Archive for March, 2013

Have you ever wondered a given chest x-ray is taken in systole or diastole ?  We should . . .  isn’t ?  Statistically chances of a  X ray to  fall in  diastole is 10-20 % more than systole as the later phase is longer . The peculiarity of cardiac anatomy is that ,  the  profile of the heart alters so little between systole and diastole  .Still the blood is pumped  efficiently into both pulmonary and systemic circulation . The left ventricle shortens by 35%  and ejects 65 % of blood . Similarly RV shortens but with  lesser quantum.

ct ratio in systole and diastole influnce of cardiac cycle on ct ratio

In a simple and elegant study  by Stephen Gammill  in 1970  published in Radiology journal,

he concluded the following about the CT ratio between systole and diastole.

  • 52 %   showed changes of 0.3 cm
  • 41 per cent showed alterations of 0.4 to 0.9 cm,
  • Only  7 per cent  showed a significant  variation of 1.0 to 1.7 cm in transverse cardiac diameter.

(I wonder why any follow up studies on this vital issue is scarce !)

xray chest 002

In spite both ventricles contracting during systole the radiological transverse cardiac diameter is relatively undisturbed ! 

Importance of  Rotary , Twist ,Torsional  and Longitudinal motion

The fact that CT ratio does not alter significantly in most ,  imply the heart has some other  kinetic motion which does not compromise the transverse diameter during systole. They are the rotary , and twist  motion .The relative constancy  of  CT ratio  is a good evidence  for existence for such alternate motions .We have since  confirmed  this  by sophisticated echocardiographic techniques .

Another evidence for rotary motion  recognised in the bed side when the apical impulse hits you in the fingers even as the ventricle is supposed to go away from chest wall during systole . This is  the torsional  movement of  LV  apex  and adjacent inter ventricular septum .



Coming soon

Inspiratory and expiratory  x ray chest and  the effect on cardiac contours .

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In the early 1980s , when cardiac physicians were confronting how to tackle intra coronary thrombus , one man from Japan  was  looking directly at the ground zero with fiber-optic coronary angioscope .He  provided live images  of coronary plaques and thrombus (long before the IVUS and OCT era) because of technical difficulties it did not get into  clinical utility  but gave us vital information like plaque morphology and behavior.

  • The concept of red and white thrombus
  • The yellow lipid enriched vulnerable plaques
  • Post lytic  clot surface
  • The fibrin strands within the clot etc.

coronary angioscopy Yasumi Uchida

The angioscopes have now given way to IVUS and OCT which provide indirect vision of the coronary arteries .Uchida has written a book tilted coronary angioscaopy which is a must read for all clinical cardiologists.

I think Japanese are  leading in this aspect of cardiac Imaging .Yasunori Ueda is another person who has  done lot of work on angioscopy . here is an  Image from his paper. Exciting  stuff  is isn’t !

coronary angioscopy  Yasunori Ueda www.invasivecardiology

Image source : Yasunori Ueda http://www.invasivecardiology.com




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Is Transient Ischemic attacks (TIAs)  belong to the  exclusive domain of cerebral circulation ?  Can it occur in the coroanry arteries ?  If so what situations ?

This is a presentation in one of the cardiological society of India annual scientific sessions . A pdf download is  provided

transient ischemic attacks attack of heart coronary tia

Download  a PDF presentation

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Primary PCI is presumed to be the ultimate  , undisputed reperfusion  strategy  in STEMI .  Still , time and again one study or  other strips down  this   “Numero Uno”  status of pPCI  .  If it is really supreme ,  such awkward  situation shouldn’t arise  too often . More importantly , the  major reason for  dubious real world record of  pPCI  goes beyond  the time and logistic factors (which is considered the only issue  for pPCI by most interventionist ! ) There is something more to it that is invisible ! (Is it the no reflow ?)

The nearly flawless study from Belgium ( STREAM Just released in ACC 2013/Sanfransisco ) , pre-hopsital or early fibrinolysis has proven to be superior in the prevention major end points at 30 days .

  1. Death
  2. Re-infarction
  3. CHF


The major surprise was pre-hospital  fibrinolysis  showed less  incidence of cardiogenic shock . ( pPCI

group had more of this ( 4.4 VS 5.9 %  in STREAM )

Now . . .  shall I make a provocative statement ?

while pPCI may be treatment of choice for cardiogenic shock . . . but it may  also confer a risk of cardiogenic shock in otherwise low risk MI !

Caution  and  conclusion

STREAM population applies strictly to 1 to 3 hour time window . It does not apply to either before or after that ! Simply put,we do not have  guts to compare fibrinolysis and pPCI  in patients who arrive  within one hour into a facility where 24 hour cath lab facility is available .  We call it unethical to do a study like that !  I personally feel it is really unethical  if we do not do a study in this time frame . The reasoning is  simple and very personal .In a  large  Government  hospital   where  we do not have primary PCI program  our net mortality for STEMI never exceeded 7-8 %  over a period of 10 years  , Which  is almost at par with global data on pPCI. (Our door to needle time is an unbelivebale  8-12 minutes ! that  too only streptokinase !)

