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Time to tweak the definition of “Professional incompetence” in medical practice.

January 28, 2020 by dr s venkatesan

 

 

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Please mind this “Acute coronary error”

January 23, 2020 by dr s venkatesan

Science is a journey in pursuit of truth. Hence, we search for it again and again.  (Thus, recurrent search becomes Re-Search)

As we try to progress in our knowledge towards absolute truth,  we need to admit our errors first. I think, one such error is blinking right in front of us in the vibrant corridors of coronary care and cath labs every day!  It is about the definition with which we deal the success of primary PCI. (A supposedly revolutionary acute coronary therapeutics  this century)

Waiting for the day . . . when all those fancy primary PCIs that leave the myocardium hurt (& retire ) with significant LV dysfunction to be reclassified as clear cases of primary PCI failures.

Posted in acute coroanry syndrome, Cardiology -Therapeutic dilemma, Uncategorized | Tagged , , |

Understanding a myth called “Systolic decapitation” in Aortic stenosis is tough !

January 3, 2020 by dr s venkatesan

Severe aortic stenosis will cut off the systolic BP and hence classical pulsus parvus et tardus occurs. This is what , we have been taught all along.

How for it is true?  

One thing is clear from clinical observation. Systolic BP need not be low, often its normal even in severe Aortic stenosis. The issue becomes curious when  high BP is associated with severe Aortic stenosis. This can happen by a variety of mechanisms.(Aging/Loss of Aortic elasticity /Pressure recovery/Hypertension)  I think, there have been little correlative studies of pulsus parvus with central aortic pressure.

Can Aortic stenosis be a cause for systolic Hypertension?   (This academically murky question rose after I stumbled upon this paper )

This paper from the journal of Human Hypertension which was published many decades ago.It sincerely documented high BP in spite of severe AS . The most crucial aspect of this study , however, was the fact that hypertension was completely corrected after Aortic valve replacement. The authors attributed to this high systolic BP as the transmission of LV chamber pressure. This is a frontal attack on the traditional concept of pulsus parvus and systolic decapitation in LVOT obstruction.

I am not sure, whether knowledge always breeds knowledge. Medical science is equally affected by new-onset Ignorance or not recognizing past knowledge.( Like this paper of 1996.) I think this study is done with a good scientific basis and unable to find any serious flaws. Hats of to the authors. This could lead to a further breakthrough in our understanding of transvalvular gradients in Aortic stenosis and the poorly understood vascular- valvular Interactions. With, catheter-based TAVRs become so common, we can exactly measure the pressure dynamics in the Aortic root pre and post valve replacement. (* My take is , systolic BP in severe Aortic stenosis  is preserved until the onset of LV dysfunction)

Reference

1.Ie E, Mook W, Shapiro AP. Systolic hypertension in critical aortic stenosis and the effect of valve replacement.J Hum Hypertens. 1996 Feb;10(2):65-7.

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Pulmonary valvotomy for Tetrology of Fallot : Will soon become a worthy option

December 24, 2019 by dr s venkatesan

Catheter based interventions in TOF  has caught the imagination of  Interventional cardiologists.decades ago. (Quereshi reported first in 1988 Royal Liverpool hospital ) .Somehow it could not develop into a full-fledged modality. The key issue in TOF  is,  RVOT obstruction is infundibular with some degree of valvular involvement. While the valvular component is amenable for easy correction by balloon, the infundibular stenosis requires some form of cutting or splitting. Embryologically,  the malalignment of IVS is the primary mechanism of obstruction. The balloon catheter is will find it difficult to tackle the alignment defect. .Obviously, surgeons can do a comprehensive RVOT reconstruction.

Things are beginning to change. Cutting balloons are available. Various dedicated VSD devices are being developed. Closure of large sub-aortic VSD  followed by  RVOT dilatation appears challenging task but distinctly possible in the near future.

Few cases of palliative RVOT dilatation with a balloon  in critical TOF  is been attempted We hope, in the coming decades at least simple forms of TOF are conquered by the interventional cardiologists!

Hardware: A small profile  coronary  cutting balloon  from Boston scientific .

