Archive for February, 2019

Not every one feels the palpitation during tachycardia / Bradycardia /VPDs , Why ?

Palpitation is awareness of one’s own heart beat. It is a complex perception of sensation at cortical level (like dyspnea) . It can occur during physical and mental exertion.However , if it occurs without any physiological reasons , it becomes abnormal. It can mean an abnormality  in heart rate , rhythm or  raise in stroke volume. The first rule of palpitation is both tachycardia and bradycardia can cause it. Tachycardic palpitation is due to valve motion and bradycardic palpitation is due to both motion and increased stroke volume.

The most common mechanism proposed for palpitation is hyperactive anterior mitral leaflet

How and where  does the sensation of  palpitation felt ?

Does  it originate in  the chest wall ?  or Is it the vibrations spreading along  the flow of blood in great vessels ?  or Simply  represent  the vigorous valve motion  sensed by Intra cardiac receptors ? How it is  transmitted to spinal cord where it’s felt at cortical level  ? We are not clear yet. Paccinian corpuscles is thought to sense these vibrations and hand over as electrical signals  to spinal cord either directly from cardiac valves /walls or indirectly from chest wall.

Paccinian corpuscles are predominantly present in sensory nerve fibres located in the dermis of skin. It is also observed in nerve ending to joints, Chestwall, blood vessel and also heart .They act like pressure as well as vibratory receptors * The exact reference for Paccinian corpuscle to be present within the heart is not available to me. Readers may contribute,

Importance of age and gender and IQ

Palpitation is primarily a symptom of young age where the heart is supple and more dynamic. Women tend to perceive more for some unknown reason. Elderly people rarely complaint about palpitation .It could imply aging  with or with out autonomic dysfunction which suppresses transmission of palpitation signals to brain.Chest wall thickness also matters. My guess would be, Chest wall thickness, epicardial fat pad could absorb the vibratory  energy  and chest wall receptors fail to recognise it. One curious observation is,  palpitation is described in a succinct manner by certain patients only. Since , it essentially involves  higher cortical senses , we believe spatial intelligence of the patient  may also be important.

Why Irregularity in heart beat is well recognized?

For the given heart rate , irregular rhythms are felt  more often as palpitation than sinus tachycardia. This is the reason single ectopic beat is easily felt than  sustained tachycardia. A common sequence of  palpitation due to ectopic beat is , a suddenly  missed beat, subsequent pause and forceful post ectopic beat.

Valve morphology and impact on palpitation

Mitral stenosis patients can feel their loud first heat sound (S 1)  or varying  S1 during atrial fibrillation as palpitation; Mitral valve prolapse with redundant , hyper kinetic motion is probably most common cause of benign palpitation.

Sclerosed  and calcific  valves attenuates palpitation. Calcific mitral valve in mitral stenosis make both S 1 intensity and opening snap feeble .These patients are less likely to feel palpitation .

Individual valve pathology can generate palpitation as in Ebstein anomaly , which has a the large sail like septal leaflet that flutters to create palpitation(Apart form pre-excitation syndrome common in this condition) As a general rule ,It is possible semi lunar valves are less likely to cause palpitation than AV valves as the latter only exposed to direct contractile pressure of ventricle.

Right vs left heart origin and localised palpitation

I am not sure one can differentiate left heart from right palpitation. But.palpitation arising from right ventricular  volume overload and increased pulmonary flow like in ASD  are associated with direct local sensation over pericardium . Mitral valve motion can not be localized by  patients .However apical impulse can be felt.Neck pulsations invariably mean high flow states. Venous cannon waves due to high pressure tricuspid regurgitation can be felt with each heart beat (RV systole)

Exertional vs Non exertional palpitation 

Palpitation occurring during exertion often imply its due to excessive handling stroke volume or (Pathological regurgitant volumes) Stenotic lesions are less likely to cause palpitation during exertion it’s never an absolute rule. Exercise Induced arrhythmia always happen in any valve lesions.

Relation with LV function

A dysfunctional ventricle cannot  generate forceful contraction and hence palpitation is uncommon symptom. Cardiomyopathy presents with more of dyspnea rather than palpitation .Even,  an episode of AF do not cause palpitation in such patients .They simply feel breathless (Dyspnea ? Or is it a palpitation equivalent ?)

