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Does Intentional harm happen in medical profession ?

Posted in Uncategorized, tagged on March 27, 2016| Leave a Comment »

I don’t know the answer, rather I am afraid to answer that question.

Read this article , that may  help find answer to this forbidden question.

medical ethics inappropriate medical care

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What ails the “Noble” profession ?… Is it the “erring” medical Intellect !

Posted in Uncategorized, tagged , , , , on January 31, 2016| 2 Comments »

medical education critics cardiology evdnce based medicine growth ethics

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Happy new year to all . . .thanks to wordpress for making this possible !

Posted in Uncategorized, tagged on January 1, 2016| 1 Comment »

On this special day , wishing all the readers and followers of this blog  an energetic, creative , insightful and  of-course a happy new year 2016 !

Just wanted to share the 2015 annual report of this site with the readers.

wordpress annual report dr venkatesan

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Is there hemodynamic advantage for co-dominant coronary circulation ?

Posted in Uncategorized on December 20, 2015| Leave a Comment »

Co-dominant coronary  circulation is defined as , when  posterior crux of the heart receives twigs from both right and left system making this water shed area with advantage of twin innervation.They essentially supply  inferior and posterior aspect of both left and right ventricle including the posterior aspect of interventricular septum.

Traditionally inferior and basal aspects of heart are perceived (wrong tough !) as less important  than anterior  surface of heart.Infero posterior MI can be extensive and cause significant LV dysfunction and poor outcome. Longitudinal function (AV grooval velocity) and Mitral valve function  is critically  dependent on  posterior circulation.

Is there an advantage for co-dominant circulation  with reference to ischemic mitral regurgitation ?

Obviously ,one would expect there is some advantage in co-dominant circulation when ACS occurs  either LCX or RCA.It could theoretically  protect against development of MR as posterior  papillary muscles could receive supportive twigs from its companion.

However , there is a caveat .The antero-lateral papillary muscle normally has twin blood  supply from LAD(Diagonal ) and LCX (OM) . But in co-dominant circulation this pap muscle is  at risk of becoming single blood supply as the dominant RCA has a trade off with OM with its large PLV branch. It is likely in   co-dominant circulations if LAD is the culprit outcomes are likely to be worse.

Final message

A rare  study involving  more than 200,000 patients which specifically addressed this issue  of dominance and outcome , threw some surprising  findings. In concluded  PCI outcomes  with left or co-dominance has a worse outcome than Right dominant system.

Reference

1.Left and Codominant Coronary Artery Circulations Are Associated With Higher In-Hospital Mortality Among Patients Undergoing Percutaneous Coronary Intervention for Acute Coronary Syndromes . Report From the National Cardiovascular Database Cath Percutaneous Coronary Intervention (CathPCI) Registry  Nisha I. Parikh, Emily F. Honeycutt, Matthew T. Roe, Circulation: Cardiovascular Quality and Outcomes. 2012; 5: 775-782  2012; 5: 775-782

2.Papillary Muscle Perfusion Pattern A Hypothesis for Ischemic Papillary Muscle DysfunctioPaolo Voci, Federico Bilotta, Quintilio Caretta,Circulation. 1995; 91: 1714-1718

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One minute survey on STEMI : Can you manage STEMI effectively without knowing coronary anatomy ?

Posted in Uncategorized, tagged , , , , , , , on December 15, 2015| 2 Comments »

 

Verdict ?

Only complicated or high risk  STEMI,  would require immediate anatomy based management. Please note, this population at worst is never beyond 20 % of all STEMI. Hence more than majority of  patients  can be managed effectively without CAG.

My reasoning tells me,though knowing the  coronary anatomy appear vital  , it is rather the physiological impact of those  anatomical lesions  that will determine the outcome. So,post STEMI, if at all , we need to investigate, it should be about the  adequacy of the over all blood supply to left ventricle.This is done by a pre or post discharge sub maximal stress /nuclear test .If it’s negative with a good exercise tolerance  CAG will never be required as any critical flow limiting lesion ( that would require intervention  )is excluded with near 100% surety.

