An unusual cardiac arrhythmia : This ectopic beat * arises right from sinus node itself !

This is an  ECG which  I reported  yesterday in my clinic . I thought it was a  near perfect example for sinus node premature beat .

(Of course I need to explain  why the  P morphology  slightly  differs )

A  sudden unexpected  QRS  complex is often called as  ectopic beat . If it occurs prematurely (ie earlier than anticipated )  it is called as premature beat. If it occurs late it is refereed  to as escape beat .Please note the difference is not absolute .

Sinus node is a dramatic bundle of energy with divine powers that  drives rhythm of life !

The pacemaker cells are arranged in a compact fashion with  differential properties from cranial cells firing fast and caudal cells little slower. The neural control is under constant Neuro/electro/humoral  servo control mechanism.It is well known the pacemaker shifts it’s firing location within the SA node in fairly regular fashion .The entire SA node has rich adrenergic and  cholinergic  innervation , with  a dominant control by the later . (This is  why the intrinsic heart rate is  in the tachycardia  range (around 116 )  when SA node is denerved  pharmacologically )

SA node ,  being  a complex structure ,  it is not surprising to note  few beats to fire  slightly late  or  prematurely.If it occurs late it is called sinus pause ,  if it occurs early it is sinus premature beat , if  both occurs  interchangeably  we refer it as  sinus arhhytmia. (Read  about sinus pause here)

What is the clinical significance  of   SPD ? (Sinus premature depolarisation )

It is a  very benign entity that it is  merely an  academic fascination . By  stretching my  imagination  I  can  correlate  it  with few possible  clinical issues.

• May be it has potenital to trigger a  SA nodal reentry tachycardia  or In appropriate sinus tachycardia/bradycardia.
• It may be imporatnt in sinus node modification process.
• However ,the main issue is  thee  cardiac physicians  in their enthusiasm should not mistake it for some serious  cardiac arrhythmia !

Related article

http://drsvenkatesan.wordpress.com/2009/04/14/can-premature-ectopic-beats-occur-in-sa-node/

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Does radial coronary Interventions increase stroke risk ?

The link between brain and the  hand  starts right from fetus .  It is a well known fact  vertebral artery   competes with hand blood flow  . In the right side , there  is one more  vascular issue !  .Bracho cephalic  artery  arises  directly  from aorta and supplies the  right  hand and  right half of brain.

It remains a mystery  why left brain  is   blessed with a  separate  origin ,  while right has to share it with blood meant for hand  .It is beyond science  . . . isn’t

It is possible the left hemisphere  of brain   has more   purpose   to be alive  ,  with bulk of the cognition work to do . Hence   God created a  separate  supply to it !  Of course , he  would   have never  thought ,  the  possibility of  his ” mean” creations   adventuring  within the   arterial tree  !

Click over the Image for animation

Please remember  whenever  we   play with   catheters and wires  through   radial route , we  are  hugging  and scraping   the artery meant  for cerebral circulation !

Final message

Femoral Interventions  enjoys a proven  track record. Currently ,  radial route has virtually taken over with  few  advantages . However , the  overall stroke risk in the two approaches  remain  low but genuine (.4 %) .It may be true , arch manipulation is more  with  femoral but  the threat to  vertebral and brachiocephalic circulation  is more with radial .  When the available evidence are  not conclusive  and  new ones are not forth coming  . . . it is wiser to rely on common sense !

Reference

I think  this 2011  study  from the  prestigious stroke journal  has convincingly answered the issue

It concludes , the right radial approach  is indeed risky  to develop cerebral  micro embolism   when compared to right femoral

A Review article in  Circulation

Other references

1.http://stroke.ahajournals.org/content/38/7/2176.full.pdf+html

2.Transient Cortical Blindness after Coronary Angiography Journal of International Medical Research. 2009;37:1246-1251,

3. Stroke and Cardiac Catheterization Circulation. 2008;118:678-683,

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What is the mechanism of ventricular tachycardia in hypertrophic cardiomyopathy ?

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 .

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 .

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

//

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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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The hidden link between Mitral annular calcification and CAD !

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  !

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).

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.

Benjamin EJ , Plehn JF, D’Aagostino RB, et al . Mitral annular calcification and the risk of stroke in an elderly cohort.

N Engl J Med 1992; 327 :374–9.

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

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 .

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What happens to CT ratio during systole and diastole ?

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.

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 !)

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 .

Reference

http://radiology.rsna.org/content/94/1/115.abstract

Coming soon

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

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Transient Ischemic attacks (TIA’s) of heart

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

Download  a PDF presentation

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What is the Ideal time window for rescue PCI ?

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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“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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