A 50-year-old man was referred for dizziness, bradycardia and dysphagia .He was very clear in describing his symptoms and  landed up in Gastro- enterology  OPD , from there was referred to my clinic for cardiac work up . His ECG showed a sinus bradycardia HR of 48 /mt.


Echocardiogram revealed a structurally normal heart as we expected , but was surprised to spot suspicious shadow in para-sternal long axis view , beneath left atrium.

A well demarcated large mass compressing left atrium.  Trans Thoracic Echocardiography  may not be looking at the heart alone ,(Its technically Thoracic Ultrasound though we may refer it as Echocardiogram   )

  • Aortic aneurysm ?
  • Mediastinal teratoma?
  • Bronchial adenoma ?
  • Esophageal mass ?

The Answer is none of the above

As I was wondering what it was, the staff nurse in charge threw a heavy folder with well worked up gastro Investigations.

That moment , diagnosis became obvious , without a need for further scrutiny to my medical acumen.

Note: The barium swallow of the Esophagus reveals the Intimate relationship between the food tube and the heart as it descends vertically downwards posteriorly  . Realise , how the proximity of these two structures could  confuse a physician when symptoms spill over on either way. (I would have expected a lateral view to show the compressive effect of Esophagus on the left atrium the radiologists felt its not important !)

Yes , it is Achalasia of the cardia , dilating the lower end of esophagus with fluid /mass effect  , compressing the posterior surface of Left atrium.He underwent a myomectomy surgery.

Why bradycardia  ?

There is well described esophago-vagal reflex reproducible by stressful swallow or balloon inflation in the lower end of esophagus at D7 level.(Ki Hoon Kang,Korean J Intern Med. 2005 Mar; 20(1): 68–71.)

Achalasia cardia is known to be associated with symptomatic bradycardia, dizziness, and rarely swallow syncope,though this patient didn’t have a classical syncope.The bradycardia is probably due to high vagotonia, (Hugging effect on posterior surface of heart known for rich innervation of vagus.) . Complete reversal  of bradycardia after esophago -gastric surgery is expected.

Implication for cardiologists

There has been instances of patients with esophageal syncope and reflex bradycardia getting permanent pacemaker therapy. I think , clinical or sub clinical esophageal disorders should be included in the work bradycardia before labelling them as intrinsic sinus node dysfunction .(Ref 1,4)

Final message 

The field of Cardiology  is often referred to as a super specialty atleast in India . I disagree with it strongly. Cardiologists are neither super(eme) nor special .We need to be reminded  its afterall a sub-specialty of Internal medicine and each specialist should undergo retro-training in medicine periodically .This patient is a typical example of a gastric problem entering the domain of cardiac Imaging.Strong foundations in symptom analysis and some degree of medical  curiosity will enable an occasional cardiologist to make a correct diagnosis belonging to a remote foreign specialty.


1. Palmer ED. The abnormal upper gastrointestinal vagovagal reflexes that affect the heart. Am J Gastroenterol. 1976;66:513–522. [PubMed]

2.Armstrong PW, McMillan DG, Simon JB. Swallow syncope. Can Med Assoc J. 1985;132:1281–1284. [PMC free article] [PubMed]

3.Turan I, Ersoz GBor S..Swallow-induced syncope in a patient with achalasia
4.Dysphagia. 2005 Summer;20(3):238-40  4.Basker MR, Cooper DK. Oesophageal syncope. Ann R Coll Surg Engl. 2000;82:249–253.

Some of the noise bites from a busy cath lab after a  mid noon angioplasty

         Oh’  that  looks bad , whats that projecting !

There is some haziness too ,

            Make sure its not a flap,

  Better to do IVUS or should I OCT ?

           Shall I  post dilate with NCB ?

Should we cover with  another stent ?

           I think we can manage with Tirofiban or Reopro 

Call the chief ! suggested a first year resident,that seemed to be the most reasonable noise bite among all .Yes, the final command came from the chief cardiologist after a 10 second glance over the workstation ,”Guys,  forget it , . . its acceptable  pinching, DAPT will take care of it , just ensure adequate ACT till night , put the next case . . .on table” !

