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Why ventricular tachycardia has wide QRS complex ?

December 4, 2019 by dr s venkatesan

Why VTs have wide QRS complex?

Brief answer: VT  usually presents with wide QRS tachycardia because it originates in ventricular myocardium, travels muscle to muscle instead of the normal conduction system. However, VTs need not be wide always, if it captures the conduction system early and more proximally it can be as narrow as SVT.

Further reading: Only for cardiology fellows 

Two empirical statements are made here. (The scientific chances of both being reasonably correct are fair)

  1. 80 % of wide QRS tachycardia by default is VT. That means 20 % of wide QRS is not VT. We all accept that.
  2. 80 % of narrow QRS tachycardia is SVT. It may also mean, up to 20 % of VT can be narrow QRS.

It’s obvious, not all VTs are dramatically wide. When it is not wide, they test our knowledge and patience. Let us be clear about the factors that determine the QRS width during VT. Once we know this we can have our own inference.

What determines the width of QRS  in VT?

1.Origin of VT 

The focus of origin is extremely important. Pure myocardial focus distal to the conduction system is invariably very wide. We know VTs originating right over the fascicles are narrow.

2.His Purkinje breakthrough

The time taken to capture the normal septal conduction system is a critical determinant of QRS width during VT.This makes the VT from septal origin narrower.VT arising from the free walls obviously takes a longer time to engage the HIS Purkinje system. Imagine , If VT originates from the lateral mitral annulus,  how much time it may take to reach RV free wall and lastly RVOT. Here the VT will become bizarrely wide.

3.The structural integrity of His Purkinje

It is important to emphasize a fact , even if the VT captures HIS Purkinje early, if they are diseased , still the VT will be wider.(Example bundle branch reentry in DCM in which VT keeps going around the conduction system still, it’s wider)

4.Course 

Length of the re-entrant circuit. Macro reentry is expected to be wider. Focal or micro reentry will often be narrow, provided the distal circuit is not diseased.

5. Scars as barriers and boulders 

If the VT circuit is interrupted by random scars en-route (from origin to exit) the  VT width prolongs. (Evidence for scars is often visible in sinus rhythm ECG as notches /slurs or fragmentations in QRS )

6.Exit point of VT

This is a poorly understood term (at least for me) It is believed,  VT can exit only epicardially. The line joining the focus of origin and the exit point is expected to decide the QRS axis. The problem comes when VT breaks out multiple paths and possibly sub-endocardial as well.

7.LV dysfunction 

A severely dysfunctional ventricle can stretch the QRS irrespective of conduction system integrity.

8.The Ionic milieu of cells Interstitial resistance

We know,  biological current is nothing but Ions in motion. So, no surprise it can alter the QRS morphology. The classical example is hyperkalemia , that can make ECG a wide and blunt sine wave. Local acidosis, hypoxia also influence the QRS duration.

9.Drugs 

Any drug which has class 1C or 3 properties can slow the VT circuit velocity. Typically flecainide is well known to make QRS wider. Amiodarone may  reduce the ventricular rate. in VT instead of reverting it. Apart from this these drugs depress the ventricular myocardium severely and prolong the QRS width independent to its action on the conduction system.

10.Mechanism  of changing width 

VTs can have varying QRS width as reentrant circuits change or experience slow conduction due to autonomic influences. VT with downstream aberrancy is also possible as the VT rate by itself influences the conduction property distally.(Just lie SVT with aberrancy)

A paradox about the width of QRS in VT

A curious phenomenon is often seen, when VT occurs in patients with baseline ECG which is already wide (As in an ischemic dilated cardiomyopathy with LBBB/RBBB). Here, the VT  prematurely stimulates viable muscles distal to the diseased HIS  Purkinje system (Which they are deprived of early activation of till then) .They seem to relish the early arrival of electrical impulse by brisk activation that converts wide QRS complex to narrow one. (This  behavior is one of the principles of cardiac resynchronization therapy where we attempt to rewire the heart with multiple leads and shrink the QRS.)