New age palpitation

With so many foreign bodies and accessories entering the heart  it’s not surprising for patients to feel amusing sounds and vibrations hitherto unknown in human body.

  • Prosthetic valve clicks (Sounds from mechanical valves can be  annoying .Tissue valves, TAVR are more quiet)
  • Abnormal electrical activity  from pacemakers and ICD coils.(Apart form pacemaker mediated muscle twitches)
  • Now, we have entire mechanical LV assist devices  working inside the heart with a 24/7 motors .(LVAD hum its called) Very soon heart is going to become a noisy place and patients would learn to ignore these abnormal sounds

Pleasant physiological palpitation

What brings the unpleasantness during palpitation? (applies to dyspnea as well). It is purely state of mind. While, palpitation due to extreme fear is unpleasant , palpitation due to pleasant emotional arousal (Often referred to as flying butterflies ! (Is it the wings of AML ? ) within the chest  as we hear from some of young  women & men ).Since they know the reason why they get it, cortical input welcomes it ,converts them to pleasant  beats .The Non-academic stuff  is intentionally made to understand how the limbic system and Hipocampus  areas of brain can modify the incoming signals of palpitation that comes from down under.

Thoughts to ponder 

Does post heart transplantation (De-nerved heart) patients experience palpitation ? Again, I am not sure .If palpitation is carried by cardiac nerves it should disappear. Of-course , 30 % of transplanted heart do get re-innervated. When you get a chance to meet a heart transplant patient you ask yourself and find the answer.

*Please be reminded Anginal pain almost vanishes  post transplant.In fact ,there have been instances of cardiac auto-transplant for refractory angina in the past.

Final message

Though all of us can list causes of palpitation without any difficulty , we rarely dwell into exact  the mechanism of genesis of this symptom and  its perception. As we enjoy flying in an exotic world of cardiac  interventions  . . .  the principles of  practice of medicine also expect us to take adequate efforts to understand fully the cardinal  symptoms of our patients . After all , they are the true teachers of Medicine. It is because of their pursuit for explanation for their symptom (Often vague though)  we make our professional progress.

Further  reading

John T.Shepard  The Heart as a Sensory Organ JACC Vol. 5, No.6  June 1985:83B-878

(The heart has variety of sensory nerve endings , still to be explored)

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Significant MR is a contraindication for PTMC. However,  If MR jet is central , and mild (some times little more than mild as well ) PTMC can be safely done. The MR may not worsen .It may even disappear.

Note: Eccentric MR jets are indirect evidence for sub valvular disease. Its very likely to get worsened and may require a mitral valve replacement .

Here is patient with severe mitral stenosis, the MR is in all probability safe.

Angle of eccentricity 

One must realise , the eccentricity of a jet is not very objective .What may appear as central jet in long axis may be wall hugging in 4 chamber view. This is very important to recognise. Further , even central jets can reveal a invisible eccentricity detected only on 3D MR jet reconstruction.

One simple way to ascertain central jet is to  check whether the MR jet align in the same angle as diastolic color jets of MS into LV inflow . (Looking carefully ,the diastolic color jets also provide us info about sub-valvular disease )

More anatomical distortion in this patient 

Incidentally , this patient also had another anatomical adversary  ie ,the bulge of IAS into right atrium. This can happen two ways .Septal aneurysm or a normal septum bulging to RA due to raised mean LA pressure.



Miral stenosis with Atrial fibrillation showing the changing mitral inflow jet .



The radius of curvature of IAS bulge Indicates its more of septal weakness that contributes than the raised pressure. There is a small risk in these patients the IAS flap may give way during the procedure and a small ASD may be created .(Hemodynamically may not be significant though)


How does the MR disappear after balloon dilatation ?

If you ask this question , it means your are a thinking cardiology fellow , good.

Guess your answer. Its all about physics of  MVOs behavior  in systole and diastole . The mitral valve tissue attachment and adhesion causes not only a  diastolic narrowing but also a fixed systolic regurgitant orifice.Once you relive it the leaflets begins to co-opt normally without a systolic leaky orifice.

