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Total anomalous pulmonary venous connnection (TAPVC) : An Illustration

April 28, 2013 by dr s venkatesan

TAPVC Total anomalous pulmonary venous connection left vertical vein

An animated version

tapvc total anomalous pulmonary venous conncetion vertical vein

Posted in cardiology congenital heart disese | Tagged , , , , | 1 Comment »

What is the “Fundemental difference” between coronary stenting and Aortic stent grafting ?

April 28, 2013 by dr s venkatesan

stent graft vs coronary stent principles aortic stent graft 002

Posted in Aortic stent grafing | Tagged , , , , | 2 Comments »

What is the mechanism of ventricular tachycardia in hypertrophic cardiomyopathy ?

April 26, 2013 by dr s venkatesan

In HCM every myocyte is  genetically made  defective . Myofibrils are in disarray every where . Still , can we identify some vulnerable zones that acts as arrhythmic  focus ? If that is possible , we  have a opportunity to abate that focus .

In HOCM  , which is the most stressed area ? LVOT ?  Septum, ? When we say stress , it can mean either mechanical or electrical .

VENTRICULAR TACHYCARDIA 002

Does electrical instability involve the same zone as mechanical stress ?

How often VT originate from LVOT in HCM ?  For this we have good clinical model _, the patients who underwent alcohol septal ablation.

What happens to the incidence of VT  post septal  ablation  ?

“It is reported  post septal ablation the incidence of SCD  becomes  equal to general population” (Read the paper below )

If that is true , it is obvious the  arrhythmic  focus is also ablated along with LVOT myocardium .

Outcome of HOCM after alcohol septal ablation

Though many studies claim  so !  It  fails to convince us  .  HOCM is a diffuse disease of  myocardium.  Even a cluster of myocyte disarray  with fibrosis   can be a future focus  irrespective of it’s location .

However ,  it is always possible relieving the mechanical stress of the LV can definitely reduce the likelihood of an electrical event .(Even if the arrhythmic focus is intact elsewhere !)

* We know RVOT is  developmentally arrhythmia prone zone . We also know HCM involves RVOT (After all ,  IVS  is legally shared by both ventricles !  ) . Some of  the monomorphic  VTs with LBBB morphology may originate from RVOT in HCM .

Management of recurrent VT in HOCM

  • Drugs (Amiodarone/ Calclum blockers/ Beta blockers/Disopyramide)
  • ICD- (Probably mainstay  )
  • Very rarely ablation (If localised focus is well documented )

Reference

1.A case report for successful ablation of  VT in HOCM   http://www.ncbi.nlm.nih.gov/pubmed/9255687

2.http://www.ncbi.nlm.nih.gov/pubmed/23076968

//

Posted in cardiology -Therapeutics, Cardiology -unresolved questions, Cardiology-Arrhythmias, Infrequently asked questions in cardiology (iFAQs) | Tagged , , , , , , , , | 1 Comment »

Why stress & obesity related hypertension . . . is not considered as secondary Hypertension ?

April 26, 2013 by dr s venkatesan

Systemic hypertension (SHT )  is the commonest  clinical entity encountered in cardiology consultations . 95 % of  HT is considered primary. The remaining 5 %  form the most important class of HT (Secondary to renal parenchymal, vascular , endocrine,  etc)

How  intelligent is this traditional classification of HT  ?

The incidence of primary and secondary  HT varies depending  upon the level of investigation we do . One of my  regular patient  who gets to me for  HT .He  is 42 year old man  works in financial institution  with lots of work stress and he was marginally obese as well .  He was investigated for all known cause of secondary HT and every parameter  was found to be normal and was being treated as   primary HT.

When he was about to leave my clinic he  bowled  this google !

Doctor , why do  you call  mine as  primary HT   ?  . . . When you yourself  say  my stress and weight is responsible for  high blood pressure ?

Primary vs secondary HT

Valid question is it not !  . .  . I told him   “somehow”  ,   we have not  been taught   in medical schools  , to consider stress  of life  as a factor  responsible for  developing secondary  HT !

Final message

Strange  definitions in medicine continue .  Not every one with high stress  levels develop HT  .There  are  some unknown factors operating  .Till we know that we  will keep calling them as primary HT .

( Who  knows the  man  who raised this question  may   show up  with adrenal hyperplasia  or a renal parenchymal dysfunction 5  years down the lane !)