*One more mechanism of wide QRS sinus rhythm becoming narrow during VT is due to a concept called source -sink relationship. The VT delivers enough energy overcoming His Purkinje resistance downstream. (This property is used in HIS bundle pacing )

Postamble

*Forget about wide vs narrow QRS debate. A significant chunk of VTs falls within intermediate width QRS(100-120ms) . Whether to label these as wide or narrow QRS  squarely lies on whims of the reader. (Should we take the widest QRS in 12 lead ECG?  Pre-cardial  vs limb lead  etc are not clear) Unfortunately, we don’t have a separate algorithm for this category. This issue demands a separate discussion.

 

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How common is the progression of non-culprit lesion after PTCA ? What is the significance?

November 24, 2019 by dr s venkatesan

Whenever a patient is getting discharged after a PCI, the treating cardiologist often faces this situation.

So, you fixed the block in my coronary artery doctor. Thank you so much. Now, I can have a peaceful life, free from  future heart problems. “Am I right doctor”?

I wish I can answer “Yes”  to your query but I can’t for the following reasons.

I have fixed only a lesion that caused maximum obstruction. Atherosclerosis is a diffuse disease and you have minor plaques scattered across your coronary artery. These can grow at its own will. So you carry a definite risk remote from the current problem. (Don’t get frightened, read further, you have definite solutions to reduce this risk.)

How common is the progression of native vessel disease?

It varies from 10 to 40%. Mind you, the exact incidence directly depends upon the compliance of medical management, risk factor reduction, and adaptation to a new life healthy lifestyle. In effect, you (the patients) decide the incidence.

One surprise phenomenon (though unproven) might happen. Since the tightest lesion is jailed with a scaffold the minor lesion is preselected to an accelerated process of atherosclerosis if medical treatment is not properly followed.

Dr.Zellweger from the university hospital, Basel, did an extraordinary study with 400 patients, meticulous 5 years follow up with SPECT and found remote lesions accounted for 40% of future events (Basel Stent Kosten-Effektivitäts Trial [BASKET]) The other study by Glazer and concurred with this. These studies reiterate the importance of taking care of the entire coronary artery instead of focused piecemeal care by scaffolds.

Does a proximal DES protect a  distal lesion in the same artery by the drug effect?

It is a good thing to happen at least on paper. A proximal LAD with the latest generation Everolimus coated stent is expected to keep the distal LAD drugged for few months at leas.( with anti-mitotic activity) Thus preventing the progression of distal lesions.

No, I can’t believe this.In this era of momentary touch on sidewalls of artery by drug-eluting balloon (DEB) shown to do wonders, anything is feasible. Chacko’s (Ref 2 : JACC CV Interventions 2009)observation has a possible answer for this. It showed BMS vs DES didn’t make any difference in remote lesion progression.

Final message 

These studies reaffirm one vital truth. Stents are temporary solutions to a permanent, systemic disease of the vascular system .Stents are indeed a major revolution in CAD, “if and only if” it’s used in a highly selected CAD population. Global attempts to project cath labs as a tool to control human atherosclerosis is a typical example of flawed science. The only effective way to tackle this menace is to faithfully follow overall healthy living,  assisted by drugs.

This is the Editorial in response to Zellweger’s article

 

Reference

1.Glaser R, Selzer F, Faxon DP,Clinical progression of incidental, asymptomatic lesions discovered during culprit vessel coronary intervention. 2005 Jan 18;111(2):143-9 2004 Dec 27
3.

Postamble

One of my patients asked some time ago. If stents are the definite remedy for severe arterial narrowing, why not stent all my lesions (even the minor ones ) prophylactically doctor, so that it will not become tight at a later date?

That’s a good query. Your doubt is genuine , appear logical as well. But, unfortunately, it will be the most dangerous thing to do*. Metals are never friendly with the coronary arterial wall. We should use it extremely judiciously and only with tight flow-limiting lesions. These metals require annual (rather permanent) maintenance. Its taken care by multiple antiplatelet drugs. If for some reason your maintenance is erratic or the drugs fail to act you are at more risk of a future event.

