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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 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 reduces may 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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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 RSelzer FFaxon 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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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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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

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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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The term Ischemic cardiomyopathy(ICM) was originally coined by Dr. Burch from Tulane University, New Orleans, USA in 1970. For many decades there was skepticism regarding the existence of such entity. WHO classification over the years never included this term. ESC working group of 2008 (Elliott P, European Heart 29(2):270–276) decided not to include CAD as a cause for cardiomyopathy. Even the current MOGES system doesn’t invoke CAD as a cause for cardiomyopathy. But, I am sure, most of practicing cardiologists would agree, there is a need for such an entity.

Why there is much reluctance to diagnose Ischemic cardiomyopathy as a distinct entity?

It is because of the basic principle, that cardiomyopathy should be a primary disease of cardiac muscle. (or at least secondary ).The presumption is, Ischemia per se doesn’t lead to muscle disease as such. It is just nutrition deprival.

Does this justify?

No, not at all. When a cardiac muscle is chronically deprived of nutrients it goes for necrosis, dilatation, scarring and dilatation, and progressive LV dysfunction. At some stage, it becomes true muscle disease or its equivalent (Secondary cardiomyopathy).In fact, adverse remodeling, Infarct expansion, extension lead to myocyte disarray, slippage and apoptosis, and cellular and interstitial fibrosis. All these changes are similar to Idiopathic (Postmyocarditis)cardiomyopathy.

What happens in the real world?

Even though there was some hesitation to diagnose ICM in the past, gradually the term shrugged of its taboo in academic circles. In heart failure clinics the only question seems to matter for everyone is, Is it Ischemic or non-ischemic DCM? Surgeons and EP guys also actively pursued the term Ischemic cardiomyopathy while they are selecting patients for CABG or CRT/ICD etc.

Further, in the research world involving community-based heart failure cohort, they required a basic distinction between the group of Ischemic from Non-Ischemic cardiac failures.

DUKE university definition (By Felker et al)

I think DUKE ended the controversy in the Nomenclature of Ischemic cardiomyopathy. It suggested the following to diagnose ICM (Read REF 2)

  1. LV dysfunction < 40% EF
  2. >Atleast one significant proximal coronary lesion (Usually 2 or more)
  3. With the history of MI or Revascularisation

* We are analyzing our data (Madras medical college, Chennai India) and propose to write WHO/WHF to include the following additional criteria to diagnose ICM.

4. At least 6 months should be elapsed between the MI and diagnosing Ischemic cardiomyopathy,

5. Must have significant LV dilatation & global Hypokinesia(With or without regional variation).

6. At least one episode of clinical heart failure is required before labeling it as Ischemic cardiomyopathy.

Other definitions that endorsed Duke

STITCH criteria *Surgical therapy in ischemic DCM study ICM was defined CAD with cut off EF < 35% with triple or double vessel disease.

iFAQs in Ischemic cardiomyopathy

1. Can we diagnose ICM without a history of MI?

This is tricky. As we all aware its very much possible as in silent MI of diabetes. One more possibility is even chronic coronary syndrome with microvascular dysfunction can lead to ICM.

2. Can Ischemic cardiomyopathy present as HFpEF or RCM?

While most Ischemic Cardiomyopathy present as DCMs with HFrEF, It is currently not clear how much of Ischemic heart failure present as HFpEF and if so they can’t be included technically as Ischemic cardiomyopathy in spite of the fact they present as HF.(as EF would be >50%)

3.When does a Post MI failure become Ischemic cardiomyopathy?

If the definition of STITCH or DUKE is applied, any acute STEMI can fulfill criteria of ICM. Hence it advisable to have a time limit say 6 months following MI to be referred to as Ischemic DCM. Pathologically to call it true cardiomyopathy, scarring, dilatation is required. Myocytes should be in independent self-destruction mode irrespective if hemodynamic conditions.

Response to treatment

The only purpose to diagnose ICM is to try to remove the I from ICM( ie Ischemia) Unfortunately, it is not an easy task. (While correcting Ischemia in ACS seems to be such an easy job.)