We live by perceived  knowledge  on a moment to moment basis  ! . Ignorance  tries  to lock the doors of knowledge .

But we  continue to open new doors . That is the  only  purpose of medical research !

Posted in Hypertension | Tagged , , , , , | Leave a Comment »

When anterior epicardial fat . . . generates Q waves . . . diagnosis of ASMI gets busted !

April 24, 2013 by dr s venkatesan

Q waves are  neither  sacred  nor sinister waves . It represents   either of the  following .

  1. Electrical activity that goes away from the recording electrode.
  2. Or whenever there is a  electrical insulation or hurdle that interrupts the flow  of current  towards the electrode ( and if it is sustained )  it  can result in q waves (Minor interruption produces  a notch or  slurs . Please note a major slur becomes a q wave equivalent  )

Here is young women of 42 years with  a diagnosis of  old  anterior MI for   over 5 years ( Getting a dedicated care from a cardiologist!  The prescription included Imdur/Betaloc/ Statin/Clopidogrel and Aspirin )

This was the ECG . It was very convincing for  old ASMI.

epicardial fat and poor r wave in v 1 v 2 v3 q waves

It  happened ,  I did an echo for her .

epicardial fat and q waves in ecg pesudo infarct non infarct 2 q

She lacked wall motion defects even after a meticulous search .  Instead   she had a   good layer of epicardial fat measuring 9 mm .That was more localised in  anterior wall extending little to LV apex.Her EF 65 % .

*She was a  fairly obese (not gross )  individual with a BMI of 34 .The fat pad thickness was not that huge  , I thought , still it was producing the q waves . I  have seen much thicker fat pads with good R waves in ECG . I  wonder ,  is it the type of fat that adds up to electrical insulation ?

This patient was sent back to me  again  for ruling out ASMI .  Echo was  done  two weeks  later . No evidence for  ASMI  could be detected.

epicardial fat and q waves in ecg pesudo infarct non infarct fat 2 q

What is the normal thickness of epicardial fat pad ?

It is less than few mm . Exact normality is not known .(Empirically < 5mm ) it is very rare for fat deposition  in infero posterior aspect , except in morbid obesity.

What is the function of epicardial fat ?

  • Long considered inert . Now , found to be a metabolically  active lipid pool.
  • We also know  heart  consumes more fatty acid than an other organs for moment to moment energy consumption .
  • Inflammatory mediator in atherosclerosis ?
  • It may also act as a mechanical cushion effect along with pericardium
  • Rarely fat infiltration can compress the heart and may result in restrictive  AV filling defects in doppler  .(May explain the unexpanded dyspnea  in many obese patients )
epicardial fat a dynamic depot athreosclerosis

Role of epicardial fat depot in the genesis of atherosclerosis

Subcutaneous vs  Epicardial fat.

We know thick chest wall can also interfere with ECG. Epicardial fat is more likely to record  q waves than  sub cutaneous fat ,  as the insulation is more closer to heart in epicardial fat . In thick chest wall current leaks from heart and  well scattered  hence  poor R wave is more common in such situations rather than q waves !

Following things can generate  q waves (Other than Infarct  )

  1. Fibrosis-Myocardial /Interstitial
  2. LVH
  3. Thickened pericardium
  4. Thick chest wall/ Epicardial fat
  5. Air/Fluid in pericardial space

Final message

In obese men and women  anterior Q wave can be  misleading .Such  medical errors can be so convincing .

After thought

If epicardial fat can  extinguish   R waves  and  replace it with  q waves  , these  innocuous  looking fat pads has every reason to  influence the ST segment shifts during  an episode  of ACS  as well !  .  Isn’t ?  . If so  . . . how reliable is  our ECG criterias  to diagnose  acute coronary syndromes  in grossly obese men and women ?

Posted in Cardiology - Electrophysiology -Pacemaker, cardiology -ECG, Cardiology -unresolved questions, Clinical cardiology | Tagged , , | Leave a Comment »

Shocking mindset of pharma companies ! Who is educating whom ?