Adding Further controversy

pPCI  is indeed a superior reperfusion strategy . No one can dispute that .But its superiority  is not  realised  in  every patient  who gets it.  The benefits are accrued if and only if it is  used most judiciously . In Low risk , small regional  , branch vessel STEMI ,  pPCI has never been  shown superior . It is well recognised ,  upto 15 % of STEMI is likely to spontaneously abort or experience very good spontaneous recannalisation . By rushing these  patients very early into cath lab pPCI   meddles with the natural anti fibrinolytic mechanisms . It is this population who  invite all the procedural hazards. .

Is this the reason STREAM had  more  cardiogenic shocks in pPCI limb ?

I think STREAM has  strengthened the case in favor of fibrinolysis in this  ever ending debate .

I would  seriously believe  pPCI is hanging it’s superiority over fibrinolysis with a wafer thin mortality advantage . pPCI may  not be recommended in a routine fashion to all STEMI  population even if they arrive within 6 hours and able to perform the plasty fast .  Science is   . . .  after all . . .  continuing  confrontations with our  assumptions !

Counter point

STREAM is not an exclusive study comparing fibrinolysis and PCI . It is a  study comparing   Pharmaco Invasive approach vs  pure invasive approach . 80 %  of patients in the  fibrinolytic limb ultimately received PCI and  stenting . It simply doesnot make sense to conclude fibrinolysis is superior to PCI . Most of the beneficial  effects on 30 day outcome may reflect the timely PCI  in the lytic group.


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Answer :

In cardiogenic shock it is A . In all others it is probably  C.

While D may be  considered as  an  essential target criteria  for completing the  rescue PCI

Read also

Why-we-often-follow-a-reckless-time-window-for-rescue-angioplasty ?

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VPDs are such a common cardiac arrhythmia . We also know most are benign .Still modern science demands to rule out structural heart disease in any patient with multiple VPDs.

When ventricles get irritated it reacts with VPDs . ( The irritants  can be anatomical , physiological or primary electrical)

Echo can detect only anatomical irritants .We are recognising  more such focus for VPDs . Hence idiopathic VPDs  may simply reflect our ignorance !  A focused  echocardiogram is  required .

The following conditions are often observed in patients  with recurrent VPDs

  1. Posterior Mitral annular calcification (Especially in women ) –Annular VPDs
  2. Aortic valve degeneration /Bicuspid aortic valve with calcification – Cuspal VPDs
  3. Mitral valve prolapse in young -Stretch induced  Pap muscle VPDs
  4. Minimal  pericardial effusions with adherent epicarditis
  5. LV false tendons-Stretch VPDs
  6. RVOT lipid focus -Subclinical ARVD
  7. LVH and Hypertension –Fibrotic VPDs    
  8. Asymmetric septal hypertrophy
  9. Scars in MI/ DCMs
  10. infiltrations in RCMs (Any Interstitial heart disease )

(Conditions 7 and 8 are  common disorders myocardium  just included to  complete the list )

**Please note ,above mentioned entites are anatomical irritants .There is a whole lot of physiological  irritants

that can induce VPDs .  ( Hypoxia, Excess catecholamines ,  K + fluxes ,  acidotic milieu etc ) .

*** Another group is primary electrical diseases inherited channel disease can induce VPDs

Also read

A crash course on ventricular ectopics


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The tie is between “B” and “D ”

We know in hypertensive hearts LV primarily fails in diastole . Lungs get congested due to raised LVEDP .Here is a catch . . .  if diastole is  terribly dysfunctional  how can be systole be near  normal  ? (After all  . . . systole is not a  distant cousin of diastole !)

How is  that  high blood pressure maintained in spite of LV failure* ?

Is it due to  well-preserved  EF and cardiac Index ?  or Is it due to extreme levels of peripheral sympathetic activity mediated by catecholamine surge triggered by LVF.

We have attempted to measure  LVEF in patients with flash pulmonary edema and acute severe hypertension .It was a real messy echocardiography . We could not conclude much but one thing is  clear in acute hypertensive  LVF   the LV was vigorously contracting in , probably making the option D  more correct .

* The other way of  reasoning is    . . .  it is because  of high blood pressure the LVF  has occurred . LV contractility has no contribution in maintaining the high BP ( Not in line with  the age  old concept of LV contractility  a major determinant of systolic blood pressure !)

(Having said that  . . . we also see patients with severe LV dysfunction with  severely  stunned , ventricles in association with hypertension and LVF . In fact many of the reversible DCMs are due to sudden surge in blood pressure )

Other mechansims of LVF and lung congestion is

  • Extreme tachycardia and shortening of diastole
  • Mitral regurgitation
  • Assocaited  CAD unmasked by sudden raaise  in heart rate .


If  this article has confused  you a little  , It has achieved  one of it’s  objective .  !  I expect more  from   young cardiology fellows to address the issue !


This NEJM article   authored by Sanjay  Gandhi  has almost answered the hemodynamics of acute LVF and HT .

mechanism of acute lvf in hypertension flash pulmonary edema lvedp in ht nejm 2005 sanjay gandhi

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