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Whenever we have difficulty in accepting our mistakes or unable to forgive other’s mistake,or when we make big fuss about trivial events in life, I was advised to ask these three questions and Introspect.

1. Who you are?

2.From where did you come ?

3.What for, you are present in this world?

It was a really tough ask , until I saw this video. It not only stuns but also humbles us and whatever little knowledge we acquired over the years looks nothing.Yes, whenever my ego tend to bloat up… this 3-minute video never fails to get it deflated.

Just one requisite , you need to Imagine it’s you lying there instead of that girl.

Post ample

It’s good to realise, how this world suffers by actions and inactions of apparently smart people, who spend some transitory moments in this universe, sharing space with millions of non-human lives and lifeless things (Mind you, the later don’t suffer from death since they have no life!)

Thanks to Google, the technology company for stimulating us to think and find the true meaning of life.

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Identifying the culprit after a criminal event may be easy for the police.For cadiologists investigating the crime scene after a coronary event, it is a different story. (Of course, localization of IRA after a STEMI may not be really difficult.) But , when a patient is having UA  and coronary artery shows multiple lesions, we do have real diagnostic issue. The general dictum could be, tightest lesion or the complex eccentric ones with thrombus is likely to be the culprit. This has important therapeutic Implication,  as we are argued to address the active lesions first. The following study was done in 2009 trying to find the ARA solely by ECG features.

The conclusion was

The following ECG findings were helpful in localizing Angina related artery . ST depression in V3- V5 correlated  with  LAD  angina .Global ST depression was highly correlated with proximal LAD or Left main disease ( 6/6 patients). ST depression in V1 –V3 was associated more commonly with dominant LCX/OM disease. ST depression in 2 ,3 , AVF , or I, AVL  had  no significant correlation with either RCA or LAD  system.However multiple culprit lesions or diffuse inflammatory CAD should always be thought off. One more possibility is , its simply a demand ischemia or micro vascular angina were there is no true epicardial culprit lesion. 

A revisit to my 2009 IHJ article.

http://indianheartjournal.com/ihj09/nov_dec_09/509-523.html

 

IDENTIFYING ANGINA RELATED ARTERY (ARA) IN UNSTABLE 
ANGINA /NSTEMI BY ADMISSION ECG AND ECHOCARDIOGRAPHY
S.Venkatesan C.Krishnakumar .G.Gnanavelu .R.Subramanian.Geetha Subramanian B.Ramamurthy.P.Arunachalam.M.Somsundram.V.E.Thandapani.M.A.Rajasekaran.
S.Murugan , Madupraphu doss ,P.Pachiappan.
Madras Medical College. Chennai

Unstable angina( UA /NSTEMI ) constitute a  heterogeneous  group of  patients with  lesions ranging from  normal coronary  artery  to severe multi vessel  disease. Even  though  multiple active plaques are documented ,  one  critical  lesion  would be   responsible  for  the  index  episode  of  angina..  Contrary to STEMI  there is no standard methodology   to identify  the  Angina  related artery.(ARA) in UA .We under took this  analysis  to find  whether  admission  ECG  with the help of echocardiography   could  predict  the ARA  in patients with UA

26  patients with  UA  admitted in  our  CCU  were  the  subjects of  study. Patients with   post  infarction angina,  CABG ,  PCI , old  MI , left ventricular  dysfunction  were  excluded. All patients  were treated  as per institutional protocol. Echocardiogrphic analysis   of  wall motion defects (WMD)  were  documented  between  2hrs  and  24hours of admission  .CAG  was  done  between  24 hrs and  7  days. The  coronary  lesion was considered angina related  if  the  WMD  detected   by  echocardiography matched with  the  myocardial  segments supplied by the  arterial territory  containing the lesion . After locating the ARA , the patient’s  admission ECG   was  compared  retrospectively   with  CAG  finding  to study  whether  it has  any  predictive  value  for identifying  ARA.  6 patients  who  had single vessel disease the ARA  localization  was straight forward. (LAD -4 , LCX -1 RCA-1 ). In 2  patients  there was  obvious  eccentric thrombus containing plaque indicating the culprit lesion . 18 had DVD or TVD with no clearcut culprit lesion.

The following ECG findings were helpful in localizing ARA.ST depression in V3- V5 correlated  with  LAD  angina .Global ST depression was highly correlated with proximal LAD or Left main disease ( 6/6 patients). ST depression in V1 –V3 was associated more commonly with dominant LCX/OM disease. ST depression in 2 ,3 , AVF , or I, AVL  had  no significant correlation with either RCA or LAD  system.

