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Is misinterpreting scientific papers an Academic crime ? No, its not, I do it often !

June 28, 2016 by dr s venkatesan

medical ethics stastistics www.drsvenkatesan.com

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Where does Bronchial veins drain ?

June 28, 2016 by dr s venkatesan

One casual question in my class led to this search for an anatomical mystery. When we were discussing why left atrial oxygen saturation never reaches 100 % ? , it was attributed to desaturated bronchial venous blood draining into pulmonary vein.

How does this bronchial vein enter pulmonary venous circulation ? How many bronchial veins are there ? What anatomical plane it runs ?

Surprisingly, even in this hi-tech era of academic excess, literature is sparse for this basic anatomical question. It is reported (In Greys anatomy ? ) Bronchial veins are two in number and both drain to Azygos and Hemiazygos veins (systemic) rather than pulmonary veins.

So is our assumption wrong ?

May not be.We realise these are only two visible and named bronchial veins .It is learnt they probably carry only about 13 % of bronchial venous blood to systemic venous circuit.

bronchial venous drainage bronchial circulation

Image showing right and left bronchial veins draining to Azygos and hemiazygos veins.

It is assumed , remaining 87 % of bronchial venous blood drains to pulmonary venous circuit in an invisible fashion (By unnamed twigs ?) desaturating the LA blood by about one percent from 100 to 99 %. This is our current understanding. I haven’t come across any specific human research that quantifies the bronchial venous channels and it saturation . It’s gratifying to find one study specifically looked answer this question in sheep study .(Charan H.B et all Reference 1 )

where does bronchial vein drain drainage circulation pulmonary vein saturation

True physiological bronchial venous drainage seems to be different from anatomical bronchial venous circuits .

Clinical implication of bronchial venous circulation.

In physiology it may not be important . However bronchial circulation (both arterial and venous) can take many anatomical tracts when pulmonary micro vascular bed is structurally and functionally altered as in COPD, , pulmonary atresia with aorto-pulmonary collaterals , congenital left to right shunts,post Fontan circulation pulmonary AV malformations,lung tumors etc .

Hemoptysis in acute pulmonary venous hypertension is thought to be due to rupture of these bronchial veins as elevated pulmonary venous pressure reflect into bronchial veins (As in mitral stenois and other conditions. ) This again would vouch for bronchial veins draining to pulmonary veins.

Final message

As on today , it can be concluded bronchial vein drainage goes both systemic and pulmonary venous circuit.Bulk of them appear to end in pulmonary veins though clear anatomical evidence is lacking.

Postamble

Exploring human anatomy appear a grossly unfinished agenda even today, especially the micro and histo-anatomy. Teachers of basic sciences should impress upon youngsters entering the medical school to pursue translational research relevant to specific clinical problems.

Students may contact <drsvenkatesans@yahoo.co.in> for specific areas of clinical cardiac anatomy topics that still requires answers.

Reference

1.Functional anatomy of bronchial veins. Charan NB1, Thompson WH, Carvalho P. Pulm Pharmacol Ther. 2007;20(2):100-3
2.Baile EM The anatomy and physiology of the bronchial circulation.J Aerosol Med. 1996 Spring;9(1):1-6.

3. Melachrinou M1, Alexopoulos D1, Dougenis D1 .Experimental studies in the bronchial circulation. Which is the ideal animal model?J Thorac Dis. 2014 Oct;6(10):1506-12 (Free full text )

Posted in Anatomy of heart, Bronchail arterial and venous circulation, bronchial arterial and venous circulation | Tagged , , , , , | 2 Comments »

Could Ablation for AF Be an Elaborate Placebo?

June 25, 2016 by dr s venkatesan

We know, atrial fibrillation is the commonest clinical cardiac arrhythmia , that is extensively studied , subjected to exotic investigations and state of the art treatment strategies.Interestingly , this arrhythmia also drags the economics of cardiology practice of a community in a big way with heavy influence on drug , device and usage.We know, RF ablation of pulmonary vein is one of the modern ways to manage this arrhythmia.

