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Why is sudden cardiac death uncommon in women ?

March 17, 2009 by dr s venkatesan

To further understand women's heart click on the title

SCD  continues to be  the major mode of  death of  our  population . Millions of men die every year instantly .The commonest mechanism is due to primary ventricular fibrillation following an abrupt closure of coronary artery due to a thrombus.Most die , within few minutes of the event, some  before reaching the hospital , few within the ambulance  and an  unlucky few die on the CCU bed  or cath lab table even after getting the best treatment.

If we analyse the data, there is a  surprising fact !  Men form the bulk of these SCD victims.In our experience , out of 100 cases of consecutive  in hospital primary VF only  6 were females , indicating  an important  biological phenomenon to be studied.The data for out of hospital primary VF is more difficult to get , but the  log records of EMRI and emergency rescue team consistently confirm the male preponderance of primary VF .

How  does the female heart enjoys this relative immunity from primary VF even as the blood supply is acutely compromised ?

The answer  is  not known . If we are able to  decode this , one can replicate the same  model in male .

The QT paradox and incidence of primary VF

QT interval represents a combination of  electrical depolarisation and repolarisation .It is a well established   scientific  fact  that  women have   relatively  prolonged QT interval .This  is determined by evolutionary biology and  inherited characteristics of  potassium channels  during myocardial repolarisation

In simple terms, the female heart  knows how to relax slowly and prolong the electrical relaxation time.(Not mechanical)

It is also a well known  fact ischemia mediated a prolonged  QT interval is a trigger for dangerous ventricular arrhythmia.This ischemia induced QT prolongation is less pronounced in females than males as the baseline QT itself is slightly longer in women.The percentage increment of QT interval during acute ischemia is significantly higher in male .This could be one reason for the preponderance of VF in men

The billion dolor question and a real challenge for the cardiologists is

How to make a heart electrically inert during ongoing ischemia ?

  • Pain is also trigger for primary VF due to high adrenergic tone.Prompt control of chest pain make VF less likely.
  • Lignoacaine a myocardial anesthetic if administered quickly can prevent many of the primary VF.

And now , shall we  think little wildly !

What if , if  we administer lignocaine spray straight over the (or sublingually ) in every patient with  chest pain

as like a sport injury and try calm down the heart electrically !

Also read

1.Lignocaine  the forgotten hero .

2.View this video -Ignorance based cardiology !

Reference

Arrhythmias and sex hormones


Posted in Cardiology - Clinical, Cardiology - Electrophysiology -Pacemaker, cardiology -ECG, Cardiology-Arrhythmias, Cardiology-Coronary artery disese, Infrequently asked questions in cardiology (iFAQs) | Tagged , , , , , , , | Leave a Comment »

Why synthetic grafts for CABG is not popular ?

March 15, 2009 by dr s venkatesan

CABG is the most common cardiac surgery done world wide. Traditionally saphenous vein graft and LIMA are used .Now radial artery is being used often. The life of venous grafts is short, so total arterial graft is preferred.The issue here is lack of good arteries for grafting especially when a second CABG is required  .

So what  are the options ?

  • Cardiac surgeons often use synthetic conduits for many of the congenital heart diseses.
  • But some how this has never been thought as an option for CABG.
  • This may be due to small nature of the vessels, but now there has been some developments on this .
  • In future sunthetic grafts might replace the conventional grafts.

 

Chronoflex, is one such graft under trial  and is engineered to be pulsatile, biostable, torque-resistant and suturable. Once implanted, the graft is able to incorporate the patient’s own cells and tissue, so that the inner surface mimics the normal environment for blood contact. The material is also flexible, so that the graft can pulsatile like a  vein as it carries blood to the heart.

www.cardiotech-inc.com

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What is the hemodynamic impact on the left main blood flow when LIMA is grafted to LAD ?

March 15, 2009 by dr s venkatesan

CABG is tretment of choice for left main and  complex proximal LAD  lesions. So most patients get CABG in these situations.

The hemodynamic effects of LIMA graft on native left coronary artery can be tremendous and some times deterimental.