What is in store for the future ?

3D printing of live heart and designer device or deployable patches for the malaligned VSD is possible. Currently, intracardiac ultrasound would assist the procedure.

RVOT reconstruction with RVOT stenting and percutaneous valves (Melody or Right sided TAVR equivalents) is already been done in post-ICR residual obstructions or late RVOT failure

Coronary cutting balloon flextome tof pulmonary valvuloplasty coronary hard ware

Flextome -Coronary cutting balloon

Balloon pulmonary valvotomy for tof tetrology of fallot

balloon angioplasty for TOF cutting balloon

pulmonary valvotomy in tof tetrology

pulmonary valvotomy in tof tetrology 3

 Other References

1.Boucek MM, Webster HE, Orsmond GS, Ruttenberg HD. Balloon pulmonary valvotomy: palliation for cyanotic heart disease. Am Heart J. 1988;115:318-322.

2.Qureschi SA, Kirk CR, Lamb RK, Arnold R, Wilkinson JL. Balloon dilatation of the pulmonary valve in the first year of life in patients with tetralogy of Fallot: a preliminary study. Br Heart J. 1988; 60:232-235.

 3.Parsons JM, Ladusans EJ, Qureshi SA. Growth of the pulmonary artery after neonatal balloon dilatation of the right ventricular outflow tract in an infant with tetralogy of Fallot and atrioventricular septal defect. Br Heart J. 1989;62:65-68.

4.De Geeter P, Weisburd P, Dillenseger P, Willard D. Valvuloplastie pulmonaire percutanée palliative dans les formes néonatales de tétralogie de Fallot. Arch Fr Pediatr. 1989;46:117-119.

 5.Guntheroth WG. Balloon valvuloplasty as palliation in tetralogy. J Am Coll Cardiol. 1992;19:234-237.

Posted in cardiology -congenital heart disease, cardiology -Therapeutics, Interventions -Structural heart disease, Tetrology of Fallot | Tagged , , , , , , | Leave a Comment »

Does elevated RVEDP cause dyspnea ?

December 18, 2019 by dr s venkatesan

Exertional dyspnea disproportional to the effort is the most common (cardinal)symptom of heart disease. Whenever we discuss the mechanism of cardiac dyspnea , we primarily attribute it to left heart disease, elevated LVEDP and the resultant pulmonary congestion.Conventional teaching in the past (may be in the present too !) doesn’t implicate raised RVEDP in the genesis of dyspnea.

It’s good to recall , the sensation of dyspnea is felt at the peri -Amygdala nuclear zone after complex processing with various cortical and sub-cortical level .It is subjected to as many afferent triggers other than J receptors in pulmonary micro circulation. (Eg Exercising skeletal muscle). It is believed, mechanical stretch receptors exist within the walls of heart along  the sub-endocardial aspects of chamber.

(Muscle spindles which are the sensors of muscle tension are extensively noted in skeletal muscle that contribute to the origin of dyspnea .We are not yet accruing enough evidence  whether cardiac muscle do have the same muscle spindle or it’s equivalents to cause dyspnea when stretched. However, we clearly witness in the practice of clinical cardiology , isolated elevation of RVEDP ( also RVSP ) to cause significant dyspnea in specific clinical situations.

Potential causes for Isolated Right ventricular dyspnea

  • Pulmonary hypertension  (COPD included* where in it could be a combination of lung and cardiac dyspnea)
  • Acute pulmonary embolism
  • RV Infarction
  • Acute rupture of sinus of Valsalva aneurysm (RSOV) Here RVEDP is often > LVEDP and dyspnea is due to the acute stretch of RV
  • Isolated normal pressure TR(RVEDP is low still cause dyspnea  due to volume related RV triggers)
  • Any RVOT obstruction (Classically valvular pulmonary stenosis)
  • Does RV dilatation without elevated RVEDP cause dyspnea ?  Though right ventricle is developmentally and hemo-dynamically better suited to handle volume , still, it  struggles to manage sudden increase in volume .(Another clinical example is seen in patients who are on dialysis)

*RV diastolic dysfunction is still a Infantile hemo-dynamic concept .Whether it can raise RVEDP significantly during exercise and Independently contribute to dyspnea is at best a hypo-science.

