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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 pateint  who is likely to develop the first clinical event (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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Pericardial effusion can be detected in many normal pregnancies. The Incidence is up to 40%.The normal fluid within the pericardial sac is around 25ml. A thin sheet of echocardiographic fluid collection in diastole up to 5mm is considered mild.

A trace  or minimal effusion may be a better terminology that describes most physiological pericardial fluid compartment. They have no physiological significance.Mechanism is due to overall increase in size of vascular compartment and especially the right heart volume overload.

Pericardial fluid drains through systemic pericardial veins and lymphatic channels also drain into venous system through thoracic duct . In pregancy these drainage pumps work overtime at its peak capacity. It’s natural it might get fatigued and show some residual fluid collection which should never exceed mild.

We also know thyroid hormones is one of the housekeeping hormones within the pericardial space.Physiological hypothyroid state is possible.Effusion in true pathological Hypothyroidism causes secondary dyslipidemia. Here, some unknown lipid sub-particles clog the lymphatic and cause pericardial effusion which is actually a part of widespread systemic edema. (Myxedema)

https://www.ncbi.nlm.nih.gov/m/pubmed/12756478/

Reference Hurst’s The Heart Valentine Fuster  Mcgraw Hill, 14th edition Page 2347

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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.

 

img_20190214_184238254084131.jpg

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

 

img_20190205_163719776750314.jpg

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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