Following principles apply.

  • Medical management of HF/Ischemia is the key.
  • It is advisable every patient with cardiomyopathy should undergo coronary angiogram to rule out ICM.
  • Effect of revascularisation remains equivocal.
  • Viability of remaining muscle mass must be documented. (At least one-third of total cardiac mass should be viable.(Not very easy to prove though)One may use Doubutamine /Nuclear stress/PET etc) .It’s very important to realize even if the viability is demonstrated, the area that shows viability must be supplied by an artery that has a revascularisation eligible lesion.
  • STITCH can be called as a negative study (meaning positive outcome for patients if the patient doesn’t receive CABG in mulitvessel CAD and LV dysfunction ).However , STICHES (Extension of stich showed some long term benefits) The probable reason for CABG not helping much in ICM is the muscles didn’t get further useful life, either because it’s fully dead or extremely viable, that revascularisation made no impact.
  • CRT/ICD is known to prevent SCD and improve the functional class.
  • Heart transplantation is a life-modifying specific strategy.

Final message

I agree, many times our valuable time is wasted in renaming /Altering /relabeling a disease /process or pathology without any useful purpose. Medical nomenclature and classifications are done to make diagnosis simpler, choose an appropriate therapeutic modality and make a positive impact on the outcome.

In that sense, segregating ICM from other causes of cardiac failure do help in choosing a specific management strategy.

Let us welcome MOGES, It is the most comprehensive cardiomyopathy classification system (Like TNM classification for cancer). Still, I am not clear why it hasn’t included CAD in that system. Thanks to Dr. Burch who thought of this 50years ago.

Reference

1.Burch, G. E., Giles, T. D., & Colcolough, H. L. (1970). Ischemic cardiomyopathy. American Heart Journal, 79(3), 291–292.

2.Felker G.M, Shaw L.K, O’Connor C.M (2002) A standardized definition of ischemic cardiomyopathy for use in clinical research. J Am Coll Cardiol 39:210218

History of cardiomyopathy classification

The landmark thoughts originated in 1972 .When Goodwin and Oakley defined cardiomyopathies as the heart muscle diseases of unknown cause and described them as dilated (DCM), hypertrophic (HCM), and restrictive (or obliterative) (RCM) cardiomyopathy types.

WHO adopted it mostly and suggested Primary and Secondary cardiomyopathy in 1980. In 1995 WHO revised it.

The current MOGES classification doesn’t mention about Ischemic etiology

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Master health checks* , superficially look like a perfect modality to practice the greatest medical concept ie “Prevention is better then cure” .Let us detect all human diseases early , prevent its progression, regress it or completely cure it . Absolute bliss is it not?

Why then articles such as this one should ever get published, that too in one of the prestigious journal of medicine?

*Master health check .( Also referred to as annual General health checks.)

Master health check up geenral cochrane bmj editorial

While the title itself is provocative, it adds a tag line which is still more a shocker.

There are specific well-researched reasons for this preventive health check fiasco.The masters, who were originally the guardians of health soon became disease mongers.In the process, the primary aim of propagating the doctrine of “prevention is better than cure”, could not reach its desired goals. Instead of ignoring and reassuring the minor deviation of biological data and Imagery generated, they became a perfect feed for the hunters who are after the trivial and non-existing illness.

Final message

Good intentioned health checks are always welcome in selected high-risk population say pregnant women/children of developing a world (As in endemic countries of rheumatic fever) Also cancer , CAD , screening in people with a positive family history can be critical.

However, when these masters of health deviated and started making a living out of apparently healthy people. ( The side effects reached monstrous proportions hiking global health cost in a meaningless way).People, especially in counties with poor resources, are the ultimate sufferers, as the cost and efforts are diverted, to fix the health of healthy, while people with true illness continue to struggle.

Will the WHO* wake up and intervene against this skewed practice of routine master health checks in healthy, that are rampant in both rich and poor countries. Ideally, doctors should order preventive health assessment for those who may need it.

There are enough grounds for public Initiated periodic walk-in health checks to be banned (or at least restricted)

*WHO is world health organization

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