Dr.S.Venkatesan MD

Calibrated PTCA guidewires : A simple Innovation can make cardiologist life lot easier !

October 13, 2013 by dr s venkatesan

It is estimated nearly half a million PCIs are done all over the globe every year .Evaluating diagnostic angiogram is a critical vital step, but often times it is given less time and left to fellows .This is done mostly offline by Image processing software. Curiously , lesion assessment becomes a causality to the visual acuity .It ends up with lot of whims , intuition and bloated egos of senior cardiologists !

Technical issues

The fundamental flaw in the lesion assessment is ,there is a dissociation in choosing the “best view” for lesion morphology and length . Size need not be well assessed in the same view as morphology . For example , LAD is fore shortened in LAO caudal view , length measurement would be erroneous , still morphology may be well delineated .(Vice versa in RAO caudal view )

Other source of errors

Reference catheter may be far away in the Aorta , and confer a magnification error . This becomes important especially in ostial lesions and associated major branch lesions. The computer uses the edge detection algorithm which carries an inherent error .

Advantage of guide wire as a scale

Instant online measurement
Always on . Repeatedly used in multiple views .
You can’t ask for more accuracy .The scale is within the coronary artery hugging the lesion
The end on view is effectively nullified .
Magnification factor do not operate.
Finally , and most importantly in complex tortuous , tandem lesions few mm errors can be disastrous .These calibrated guide wires will make our life lot easier.

Final message

Measuring a coronary lesion remains a delicate issue . If only we have radio opaque rings every 1mm or so in the distal end of the guide wire , we can measure the lesion instantly and most accurately.

This will definitely make our life not only simple but help our patients with accurate stent sizing and avoid costly geographical miss (or inappropriately long stent that increase metal load .)

After thought

I do not know whether any of the existing guide wires have this facility .(I guess it is not . . .then , let this idea be patented in my name !) After all , It is a mean task for all those mighty coronary hardware companies to add few radio opaque rings to all PTCA guide wires!

Medtronic, Abbot, Boston are you listening ?

And . . . your opinion please !

Posted in Cardiology -Interventional -PCI, carotid interventions | Tagged calibrated guidewires, coronary stenting, lesion length assessment, morphology of lesion in ptca | Leave a Comment »

Unusual tips in PTMC : How to cross a critically narrowed mitral orifice ?

October 12, 2013 by dr s venkatesan

Click over the Image for animation

Posted in Cardiology - Animations, Cardiology -Non coronary Interventions -PTMC, cath lab tips and tricks, PTMC -Tips and tricks | Tagged difficult ptmc, how to cross a crtical mitral stenosis, inoue balloon, mitral valve crossing, mitral valvotomy, percutaneous mitral commissurotmy, ptca balloon during ptmc, ptmc, subvalvular fusion in ptmc, tough ptmc | Leave a Comment »

Why we take LV end-systolic diameter(LVESD) in mitral regurgitation assesement ?

October 11, 2013 by dr s venkatesan

Regurgitant lesions of cardiac valves are often tricky for the heart . Myocardium shows “love- hate” relationship with these leaky valves. Some of them are “sort of” stress relievers for LV . A mild MR will make the LV comfortable in terms of wall stress. When the wall stress is reduced the contractility increases and LV EF may raise a little.Hence EF is never going to help us to assess true LV function in MR .

LV end diastolic dimension(LVEDD) is a preload dependent parameter .A patient with 6.5cm LV EDD may still have good contractility and he may reach even a 40mm LV ESD, implying an intact LV function.

LV function should be best assessed in systole .(After all , systole is the prime function of heart) .Further , it should be assessed when the LV is free from influence of the all loading conditions of heart . (Note : The initial part of systole depends on after load. As the systole progresses the influence of after-load lessens .In the pressure volume loop* , the point at which loading conditions are least operative is end systole.)

* Please realise , heart is a dynamic organ there is no true load independent point in cardiac cycle as pressure and volume are eternally coupled.