Iam sharing this article from medscape by an EP specialist Dr. Jhon Mandrola , surprisingly exposes our fundemental ignorance about this arrhythmia and the near futility of certain procedures.

http://www.medscape.com/viewarticle/865209?src=WNL_infoc_160625_MSCPEDIT_v2&uac=44538BX&impID=1137861&faf=1

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Don’t hunt for non-existing culprits in STEMI crime scene !

June 22, 2016 by dr s venkatesan

Scientific cardiology has forced us to believe ACS management must be catheter based and all others are inferior  and  those who pursue the later , carry a risk of  being labelled as unethical in near future. However ,experienced cardiologists will know  where the truth lies.

Now,in the interventional cardiology board rooms  there is a big  debate going on regarding the value of early total revascualrisation in STEMI with multivessel CAD.Suddenly , every lesion looks suspect ( Ex,current or future culprit ! ) and all stentable lesion are stented  either in an emergency or semi emergency fashion (The new age post PCI dialogue goes something like this “I have tackled one culprit , other one seems to hide in LAD ,  we will arrest it  next 48 hours or so* ? ( This is the concept of  deferred or staged  non-IRA stenting )

*Ironically it brings   one more dubious therapeutic time window in ACS !

ptca ira non ira multivesssel pci

The recent  studies like  PRAMI, PRIMULTY ,CvLPRIT are trying to find out an answer to this issue  and suggest acute multivessel PCI may be  good strategy. Some of them advocate a FFR guided non IRA intervention , knowing fully well micro-circulatory bed is completely altered by the index acute thrombotic event.( Mind you , for FFR,  we need to induce maximum hyperemia with Adenosine in a highly varying local autonomic milleu within the thrombus clogged capillary network)

Final message ( Intentionally biased !)

Till we learn or unlearn  it is vital to go with conventional wisdom.Don’t pursue a random hunt for coronary culprits in acute phase of  STEMI.Many of them are innocents and likely to suffer in cross fire.Tender coronary arteries need some rest,peace and time to heal thyself  . Just keep away , they will definitely say big  thanks with folded hands !

Reference

1.Gershlick AH, Khan J, Kelly DJ, et al. Randomized Trial of Complete Versus Lesion-Only Revascularization in Patients Undergoing Primary Percutaneous Coronary Intervention for STEMI and Multivessel Disease: The CvLPRIT Trial. J Am Coll Cardiol. 2015;65(10):963-972.

Posted in acute coronary syndrome, Cardiology -unresolved questions, Primary PCI | Tagged , , , | Leave a Comment »

ICDs are not foolproof devices for Long term VT management : Most need antiarrhytmic drug or ablation support !

May 6, 2016 by dr s venkatesan

ICDs are revolutionary devices in the management of patients at risk for electrical sudden death .Its is indeed a boon for patient’ s with a primary electrical disease with occasional risk for VT.

Unfortunately , the usefulness of ICD in patients with severe mechanical dysfunction is marginal at best as these patients succumb sooner or later inspite of ICD, especially if the episodes of arrhythmia is more.

This is understandable as electrical events are directly linked to primary mechanical problem and one begetting the other.Of late , we realised these patients require some methods to stop the arrhythmia generation in the first place rather than terminating it after it manifest.

ICD may be great devices but it simply does nothing in preventing an episode VT.It trys to battle the fire after its ignition.Not a great concept to be pride upon.At best it can be called as back up safety device.So , for long term therapy it seems we need additional support system to ICD .

This can either be RF ablation or medical therapy (Amiodarone ,Sotolol, Mexiletene).It is likely , intensive anti -arrhymic therapy is essential in most.In some patients all three modalities(ICD, RF ablation, drugs) will be required for complete protection.

The VANISH trial has added important data on this issue .

http://www.nejm.org/doi/full/10.1056/NEJMoa1513614?query=OF

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Yes, Its official , medical mistakes consume more human lives . . . and threaten to displace cancer and heart disease for the top honor !