That’s fairly common chat session in any high volume cath centres (Which ended abruptly  in this case with the chief’s uttering)

Does any body know  what the chief meant by  the term pinching ?

  • Is it the  pinch of Intimal fold ?
  • Is it pinch of plaque ?
  • Is it a flap ?
  • Is it a plaque prolapse within the strut ?
  • Or just a evaginated thrombus
  • A subintimal calcium speck ?
  • A longitudinal stent deformation?

Any one knows the histology ? Is there any natural history  study of such pinching ?

Iam afraid no one knows . But common sense tell us it can be anything  between a totally benign entity to  Imminent nidus  for an acute stent thrombosis , depending upon the patient’s destiny and physician’s luck !

How does one make a decision in such an uncertain situation ?

The decision to leave that pinching is taken by any  cardiologist  based on his past experience or  Inexperience or both. Some do IVUS/OCT , many don’t . Whatever the decision  ( empirical or scientific ) its  going to be tentative  and  outcome is any body’s guess.

Final message

Coronary arterial pinching is a dangerous cath lab slang used exclusively by expert Interventional cardiologists , often after a hurried PCI ! It may sound  innocuous .To label a protruding plaque as a “safe pinch”demands heavy courage that is an essential requirement  for a successful Interventional  cardiologist , which most of them are blessed with !


1.No Reference as such :There is no specific study about histology of coronary pinching  .Though , IVUS and OCT data are available for various post PCI shadows , it never addresses the issue of pinching specifically as no one is clear about what they mean by it.  Hence ,we are planning to decode this long pending mystery with our own  PINCH-iVUS  study.

2.This article from Circulation Imaging  new generation IVUS could reveal  histology of pinching


Professional competence is defined as doing things, always in the Interest of patients. It’s generally believed small hospitals are not competent enough to treat cardiac emergencies . . .Do you agree with that ? No, Its largely a myth . Do you know there is a absolute  lack of proficiency  threatening to plague our country’s coronary care system. ? It’s the professional  Incompetence by the space age, star hospitals (mis)managed by masters of the noble business. None (am I right ?) of this hospitals either monitor or publish the outcome of their treatment.

Backed by pseudo scientific data , amplified by unrealistic expectations of ill Informed patients , some  hospitals are avoiding Initial emergency treatment of acute MI  , instead they waste time ( load DAPT ofcourse !) in securing the finance  for the costly Invasive procedures or refer them out of their premises if they can’t afford for it.In the ensuing emotional and financial melee many of the ill-fated patients lose vital  time window of thrombolysis as well ! and carry risk of fatality or damaged myocardium.

Every stake holder in the current  coronary care system simply assume the enforced modality  must be far superior because they administer the most modern and costly treatment suggested by few high intensity cared clinical trials originating from west. The wisemen who run the corporate hospitals  never realise medical competence and outcome is not entirely defined by science. Their primitive cognition wouldn’t allow to think beyond business equations either.

Please believe me, time and again, I have witnessed patients reaching Government hospitals  after being shunned away by  big (Some times even medium sized )  hospitals who boast themself only as PCI enabled care. Even if they want to lyse they stock only the Tenekteplace .

I think tragedy  is a lesser word to describe the scenario , where a distressed family is trying to arrange  for a Rs30,000 shot of Tenekteplace when thirty times cheaper still equally efficacious (Rs 1000 Streptokinase)  is concealed from their visibility .The Govt should urgently look into instances of large private hospitals avoiding Govt insurance scheme patients  even in  cardiac emergencies ! To label our poor patients as unaffordable ones is a outright misnomer, rather its the rich hospitals that are “not affordable” to lose profit and treat our countrymen , in a cost effective manner is the reality !

Who is Poor ? You decide.

Two forbidden things in coronary care

 1.Cajoling  and manoeuvring a distressed  family for a primary PCI as a routine treatment  hyping its beneficial effect and underplaying the true advantages of thrombolysis in largely technical jargons is the current norm in most coronary care units.