April 21, 2013 by dr s venkatesan

News : It seems the pharma companies are worried   about  the new MCI  (Medical council of India ) guidelines  that restrict  sponsorship  for conferences and freebies to individual  doctors  . They think it is a  big set back  as it  may interfere with doctor’s  education and knowledge  !

ethics and pharma compnaies

They have proposed new amendments and  has asked  the health ministry to advice the MCI accordingly .(ie To help them bring back  the corrupt and bad practices  that  influence  doctors prescribing behavior  !)

It is true , for the  growth of medical science , we  require some sort of  a business model and  tax holidays for the companies for true  &  land  mark discoveries  . Currently the MCI allows to sponsor  medical  events or a conference  for an institution or organization .  But  what these companies want is  official permission to provide  incentives to individual doctors and influence them  ! .  More shockingly  they said  doctors knowledge will  suffer without these industrial support . It is an outright insult to all doctors who get educated  for over  decades* . In fact the heads of pharma companies require  few lessons from the medical fraternity  ,  how many drugs with  dubious scientific value  is playing havoc in  health of  the society !

Of course ,we can not blame the pharma companies  for  all . It is a collective evil.

Counter point

*This  is a  second  slap on the face of  medical profession  !  I am  sorry to say this ,  many of us ( Including  the blogger  ! )  are some way responsible for this state of affairs  . Shockingly ,  few of  our  colleagues are  proud  to  have illicit relationship with drug companies !  Younger generation   no longer consider  this as an offense  , since they are born and brought up with  capitation fee as their principal fodder. Commercial forces  has taken over  medical  profession . Many of the  colleges are owned by business barons and alcohol vendors  in India . It is a well known  fact , MBBS seats are now  sold for 50lakhs (like  3 bed room flats )  . Agents transact black money in secret basements of   medical colleges  once considered  as  temple  of  the  noble profession .

So what is  in-store  for the future ? . . .  Self regulation is best  regulation   . . .   Mahatma told us ! . It  may be  the most idealistic     solution   . . . but  currently   it appears   self  regulation is  as bad  as no regulation !

Link to the article

http://articles.timesofindia.indiatimes.com/2013-04-19/india/38673588_1_pharma-companies-pharma-industry-doctors

Posted in bio ethics, cardiology-ethics | Tagged , , , , , , , | Leave a Comment »

The hidden link between Mitral annular calcification and CAD !

April 19, 2013 by dr s venkatesan

Why should mitral  annulus gets calcified ? .  Degenerative  calcification can be benign in  elderly .  If it occurs prematurely (say < 55 years )   there is enough reasons to worry .  This may represent a systemic vascular inflammation and  is considered a surrogate marker for athero- vascular -sclerosis .  A study from Cidar Sinai  , Los angels  has well documented the link way back in 2003  !

mitral annular calcification mac cad link

This is a  large study involving  17 735 patients (who were investigated for symptoms of CAD )   were screened.

The incidence  of MAC was high (As expected !)

  • 35% > 65 years
  • 5 %  < 65 years
Angiography  revealed more surprises .
  • The incidence of angiographic  CAD among those who had MAC and no MAC   was  88% v68% respectively ,( p = 0.0004),
  • Left main coronary artery disease  was (14% 4%, p = 0.009)
  • Triple vessel disease  was (54% v33%, p = 0.002).
mitral annular calcification www_drsvenkatesan_co_in

Image source  S.Atar ,  Heart 2003 : 89, 161-164

Conclusion
This study concluded ,  CAD is more aggressive in patients with MAC. It can  also be  an independent  predictor of  high risk CAD .
Further Implications  of MAC
  1. MAC is more common in women, especially diabetics .
  2. Degenerative Mitral regurgitation  is common ,rarely  mitral stenosis
  3. Recurrent VPDs and even  trouble some mitral annular VT is possible
  4. Extensive calcific lesions in coronary  artery is also reported with MAC.
Link between Stroke and MAC .
This was well proven by this paper  published in  NEJM in 1992.
MITRAL ANNULAR CALCIFICATION AND STROKE NEJM EMELIA BENJAMIN 1992

Posted in cardiology -Therapeutics, Cardiology -unresolved questions, cardiology women, Cardiology-Coronary artery disese, echocardiography, MVPS, valvular heart disease | Tagged , , , , , , | Leave a Comment »

How to Image LSVC by Echocardiography without contrast ?