May 5, 2016 by dr s venkatesan

We all know to err is human , but most of us probably won’t agree medical mistakes , (bulk of which happen in the name of practicing state of the art of science ! ) could be the dominant theme in modern medical care !

BMJ exposes this  well known secret with the help of most authentic data from an apex scientific body CDC , Atlanta .

Reference

http://www.bmj.com/content/353/bmj.i2139#

Posted in bio ethics, Cardiology -guidelines, Cardiology -Patient page, cardiology -Preventive, Cardiology quotes, medical quotes, Uncategorized | Leave a Comment »

Which is the “side branch” for Left main ?

May 1, 2016 by dr s venkatesan

Bifurcation lesions (BFL) remain a true challenge to interventional cardiologists. For over two decades , at least a dozen strategies are being tried to conquer it without true success . . . if iam allowed to say that.

We often talk about side branch in BFLs.Ironically , the importance of side branch is largely determined by our cortical linguistic perception of the word “side”

The much famed Medina classification does little to clarify the importance of side branch with reference to left main vs non left main bifurcation lesions.

In true sense , both LAD or LCX can be side branches in left main BFL depending upon how one views it.
Commonsense would tell us, since LAD is a major vessel , LCX gets the side branch tag by default.

However, If LAD is diminutive, or its serving a infarcted , non functional zone and if LCX is really big and dominant, it has every right to reject the humiliation of being refered to as a sidekick.

Note , in non left main BFL there is no much confusion since main branch continues as main and side branch just exit.

Final message

Interventional cardiologists use the term “side and main branch ” in variety of ways .Though, it could mean vitally important things , oftentimes its simply semantics prevailing over complex coronary hemodynamics.

Posted in Uncategorized | 1 Comment »

Unlearning cardiology :Diabetes is not CAD equivalent

April 30, 2016 by dr s venkatesan

There can be no debate to call diabetes as major cardiac risk factor . But , how about calling all diabetics to be deemed (Rather doomed ) to suffer from CAD and label them  with a fanciful terminology as CAD equivalent ?

This is what happened few years ago.From the beginging it was a controversial concept. The argument in favour of it was , many diabetics will have micro or macro vascular disease  process in coronary or peripheral disease which are sub-clinical .One major   study from Fiinish population  in (NEJM 1998 ;Ref 1 ) suggested this possibility and was dissiminated without proper scrutinty . The same Finnish group ( I need to confirm this as few authors are same in both studies !)  has comeout with 18 year old data (1998-2016 ) and conclude their earlier conclusion could be wrong after all (Reference 3 )

Premature conceptualisation can be rampant and crucial time is wasted in unlearning. This emphasizes an important aspect of medical learning what I call as “discontinuing medical education” (DME) that would make sense in the future for sure !

Reference

1. Haffner SM, Lehto S, Rönnemaa T, Pyörälä K, Laakso M. Mortality from coronary heart disease in subjects with type 2 diabetes and in nondiabetic subjects with and without prior myocardial infarction. N Engl J Med. 1998;339:229–34

2.Type 2 Diabetes as a “Coronary Heart Disease Equivalent”An 18-year prospective population-based study in Finnish subjectsdoi:  Diabetes Care  2005 vol. 28 no. 12 2901-2907

3.Auni Juutilainen, Seppo Lehto, Tapani Rönnemaa  Jamal S. Rana , Jennifer Y. Liu, Howard H. Moffet Diabetes and Prior Coronary Heart Disease are Not Necessarily Risk Equivalent for Future Coronary Heart Disease Events  Journal of General Internal Medicine April 2016, Volume 31, Issue 4, pp 387-393

 

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Comical concepts in cardiology : Prehospital thrombolysis is great , but its “no good” inside the hospital !

April 26, 2016 by dr s venkatesan

This happened  recently in one of my private ER visits. When I asked my fellow to lyse a patient with STEMI who arrived within 20 minutes after the onset of chest pain to our CCU.