2.Another issue is , after confused confabulations with the duty medical officer,  if a rare patient family  choose the option of thrombolysis , comes the next googly*.  Many noble minded hospitals do not stock the low-cost and equally efficacious thrombolytic agent and offering  only the costly option to the anxious families when the myocardium is on fire.

Hospitals that  practice these two coronary protocols  need to be shamed and labeled as  “Coronary Incompetent  ” In spite of having 24/7 cath labs.  (Realise , they are just like  any remote rural hospitals , at least  the later can’t be faulted  as they don’t  withhold  a  reperfusion strategy  !)

Final message

I think , mindless proliferation of cath lab based cardiac care , which follow this theme , ie  “Thrombolysis incapable but PCI capable “ are  biggest threat to coronary care in our country ! For the best coronary care for any country ,what we need is efficient prehospital thrombolysis team .We have conveniently forgotten the great study of CAPTIM wherein the ambulance drivers replicated the same effect of primary PCI performed by highly trained cardiologists in modern labs.

In India,  primary health centers which is within  few km reach of entire population  can be designated as static ambulance equivalents  with basic resuscitation facility . If a multipurpose health worker can be trained to lyse, with remote supervision that will accomplish  90 % of what the cathlab guys can achieve ! Selective shifting is suffice.

Postample :  Ofcourse, not doing  pPCI for high risk or complicated STEMI is unscientific and we need to have proper consenting and referring frame-work for such patients.

Counter point : One of my colleagues asked me ? Why do I enjoy attacking the established scientific practices ?  May be I have a problem , yes, but  I think in a  true medical democracy we have right to debate anything , absolute truth is a ongoing journey !



*Googly:  An unplayable ball delivered to a batsman in the game of  cricket.

A 45 year old man came with  recent onset breathlessness.His left ventricle was dilated along with left atrial enlargement.The LV EF was 42% (By current definition mid range preserved systolic function( Circ Heart Fail. 2016 Apr;9(4))

But, he was severely symptomatic because of combined  systolic and  diastolic dysfunction.Diagnosing and grading diastolic dysfunction has been extensively done in last decade.Now , we realise without significant diastolic dysfunction symptoms of pulmonary congestion can never occur in patients with DCM.

We don’t require complex tissue Doppler parameters to diagnose high-grade LV diastolic function.Just have a look at LA dimension,  concentrate the E to A ratio. A tall E that humbles the A by more than 2 to 3 times is clear evidence for  LA mean Pressure exceed  18 to 20 mmhg or so.

This , in combination with dilated LA is a marker of chronic severe diastolic dysfunction.The fact that A is diminutive in no way takes the Importance of Atrial contribution to LV filing at this critically compromised LV status.

Note E:A ratio is 3:1 .This simply means the early (and mid to a certain extent ) diastolic pressure in LA is high and most of the filling takes place before Atrial contraction .There is one more reason for diminutive A . Atrial contractility fails to prevail over E in late diastole as LV end diastolic pressure is significantly high in these patients with diastolic dysfunction.

A dilated left atrium is an Independent marker of significant LV diastolic dysfunction (In the absence of MR) .When does LA begin to enlarge in diastolic dysfunction ? There is uniform rule.Generally LA size more than 4.5cm indicate grade 3 or 4 LV diastolic dysfunction.

LA size and Pulmonary congestion 

It’s a paradox , a roomy  LA dampens the LA pressure curve and A reversal into lungs may not happen.

*AF irony on A reversal

Logic might suggest , loss of atrial contraction might attenuate A reversal and less blood flooding into pulmonary veins.No, It doesn’t happen that way.If  AF is precipitated for any reason its going to be “switch on”  for acute pulmonary edema.

What is the relation between systolic and diastolic dysfunction in DCM ?

We find about 30 % of DCM has documented resting diastolic dysfunction.This is actually a underestimation of true diastolic dysfunction as it can very well manifest only during exertion.