  • One of the consistent observation has been , the moment LIMA is bypasssed into distal LAD the antegrade flow through left main is reduced .This is still more significant if circumflex is also grafted .
  • For inital few weeks there is competition between LIMA flow and LAD flow and invariably LIMA wins  , and native leftmain or LAD  flow regresses and many times  closes totally.
  • Some studies have observed accelerated left main and LAD atherosclerosis.
  • The native LAD and leftmain could be a source for thrombi and atheromatous debri and these migrate distally and have potential to block the LIMA entry point  into LAD
  • The advantage of having a patent native left main and LAD  is that if the LIMA  graft occludes later on native circulation may assist.

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Common myths in cardiology : Presence of viable myocardium does not mean it demands a revascularisation

March 15, 2009 by dr s venkatesan

Post myocardial infarction revascularistation either by PCI or CABG forms the bulk of the coronary interventions world wide.There has been considerable controversy in selecting the patients for the procedure.

Certain basic rules are to be applied.

  • Never do any thing on a totally asymptomatic and fully functional patient.(Functional , means good exercise capacity of atleast( 10Mets).Just medical treatment with good doses of statins, beta blockers will do.
  • If a patient has persistent angina  following MI  ,the issue is relatively simple as  they are  candidates  for CAG  and intervention .
  • The issue becomes little complex when the primary complaint is breathlessness and echo showing  LV dysfunction.

This dilemma is due to a  simple fact

coronary revascularisation has a  great impact in relieving angina but has  less impact in reversing

left ventricular  dysfunction

So,  how do you approach a patient with LV dysfunction and exertional  breathlessness and absolutely no chest pain ?

  1. Do a  CAG
  2. Assess the lesions if any (Some times,  to our surprise there may not be any critical lesions at all ! )
  3. If there is / there are critical lesions try to corroborate with infarct segments.(Use Echo for this correlation)
  4. Don’t bother much,  if a  vessel has a lesion  that is supplying a scarred myocardium.
  5. If there is gross LV dilatation, mitral regurgitation and LV clot refer these pateints  may benefit  from surgical management

One of the rules written by the cardiology community over the past few decades has been

We must document viable myocardium before doing a revascularisation procedures on them.

This rule was self imposed ,  to prevent inappropriate revascularisation in  post MI population.

So , a  gamut of investigations (Both invasive and non invasive came into vogue) to identify viable myocardium in post MI population. Stress echo, Thallium-sesta MIBI, PET  to name a few .

Even after liberal usage of these invesitgations , we realised ,  the confusion in the  optimal selection of candidates for revascularisation has not settled.

In fact,  the correlation between viabilty and subsequent interventional benefit is  inconsistent .Not withstanding this  issue  ,cardiologists inspite of the negative results of OAT and TOAT trials ,  started  opening or by passing any occluded vessel irrespective of viability status.

Unanswered  &  Unasked questions in myocardial revascularisation ?

1.Why viable myocardium is viable even in the adverse compromised vascular  environment ?

It  is viable for the simple reason it has some capacity to be alive . By it’s inherent survival capacity (Survival of the fittest ) or it somehow gets the nutrients by cell to cell perfusion.

2. It is viable allright  ,  why it is not contracting ?

Because ,  it is biochemically and metabolically alive (Can be documented by FDG PET scan mismatch ) but it can not synthesise adequate ATPs to make the muscle contractile.

3.”Viable myocardium is viable ” what more you want from it   ?

Simple viability is not suffice . How to make it mechanically active and contractile ?

4.Is viable  myocardium    synonymous with ischemic myocardium ?.

No,  it is not (Contrary to the popular perception ) .

5. Is it not  common to find dysfunctional segments with good TIMI 3 flow ?. So what is the purpose to document viability ?

It is not suffice to simply document viable myocardium but it is an absolute necessity to prove this viable segment is also  critically ischemic .

7.If angina is  a sign of viabilty why most of viable myocardium is painless ?

This again confirms the fact , much of the viable myocardium in the post MI phase is not ischemic but” still dysfunctional” waiting for healing time. This concept  was  introduced with great fanfare* as  stunned myocardium ,  20 years ago , which was subsequently rejected my mainstream cardiologists , as this concept tend to  restrict the  freedom of interventionists. * Even though ,the concept was genuine and proven scientifically !

6.Are we  certain , the  viable ,  non contractile myocardium  (Which we painstakingly document )  will get back the contractility once the  segment is    revascularised?

Absolutely not. (With lot of PET study doumentation )  This,  we can not guarantee even in ischemic, viable segments  ,  while in the  non ischemic, viable segment it is all the more unlikely.