(* This is what has  happened (happening) in the past, that demanded urgent publication of appropriate usage criteria)

Now, the current belief among the “fair thinking cardiology community” is dramatically changing. It’s leaning towards non-stent management even with significant flow-limiting obstructions in otherwise stable patients(SIHD). This belief is accruing more and more evidence base (The COURAGE 15 year follow up / ORBITA/ISCHEMIA)   All these studies confirm the emerging doctrine and bring back some semblance of sense into the cardiology community.

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CAD management in cross roads : Ischemia vs Ignorance driven PCI ?

November 21, 2019 by dr s venkatesan

*ISCHEMIA trial breaks not in NEJM or Lancet but in Washington Post and Wall street Journal

After three decades into cardiology profession, one thing is very clear. We work so hard to create pseudo-knowledge and struggle with it for so long and feel awkward and guilty to come out of the mess. But we have to  . . .  in the overall interest of mankind, isn’t?

We aptly call the whole process as continuing medical education, but in the melee, often we ditch some of the precious gems as obsolete. (This tempts me to suggest discontinuing false education is also an option for medical knowledge seekers !)

Confucius has something to say about this issue , which appears more relevant to the medical profession in current times.

Postamble 

We don’t know what’s in store for 2020

Posted in acute coroanry syndrome | Tagged , , , , , , |

Confabulation of a cardiologist – post ISCHEMIA trial !

November 17, 2019 by dr s venkatesan

I have never found it difficult to retrogradely cross a dangerous epicardial collateral in complex CTO. Delivering a twin stent in a partial culotte strategy for a bifurc lesion has never tested my talents. Stenting a left main across the LAD, jailing the LCX with OCT support is my favorite time pass. Crushing a calcium infested diffuse long lesion with diamond-tipped ablator appear as breezy as shopping in a mall.

But this one is really challenging 

What is that?

Understanding these four studies (Ref 1-4 ). They dogmatically say medical management confers definitive protection in chronic coronary syndromes. It stretches our limits of Imaginary Intelligence! How can a near tight coronary obstruction sitting right across your eyes, be left untouched? The latest one seems to suggest we can even ignore FFR positive lesions.

COURAGE BARI 2D ORBITA ISCHEMIA DRSVENKATESAN SHD CHRONIC STABLE HEART DISEASE PTCA PCI ACC ESC SCAI 2GUIDLEINES

It requires 4 negative forces . . . to bring one big positive Impact!

I don’t understand who is funding these negative trials and glorify it, and trying to defame the talents in me. All these studies have a huge lacuna. They conveniently exclude high-risk cases and allowed liberal cross over to PCI later on. Even the just-released ISCHEMIA trial had 38 % patient with no angina. (But why they received PCI ?) How to Interpret these trials and extract the true conclusion? .One consolation is, I know these negative trials have a very short memory and expiry date. Very soon I shall be liberated from the clutches of this negativism.

Even as I scribble this, my inner conscious is telling a completely different story. I agree we do Indulge a lot in stable Ischemic Heart disease. (SIHD).  I am yet to be clear what exactly we mean by SIHD. How is that near 90 % mid LAD guy ran 12 met exercise with negligible perfusion defect and still FFR was .7 ?

OMG, save me from this academic conundrum and help to acquire true wisdom.