Postamble :Try asking  any neurologist , how often they demand to know cerebral arterial  anatomy for managing stroke  ? You will get a real surprise answer !

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Nocturnal pauses in Holter monitoring : How significant is it ?

Posted in Uncategorized on December 11, 2015| Leave a Comment »

Holter monitoring is the Initial test for all those with documented  syncope (or Pre syncope ) with suspected cardiac arrhythmia .It is a 24 hour ambulatory  ECG monitoring , expected to pick up any electrical abnormality and its correlation with the resultant symptom if any. Though the test looks  attractive , the diagnostic yield is far less. (About 10%) .The reason being the episodes can be rare  to be  missed by 24hr sample time. We have extended Holter (48hr) , Event monitors , Loop recorders and implantable devices that can record ECG for extended periods.(18 Months ,Reveal Plus Medtronic)  that improve the yield  up to 45%.

One common issue that often confuse us  while reporting  Holter is, the  pauses that occur during day / night .

What is the significance of these pauses * ?  Nocturnal vs Daytime

Pauses are obviously significant when the patient is awake . It is generally accepted pauses more than 3 seconds during day time  (ie Heart rate of < 20/mt ) is significant . This is logical , as pauses more than that,  is expected to cause syncope ( or atleast pre-syncope ).The problem comes when you document pauses more than 3 seconds without any symptoms . Then this  difficult  question comes up ,At what degree of pause syncope occurs ? How is that some persons mange  even prolonged pauses with just giddiness.(Good overall vascular integrity and tone ! )

We know such pauses are  especially  common during sleep. How does the brain react when pauses occur  during sleep ? as there is no question of fall as such and loss of muscle tone is non existing.

*Please note ,when we say pause we mean only Sinus pause , Pauses due to AV blocks are very significant

nocturnal pauses during sleep holter

Source : Brodsky M, Wu D, Denes P,et al.Am J Cardiol 1977; .

Dramatic  pauses during sleep do occur

There has been prolonged pauses reported  during sleep without fatality . A 35 second nocturnal pause resulting in seizures has been documented by implantable  recorders.(Mairesse 2003)

Causes for prolonged pauses

  • Sinus node dysfunction
  • Obstructive sleep apnea
  • High dose beta blockers therapy

Final message

 Most bradycardic episodes during sleep are benign.This is due to depressed autonomic control during sleep. Holter interpretation is primarily done with  awake rhythm data in most individuals .So, empirically shall we fix a  5 second pause as significant during sleep ? We don’t know.While this may seem applicable even with structural heart disease , one may be vigilant while interpreting the nocturnal pauses in this population .

Caution

** Please note,  all these rhythm monitoring extravaganza is meant for people  with equivocal symptoms .Patients  with well documented syncope with ECG features suggestive of  cardiac rhythm disorders would never require these tests and go for pacemaker straightaway.

Reference

1.Use of an extended monitoring strategy in patients with problematic syncope. Reveal Investigators. KrahnAD, Klein GJ, Yee R et al Circulation. 1999;99:406–410.
 
3.Clinical relevance of arrhythmias during sleep: guidance for clinicians L J Gula, A D Krahn, A C Skanes, Heart. 2004 Mar; 90(3): 347–352
4.Arrhythmias documented by 24 hour continuous electrocardiographic monitoring in 50 male medical students without apparent heart disease. Brodsky M, Wu D, Denes P,et al.Am J Cardiol 1977;39:390–5.
For Advanced readers
guidelines for syncope nocturnal pause holter

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COURAGE begets Courage : A 15 year truth unfolds !

Posted in Uncategorized on November 12, 2015| Leave a Comment »

Effect of PCI on Long-Term Survival in Patients with Stable Ischemic Heart Disease are just out in NEJM.