April 19, 2013 by dr s venkatesan

lsvc persisitence lsvc left superior vena cava

While 2D echo visualizes the LSVC , it is the color Doppler flow (in blue ) that confirms the flow going away from transducer towards coronary sinus .Please note , if the LSVC shows red flow it indicates the left vertical vein and the flow is from below up .This is supra cardiac TAPVC . It makes immense embryological sense to understand LSVC and and left vertical vein are both same entities only the connections are different .

Click over  for a high resolution Image

Posted in Echo library and gallery, echocardiography, Infrequently asked questions in cardiology (iFAQs) | Tagged , , , , , | 1 Comment »

Does PCI convert “A positive stress test” into “Negative” in all patients with CAD ?

April 9, 2013 by dr s venkatesan


Those who answered  “Yes” ,  can leave this article . Those who answered  “No” read further .

* Logic would tell us myocardial revascularisation should correct  stress induced ischemia and it  should disappear promptly  . This does not happen in all cases  real world  ! That is  why medicine is  different  from mathematical science .

Some of the  reasons for  persistence of stress positivity even after an apparently successful PCI are  . . .

  1. Incomplete  correction of ischemia. (Ideally  to be referred as failed PCI )
  2. Error in Identifying culprit 9Angina related artery ) .Common feature of poorly worked up  multivessel CAD.
  3. Re-stenosis /Re-occlusion
  4. Doing very early stress test without giving time for revascularisation to work *
  5. Rapid progression of non culprit lesions .(Sub -optimal medical management )
  6. Chronic N0-Reflow phenomenon  surrounding  area of infarct .(Especially in  PCI of CTOs)
  7. Dyskinetic  or grossly remodeled ventricular segments  can result in non ischemic positive EST response (ST drag **)
  8. Associated systemic conditions especially  Anemia/ SHT & LVH -(False positive )
  9. Many diabetic patients may  continue to show stress ischemia due to  small vessel disease.
  10. A  patient with  syndrome X  characters  can have incidental  epicardial lesion as well . In such a patient EST will always be positive .

* Optimal time to do  EST  for assessing the  efficacy of  PCI/CABG is not established .Six months may be the reasonable point .If done within 2- 3 months it may  end  up  in embarrassment for the Interventionist . (So only it is kept at 6 months , this also help us  greatly  as  we can always blame it on poor life style control and progression of  the disease !)

** No reference  for this  , a  personal observation .We know  Q leads following MI ,  will show ST elevation during stress test especially if the segments are dyskinetic  . In leads diagonally opposite to q leads ,  ST depression is observed . This may not be  a evidence for true  ischemia . It probably represents   ST drag due to mechanical stretch .

Posted in Cardiology - Clinical, cardiology -ECG, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, chronic total occlusion (CTO), Clinical cardiology, cto chronic total occlusion, Diabetes and Heart, excercise stress test .EST, Infrequently asked questions in cardiology (iFAQs) | Tagged , , , , , , , , , | Leave a Comment »

Bifurcation angle is what ?

April 7, 2013 by dr s venkatesan

bifurcation angle

  • At any branch point three angles are possible .True bifurcation angle is formed between LAD and LCX .
  • The angle between LM and LAD or LM and LCX can also be important in specific situations ,especially when we encounter short left mains and Medina 1,1,0 lesions .
  • Major bifurcation angle can  occur in mid  segments  as well ,  between LAD / major Diagonal  , LCX and OM.
  • Logic would tell us the  left main  bifurcation  angle is relatively fixed by the anatomical AV and IV grooves. Still early course of LAD and LCX can be out of grooves.
  • Further ,the bifurcation angle is imparted some amount of dynamism by cardiac cycle . It can vary between 80 -120 degrees (LAD/LCX).
  • Most importantly various  angiographic views can alter the true angle (by illusion ) in dramatic fashion . RAO caudal view appear ideal to measure it. (LAO caudal make every bifurcation angle obtuse !)
  • Acute angled bifurcations are prone for stent related mechanical issues both during deployment and in the long term outcome . (When two stent technique is used) This is because ,  acute  angled bifurcations has a tendency to drift the carina , and  encroach  the lumen  which can create new  turbulence . Of course final kissing balloon is expected to reduce this hemodynamic side effect at least on paper !

Posted in Cardiology -Interventional -PCI, cardiology -Therapeutics, cardiology- coronary care, cath lab tips and tricks | Tagged , , , , | Leave a Comment »

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