Reference

1.Weintraub WS, Spertus JA, Kolm P, Maron DJ, Zhang Z, Jurkovitz C, et al. For the COURAGE Trial Research Group. Effect of PCI on quality of life in patients with stable coronary disease. N Engl J Med. 2008;359(7):677–687. [PubMed] []

2.BARI 2D Study Group. Frye RL, August P, Brooks MM, Hardison RM, Kelsey SF, MacGregor JM, et al. A randomized trial of therapies for type 2 diabetes and coronary artery disease. N Engl J Med. 2009;360(24):2503–2515. [PMC free article] [PubMed] []

3.Al-Lamee R, Thompson D, Dehbi HM, Sen S, Tang K, Davies J, et al. ORBITA Investigators Percutaneous coronary intervention in stable angina (ORBITA): a double-blind, randomised controlled trial. Lancet. 2018;391(10115):31–40. [PubMed] []

4. International Study of Comparative Health Effectiveness With Medical and Invasive Approaches – ISCHEMIA

 

 

Posted in acute coronary syndrome | Tagged , , |

New cause for differential cyanosis : The North-South syndrome

November 12, 2019 by dr s venkatesan

Differential cyanosis classically occurs in PDA with reversal of shunt when raised PA pressures /PVR is able to supersede the systemic Aortic pressure and drive the blood from LPA to descending Aorta bringing down the lower limb saturation.

Of course,  this can be undone by the presence of any other intra-cardiac shunts or aberrant left subclavian that arising from the desaturated descending aorta.

Other causes of reversed differential cyanosis 

Where the upper body is cyanosed (desaturated) and the lower half is not. There is a conventional list of conditions.

  1. Transposition of the great arteries (TGA) with patent ductus arteriosis (PDA) and elevated pulmonary vascular resistance
  2. TGA with PDA and pre-ductal aortic interruption or coarctation
  3. Supracardiac TAPVC* + PDA
  4. Anomalous right subclavian artery connected to hypertensive ductus through RPA

(*This occurs due to streaming effect ) Highly saturated superior vena cava (SVC) blood into the right ventricle, reach MPA / through a PDA, and to the descending aorta, with streaming of more desaturated blood from the inferior vena cava (IVC) into the LA through PFO (Ref Yap S H Pediatr Cardiol. 2009 )

Now let us add one more cause for  reversed differential cyanosis in the Modern Era

It is seen with ECMO in VA connection (Often reported in babies ) . The Aorta has high oxygen content entering from the femoral cannula going up into the Aortic arch., while deoxygenated blood from LV (because of failing lungs) reach antegradely to the Aorta. Ideally, the ECMO is expected to supply the entire aortic arch and hence oxygenation is uniform all over the body. It rarely happens as some amount of flow will come from LV unless its in asystole. However, If the severely dysfunctional heart tends to recover & lung oxygenation is very poor as well, the LV stroke volume competes with highly oxygenated blood coming from below ( femoral inflow ) into the Aorta , creating a watershed zone . This makes the deoxygenated blood perfusing upper half of the body and hyper oxygen saturation lower half. This is been referred to as North-south syndrome or (Harlequin syndrome the famous Italian comical character)

How to manage North-South syndrome?

  • Try to Improve the oxygen perfusion with high-frequency ventilation(This is logical first step , to improve the native lung function)
  • ECMO flow rate may be increased and overdrive the LV ejection .(This can be counter-productive as we are hitting a recovering ventricle)
  • Converting to VV ECMO if the hemodynamics allows. This is possible as North-south syndrome is a sign of recovering cardia function VV ECMO will convert it into a primary lung support

Reference

ECMO review article

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Is LV dilatation (with normal EF) Indicate LV dysfunction?

November 2, 2019 by dr s venkatesan

LV dysfunction is one of the most commonly used terminology by cardiac professionals.It can be systolic, diastolic or global, regional etc. But, before dysfunction sets in, the heart fights. The Left ventricle can behave in many different ways when confronted with stress. It increases the force of contraction, elevates it’s Intra cavitary filling pressure and still accomplishes its task of pumping adequately. Further, It can build fresh muscle (LVH). It can double up with more heartbeats. (All these factors are referred to as cardiac reserve mechanisms)

These reserve mechanisms can be activated in the short or long term. In the long term, autonomic activation with neuroendocrine factors joins the compensation process.  These will work for some time till the circulatory system settles down to new homeostasis. However, they become counterproductive and becomes decompensated, ultimately heart failure sets in(Unless Intervened)

 

Is LV dilatation a mechanism of cardiac reserve ?