The results are as expected !

“Let us get more Courage , to say no when we want to say no !”

Reference

http://www.nejm.org/doi/full/10.1056/NEJMoa1505532?query=TOC

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A classification for “Polymorphic ventricular tachycardia”

Posted in Uncategorized, tagged , on October 16, 2015| Leave a Comment »

A  classification of  Polymorphic VT .

It can be classified according the etiology,  morphology  or hemodynamic stability . However , for some reason classifying  PVT with reference to the preceding QT interval and  the manner in which  tachycardia twists its axis along the qrs axis has been the most popular theme . ( Obviously ,the classification  process should  evolve further , and management strategies should be linked with it )

classification of polymorphic vt, torsades de pointes , long qt syndrome

Read a related article :Different Avatars of polymorphic VT

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What are the causes and mechanism of diastolic mitral regurgitation ?

Posted in Aortic regurgitation, Hemodynamics, Infrequently asked questions in cardiology (iFAQs), Uncategorized, tagged , , , on October 11, 2015| Leave a Comment »

Mitral regurgitation is expected to occur only in systole during  left ventricular contraction. In rare pathological states , if   LV pressure exceeds the mean LA pressure at any point in diastole , small  puffs of regurgitation into LA can occur.The genesis of this MR and its  hemodynamic  significance has generated much interest .

Causes

  1. Aortic regurgitation -Severe . (Occurs mainly in acute AR or chronic AR with decompensated LV )
  2. AV blocks (especially complete AV block )
  3. Any cardiomyopathy with severely elevated LV diastolic pressures

Mechanism

No single mechanism is  responsible.

  • Common hemodynamic denominator  is transient cross over of LV pressure over and above LA pressure curve .
  • This tends to happen often soon after the atria contracts  specifically so , if the atrial contraction is not followed by a QRS complex as in heart block .
  • The fact that its reported even in the presence of atrial fibrillation (As in some cardiomyopathy ) atrial mechanism is not exclusive.
  • In Aortic regurgitation the mechanism is  different (More of  volume dependent ,  Read below )

diastolic mitral regurgitation animationTiming of  diastolic MR

It occurs in later part of diastole as it takes a time lapse for raising LV diastolic pressure  to cross the LAP and generate a reversed ventricular gradient.

Will there be a clinical evidence for this MR ?

Its silent in most cases .Some patients with complete heart block may  generate  mid diastolic murmur . (Rytand AHJ 1946) .Retrospectively this could be due to diastolic MR

Is there a link between Austin flint murmur and diastolic MR ?

Many researchers believe the generation of diastolic murmur in severe AR is attributable to premature closure of mitral valve and the poorly compliant LV  is not able to accommodate the leaking blood and it tends to regurgitate into  LA  through partially closed mitral valve in diastole (Ochaya  S,  Am Heart J. 74 1967:161-169)

Echo features

  • Doppler flow signal in mitral inflow is diagnostic
  • Color M-mode is ideal to map  diastolic MR.

Cath correlation

Wong has demonstrated this phenomenon by direct hemodynamic  recording in 4 patients

Further research

While the field of diastology is growing , still we are not clear how significant this MR in clinical diastolic dysfunction and acute LV failure that results in flash  edema.

