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

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

Read Full Post »

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, JACC 2018, 72 (9) 1046-1059
   

   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)

Read Full Post »

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

Read Full Post »

Cath labs are probably the best place to practice preventive cardiology . . .

Practice of medicine is primarily guided by Infinite Information , plenty of Intuition, little bit of Intelligence and unquantifiable amount of Ignorance.The science of coronary reperfusion is standing example for variable mix of the above.The term no reflow is a jargan used liberally in cath labs right from first year fellow to super consultant without knowing what exactly they mean by it.

What really is No-reflow then ?

The academic definition :According to Kloner no-reflow is defined as suboptimal myocardial reperfusion through a part of coronary circulation without angiographic evidence of mechanical vessel obstruction.( Kloner RA, Ganote CE, Jennings RB. “The “no-reflow” phenomenon after temporary coronary occlusion in the dog.” Journal of Clinical Investigation, 1974; 54: 1496–1508.)

With due credits to his seminal paper, I always wonder what exactly Dr Kloner meant when he labelled it as No-reflow!

No is ok , Flow is ok , What does the adjective “re” mean to you ?

Re stands for repeat ? recurrent ? Yes , it may mean any one of it. It may mean nothing in many patients as their post PCI flow is same or found to be no better than pre PCI flow with no significant forward flow at all ! In this situation No-reflow is same as No-flow (Never flown ) in physiological terms irrespective of epicardial patency.

Literally, the term no re-flow tell us, there has been a dramatic procedure related*( or preexisting ) destabilization in distal blood flow. It can be any downgrading of basal TIMI flow. ( Example : TIMI 3 becoming Zero , or TIMI 1 becoming 3 then back to 1 or Zero.) The terms slow flow, low flow, stuttering or trickle of flow all fall under the common  category No reflow. In a crude manner one may conclude no reflow to be  masquereding term  for failed PCI.

*Mind you , No reflow can also occur with pharmacological lysis as well.(Less common)But personal experincee suggest it has a less benign course.

Mechanism of No- reflow

Many mechanisms has been proposed and disposed by experts. However , all suggested mechanisms end up in the final common theme ie micro vascular obstruction.

Can no-reflow precipitate a fresh ACS ?

Could be yes . How ? The distal thrombus migration clogs the active collateral channels at its entry point.This is probably the most unrecognised concept which is difficult to prove though.The problem is , we may not realise this as it could be silent or may just present as LV dysfunction , Infarct extension, or Ischemic cardiac failure.

Why is treatment of no reflow is so dismal ?

I think, by now you can guess the answer and get it right too !

Is no flow better than No-reflow?

It may seem a foolish question one could come across in coronary hemodynamics. The prevailing coronary doctrine, as we understand is , all ATOs need to be opened in STEMI in an emergent fashion. (Other wise patients or their myocardium can’t be salvaged )But, we also realise ATO do get converted to CTOs in a safe manner following a STEMI in a significant number. It’s the ultimate myocardial mystery when we realise even the ATO fails to damage the myocardium significantly in some patients.

Presence of acute collateralisation to IRA from non IRA is observed instantaneously and spreads rapidly towards myocardium in distress.It is observed in atleast 40% of all patients.(Ref 2,3).

The anatomical and physiological codecs of acute collaterals in ACS is secretly located close in the God’s domain.But, Interfering with it, is definitely in human domain.

Should we need to worry about the impact of PCI on these acute collaterals ?

It is estimated up to 5 grams of thrombus could spilled over to the distal coronary bed. Mind you thrombus formation is not a one time process.Can you guess where these thrombus lodge in ? We don’t know what is thrombus clearing capacity of LAD/LCX/RCA vascular bed. But. we have observed naturally formed thrombus is less likely to disseminate and migrate than the catheter and wire induced.My presumption is , coronaries show their dissent and disapproval in the only way they know, ie non stop generation of thrombus (Not withstanding our DAPT/2b 3a /Bivaluridins etc)

Acute collateral shutdown : A new concept

We are not sure if there is a collision between two streams of reperfusion that happens after a STEMI. One spontaneous from the collateral and other from antegrade(Either spontaneous or man made)

Is it benefitial, detrimental or neutral ? We don’t know the answer for sure. My understanding is some of subset of critical STEMI are heavily dependent on this life line however miniscule it may be.

It doesn’t require a double blinded study to prove what would happen when a hurried cardiologist attempt hurried PCI who often has to a change his target to thrombus instead of myocardium .

When aggression is shown on the thrombus, it’s more likely you end up in no reflow . One possible new mechanism(Proposed by the author) of No reflow is distal dissemination of thrombus debri that plugs the lateral entry points of collaterals.

This is the time , no reflow shows its violent face. Invariably hemodynamic deteriation occurs and the entire reperfusion team would seem to count their luck than expertise.

Can we perceive, predict and prevent this ?

We should , we need to , but how ? Since we know the true success rate of no reflow is miniscule, serious introspection to be done. Funnily (but realistically) one can take a famous cue from the most underrated medical specialty Social and preventive medicine .

Yes it’s “Prevention is better than cure” and mind you, if there is no cure, how important prevention becomes.Strangley , preventive cardiology is meant for lesser professionals , who and talk about diet, excercise and lifestyle.

No , it’s not . Preventive medicine needs a new defintion , rather new understanding .Its’ all about preventing an expected or unexpected adverse event anywhere.

How many of us really believe there is no effective cure for No-reflow and it is directly related to aggressive thrombus clearance strategies .

Should we argue new age Interventionists to practice preventive cardiology right inside the cath lab and do away with non-academic temptations.(Surprise , this is exactly mega trials on thrombus aspiration told us (Class 3 Indication for routine thrombus meddling)

Final message

Stable and comfortable, late ATOs need not be opened like defusing a time bomb. We will never know which side of the bomb the cardiologist is sitting.

The incidence of new onset No-reflow can be higher than what we presume.Further it can trigger a fresh ACS by whipping up the injured and resting myocardium.(Mostly attributed to late reperfusion Injury and the acute collateral shutdown.)

Postample and Counterpoint

As an interventional cardiologist, No-reflow is one among the expected complications , which are part of the profession.Never bother about these unscientific utterrings . That’s the job of critics. You go ahead and fight with the coronary artety in every case of ACS. Only weak minded unprofessionals would love to sit on a case of ACS and play a waiting game in CCU. True professionals shall look for multiple criminal targets beyond thrombus, myocardium, IRA , non IRA, doesn’t matter . Do it with confidence.Hope for the best, don’t bother too much about the endpoint.

Mind you, that’s what , we are trained and paid for and possibly respected too in this most glamorous subspecialty of Medicine.

Coming next

*Is Catheter, Guidewire Induced thrombus radically different from natural denovo thrombus ?

*How common is angiographically blind No reflow.(TIMI 3 with good and bad blush included)

*What are the residual defects and long term myocardial sequale ? (Inspite of successful tackling of No reflow )

Reference

1.Claire Bouleti et all The no-reflow phenomenon: State of the art Le no-reflow : état de l’artArchives of Cardiovascular Disease (2015) 108, 661—674
2.L YJ,Masuyama T,Mishima M, et al Effect of pre-reperfusion residual flow on recovery from myocardial stunning: a myocardial contrast echocardiography study. J Am Soc Echocardiogr 2000;13:18–25. doi:10.1016/S0894-7317(00)90038-5

Read Full Post »