What happens in AR ?

The same rule applies for Aortic regurgitation, but the parameters worsen little later than that of MR. For same degree of regurgitant fraction MR will require early surgery than AR.The reason for better tolerablity of AR is due to largely intact LA function and compliance till very late stages of AR.(In AR- it’s single chamber volume overload , while in MR it’s two chambers !)

Final message

LVEDD is not used in assessing MR as it is a pre-load dependent parameter that will not reflect true myocardial function /dysfunction. LV ESD is fairly accurate measure of LV systolic function minus all loading factors .

Watch out for next topic

Vasodilator therapy in MR and AR : How is it different ?

Posted in Cardiology -unresolved questions, Infrequently asked questions in cardiology (iFAQs), Mitral regurgitation, rheumatic heart disease, valvular heart disease | Tagged cut off for lv esd 55 mm in mr ar, lvedd vs lvesd, mitral reguritation when to operate, mr vs ar operability, pressure volume loop in mitral regurgitation, why we take lv end ssytolic dimension for assessing lv function ? | Leave a Comment »

Future directions in cardiology : A land mark review by Valentine Fuster

October 4, 2013 by dr s venkatesan

Medical research often ventures into a directionless and meaningless exercise with or without intention .The reason is simple , unlike other fields, scientists enjoy the ultimate freedom of expression.

How to find genuine treasures from this chaos ?

We need people like Valentine Fuster ,

Here is link to the article in circulation 2011 which I consider a must read for all cardiologists !

Posted in cardiology journals, Cardiology research topics, Cardiology Risk assesment, Great Men in cardiology, Great websites in cardiology, history of cardiology, Land mark articles in cardiology, Top ten in cardiology | Tagged epidemic of cad, future of cardiology, global cardiology issues, land mark articles in cardiology, preventive cardiology, promoting global cardiovascular health, top articles in cardiology, valentine fuster | Leave a Comment »

What do you mean by adequate LV function . . .Doctor ? !

October 1, 2013 by dr s venkatesan

Many modern day cardiologists consider doing echo , a mean job and leave it to technicians and fellows . Final report often ends up with a cursory glance. The culture of reporting an important aspect of LV function is reaching a new low. It is common to find the following terminologies in the echo reports in many parts of the country* (Guess it is not used elsewhere ! )

LV function good
LV function adequate
Good bi-ventricular function
LV function fair

Among these , the term adequate LV function has caught the imagination of young cardiologists ! Especially , this description often appear in pre- operative screening echo for non cardiac surgeries .

Recently ,one of my patient asked me what do we mean by adequate LV function . I told him it means nothing . . . it’s all fancy words ! but , generally it is used to imply normal LV function . . . I clarified .

Think over for few minutes . . . what do we want to convey by calling LV function as adequate ?

Does it mean normal ? or Just less than normal ?

If adequate LV function is accepted , what is inadequate ?

Adequate for whom ? For the patient ? or for the physician ?

Adequate for daily activity ? or Adequate to with-stand the proposed surgery ?

Final message

Even learned cardiologists indulge in this term frequently . This is rather a fancy and unprofessional way reporting LV function . They pass this style to their residents as well para medics .Adjectives in medical science are not banished . . . but should be judiciously used . In my opinion the term adequate LV function should be removed from all echo labs . Youngsters please watch out.

Related links in this site .

LV ejection fraction fallacies

What is LV dysfunction ?

Posted in Cardiology -unresolved questions, echocardiography, LV function | Tagged LV ejection fraction, lv function parmeters, what do we mean by adequate lv function ? | Leave a Comment »

What are the patterns of RV enlargement in various clinical entities ?

September 30, 2013 by dr s venkatesan

Right ventricle is a passive venous component of the heart .It simply acts a transit pump for blood to reach the lungs.