7. What are the chances of these viable but  non contractile myocardium  regain the contractility  by natural course ?
Very significant chances .In fact every patient recover some LV  function spontaneously over time .

Final message.

  • Revascularisation is non controversial in patients with angina
  • In patients with  primary symptoms of dyspnea  ,  it is less effective and documentation of myocardial viabilty per se will not guarantee successful outcome following revascularisation.Out come depends on  multiple factors .

Posted in cardiac surgery, Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology- coronary care, Cardiology-Coronary artery disese, Infrequently asked questions in cardiology (iFAQs) | Tagged , , , , , , , , , , , , , , | Leave a Comment »

What are the differential diagnosis for intraluminal filling defect in coronary angiogram ?

March 8, 2009 by dr s venkatesan

Intraluminal filling defect is often  observed during coronary angiogram .Thrombosis  has become the default diagnosis in most situations.This has resulted in over diagnosis of thrombosis .In fact a strategically located plaque stained by the dye is an equally common cause for intraluminal filling defect.

In fact there are many recognised caused of filling defect

  1. Thrombus
  2. Dissection
  3. An eccentric plaque
  4. Dye trapped within  plaque fissures
  5. Calcification projecting into lumen
  6. Plaque prolapse from stent struts
  7. Artifacts-End on view of  side branches
  8. Static myocardial bridges
  9. Trapped air bubble(Transient filling defect)
  10. Streaming  effect  dye may mimic a filling defect

Message

It is  not advicable  to make a  default dignosis of coronary thrombosis in all cases of intraluminal filling defects

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Some thoughts about left main disease : Why CABG will always prevail over PCI in left main disease ?

March 6, 2009 by dr s venkatesan

Why PCI  in   left main CAD is considered  an inferior modality than CABG ?

CABG is superior to PCI for the  simple reason it provides complete revascularisation virtually in all  patients with LMCAD , while PCI is possible only in a fraction of patients with LMCAD.

If  we take 100 patients  with left main  disease may be ten (At best !)   would be  suitable for PCI ! In other words PCI is contraindicated in vast majority of LMCAD  by technical criteria alone , while there can never be a contraindication for CABG in patients with LMCAD.(Except  when , comorbidity precludes surgery )

Why  PCI in  LMCAD difficult ?

It is  dependent on  technicalities

CABG does not tackle a lesion,  it simply avoids it  and by passes it ” No great brains required”

while PCI takes on the plaque frontally ,  in the dangerous  terrain of  left main artery  itself !

so,  much caution,  planing ,  logistics are required . Further ,  if there is a complication there is a potential

for catastrophe  as the only  supply line is cut off . This is the reason , cardiologists were worried to try this on

unprotected left main. (Protected LMCAD refers to left main disease following CABG  wherein atleast   LAD or LCX is  grafted )

Points to ponder in LMCAD

  • PCI is suited for isolated discrete LM disease.In realty  this is seen in less  than 5-8 % CAD.
  • LMCAD is very often associated  with  critical and multivessel distal CAD . So these patients will be candidates for CABG.
  • Left main ostium or LAD ostial  involvement makes PCI a tougher exercise
  • Calcification is more common in LMCAD that  again makes PCI difficult.

The following article in Feb 2009 is a major blow for proponents of  PCI for left main

http://circ.ahajournals.org/cgi/content/extract/119/7/1013

left-main

http://content.onlinejacc.org/cgi/content/abstract/51/5/538?ijkey=84c977d189e84327c3abbd4c1228de17dd99048a&keytype2=tf_ipsecsha

Final message

  • Conquering left main disease is an interventionist’s  ultimate dream.
  • But, before that they have  to tackle the bifurcation lesions .This is of vital importance, because 2/3 rd of left main  patients have  some form of bifurcation lesions. Current techniques , hardware  and outcomes are far below the idealistic solutions in bifurcation lesions.
  • Till that time ,  CABG would  remain the only choice for all , but for  a small fraction of isolated  left main disease where PCI may be possible.

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What is the incidence of insignificant left main disese ? How will you manage it ?

March 6, 2009 by dr s venkatesan

Left main coronary artery disease (LMCAD) often evokes  a panic reaction  among cardiologists .Not every LMD deserve that re. To  label  it as  significant, we have a criteria ,  that is 50% diameter stenosis.  So what you do , for a tapering  or narrowed left main with 40% stenosis. Isolated insignificant left main is rare *, but real incidence is not known.  LMCAD  is  most often due to  , atherosclerosis of left main coronary artery without limiting the flow.