It  is  concluded  ARA  can be  identified  with  fair  degree  of accuracy   by admission  ST segment  profile. This  observation  differs with  the existing literature which  suggest little role for ECG to localize arterial lesion in UA. In patients with multivessel CAD  with  more than one  critical lesion  a  combination of ECG  and echo features  help  us to  fix the angina related artery and possibly the lesion. This has  important  therapeutic implication.

Keywords: Angina Related Artery, Unstable Angina/NSTEMI, ECG, Echocardiography.

Postample

I am reposting this abstract again because the same paper has been plagiarised in at least two occasions and got published in predatory journals. Now, we realise Journal article shopping and trading has become a scientific scam .

Reference

This paper  from Japan analysed this ARA concept in 1996 itself with SPECT Imaging

 

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In the evaluation of syncope, history is most important to arrive at a diagnosis. Ofcourse, the first step is to confirm whether its truly a syncope or something else.(Metabolic/TIA or seizure.)We are easily carried away by the urge to order a Holter monitoring routinely. In reality, the yield is too low (<15%) .Even the utility value of Head up tilt (HUT) is being downgraded.

Paradoxically, resting ECG might give important clue in many. One need to specifically look into a set pattern of ECG. It generally falls in one the following in any patient with syncope.

This post specifically may not be exclusive but stresses the importance of resting ECG in the evaluation of syncope. by our urge (Stress testing is not included)

  1. Bradycardia( Sinus Node dysfunction/AV block) Note Brady cardias can per se cause syncope if pause >3-5sec Or it may lead to Brady (Pause) dependent escape VT.

    A pause can be a sinus arrest, Pause or SA block .If pause ends with a junctional escape it becomes a arrest.

  2. Look PR interval specifically(A bifasicular block shouldn’t be missed .It can be more dangerous than say a congenital CHB)PR interal represents condcution from SA node to Purkinje fibres in ventricel. The importance is directly linked to the location of the block than propably the degree of prolongation. Please note HV interval > 70 ms in any patient with prolonged PR is cause for concern,
  3. Preexcitation/Delta waves (Though Narrow QRS AVRT rarely causes syncope its very much possible during  Antidromic tachycardia. (AntiVRT), Antidromic AVRT or Accessory pathway with short RP <250ms need to be documented. Concealed paths are safe , but delta appearing during stress testing is extremely unsafe
  4. Post-excitation /Epsilon waves. (often noted in lead V 1, A marker of RVOT dysplasia as in ARVD. Also referred to as Fontaine wave who discovered it by bipolar cheat leads over V1 )

    Note the epsilon occurring after the qrs Indicating RVOT dysplasia

  5. Q waves (Markers of old MI -Scar Induced VT)
  6. High voltage QRS LVH /HCM /Aortic stenosis
  7. RV strain/S1Q3T3 pulmonary embolism.(Syncope is a common presentation with PE especially with minimal exertion or change in posture)
  8. Early coupled VPDS (R on T location a trigger for VT) Wedesky effect. The terminal portion of T which correspond to supernormal period.

    The significance of VPDs directly related to its prematurity than its focus of origin.The one that falls on the vulnerable period .Late phase 2 and phase 3 are more vulnerable as triggered activity

  9. Brugada (Type 1 with T inversion riskier, Camel hump less dangerous Joseph Brugada,

    Brugada syndrome -Note three types . Type 1 is typically risk prone. Please note it is the late ST declining component and the T iversion that confers the risk not ST elevation per se.The type 2 with a camel hump is confered with least risk

  10. Malignant ERS pattern (Most ERS or safe / Maligant forms infero lateral forms risky only at times of ACS not spontaneous risk
  11. J wave syndromes –Overlapping with Brugada /ERS Charles Antzelevitch,J Arrhythm. 2016 Oct; 32(5): 315–339

    ERS syndrome are so common. In the absence of sycnope, it should be ignored straight away. Recently it received too much hype among cardiologists increasing the anxietywhich is not warranted.

  12. Long QT Interval (Hypokalemia commonest, Congenital next Peter J. Schwartz,Long-QT Syndrome Circulation: Arrhythmia and Electrophysiology. 2012;5:868–877
  13. Fractioned QRS (Most often seen in DCM ischemic /non-ischemic confer VT risk usually with LV dysfunction, these are candidates for CRT-P/D as well)
  14. T wave alternans Fluctuating T waves indicate repolarisation alternans .It elevates risk of VT Narayan SM J Am Coll Cardiol. 2006 Jan 17;47(2):269-81
  15. Exercise Induced VT/ CPVT is to be considered seriously in all unexplained exertional syncope. Behere SP, Catecholaminergic polymorphic ventricular tachycardia: An exciting new era. Ann Pediatr Cardiol. 2016;9(2):137–146.