It is true , RV is dispensable in many complex congenital heart disease as we can connect the great veins directly into the pulmonary artery by Fontan , Glean and it’s clones bye passing this chamber . Still , by no means the importance of this chamber is to be underestimated. RV dysfunction and failure is the key to survival many disorders.RV shock is is cause of sudden cardiac death in acute pulmonary embolism and RV infarction .

RV is an unique muscular chamber .It is more of a triangular shape. It has three different parts connected by three different angle .There is no true apex for RV , it is connected to Inflow and outflow in peculiar fashion .

In the following table I have tired to describe of how different parts of RV behave in various disorders.

Posted in cardiology congenital heart disese, Clinical cardiology, myocardial disease, Right ventricle | Tagged arvd, ebstein anomaly, epigastric pulsation with rvh, how is rv in various heart disease, infundibular dilatation, para sternal lift, parts of right ventricle, right ventricle, right ventricle in tof, rv in tricuspid atresia, rv inflow body out flow, rv morphology in various congenital heart disease, rvot dilatation | Leave a Comment »

Clark’s classification of congenital heart disease

September 30, 2013 by dr s venkatesan

Congenital heart disease (CHD) still constitute an significant subset in cardiology practice.The moment you ask how do you classify CHD to any cardiologist , the answer would come promptly as “cyanotic and acyanotic CHD “. Such is the power traditional clinical teaching .

There is a fundamental embryological and functional classification available put forth by Clark.It lifts our understanding about congenital heart disease to a different perspective. I wish,every cardiology fellow should know this.

Link to embryological classification of congenital heart disease .

A subset for cono-truncal anomalies is also available.

cono truncal anomalies embryology of heart

Reference

Clark EB. Mechanisms in the pathogenesis of congenital heart defects. In: Pierpont ME, Moller J, editors. The Genetics of Cardiovascular Disease. Boston, MA: Martinus-Nijoff; 1986. pp. 3–11.

Posted in cardiology -congenital heart disease | Tagged clark classification of congenital heart disease, classification of cono truncal defects anomaly | Leave a Comment »

Is RF ablation possible in Rheumatic Atrial fibrillation ? ?

September 30, 2013 by dr s venkatesan

No procedure is impossible in medicine . . . but it should be useful for the patient !

Where will you ablate ? What is the purpose ?

The much hyped* ablation of pulmonary vein is never going to help in rheumatic heart since arrhythmia focus occurs at random . How can you locate a focus of AF over a huge , scarred left atrium ? ( which looks like a lunar surface sprinkled with a rocky terrain ! )

Note the huge , scarred LA .It would

be a wild guess to locate the true focus

of AF . (Image source : http://www.e-heart.org)

So , the other option was disconnecting atria electrically . In the past surgeons advocated linear or multiple incisions as in Maze and Corridor procedure after mitral commissurotomy .This helped to a certain extent , still effective , organised atrial contraction was not restored in many.

Now , some electrophysiologists tried to do the same with catheters without much benefit.* Please realise , pulmonary vein ablation even in lone and ischemic AF is struggling with a concept collision !

Can Right atrial focus trigger and sustain AF in RHD ?

Autopsy studies reveal tricuspid valve scarring in 33% of all RHD .Since RHD is a diffuse process , RA lesions can be very well be the focus . It is not an easy task to identify the real culprit focus. So ,concentrating LA for ablation may end up in futility.

There are only few studies available on RF ablation in RHD .This one from Istanbul ,Turkey and it does not favor it as recurrence rate is still significant .

rf ablation in rheumatic atrial fibrillation

Final message

Approach to AF in RHD : Opening up the mitral valve (or replacing it ) and controlling ventricular rate with beta /calcium blocker along with adequate oral anti-coagulation substantially reduce the risk of embolic events .One may never need to contemplate restoring sinus rhythm in rheumatic atrial fibrillation.

http://www.ncbi.nlm.nih.gov/pubmed/19744884

Posted in Atrial fibrillation, Cardiology - Electrophysiology -Pacemaker, rheumatic heart disease | Tagged maangement of af, maze corridor surgery in af and rhd, ptmc plus rf ablation of atria, pulmonary vien isolation rheumatic af is useless, rf ablation in rhd, RF ablation in rheumatic mitral stenosis, surgical la ablaton for atria fibrillation, therapeutics in atrial fibrillation | Leave a Comment »

Enigmatic relation between LA blood volume and LV stroke volume ?

