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

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.

It  happened ,  I did an echo for her .

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.

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 )

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 ?

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Fibrinolysis beats Primary PCI convincingly in the Belgian STREAM !

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 the same may  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 notdo a study in this time frame . The reasoning is  simple and very personal .In a  large  Government  hospital   where  we do not have primary PCIprogram  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 realised  not 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 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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There is nothing called Idiopathic VPDs . . . It may simply reflect our Ignorance !

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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“Non sustained” ventricular fibrillation : A concept paper and a case study .

Can VF be a non sustained  arrhythmia ?   This question was raised and a single case report was presented

in the annual scientific sessions of  Cardiological society of India Meet in  year 2008 in  Chennai.

I am just reposting it from my archives .

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Escape – Ectopic trigeminy :An unique ECG sign in Sinus node dysfunction

Sinus node is the electrical high command of our heart .When it gets injured  seriously (or shot down   as in sinus arrest ) there is utter chaos in the lower ranks !

This is what happened  in this patient .

The lower pacemkers can either passively release  themselves as escape rhythm or actively fire with a  ectopic focus  . Any combination of escape / ectopic  beats can  occur .If occasional sinus beats capture the ventricles things  can become further complicated .

It is obvious , this  random intra-cardiac  shooting  makes the life of the  myocardium miserable . It is a perfect setting for syncope, tachcyardic cardio myopathy , extreme brady induced VT , VF  even SCD.

*Meanwhile , It is  heartening to note  SND   rarely lead to  sudden death in spite of all the chaos .However  extreme  bradycardias  that occur in  complete heart block  does  not enjoy this immunity as fatal complications are common if not intervened .

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A chill in Cardiologist’s spine : Unnecessary intervention becomes a definite crime !

The irony of modern medical care is  9/10 times  medical negligence is  defined in terms of  acts of omission  in  required  level of care . In reality  most medical negligence acts are related to knowingly overdoing a futile diagnostic or therapeutic modality.

This irony was never understood by the public, the professionals or  even the judiciary .This remains  the most dangerous issue  facing modern medicine !

Finally some light is appearing in the horizon . A Missouri  Cardiologist is suspended for overdoing things he knows best  . . . namely coronary stenting ! 

This may bring chills over many cardiologist’s spine .

http://www.stltoday.com/news/local/metro/missouri-healing-arts-board-issues-first-emergency-suspension-of-doctor/article_205eaffd-1825-5d7d-a9de-a289c010fd65.html

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Why Prasugrel is contraindicated in TIA ?

 

Current prescribing information cautions clearly Prasugrel should not  be used in TIA  or recent  stroke (Even in  ischemic strokes -Embolic included !)

The warning  is perplexing and illogical to me.

What is your take ?

I would imagine the following  could be  the reasons.

Prasugrel  as an  antiplatlet agent is  many fold  powerful and could convert all  strokes into hemorrhagic one .

Does Prasugrel convert a TIA into stroke instead of curing it ?

Prasugrel may worsen the stroke  in case the TIA is going to end up as stroke.

Is there any thing called hemorrhagic TIA ?

Since we do not have any mechanism to diagnose Ischemic TIA from hemorrhagic TIA ,  it is better to avoid Prasugrel . It is still a mystery ,  why  clopidogrel which acts on the same receptor and can be safely given for TIA ( pro actively)

After thought

I think Neuro physicians must answer this question . ( Cardiologists  better limit their extended geographical terrain ! )

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Knowledge and wisdom check in pace maker therapeutics !

Answer

Each of the above can be important in diseased heart .The most important component seems to be Inter- ventricular  synchrony .This is closely followed by AV synchrony .In dysfunctional  ventricles Intra-ventricular  synchrony  also becomes important .In  structurally  normal hearts  none seems to be important  (This statement can be debated  )

VVI pacemakers causes  both AV  and Inter-ventricular (VV ) dys-synchrony

DDD pacemaker  may still  induce  Inter-ventricular ( VV ) dys-synchrony  whenever  RV is paced for any reason .This may happen up to 60 % of pace making time in real world.

Some more facts

*Chronic VVI pacing may  induce adverse  remodeling of both atria and may worsen LV dilatation. In contrast isolated chronic organic LBBB is well tolerated and with paradoxical septal motion rarely worsen the LV function.

**Please note the paradoxical septal motion , which is  noted in  all LBBBs is  same as inter-ventricular  dyssynchrony .

***Inter atrial synchrony is a less discussed issue .It becomes  important in diseased atria which manifest gross   intra atrial conduction blocks  , atrial inhomogeneity and AF .Onset and offset  of AF has a major impact in the way DDD pacing is going to fire .

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ECG suggests LAE . . . Echo reveals an absolutely normal Left atrium . . . what is your comment ?

This is an ECG of a 42 year old man .He was reported as  Left atrial  enlargement (LAE) and was referred for  echocardiography . His echo was normal . LA measured 2.5 X 3.1 cm .The consultant  called back the echo lab ,  to verify   the left atrial dimension .He thought he was very sure of LAE .It took  considerable time to convince him about the credibility  of the echocardiographer . He was  right after all  . . . still . . .  ECG was  also looked  convincing  for LAE !

                         Is this phenomenon  of wide P wave with normal atrial dimension  common ?

Yes it is . It  underscores  poor sensitivity of ECG in the  diagnosis  of LAE .The P wave abnormality in the above patient is due to Inter atrial block (IAB ) . This widens the p wave .

What  are the types of Inter atrial block ?

 

P wave widening is not synonymous with LAE .(Here P waves  widened   due to sluggish inter nodal pathway and inter atrial pathway .It is something like QRS widening in  bundle branch blocks  )

Final message

IAB is an important differential diagnosis for LAE . The significance of which is not entirely clear . It  is possible  IAB   precede LA enlargement  .It can even trigger AF due to  inhomogeneity.

Even though IAB was reported in 1950s  (Puech P* ) ,  it was  rarely  considered important With  increasing incidence of atrial arrhythmia in aging population , IAB is expected to  come into the lime- light again . The sophisticated electro anatomical mapping  can unravel the mysteries surrounding this entity .

Reference

*Puech P. L’activite´ electrique auriculaire normale et pathologuique. Paris: Masson, 1956; 206.

http://www.jecgonline.com/article/S0022-0736%2812%2900227-0/abstract

http://europace.oxfordjournals.org/content/1/1/43.full.pdf

Bachman bundle branch block

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Can we diagnose LVH with normal IVS thickness ?

We always look at the thickness of  Inter ventricular septum for LVH . The Normal IVS thickness is up to 11 mm in diastole .  LVH is definite if IVS measure > 11 mm .It is  certain if it is > 12mm . But , we need to realise LVH by definition is not simply wall thickness .

It is increased LV  mass .

LV mass can increase without wall thickening . This is  referred to eccentric LVH . For example in chronic  volume overload  states  (or even DCMs )  LV mass may increase without septal thickneing .

Final message

LVH is possible without IVS thickening .

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