What are the options ?

  • Leave it alone, with intensive medical management assisted by high dose statin(80mg)
  • Elective PCI with stenting , even though the lesion is not significant.

*If associated LAD  or LCX is there decision making is easier .

How  significant is a coronary stenosis ?

The significance of a coronary lesion with reference to “lumen diameter obstruction” is basically flawed. The significance of a coronary stenosis, by tradition is  based on it’s hemodynamic impact ,right from the  CASS days in early seventies.Unfortunately our mind set has not changed even after realising    non obstructive – sub critical lesion is more prone for acute coronary syndrome.  Is it not ironical to call a  40% lesion a non significant one !

So, the  significance of coronary stenosis is two fold.

  1. Hemodynamic  significance
  2. Clinical and  pathologic significance

The former predisposes to often chronic stable angina, later likely to result in ACS.

How will you approach a apparently insignificant left main disease ?

A 40 % lesion in left main is hemodynamically not significant , but pathologically very significant.It needs intensive treatment. Plaque passification with medical approach is first choice.If the lesion morphology is eccentric,  has irregular margins or involves  LAD  or LCX ostium doing a PCI or even a CABG is to be considered in spite of the lesion is  hemodynamically insignificant .

Why , PCI is   considered  “not appropriate”  for   less tighter lesions , even though these lesions  have great clinical significance ?

The answer is simple, The risks  and the  potential cost are more than the benefit !

And further ,  stents are  not innocuous devices  either  , they  always carry a risk of sudden occlusion as like  a sub critical lesion  !

Answer to the title question

True incidence is not known . Our experince (Class 1 c evidence) would suggest Left main disease constitutes up to 10 % of CAD.Among this one third would be hemodynamically insignificant

Suggested reading

Handbook of Left Main Stem Disease


edited by Seung-Jung Park

hbleftmn

//

Posted in Cardiology -Interventional -PCI, cardiology- coronary care, Cardiology-Coronary artery disese, Hemodynamics, Uncategorized | Tagged , , , , , , , , , , , , , , , , , , , , , | Leave a Comment »

How to localise focal atrial tachycardia with P wave morphology in ECG ?

March 3, 2009 by dr s venkatesan

What is the simplest and accurate way to predict  the   origin of Right atrial tachycardia(RAT)  from left atrial tachycardia(LAT) ?

Look at the P waves in V 1 ( Don’t look further ! )

  • A  negative  or  a biphasic (+/- ) P wave in V 1  is 100% specific  for a right atrial tachycardia
  • A positive P in V1 or  a biphasic ( –/+ ) P-wave in lead V1  has 100%  sensitivity  for a left atrial tachycardia

What are the incidence of left and right atrial tachycardia ?

RA- 75%

LA -25%

What are the common focus of right atrial tachycardia ?

  1. Crista terminalis (60% of all RAT)
  2. Tricuspid annulus
  3. Coronary sinus ostium
  4. Perinodal tissue
  5. Right side of IAS
  6. Right atrial appedage

What are the left atrial focus in Left atrial tachycardia ?

  1. Right & left pulmonary vein (50% of all LAT)
  2. Superior mitral annulus
  3. LAA
  4. CS body
  5. Left septum

(Please note  this rule is not applicable for re-entrant tachycardias, atrial flutter, AV nodal tachycardias)

Source :

P-Wave Morphology in Focal Atrial Tachycardia

Development of an Algorithm to Predict the Anatomic Site of Origin

peter M. Kistler  et all. 

This paper  from  Melburne, Australia is a rare gem of  an article for understanding  atrial tachycardia .This  paper won the  the Eric and Bonny Prystowsky Heart Rhythm  society Fellows Clinical Research Award, New Orleans, Louisiana, 2005.

Click on the Link  to reach the article

http://content.onlinejacc.org/cgi/content/full/48/5/1010

 
 
 
 
 
 
 
 
 
 
 
 
 
 

 

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Posted in cardiology -ECG, Cardiology-Arrhythmias, Cardiology-Land mark studies, Tutorial in clinical cardiology | Tagged , , , , | Leave a Comment »

What is epicardial ventricular tachycardia ?