No one calls LV dilatation as a reserve or compensatory mechanism. (I wonder, why not ?) I think like RV ,  LV too has some potential to reversibly dilate . The quantum of which we are unable to estimate.This happens usually in response to chronic  volume stress* like regurgitant valves or high output states. Though cardiomegaly and a huge heart convey a sinister outcome, many hearts shrink if the primary issue is corrected.(Typically in Anemia, Beri Berri. We also know LV may transiently dilate in response to some toxic /pregnancy-related cardiomyopathy.

* Mind you LV poorly tolerates acute volume stress as in Acute AR/MR

The critical gap in our understanding is about this question.

When does LV dilate physiologically and when pathological persistent LV dilation sets in (The absolute state of irreversibly lost cardiac elasticity.) We also know dilated LV will consume more oxygen due to enhanced wall stress (Laplace law) and hence its possible LV dilatation begets further dilatation. Optimal timing of mitral and aortic valve replacement in patients with AR and MR directly depend on this knowledge.

Final message

We need clarity in the following queries

  • Is LV dilatation (with normal EF ) a sign of LV dysfunction?
  • If so at what level of dilatation?
  • Since LV dilatation  occurs in diastole can we fit this entity “Isolated LV dilatation” in the already confused spectrum of diastolic dysfunction?

Let us wait for the knowledge to evolve. Young cardiologists could take up this area for research.

Posted in cardaic physiology, cardiac physiology, LV dilatation is diastolic dysfunction | Tagged , , , , |

Prolonged balloon inflation time : Surprise , why few takers for this PTCA concept?

November 1, 2019 by dr s venkatesan

I asked some of my experienced colleagues, how much time they inflate the balloon to deliver a stent? Most answers were spontaneous and unanimous “It’s hardly 10 seconds,  few said maybe up to 15s.

Can prolonged balloon inflation time reduce the need for post dilatation and prevent mal-apposition?

We know high-pressure Inflation( up to 20 atmospheres ) was a big revelation in the science of PTCA more than two decades ago. (Antonio Colombo JACC 1995  ) He proposed and proved high-pressure inflation eliminated the need for routine anticoagulation following stenting as approximation was better. He also pioneered the concept of dual antiplatelet therapy (DAPT) in the PCI arena.

Similarly, prolonged balloon Inflation  (30 to 60sec) could be another trendsetting tip to prevent malposition. It delivers more sustained pressure. Its believed the imparted centrifugal force and the inbuilt radial forces add up to the stent vessel wall Interface and prevent mal-apposition.

Is there a downside to high-pressure Inflation?

There must be few.  Potential new Ischemic events and arrhythmia. In calcium laden plaques( spur) risk of perforation may be enhanced.

Final message 

I don’t know why this concept never took off. Many of us still fear to inflate the stent balloon no longer than 10 to 20 seconds? Adhoc post dilatation with short NC balloon appears mandatory in areas of mal-apposition. Meanwhile, we also understand sustained (30-60s) high-pressure initial inflation could deliver the stent in a more synchronized and smooth fashion with a perfect metal/vessel wall interface. Further , prolonged balloon inflation times could make a routine (By the way who does routine ?)  IVUS/OCT redundant.

What do the experts say?  What does science say?  There is one meta-analysis that clearly says the advantage of long inflation time. This issue becomes much more relevant as it could avoid post dilatation which all of us know can be tricky. In fact, every balloon dilatation should be technically counted as another PTCA procedure and adds up to net total risk.