Reference

1. Wong M. Diastolic mitral regurgitaiton. Haemodynamic and angiographic correlation. Brit Heart J. 1969;31:468.
2.Different mechanisms for diastolic mitral regurgitation illustrated by three comparative cases. Sisu RC1, Vinereanu D.Echocardiography. 2011 Apr;28(4):476-9.
3.Diastolic mitral and tricuspid regurgitation by Doppler echocardiography in patients with atrioventricular block: new insight into the mechanism of atrioventricular valve closure.Schnittger I1, Appleton CP, Hatle LK, Popp RL.J Am Coll Cardiol. 1988 Jan;11(1):83-8
4.Diastolic mitral regurgitation in patients with atrioventricular conduction abnormalities: A common finding by Doppler echocardiography. Panidis IP, Ross J, et al J Am Coll Cardiol. 1986;7:768
5.Diastolic atrioventricular valve closure and regurgitation following atrial contraction: their relation to timing of atrial contraction.Okamoto M1, Tsubokura T, Kajiyama G, Clin Cardiol. 1989 Mar;12(3):149-53.
6.Diastolic mitral regurgitation in acute but not chronic aortic regurgitation: implications regarding the mechanism of mitral closure.Downes TR1, Nomeir AM, Hackshaw BT, Am Heart J. 1989 May;117(5):1106-12.
7. An auricular diastolic murmur with heart block in elderly patients.Rytand  DA; Am Heart J. 32 1946:578-598.
8. Late diastolic mitral regurgitation secondary to aortic regurgitation its relationship to the Austin-Flint murmur.ochaya  S, Igarashi  M, Schaffer  AB; Am Heart J. 74 1967:161-169

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Recannalised IRA : When God’s hand is natural aspiration catheter . . . better show restraint .

Posted in Uncategorized on October 2, 2015| 1 Comment »

“Oh , it’s a well recannalised IRA  and its flowing TIMI 3  as well.  Now, what shall we do sir” ?, An apparently worried senior resident queried after a second look at the images from a 8 hour old STMEI .Why you sound unhappy  man ?  As if recanalisation is an untoward event” ! I teased my resident !
and went on to ask . . .

What we mean by recannalised  IRA ? (Recan-IRA)

  • It is akin to natural or pharmacological angioplasty (or combination of the two )
  • It can be complete or incomplete from the IRA perspective.
  • It can either result in partial or fully salvaged myocardium.
  • It should be understood even a 30% recanlisation can result in TIMI 3 flow and result in near complete salvage
  • Even a 90% recannalisation may not accrue the same benefit if it has happened late. So its all in timing
  • Spontaneous recannalisation can some times even be  superior  to thrombus aspiration . However , some degree of residual thrombus would be present in most
  • Residual plaque burden is also an important factor that will decide the extent of angiographic recannalisation.
  • Some times the recannalisation  will make the vessel near normal with only luminal  irregularity
  • IVUS/OCT may provide accurate assessment of Recan-IRA , it’s is not logistically acceptable in STEMI setting.
  • After listening to my briefing on recannalised IRA , the fellow looked more confused than before. He bothered to ask again , what am I supposed to do once a well recannlised IRA is detected ?  Should I intervene or not ?

The term recanlised IRA generally convey a hemodynamic  meaning for a successful  early (natural plus or minus pharmacological ) reperfusion .If every parameter is fine , and the lesion is not significantly obstructing better to pause any further procedure ,  as consequences of deploying  stent in a well recannalised segment is not yet clear with a stro ng trend towards harm .The decision is to be taken on individual basis with reference to  symptoms, stability ,  residual ischemia and quantum of incomplete salvage and lesion morphology .

If you believe ,a spontaneously recannalised  IRA has provided a TIMI 3 flow , it is equivalent to well done job of natural thrombus aspiration by  a hidden hand and catheter . Consciously respect that .Most cardiologists would have  realised atleaset once ,  that any aggression on a God handled IRA can be counterproductive !

Is there a non academic angle to this issue ?

Undoubtedly yes , strangely  inspite of a positive phenomenon for the patient , recannalised IRA leads to a difficult debate  in cath lab .Suddenly , the  entire collective scientific wisdom of the cardiologist is put into a stress test. There is direct fight between reality , expectations .True patient benefits , obligations to hospitals , the parasitic  relations with device industry , do have a big say !

Final message

Practicing cardiology is simple , but when scientific and non scientific realities of life are in direct confrontation with patient welfare it becomes a huge struggle and only a determined few can win over this infinite fight against conscience !

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