of a patient who arrived at CCU with  angina  at rest .  I showed  this   ECG asked them the  management .

positive est and unstable angina

History was  purposefully blinded . 5/6 cardiologists wanted to admit the patient either in CCU or rush to cath lab.  Heparin/ Fondaparuinux was prescribed by all. Tirofiabn was suggested by few.It is a  high risk UA with left main disease some one  mumbled .

I silently listened to them and  revealed the history . This patient  has just finished the  exercise stress test , it was terminated as he had angina at peak exercise. and was  reported as  positive . A date was fixed for elective   coronary angiogram. 10 minutes later ECG totally normalised  , and the patient went home (Boarding a crowded Chennai  city bus )

The fellows realised the importance of history . In fact no body asked for it ?  I felt  bad  as  all my fellows failed in this test That reflects bad teaching on my part !

What is the mechanism of ST depression here ?

  • Fresh thrombus ?
  • Mechanical occlusion ?
  • High  heart rate ?
  • Combination of high rate and probable flow limiting lesion .

(Severe forms of  stable angina can occur at rest . So do not equate all rest angina as true  unstable angina !)

Final message

Do not label an ECG straightaway  as acute coronary syndrome when there  is  baseline  tachycardia and ST depression . Spare few minutes and apply your mind !

If  a combination of ST depression  and angina  can be taken  synonyms with UA  every EST positive fellow should be labeled as UA and admitted in CCU. Please remember any tachycardia with a fixed tight lesion will  mimic UA . Further ,  since there is no thrombus here  and there is absolutely  no role for heparin.

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ST segment elevation is the key parameter on which the fate of millions of infarct patients are recognised and managed. It is ironical we do not have standardised reference point for measuring the quantum of SR elevation .

This is especially difficult when ST segment blends with forward limb of T waves.

While we have reference point for measuring  ST depression  (Like during EST ). . . why we do not have one for ST elevation ?

Now we have adopted a rough criteria .Read below .

where will you measure st segment

How to measure ST elevation in ECG
How to measure ?
Measure The ST segment 40 ms from J point.
how to measure ST  elevation in STEMI 2
                        I lost track the source of this Image .(STEMI hand book 2012 ?)
Final message
ST segment  elevation  is  the key parameter in ACS.  Quantifying  it becomes  important in  assessing  the efficacy of reperfusion strategies and risk stratification. Fresh ST elevation can represent pericarditis, reinfarction or an early dyskinetic  segment . Unless we have  proper reference point there is  a room  for  error in this simple parameter.

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95 % of hypertension is designated as primary HT .What does it mean ?  It means  95 % of times  we do not   know what  exactly is the cause for raised blood pressure  . Simply stated  . . . it  reflects 95% ignorance .

So what is secondary hypertension ?

Secondary HT is the one,  in which we have specific reason for the raised BP.  The most important cause is Renal  ,  endocrine etc.

When will you suspect renal HT ?


How is secondary HT different ?

  • Occur at relatively at young age (<45)
  • It is generally more severe.
  • Diastolic BP is proportionately  higher ,
  • End organ damage is more.
  • It is very unlikely primary HT to present as acute LVF.  One rule of thumb is ,  if diastolic blo0d pressure is > 120 never diagnose  primary HT . Some amount of renal component is very likely.

Is stress related HT a form of secondary HT ?


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Heart disease was  once considered as   rich man’s disease  . . .  It’s no longer  true .  We in India ,  are witnessing an epidemic of CAD . The reasons are  varied  . Apart from  conventional factors ,   social   factors  like changing demographic pattern  ,  life style , ethnic  risk  like  south  Asian metabolic profile are responsible .

While  Rheumatic heart disease (RHD ) continues to be a huge burden , CAD  is  the number one  cause for cardiovascular morbidity and mortality .

CAD affect the poor and rich with equal vengeance . The later is better equipped financially to tackle it . Of course ,  it has resulted in maximum inappropriate interventions. The poor (or borderline poor ) have  no  other  option  but  to knock the doors of Government  hospitals. It is heartening to note, various state  Governments   are  gradually involving insurance schemes.