Though generally , there is good correlation of grade of diastolic and systolic dysfunction in terms of severity , some of the patients show severe diastolic dysfunction out of proportion with systolic dysfunction.

Note : In the above patient it’s actually a fairly preserved systolic function but still has advanced diastolic dysfunction.

Grading of diastolic dysfunction .Image courtesy MM Redfield et al: JAMA 289:194, 2003. Note E:A >1.5 is

Final message

Relying on E:A ratio to diagnose diastolic dysfunction  may appear  amateurish for some of us .The rampant reporting of E>A for grade 1 diastolic dysfunction has made this parameter a “Doppler cliché”. But , the fact of the matter is,  it does help us confirm severe (Grade 4) diastolic dysfunction when E stands  tall and towering over an almost dwarfed A.

Clinical Implication

Please realise ,In patients with DCM  when you find an  A that is too diminutive in combination with  a menacingly tall E , it may be prudent to raise diuretic dosage. It’s a sure signal for impending pulmonary edema.

Queued queries 

Can DT and IVRT normalise with progressive diastolic dysfunction ?

Continue Reading »

Technology is a great equalizer.Never in my dreams, I would  have thought as I drive through the dense Nilgiris forest , a satellite  located 36000 Km up in the sky would guide  me through  every turn and bend most accurately.

The curvy roads are coded with  live traffic  flow in Red ,orange & green . That’s “Google map”  for you. (By the way, proud to note Google runs with an Indian CEO who hails from my city Chennai !)

Now , coming to academics , . .Some one thought,  if the traffic in the entire globe can be monitored with few clicks,  How about  adding live traffic data to the otherwise  dumb anatomical coronary angiogram images we get in a non Invasive  CT scan ?  We can even color code the different segments of coronary artery based on the velocity profile and pressure drop. That is CT- FFR . Now technology is  available to get online live FFR as well. (Siemens )

Live coronary traffic blood flow 

Fractional_Flow_Reserve_Coronary_CTA (1)

Heart flow the newest technology in coronary Imaging and  non invasive Quantitative assessment is possible .It provides direct information about how to navigate the coronaries and intervene only the reddish areas  leaving the greens untouched.


Its called computational fluid dynamics .A super computer calculates live FFR for the entire segment by measuring the drop in  CT density data in Hounsfield units and translates into pressure equivalents and hence non invasive FFR.This modality has been approved by FDA.The heart -flow and Siemens has come out with onsite CT FFR.

Reality check :Have we conquered the coronary physiology ?

Trying to  understand coronary flow with a engineering mind-set is Insulting the complexities of biology. Be reminded , Invasive FFR is assumed as a gold standard, Inspite of the fact that , its blessed with flaws in concept , techniques ,(Hyperemia vs no hyperimia) and lesional variation . Now ,what is the big deal , a non invasive CT -FFR  is compared Impure gold standard  and claiming a breakthrough ?

Of course,logic would suggest,if both FFRs are flawed why not use  a less invasive one that is CT -FFR. It can atleast save time, cost, and potential procedure related issues.May be ideal in ACS situations were catheter FFR can destabilise the patient.Further, it can provide  continuous live information in a hybrid lab , hence post procedure FFR is readily assessed . (Converting Red coronary into Green ones  would become cardiologists new moto!)

Final message

The point of contention for the modern day  cardiologist is ,they have realized (Not all ofcourse !) in a harsh way that , they must use a physiological confirmation of a lesion severity before indulging on fixing it with a metal. Whether CT-FFR will increase the number of angioplasties  or reduce will remain a mystery . Whatever it does , it should do it for appropriate reasons . We know any technology has a shelf life and If MRI can provide the MRI-FFR (Journal of Cardiovascular Magnetic Resonance January 2014, 16:O55)  , CT will be pushed back for obvious reasons (Prohibitive radiation hazard)


Status of MRI based FFR 

Brugada syndrome is  as an  Inherited sodium Ion channel defect leading to loss of /or reduced sodium channel function.This specifically causes RV epicardial Imbalance of In-flowing(depolarising)  and out-flowing (repolarising)current , potentially triggering ventricular arrhythmia. This happens either spontaneously or during electrical stress times which include, fever, various drugs , adverse autonomic fluxes etc. So far,  we have been thinking it as primary electrical disorder with no macroscopic/ histopathologic  defects.