Role of muscle spindle and mechno-receptors

 

Muscle spindle

structure of skeletal muscle spindle. Though we don’t have a highly developed spindles in smooth muscle and cardiac muscle we have evidence to suggest cardiac neural ending do have mechano-receptors with afferent connection through visceral neural plexus that can trigger both heart rate and respiratory centers Further reading : Neuroscience. 2nd edition. Show details Purves D, Augustine GJ, Fitzpatrick D, et al., editors. Sunderland (MA): Sinauer Associates; 2001.

Bain-Bridge reflex: The hidden link in right heart dyspnea

Bain-Bridge reflex is a 100 year old concept. still helping us to understand the basics of right heart hemodynamics and how adjustments with acute volume loading take place.He proposed that  veno-atrial stretch receptors are located  primarily in great veins as it enter ,right atrium (RV as well).

This gets activated through vagus and stimulates  in brain-stem sympathetic system and increase the heart rate to handle the excess blood reaching the heart. How often we feel the symptom of palpitation  whether due to this reflex ( when it is operating) is not really tested. But, what we can infer is , the surge in sympathetic tone perceived can be perceived as  dyspnea.

*Clinical Relevance of the Bezold–Jarisch Reflex and its possible interactions with Bain Bridge reflex is a different topic.

It is interesting to note many of these reflexes cause hypo-tension, bradycardia and hypopnea (Even near Apnea.) The word dyspnea is surprisingly not used .It is highly plausible many of the unexplained dyspnea we see in otherwise healthy population is attributed to acute or chronic volume overloading or under-loading of right heart.

Role of PFO in right heart dyspnea

PFO is a natural decompressing orifice in the IAS guarded by a flip-flap safety valve which is a remnant of septum primum .Though it can flow either way , since the flap of the valve is larger in LA side,  it gets closed when  LA pressure raises but opens up , if RA pressure raises making it more often a right to left shunt at times of elevated RA mean pressure. In isolated right heat pathology , this communication shunts  right to left and  adds a new dimension to cardiac dyspnea (Now, It becomes a hypoxic /biochemical dyspnea over and above the right heart stretch related dyspnea )

Other mechanisms in right heart dyspnea

Pulmonary arterial stretch and altered QP : Role of ventilation perfusion mismatch should also be considered as a cause for dyspnea in isolated RV pathology. The term V/Q mismatch is a poorly understood term fro me. My Inference is, since RV contraction  provides the Q in the equation V/Q .Whenever Q falls V has to fall to maintain neutrality causing net hypoxia and dyspnea.

Final message

Dear fellows, never hesitate to attribute the origin of dyspnea,  to elevated RA mean pressure /RVEDP. It is due to RA/RV stretch secondary to volume and pressure overloading with a perfectly normal pulmonary capillary wedge pressure or LVEDP. As in the left heart ,this occurs both in pathological as well as perfectly exaggerated physiological times.

Reference 

1.Bainbridge FA. The influence of venous filling upon the rate of the heart. J Physiol. 1915 Dec 24;50(2):65–84. [PMC free article] [PubMed] []

2..A J Crisp, R Hainsworth, and S M Tutt  The absence of cardiovascular and respiratory responses to changes in right ventricular pressure in anaesthetized dogs. J Physiol. 1988 Dec; 407: 1–13(This paper actually undermines the importance of RV receptors. It is still perplexing to note both the inflow into RV (ie RA  and the out flow  pulmonary artery circuit has richly innervated by receptors , its difficult to accept why we  have failed to get much evidence for RV stretch receptors) Its potentially great area of research for cardiac physiologists. That will be a tribute to the greats like  Bain Bridge and Bazolds Jarich.)

Posted in Cardiology - Clinical, Clinical cardiology, Uncategorized | Tagged , , |

“Loud S1” and “Opening snap” in mitral stenosis : Do they always go together ?

December 10, 2019 by dr s venkatesan

 

Posted in clinical cardiology -Murmurs, opening snap | Tagged , , , |

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

 

 

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