Final message

Though there are clear contraindications ,suitability of mitral valve for PTMC is more of a personal experience and confidence. A MR jet of grade 1  may be acceptable. A huge LA, Distorted IAS anatomy, a clot confined to LA appendage are relative contraindication only. The puncture site on IAS , minimal manipulation guide wire within LA, a gentle over the wire technique to cross mitral valve or some of the tips for success.

Never hesitate however to refer complex cases of mitral stenosis to the surgeons. Of course , you can’t insist them to do a valve preserving OMV .It is unfortunate(They have good point of argument as well)  most of the surgeons have have made Mitral valve replacement as a default modality

Post ample :

When we were cardiology fellows , we used to have a mitral valve scoring system for suitability for PTMC. Its called Wilkin’s score. Its a purely an anatomical score. (I guess still its expected in Board exams) What we need is comprehensive anatomical and physiological assessment of mitral valve. With due respects to  published literature this scoring system lacks  two  vital parameters we look before PTMC , namely the extent of commissural calcium  and degree of MR.


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Cardiologists are grappling with at least  half a dozen time windows  in the management of STEMI. (It can be combinations of any of the following :Symptom – DAPT Loading – Door – Needle /Balloon-Sheath, wire crossing etc ) Time windows are Important in choosing the right (or no)modality of re-perfusion . Though superiority of  primary PCI  is thought to be established in academic community , it  may not be in real world. Published studies that suggest pPCI is superior to lysis at any time window  still lack good evidence.

Why is this long drawn confusion  ? 

One of the important determinant of outcome in STEMI , is the thrombus organisation (hardening )time . Some how we have assumed PCI can tackle hardened thrombus  much better than lysis (In fact the outcome in late PCI is as bad or good as lysis in terms of true myocardial reperfusion in this population.This fact will not be visible in scientific data that’s read superficially .One has  to  mine deep for the truth) (Claeys MJ,. . Arch Intern Med. 2011;171(6):544–549)

Two more virtual pathological Time windows.

While we are preoccupied with certain time windows in STEMI  ,may I suggest  two more  Invisible pathological windows. I don’t know , whether these are presumptive theoretical stuff ,  but understanding these time windows will sharpen our decision-making skills in STEMI.

1.Symptom to  ATO time (Acute total occlusion) 

ery gets occluded(ATO ).This is truly Invisible time window .( Pre-Infarction angina  to Infarct time ) Taking the last episode of most Intense pain need not refer to beginning of ATO / Infarct pain. (ACS being as dynamic process in a 24 hour time span an angina  can even be post Infarct angina!)

2. ATO to thrombus organising (hardening) time

It is obvious time is primary factor that correlates with thrombus organisation. But there is much more to it. It’s not the fibrin organisation alone that makes a thrombus hard. ATO gets reinforced by plaque and tissue material ( like steel rods  inside cement) In other words no one really knows  when does the thrombotic process begin or end  and  hardens thereafter. But we know for certain is  tackling a hard thrombus is difficult for both modalities currently we have lysis and PCI*

.(Almost forgot the third modality,  yes its humble drug heparin(.It can do wonders little slow though , Slowness doesn’t matter beyond 24 hrs is it not ?) Now there can be a role for Warfarin also to get rid of chronic IRA thrombus (Moon JY, N The role of oral anticoagulant therapy in patients with acute coronary syndrome. Ther Adv Hematol. 2017;8(12):353-366.)

There are excellent studies that correlated time window to thrombus hardness.At least in  50%  IRAs with time  window less than 12 hrs have thrombus age more than 24 hours Some of the thrombus material aspirated has been shown to be many days old (Kramer et al PLoS One. 2009;4(6):e5817)

Image source : Miranda C.A. Kramer Relationship of Thrombus Healing to Underlying Plaque Morphology in Sudden Coronary Death Volume 55, Issue 2, January 2010

How to arrive at the age of the thrombus  ?

It’s a difficult task to guess the age of thrombus with help  symptom onset and ECG .  There  can be 50 %  error as discussed earlier.

Is coronary angiogram helpful ?