September 30, 2013 by dr s venkatesan

Normal left atrial (LA) volume is about 22ml/sq.meter body surfacearea at all ages.Maximum LA volume in physiology is about 46ml in females and 56 ml in males( Average 35 ml)

LV stroke volume for each beat is about 70 ml . . . so where does the remaining 35ml come from ?

Answer .

Pulmonary veins ?
Residual LV end systolic volume ?
Mix of the two ?

It is logical to assume about 35 ml of fresh blood from 4 pulmonary vein* rushes into LV with every diastolic cycle .It never stays in LA .It just uses LA as a transit route ,

*In diastole the four PVs,LA and LV all act like one single chamber .

Is this reasoning correct ?.

If we believe the continuity equation this explanation is correct . However still what we need to know the fate of residual LV volume (End systolic LV volume which is also about 35 ml that would be in queue for ejection into Aorta for the next beat !)

Further , we know the LV end systolic volume is not constant .During exertion it can reach negligible levels (<10 ml) .At times of vigorous contractions it can touch near zero as well . Then , It become vital for the pulmonary venous reservoir to be act as a major donor for LV blood volume for every ensuing beat.

If the hemodynamics of pulmonary vein LA interface is tricky even in physiology , one can imagine the complexities if the LV diastolic function and left atrial compliance is affected

Debit and credits of LV end -diastolic volume .

Let us assume LVEDV is about 1o5 ml .LA blood volume is roughly one third of LV volume .For every beat equal amounts of fresh blood from pulmonary vein . These two (LA+PV) adds to the residual blood in LV to make LVEDV 105 ml . From this 70 ml is ejected as stroke volume leaving behind 35 ml.

lvedv lvesv stroke volume wiggers cycle left atrial volume pressure volume loop residual diastasis

Image template from http://www.cvphysiology.com

Further questions

LA Chamber volume and blood volume need not be same .What I struggle to understand is , total anatomical LA volume measures 35ml , while the amount of blood it is supposed to hold is also about the same .Does it mean the LA is completely filled with blood . . . air tight !

Will the LA compliance make it accommodate twice or thrice the blood volume during exercise ?

What is quantum of residual end diastolic LA volume ?

Reference.(Normal LV and LA volumes )

Posted in cardiac cycle, cardiac physiology, cardiac volume, Cardiology -Hemodynamics, Cardiology -unresolved questions | Tagged cardiac cycle, componets of LV stroke volume, end systolic lv volume, la volume vs lv volume, relationship between la volume and lv volume | Leave a Comment »

Obesity paradox in CAD and CHF

September 30, 2013 by dr s venkatesan

Obesity is a major cardio vascular risk factor.We earnestly believe this by evidence from Framingham and other studies.However , epidemiological truths can be dissociated from individuals .

We now understand some of the obese patients fare better in CHF outcomes apparently because of the obesity ! Even patients who undergo PCI show some benefits.This concept is being proved in large data base of > 200,00 patients.

Possible mechanisms

The lay man’s logic may apply (Science hidden somewhere !) Obese persons have basically a large heart with better cardiac reserve and muscle mass .These hearts are pre-conditioned to extra burden of MVO2 in it’s life time . So it is able to tackle hypoxia better, takes more time to get fully exhausted .After all heart can consume fatty acids for it’s energy requirement.

Adipose tissue may also secrete favorable anti-inflammatory chemicals , though majority of adipocytokines are detrimental except adiponectin .Paradoxically the tumor necrosis factor TNF (Same as cachectin or Interleukin 6) is less in obese patients .

Reference