He was reluctant and surprised, seemed to suggest  thrombolysis is a banished indication.

I asked him , whether he is aware of any study  that showed early , fast pre-hospital thrombolysis is as good as primary PCI ?

Yes sir. . but these studies clearly say it is useful only if its done prehospitally sir, not inside the hospital or coronary care units. 

I told him to think CCU as an ambualnce ,consider the patient is  in transit and  lyse him.

He was amused , as it looked  a comical concept and an unscientific uttering from a professor !

Still, he was courteous enough to follow my advice.The  patient stabilised within 6 hours and the ST segment  resoluted to near 100 % , No LV dysfunction.Discharged in 48 hours.

Final message

I realised in a harsh way , modern day scientists driven by evidence would struggle to regain the lost common sense ! There is a real risk for  irreversible damage to our faculty of wisdom !

STREAM trial nejm

 

http://www.nejm.org/doi/full/10.1056/NEJMoa1301092

 

 

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When STEMI dressup like NSTEMI. . .Cardiologists can easily be fooled !

April 22, 2016 by dr s venkatesan

The ECG changes in ACS can be  “as dynamic as”  an occluding thrombus. The initial events include sudden total occlusion, early lysis, a trickle of flow, partial re-occlusion, reflow, no-flow, etc. The extent of transmural vs sub-endocardial ischemia, the competing force of re-perfusing vs necrotic wavefront, would define  ECG findings. This makes the ST segment labile in the early hours of ACS. This is also the basis of some cases of  STEMI evolving into NSTEMI and vice versa.

A 65-year-old man  presented to with this ECG,

 

img-20160423-wa0012_1.jpg

Does this ECG allow you to go ahead for thrombolysis? It actually looks like NSEACS with ST elevation in AVR suggesting left main lesion

The initial diagnosis of  NSTEMI was made, and hence thrombolysis was not considered. Even as the fellows were mulling over the diagnosis, one of them could find one more ECG available taken a few hours ago in another hospital.

It had something on it ,

img-20160423-wa0009_1_1.jpg

This ECG taken a few hours ago, shows ST elevation in 1 and AVL, and few VPDS in the chest leads unmasks the anterior ST elevation.

The moment we saw this ECG it was decided to go ahead with thrombolysis.The final ECG after thrombolysis with (Streptokinase) showed further stabilization. The question of thrombolysis in NSTEMI though not indicated in general, in selected situations we need to Introspect!

img-20160423-wa0011_1.jpg

How to manage a patient who presents as NSTEMI but had STEMI a few hours ago?

Four ways to ponder!

  • This patient should not be lysed as we have to treat the current event, not the past.  ,(Its NSTEMI and no need for lysis) Just heparin, dual antiplatelets. That will do.
  • One can go ahead with lysis as there is evidence for STEMI in prior ECG.
  • There is ST elevation in AVR even in the second ECG and so you have to thrombolyse !
  • “Come on guys, . . . don’t live in the primitive era of managing ACS in CCU . Forget the ECG take him to the cath lab , suck out all thrombus and deploy a stent and come out”.

* The last one , though appear practical (and most of us would love that ) is an unprofessional way of practicing cardiology. Management of ACS requires sound principles of ECG and its correlation with the Intra-coronary and myocardial pathology.

What happened to this patient?

He did well, free of angina with minimal LV dysfunction. He was discharged. Will be reviewed later, for further evaluation. This is a typical example of a patient with ACS managed successfully without entering the cath lab.(A forbidden practice and a potential coronary blasphemy )

Final message

ECG changes are as dynamic as the Intra-coronary blood flow in ACS. Multiple factors determine ST elevation or depression. While thrombolysis is reserved for STEMI,  NSTEMI has little or no benefit to accrue with thrombolysis. However, this is applicable only for de-novo NSTEMI  and may not apply for  STEMI in transition into NSTEMI as in the above patient.

 

Posted in acute coronary syndrome, Cardiology -Therapeutic dilemma | Tagged , , , , | Leave a Comment »

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