There is no good clue to differentiate fresh from old thrombus by just looking at angio shot. Some experts are able do it (Guess it ?)

Poke and feel with guidewire  : This is probably the best way to tell whether thrombus is fresh or old (Still not fool proof ) Most of us do this in STEMI . All is well if guide wire cuts through  smoothly and nice flow is established.(What we call guide wire angioplasty) Procedure is completed with or without a stent ( &residual lesion) .This is the most gratifying and desirable outcome of primary PCI. (Note : Hardness of thrombus can be overcome stiff wires and force.That doesn’t make it a fresh clot ! This is where we may end up with No-reflow)


Image courtesy : Karim D. Mahmoud & Felix Zijlstra Nature Reviews Cardiology volume 13, pages 418–428 (2016) Various forms of thrombus aspirated during primary PCI.

When poke test fails  . . . be ready for a long haul or quit

Thrombus is not a single aged mass of blood. It has lawyers of clot with different maturity  ( like shells over earth ).Hence poking has its own side effects too.Some of it can be violent.When  deeper layers of old thrombus is exposed to fresh blood it can create fresh  cycle of clot activation.( Ofcourse we fight it out with DAPT and heparin) Winner of this fight can never be predicted. To conquer the thrombus or quit is directly linked to the cardiologist wisdom.

What about OCT/IVUS ?

They could help us to assess the morphology of thrombus and give  us Indirect clues about the age of thrombus. Some of the experts say they use it efficiently . My opinion is it adds more glamour than true enlightenment .(Mind you , we need to  cross , clear and flush the vessel to complete OCT. The fact that we are able to complete OCT in STEMI settimg would mean  thrombus is  fresh .In that way it may be useful but without a true purpose.)

Thrombus aspirate analysis : Its more scientific way of arriving at the age of thrombus (Any one want to do carbon dating on this ?) , This again lacks practical use as we need to assess  the thrombus age before poking to avoid subsequent complications. It is also not clear whether thrombus in STEMI is more of RBC and fibrin and net platelet content can’t be quantified.This especially true in stuttering ACS where NSTEMI is threatening to become STEMI or vice versa. (Platelets love to hug each other at high shear force , RBCs do the opposite )

Is the Consistency of the thrombus uniform ?

Here comes the importance of the length of the thrombotic segment. It’s estimated the length of the thrombus segment can be anywhere between 1 cm to entire length of the coronary artery distal to the site of occlusion .The initial proximal part may be soft as its directly exposed to DAPT and heparin.The distal thrombus is flushed only with collateral or a trickle of flow from anti-grade .So ,very likely the distal thrombus is harder than proximal.

How does DAPT loading and subsequent heparin interfere with thrombus organisation ?

Loading DAPT has a definite impact and prevents hardening.(But, one issue is it shouldn’t have been happened before administration)

What is the natural history of organised hard thrombus in IRA ?

  • It transforms  into a CTO.(Many of us believe this is dominant theme)
  • Late total recannalisation – 20% by 30 days
  • Partial recannalisation  (More than 20 % ?)
  • Since wide-spread use of predischarge PCI , true natural history is masked.

Final message

Taming STEMI with pPCI  is not always  a time sensitive emergency procedure . It’s important to recall STEMI patients can harbour thrombus with different maturity .We know STEMI can occur even in  patient with chronic thrombotic process also (even a CTO) . This is proven by a simple fact people walk in 3 days after MI casually. Further, during pPCI both early and late arrivals have equal difficulty though they carry different set of problems tackling the IRA.

If we really  believe principles of coronary care is aimed at tackling coronary thrombosis , wisdom  lies in  judicious use of both CCU and Cath lab facilities .Never hesitate to rush back the patient to CCU for a quick lysis (Or Intra coronary) and avoid the potentially prolonged  battle against huge mass of hard thrombus.



Post-ample : A quote 

Importance of  early arrival of STEMI patient to nearest hospital is huge , not because of the possibility getting an emergent PCI . Rather, it is  due to fact that simply reaching the nearest coronary care center dramatically reduce the mortality.(My guess is , this mortality benefit should be more than Lysis/pPCI put together)

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Let me see how many find sense in this Nonsense !

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