February 15, 2009 by dr s venkatesan

Ventricular tachycardia as a group , constitute a major  group of cardiac arrhythmias. Most of the VTs are managed  by cardioversion  followed by medical management.  Few require , implantable defibrillator when there is severe LV dysfucntion .(ICD) Localising the origin of  VT and subsequent , ablation is the treatment of choice in some of the  patients  with VT.

Traditionally VT was thought to arise fro the endocardial aspects of myocardium. Now  we realise many times VT originate from the epicardial aspects of  ventricle.

Epicardial VT : Defintion

Epicardial ventricular tachycardia (VT) is defined as VT in which the critical sites of the reentrant circuit (or the ‘sites of origin’) are located exclusively in the subepicardial tissue, as shown by entrainment manoeuvres or VT that is terminated within 10 s with standard radiofrequency (RF) pulses, or both.  E. SOSA,M. SCANAVACCA et  all  http://www.springerlink.com/content/w608142674154tp5/ 

 

 How to recognise epicardial origin of VT by surface ECG ?

  • Terminal S wave in V2 and q in lead 1 strongly suggest VT of sub epicardial origin.
  • Pseudodelta wave 
  • Intrinsicoid deflection time of  85 ms
  • RS complex duration of  >120msec

Suggest   epicardial origin of the VTs.

Important Links

http://www.circ.ahajournals.org/cgi/content/full/113/13/1659 

Berruezo      criteria ,http://circ.ahajournals.org/cgi/content/full/109/15/1842  ( Must  read)

http://cogprints.org/4222/2/tada.pdf

 

What is the clincal significance of epicardial VT ?

Endo cardial ablation  not likely to be successful

Trans pericardial approach may be needed.

Posted in cardiology -ECG, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, Uncategorized | Tagged , , , , , | 1 Comment »

What is isolated diastolic hypertension ?

February 8, 2009 by dr s venkatesan

idh

  • Hypertension  is  major determinant of cardiovascular health  of our global population
  • Millions suffer,   hundreds of societies ,  and as many guidelines , and drugs are still struggling  to control the menace.
  • An important sub group of HT , (ie IDH ) population has been neglected and never received the scientific interest , which it deserves !
  • In our study it occured in 7.2% of all HT  patients.
  • JNC,  the world authority on HT never considered  IDH as a separate entity, and as of now there is no specific guidelines.
  • And the irony is complete . There is not  a  major study available to analyse the differential effects of anti hypertensive drugs on systolic and diastolic blood pressure.

If  a patient with the BP of 120/96 asks you , “Doctor , will the drug,   you have prescribed , selectively lower my diastolic blood pressure ” what will be your answer ?

A clear ,  I don”t know !

The following paper was presented in the World congress of cardiology Sydney  2002

Isolated  Diastolic Hypertension

S.Venkatesan,S.D.Jayaraj.Gnanavelu, Madras Medical College. Madras, India.

Abstract : Systemic  hypertension  continues to  be a major determinant of cardiovascular  morbidity. While isolated systolic hypertension(ISH) has been identified as a specific clinical entity, isolated  diastolic  hypertension(IDH) has not been reported as a separate group. When we analysed our data from our hypertension   clinic  we found  a distinct subgroup of patients who had  elevated  diastolic blood pressure   with  normal systolic pressure. We report the clinical profile of these patients. 440 newly registered hypertensive  patients between the year 1998-99  formed the study population. All  patients with secondary hypertension  were excluded.. IDH  was defined as  diastolic BP more than 90mmhg and systolic BP less than 140mmhg.

IDH was present in 32(7.2%) patients.  The male female ratio was 3:1, mean age was 42(Range32-56) The mean diastolic pressure was 96 mm (Range 90-110).The mean systolic pressure was 136mm(Range 128-140). LVH was observed in 4 patients(12.5%). Diastolic dysfunction was detected by echocardiography   in 20patients.(62%)

We conclude that isolated diastolic hypertension  constitute a  significant subset among  hypertensive  patients and they need further study regarding the pathogenesis, clinical  presentation and  therapeutic implication.

Link to PPT  will be available soon .

Posted in cardiology -Therapeutics, Cardiology -unresolved questions, Cardiology hypertension, general medicine, Infrequently asked questions in cardiology (iFAQs), My presentations | Tagged , , , , , , , , , , , | Leave a Comment »

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