Reference

1.M. Saad, M. Bavineni, B. F. Uretsky, and S. Vallurupalli, “Improved stent expansion with prolonged compared with short balloon inflation: a meta-analysis,” Catheterization and Cardiovascular Interventions, vol. 92, pp. 873–880, 2018. View at Google Scholar 

2.https://www.researchgate.net/publication/317175130_Shorter_duration_of_balloon_inflation_time_results_in_greater_malapposition_during_PCI_with_DES_in_patients_with_stable_coronary_artery_disease_a_randomised_control_trial_of_the_second_STent_OPtimisat

Posted in post dilatation, Tips and tricks in cath lab, Uncategorized | Tagged , , , |

How to assess diastolic function in patients with atrial fibrillation by Echocardiography ?

October 23, 2019 by dr s venkatesan

Assessment of LV diastolic function primarily depends on the Doppler flow profile across the mitral valve and also to be noted are the 2D features of LA and LV for associated abnormality like LVH, LAE etc.

Why diastolic dysfunction assessment difficult in AF ?

Since most diastolic doppler mitral inflow parameters involve analysis of atrial contraction A wave, atrial fibrillation makes it difficult to assess diastolic dysfunction. Since we have only early diastolic velocity to assess, the changes confined to this E velocity is of paramount importance. This E velocity again is subjected to cycle length dependent alteration in both its acceleration and deceleration time , making things still more complex.

However, the following features help diagnose diastolic dysfunction in AF

  1. Lack of significant  E velocity variation (<20%)  Inspite of significant RR interval change.(This implies mean LAP is kept high irrespective of cycle length suggesting elevated baseline LAP)
  2. E deceleration time (<140ms) (In long cycle)
  3. Propagation velocity in color M Mode(Vp)  <45cm/sec might help (RR interval dependent, measure in the long cycle)
  4. E/e” in a single beat by dual doppler probe (Ref 1)  > 10 indicate diastolic dysfunction that correlate with PCWP> 15mmhg (Ref 1)
  5. Finally (and curiously ) presence of AF by itself may imply significant LV diastolic dysfunction. It could be due to an increase in atrial strain and afterload of LA (ie pre A-LVEDP) (Of course, It should be in the absence of mitral valve disease)
  6. LA dimension in AF*

*LA dimension is a very good sign of chronic elevation of LAP and diastolic dysfunction in the absence of mitral valve disease. However, AF can dilate the LA making it a less useful parameter. But, it should be noted in AF both RA and LA dilate together.So,  a disproportionate LA>RA (or if RA is normal size ) could still be a marker of baseline LV diastolic dysfunction.

 

Reference

  1. Kusunose K., Yamada H.,  Nishio S., et al.  Clinical utility of single-beat E/e′ obtained by simultaneous recording of flow and tissue Doppler velocities in atrial fibrillation with preserved systolic function. J Am Coll Cardiol Img 2009 2:1147–1156

 

Posted in Atrial fibrillation | Tagged , , , , , , , |

Is FFR heart rate dependent ? If yes, how significant it is?

October 2, 2019 by dr s venkatesan

FFR is the ultimate hemodynamic test that measures the physiological Impact of lesions. Just pass a manometer tipped wire across the lesion and note the pressure drop (with or without Adenosine) All you have to remember is two cut off values  .8 for FFR and .9 for IFR. Abracadabra . . . yes you got the answer , whether to proceed with PCI or not? It’s as simple as that. We are no longer blind to physiology to which many coronary purists often criticize us.

ffr ifr fame study

Coronary physiology simplified

Now , answer this question.

Is FFR heart rate dependent? If yes, how significant it is?

This simple question on coronary physiology caused the maximum distress  to  a large expert cardiologist group

Some of the answers

  1. No, it doesn’t.
  2. I think it may be affected.
  3. Yes for sure, but it’s not significant
  4. Yes, it’s an important limitation

My Answer

It has to be yes, right, however minimal it may be. My interpretation of truth in FFR is, it can have a massive influence* . (*Unless you are sure (we can never be ) about achieving maximum hyperemia or this hyperemia is the same as physiological exercise.) In fact, the whole concept of FFR lies in the fact that it should induce enough HR raise that should be used as a surrogate marker for maximum hyperemia. Ideally, like stress testing, we need to test FFR at maximum heart rate and minimal heart rate. The difference could be documented as FFR max-min. This will throw new light into the physiology of microcirculation.