Newer Insights are emerging

But, how is this primary electrical disease , harbor a well demarcated  RV epicardial phenotypic substrate ? .  . . ablation of which eliminates the VT.

Zone of probable structural defect over RV epicardium (Pink zone) amplified by infusion of Ajmaline. Note the ECG showing typical ST elvation lead V1 to V3 .(Image courtesy Carlo Pappone et all  )

A recent study from Italy from the original founders  (Brugada team Ref 1 ) has confirmed RF ablation of RV epicardial tissue  is indeed feasible in many and should be considered in high risk Brugada syndrome. (Then should we suggest , ICD is no longer a choice in Brugada ?)

MRI findings in Brugada has shown some structural defects .(Ref 3,5) .It seems  Brugada is an Inherited electrical cardiomyopathy with a structural defect. (The overlap between ARVD and Brugada syndrome appear more real than we thought before ! (Ref 7 )

Final message

Still , Brugada is more of a electrical disorder,  but soon we may refer it as structural heart disease.


4.Catalano O,Antonaci S,Moro G,Magnetic resonance investigations in Brugada syndrome reveal unexpectedly high rate of structural abnormalities. Eur Heart J. 2009;30:22412248Abstract/FREE Full Text/Google Scholar
A best review comparing Brugada vs ARVC

An event that happened recently  that shook my country’s  collective conscience .It was, loss of  hugely popular and beloved  President of India , Dr Abdul Kalam on 27-07-2015. He was 84.Death came in a most dramatic way when he fell down midway  during his lecture to students of Indian institute of management ,Shillong in the state of Megalaya.


Indian President Kalam addressing the students snapped moments before he dropped down dead due to cardiac arrest

What is the implication of this VVIP’s death for  cardiac Academic ?

I believe , there is lot .The presumed cause of death was cardiac arrest . As we know , it must have been an instant electrical death as the local medical personnel  couldn’t  revive him after an Initial  CPR and later shifting him to state of the art facility . The ex-president was known to have a good health record and the heart should have been normal until prior to the cardiac arrest.

Now coming to the key question what is the chances of survival of cardiac  arrest ?

While there have been many survivors  of cardiac arrest within hospital premises  and coronary care units . . . still ,  life cannot be  guaranteed even if prompt CPR is initiated .

It’s the height of  Heisenberg  irony,  some lives can be saved  even when cardiac arrest happens out of hospital , while it’s also a fact deaths due to cardiac arrest happen right inside the cath lab where all emergency strategies are in place .

How much delay is permissible in resuscitating cardiac arrest ?

Cardiac arrest is nothing but activation of  the switch of death . Evey second is important . Experience suggest if reversed within first 2 minutes maximum survival is expected .Beyond 5 minutes and within 10-15 minutes most deaths will ensue.Up to 20 minutes survival is possible though with a risk of brain permanent brain damage.

A  recent study  from Sweden which addressed this  issueand  confirmed a  dismal fact  that even in the presence of best emergency care system,  survival is meager  4 -8% . However , the positive outcome was , If the bystander does some form of CPR till the arrival of  emergency service reaches the spot it can go up to 10.5 %.

cpr cardiac arrest

It is very clear , surviving an unexpected cardiac arrest is in the domain  of  God , still  we must encourage lay persons  to know and learn the techniques of CPR. The protocols has been simplified now , to include chest compression alone as the Initial measure.

Coming back to the question of death of our president,  as some one asked me direct question if the death could have been prevented ? , I said , yes if God willing !


Note : Cardiac arrest in patients who are at high risk with underlying heart disease (structural or genetic ) will require implantable cardiovertor  defibrillator ( ICD ) that can save thousands of life every day across the globe .