What next after ECG ?

After ruling out neuro cardiogenic syncope by history, one has to perform a good quality echocardiography that can clinch structural heart disease .In cardiomyopathies like ARVD or RCM MRI studies will be of immense value especially the LGE/DEMRI that picks up the scars and fibrosis as in sarcoid or tuberculomas etc. Event recorders are popular, may have a slightly better yield than Holter.EP studies are required in few as diagnostic or more commonly as a part of therapeutics.(Please note, EP lab Induced polymorphic VT has Zero diagnostic value as any normal human heart can be induced to VF by repetitive stimulation)

Management

The main purpose is to exclude serious primary electrical and or structural heart disease. However, fortunately, the most common cause of syncope is neurogenic or reflex mediated. It requires reassurance and fluid repletion Fludrocortisone,/Midoridine (Alpha receptor agonists are promising) Pacemaker/ICD is indicated in few with brady/Tachy -Brady .ICDs/RF ablation are Indicated in Ischemic VTs channelopathies with inherited VT/VF like Brugada. One important question still not clearly answered is when to refer a patient with syncope to Electrophysiologist. ? For me , it appears only a fraction may need it.

Further reading (2018 ESC guidelines)

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A middle-aged man a Biotech engineer, who is just back from his annual health check, sitting in front of me with a deeply anguished face and said “Doctor my LDL is 130mg, and my diastolic BP is 90 mmHg and fasting sugar is 120 mg .I am very much worried about my future”

Wait , let me go through your file, I said ,

Isn’t a serious Issue doctor?

No, its not ,

But , doctor, I have read about ASCOT, SPRINT and HOPE-3 trials. I guess they tell us to keep the LDL, blood sugar and diastolic BP all these three parameters around 80. Isn’t doctor? He went on to add, that his old fashioned family physician has asked to continue the beta blocker. He said he is also aware of the fact, how JNC has ditched the beta blocker to the graveyard since they don’t do anything to central Aortic pressure. He continued, “Last year my routine coronary calcium score was beyond 300 . Shall I go for a regular coronary angiogram to ensure my SYNTAX score is around zero doctor” ?

I was quite shocked with his academic prelude, and asked him, by any way, he is a physician or a cardiologist?

No doctor, I am purely a non-medical man but follow all health related stuff from wall street medical bulletins. I am a busy man, still, work out regularly. I have important targets, ambitions to fulfill and lot to achieve in life. But, this LDL and BP is really bothering me doctor.

Yes, I got it . . . I understand your anxiety. Don’t get worried about all these biochemistry and hemodynamics. They are just numbers. Some of them will fluctuate to the tunes of your wall street as well.

Really Doctor?

Yes, we are all unlucky, in one sense you know. We are living in a man-made (scientifically) insecure environment. Great men in the past never had to bother with these silly numbers that currently define health. Alexander the great , neither had his Macedonian master health check nor he looked up for his lipid particles, (he was counting his horses Instead) Did Chengiskhan ever knew about his BP ?

Medical ethics master health check up holistic medicine life style nutrtion

If only these men were worried about these fancy number the world history would have been rewritten.

They didn’t even know an organ called the heart that is pumping 5 liters of blood every minute, until Harvey found the circulatory system 1000 years later. Still, they conquered the world. If we take world history millions of men and women have tasted the pinnacle success without really bothering to know their periodic Individual organ function status.

Here is one more story from my country, The Raja Raja Chola the great built this biggest Hindu monument called Brgadheeswara temple in Tanjavur ,Tamil Nadu , India in the year 1010 .

Raja raja cholan

A fictitious query – Who did FFR for Raja Raja Chola (947-1014AD) when he had vague chest pain from suspicious LAD lesion just after his war with Rashtrakuta empire .He went on to Live for 67 years conquering much of India without a single health check and ECG in his life time

It was an unparalleled kingdom of South India where millions of happy men and women who lived a healthy life with absolute faith and trust in their village healers who did the magic with Indigenous leaves, herbs, secret medical formulas based on ancient wisdom.

Longevity with a purpose

The anxiety to live long often keeps our lipids , sugar and blood pressure high . . . and sets a vicious cycle. Today ,this has become a perfect ground for the saviors of health care to trap us in a cartel who are conferred with an almost divine power of defining who is healthy and who is not.