Still , many struggle to find the required  finance for  a major cardiac intervention. It roughly costs 100,000 rupees  for PTCA  .While  PCI is required in all symptomatic ,  critical coronary occlusions , still . . .  majority of the  CAD in general population  do not require it . There are 675 cath labs in India performing 180000 angioplasties every year  on an average of   15000  PCI per month ( 500 /day )  This is grossly inadequate . We  have huge potential

What is the hurdle ?

  • Expertise ?
  • Hard ware ?
  • Awareness ?

No  . . . it is all about  financial resources

Recently I stumbled upon an  advertisement on Times of India

cardiology ad ptca

Disclaimer: This article does not in any way defame any hospital that offers the scheme.It just want to debate the concept.

Hospitals  want  to  market the procedure . Convert angiograms  to angioplasties . That’s   corporate boardroom mantra  . And one fine day ,  bankers and medical doctor sat together and brought a brilliant idea.

Why not do the procedure  on credit and  push the patient  life long  into a financial debt !

Wonderful idea  . . . many thought .Thus came the financing scheme for  cardiac procedures.

Final message

Financing a poor patient  with good intention is welcome. But, there is big caveat .In a vast country   with high  illiteracy , inappropriate  procedures   may be thrusted upon  on   the  poor  souls.

After thought

Now ,  our patients   have  one more  risk parameter to  assess   ” Number of remaining EMI( Equal monthly instalment )  and incidence of stent thrombosis”   “Accumulated  interest  and angina”   What a wonderful way to provide cardiac care !

I can recall a  patient who sold his livestock  (his sole income source ) for undergoing a open heart surgery and lost his life as well in the process  leaving the family stranded !


The only solution is  to  provide  a strictly regulated Govt sponsored  insurance scheme.  High tech procedures should be  continuously and meticulously  audited for cost effectiveness .


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Ventricular tachycardia is a common cardiac arrhythmia. The significance of which can be very dangerous to relatively benign  depending upon the etiology and underlying heart disease . The ECG during VT is rarely useful to identify the etiology .Often times  ECG after reversal will  throw more light .

What are the ECG clues one should look for once VT is  reverted ?

  • Any evidence for old MI
  • Low voltage QRS/ LBBB/RBBB may indicate DCM
  • LVH -HOCM features
  • VPDs – Multiple , LBBB morphology / suggest  RVOT  VT
  • QRS slur or notching  indicating scars
  • Epsilon waves indicate  ARVD
  • RBBB pattern would  suggest  Brugada
  • Prolonged QT interval
  • Tall  T waves/ U waves /  Inverted  T -and other electrolytic abnormality.
  • Delta waves would indicate anti-dromic tachycardia.

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It happens only in India


About  150,ooo people die in road accidents in India every year . . . highest in the world !  Myocardial infarction  kills  only slightly  more !

Image courtesy : Times of India , 18th April 2013 . Picture  by  S.L. Shanth Kumar .


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We are taught in  medical schools  early in our career ,   ventricular premature  depolarization (VPD ) takes  LBBB morphology if it arise from right ventricle , and  RBBB morphology if it arise from left ventricle .This is a rough rule of thumb.

Why this rule is  unreliable ?

VPDs have a focus of origin—–a short circuit——and an epicardial  breakthrough . All these together influence the morphology. Within  the left ventricle , a deep endocardial focus  can  behave  vastly different  from superficial epicardial focus  . The  course of VPD is influenced by the myocardial status ( scars etc ) . Further,  the electrical  properties of  interventricular septum is shared  by both ventricles .

  • Generally – LBBB morphology  has  more localizing value .
  • Most RV focus have LBBB morphology (but not vice versa!)
  • LV focus can either have LBBB or RBBB

What happens to  a VPD  arising from  interventricular septum ?

IVS is  not only shared by both ventricles , it does  not have  true  epicardial  surface  (Both side  bordered by endocardium ) In most septal VPDs , breakthrough occur on either side of the ventricle  . However , It  keeps trying  to break through  epicardial surface  !  .  Hence , septal VPD  is like cat on wall situation .So the morphology varies quiet frequently.Further , the VPD can capture  the specialised conduction tissue occurs  more commonly with septal VPDs. This can alter both the width and morphology of QRS.

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