Should we need to create a heart rate corrected FFR?

Yes , I think we need to do it or else should report at what HR we are reporting the FFR. If FFR falls at a high heart rate and maintains at low it implies a significant lesion. So don’t get fooled with FFR of .9 measured at an inadequate heart rate.

IFR to replace FFR : On what basis?

Meanwhile, new generation coronary flow quantification tool IFR jettisoned Adenosine and simply measure diastolic instantaneous flow at resting state. This makes a mockery of coronary physiology, without a true debate about heart rate dependence of trans-lesional flow.

Impact on clinical practice

Even as we struggle to answer the fundamental question of the influence of Heart rate on FFR, many landmark studies had been done. They have ratified FFR as the most physiological modality to assess coronary lesion. Important guidelines have been written based on these studies. No one will ever know, the true impact on the current cardiology care,  had we included heart rate adequacy /correction as an essential criteria in those FAMEd studies we hype about.

Counterpoint.

All is well with FFR.It has been tested with various heart rates.

FFR at peak hyperemia means there is no further HR rate induced potential microvascular reserve. So a properly administered optimal Adenosine augmented FFR should not bother the HR variability. (But its only theory)

If FFR is ok . . . IFR should not be ok is it not?, For the simple reason, there is no hyperemia in IFR , what is the use of knowing resting flow reserve (RFR)

Reference

1.Przemyslaw Kwasiborski, Wojciech Czerwiński, Paweł Kowalczyk, Influence of heart rate on the FFR measurement – experimental and clinical study

Journal of the American College of Cardiology Volume 70, Issue 18 Supplement, October 2017

 

Postamble with a slice of History 

FFR is as old as the concept of PTCA. In fact, the original balloons used by the great Gruentzig’s * had a central port for pressure recording through which he measured both proximal and distal pressure curves to guess the significance of obstruction. After each inflation, he checked  whether both curves are drawn together which he speculated to indicate a successful procedure physiologically.

*What a stunning scientific mind the father of Interventional cardiology was blessed with, still inadequate for the Nobel committee to get convinced.

Posted in fame study ffr, quantitative coronary angiogram | Tagged , , , , , , |

FFR negative & OCT positive LAD lesion: What shall we do ?

October 2, 2019 by dr s venkatesan

Rules of the PCI game 

  • Mind the physiology. It is the new norm in selecting the lesions for stenting.
  • Now, If physiology is ok, you have to mind the Anatomy and vice versa.
  • If Anatomical (severity of block )is ok, then, you have to mind the morphology and vulnerability.
  • Finally. and most importantly mind the patient’s symptoms and clinical scenario.

So what should we do in a case of 70 % LAD with  .9 FFR ? (Still shabby looking, eccentric plaque, looks vulnerable  with a thin cap on OCT)

  1. I will stent, no doubt.
  2. I shall wait, and treat with Intensive optimal medical management (OMT).High dose statins will surely seal the cap.
  3. I will defer and watch.
  4. I will teach the patient and their family the basics of coronary hemodynamics and accept their decision.
  5. I simply leave the LAD for God to heal.

Which is correct?

All can be fair depending upon the clinical scenario.

In the ACS setting, one can’t afford to ignore these lessons.

Many would argue even in CCS setting it need to be tackled with PCI.

But isn’t also a fact, (maybe, we have been taught wrong as well ) non-flow-limiting lesions are more at risk in terms of ACS risk.

Hmm . . . then why we Insist to celebrate the concept of FFR  and its magic cut off of .75?

Do we practice coronary care at its height of confusing times ? or Am I make it appear so? 

Watch this, (https://rutherfordmedicine.com/videos )It might help you to get a better answer. Its called FORZA study. freshly delivered at TCT 2019, San Francisco.It compares FFR vs OCT guided PCI

 

 

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