Many times philosophers have felt longevity and the urge to live long, lacks a matching and meaningful purpose. Lack of purpose, as well as extreme obsession with a purpose, are equally dangerous. The purpose of life can never be equated solely on the longevity of our life. Life long fear and anxiety about possible illness and death is not welcome.

Human life span is mystical journey determined by genes as well the environment and its interaction with each other (Epigenetics) It’s destined to face challenges.Substantial of them can be managed without anyone’s help. I will be happy if you don’t ever need the help of cardiologist to get rid of fear and anxiety induced by general health awareness.

Isn’t prevention better than cure Doctor? I came for a possible coronary angiogram . . . but you have really confused me doctor!

No , I am not doing that Intentionally. From your angle its prevention of potential hidden disease. I am talking In a larger perspective, Master health checks many times end up as medical witch hunting. I am bothered about technological contamination that is all too pervasive among the health care system, especially manifesting as new non-existing diseases. (Skewed and tinkered normal curve )

We, the modern men . . . with all six senses intact, tend to make our life miserable with all these digitized biological data and deeply mined medical images from Innocuously good organs. Some times, we seem to more worried about artificial intelligence and least bothered to know the advantages of being naturally ignorant.

Life is not live data that is in motion. Have a good purpose in life, be physically active, think right, eat well, life shall be lived with peace. Please realize many pockets of the world had been more peaceful, healthy, and cultured in the past, than the current glorious and glamorous times. Of course, life expectancy has definitely prolonged with breakthroughs medicine but It’s not clear it has any positive impact in terms of overall global well being.

Please wake up , you are in the middle of patient consult story … Doctor!

Oh yes , thanks. As a parting advice, I sermonized, homo-sapiens are generally programmed to live for about 100 years except in a fraction who have either true incurable disease or those who succumb to a bad fate.

I realized , what should have been a simple prescription for an ARB +Thiazide + Statin and a stress testing , turned out to be an unsolicited compulsive lecture on life’s purpose, and philosophy etc I said sorry to my patient.

He silently got up. His body language was clearly not convincing enough to suggest, he has accepted my confabulations. He left the clinic with a humble thanks probably looking for a more saner physician!

.

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Somehow the concept of  Evidence based medicine (EBM )never excited me in spite of great strides it has made. Probably the main reason for this is, EBMs origin, quality, and credibility is currently severely compromised. (Though It appears to ooze science 24/7 and make us believe in it too !) Herewith, sharing some of the forbidden thoughts(with lots of pun)  for a (un)successful practice of EBM. This is definitely not meant for young and novice medical professionals. Strictly for the ones who can segregate sense from non (S)

Evidence-based Doubting 

 

Reference

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Yes, Its “evidence-based fun”. Forget all those anti-platelet trial dramas … showing in the cardiovascular theatres near you . There is only one genuine drug , that’s the good old humble Aspirin . Mind you ,none of other  actors can ever be imagined for primary prevention.

By the way , there is absolutely no controversy for the role of Aspirin in secondary prevention after established CAD.(We know , how Aspirin has taken up a critically  Integral role in saving the life of the stents  as well as  patients,  post PCI)

Oh , what a disgrace for this drug when it comes out of the glamorous cath lab zones. Its use is often frowned upon for preventing simple CAD. (All due to a single factor, fear of bleeding ? No , its exaggerated in most studies)

Overlap between Primary and Secondary prevention 

In primary prevention of CAD , what do we attempt to prevent? How do you differentiate established CAD from  “Established coronary atherosclerosis  but Non-established CAD ?”

The fundamental flaw in this perceived controversy is in our inability to define what is significant CAD in the asymptomatic population.Do we need a clinical event to say, established CAD?

For the attention of  evidence-based script writers , a long query  . . .

“How much evidence we have to conclude , that a  patient with manifest clinical CAD carry more risk for a recurrence than an asymptomatic  high-risk patient who is likely to develop the first clinical event (which happens with a  bang that could be a major ACS ) due to underlying silent Atherosclerosis.?  

Reference 

Click  here to for more  unscientific review on primary prevention of CVD.

 

 

 

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*When I tried to condense three decades of my learning into the medical profession in three lines, I scribbled this. Sorry folks, if It doesn’t sound scientific for some of you! 

By the way, What is successful medical practice? Success for the Doctor, patient or both?  The answer to this question is never simple. 

 

 

 

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