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Welcome to the  future of  valvular heart disease . This is just the beginning.Expect more dramatic break through  . (Already mitral valve prototype is in advanced stages of development .)

Currently we have two approved percutaneous aortic valves for use in isolated Aortic stenosis. The Edwards valve is popular in  USA  ( 2011 ) and Medtronic  is used extensively in  Europe (From 2007)

Though both valves appear suitable .There are major differences in the concept , design , and technique of implantation .

tavi edward sapiens vs medtronic core valve

Reference

Major  issues to be addressed. Late onset Para valvular leak :
Please remember, these valves are not sutured around the aortic annulus ,  which our surgeons do it meticulously . The force that keep the valve  within the  aortic root is nothing but the disease process itself . The stiffened, elastic aortic root .(Does it appear  foolish to expect the diseased  aorta to hold the valve in situ ? but that is the reality  ! )
If the aortic root  dilates  for  some reason  which is very likely in  atherosclerotic  process    the very foundation of valve is shaken and para valvular leak is certain.

Dear Cardiologist, why don’t you spare that extra minute in cath lab?

clock

Suddenly  . . .  a primitive ,  common sense based question is asked!  How many seconds are required to optimally dilate and deploy the coronary stent ?

This simple and elegant study from the prestigious CCI journal tries to answer.

cci journal ptca pci balooln inflation time

Highlights

  • 105 patients, 150 lesions , Three different stents were used
  • Cypher Select (55%)  , Xience V (30.%), Taxus Liberté (15.%)
  • Three  balloon inflation timing
  • 5, 15, 25 seconds
  • Complex lesion (B2) formed 26 %

balloon inflation time pci ptca

 

This paper concludes, duration of stent balloon inflation has a significant impact on stent expansion. Stent deployment for >25 sec is recommended.

It again keeps the vital answer to our guess! Can we inflate it for 60 seconds  ?

Final message

This seemingly simple paper conveys a strong message.

Time is every thing , . . . we have to be fast . . . where we need to  (Time is muscle)  and we have to be slow where we  need to*  

Reference

http://onlinelibrary.wiley.com/doi/10.1002/ccd.23343/abstract

Further questions ?

  1. Can post dilatation be as  efficacious   as that of  stent- balloon  dilatation ?
  2. In difficult lesions  , the sum of  “Pre  / Per / Post”  balloon dilatation  gives  us net inflation  time(NIT)  Does it  add any sense to our understanding of optimal stent deployment  ?

Answer

Each of the above can be important in diseased heart .The most important component seems to be Inter- ventricular  synchrony .This is closely followed by AV synchrony .In dysfunctional  ventricles Intra-ventricular  synchrony  also becomes important .In  structurally  normal hearts  none seems to be important  (This statement can be debated  )

VVI pacemakers causes  both AV  and Inter-ventricular (VV ) dys-synchrony

DDD pacemaker  may still  induce  Inter-ventricular ( VV ) dys-synchrony  whenever  RV is paced for any reason .This may happen up to 60 % of pace making time in real world.

Some more facts

*Chronic VVI pacing may  induce adverse  remodeling of both atria and may worsen LV dilatation. In contrast isolated chronic organic LBBB is well tolerated and with paradoxical septal motion rarely worsen the LV function.

**Please note the paradoxical septal motion , which is  noted in  all LBBBs is  same as inter-ventricular  dyssynchrony .

***Inter atrial synchrony is a less discussed issue .It becomes  important in diseased atria which manifest gross   intra atrial conduction blocks  , atrial inhomogeneity and AF .Onset and offset  of AF has a major impact in the way DDD pacing is going to fire .

This is an ECG of a 42 year old man .He was reported as  Left atrial  enlargement (LAE) and was referred for  echocardiography . His echo was normal . LA measured 2.5 X 3.1 cm .The consultant  called back the echo lab ,  to verify   the left atrial dimension .He thought he was very sure of LAE .It took  considerable time to convince him about the credibility  of the echocardiographer . He was  right after all  . . . still . . .  ECG was  also looked  convincing  for LAE !

left atrial  enlargement by ecg limitations sensitivity

left atrial  enlargement by ecg limitations sensitivity  echo la dimension

                         Is this phenomenon  of wide P wave with normal atrial dimension  common ?

Yes it is . It  underscores  poor sensitivity of ECG in the  diagnosis  of LAE .The P wave abnormality in the above patient is due to Inter atrial block (IAB ) . This widens the p wave .

What  are the types of Inter atrial block ?

inter atrial block europace 1999 de luna

 

P wave widening is not synonymous with LAE .(Here P waves  widened   due to sluggish inter nodal pathway and inter atrial pathway .It is something like QRS widening in  bundle branch blocks  )

Final message

IAB is an important differential diagnosis for LAE . The significance of which is not entirely clear . It  is possible  IAB   precede LA enlargement  .It can even trigger AF due to  inhomogeneity.

Even though IAB was reported in 1950s  (Puech P* ) ,  it was  rarely  considered important With  increasing incidence of atrial arrhythmia in aging population , IAB is expected to  come into the lime- light again . The sophisticated electro anatomical mapping  can unravel the mysteries surrounding this entity .

Reference

INTER ATRIAL BLOCK

*Puech P. L’activite´ electrique auriculaire normale et pathologuique. Paris: Masson, 1956; 206.

http://www.jecgonline.com/article/S0022-0736%2812%2900227-0/abstract

http://europace.oxfordjournals.org/content/1/1/43.full.pdf

Bachman bundle branch block

Critical  and intensive medical care is meant for supporting  an  individual organ (or multiple organs )  at times of extreme distress ,  till the  healing process  prevails over .Later , the patient  shall be shifted safely out of the unit .

Whatever be the modern technology , the single most important factor that  determines the success of ICU outcome  lies within the  patient body ( One estimate says  patient factor constitutes almost  85-90% -Dukes medical center )

Ironically , the modern gadgets, drugs , devices  threatens  . . .  rather  fights . . . with this  inherent  patient fighting  mechanism . We will  never-ever know how many cellular switches are turned on by our biological high  command ,  that compensates  and tries to restore  body  homeostasis.

critical care unit icu ccu.jpg evidecne based medicine modern medicine

Here is a  personal experience with a patient management scenario in an ICU  . The  patient is none other than my father !

He  is a 82 year old man who has  developed a acute febrile illness which rapidly degenerated into  acute respiratory failure  and  X ray  showing  infective bilateral pneumonia  and  probable ARDS  .He was on ventilator for 4 days  and subsequently weaned  off but still  heavily dependent on oxygen . His lung is wet with crackles and wheeze intermittently . His cardiac function was excellent . In one of the episodes of hypoxia he  developed  , mild shooting of blood pressure and minimal ST changes .  Alarmed  by this he was started on  beta blocker , for the first time  . It  was titrated up to maximum doses for a suspected ischemic  episode .

It is  well-known , ECG changes are extremely common in hypoxia , tachycardiac  stressed individuals .

Sympathetic  blockade  is important , only  if ,  it is an inappropriate surge  . When the body fights a disease it is the only major biological weapon available to him .How is it justified to block it ?

When this was discussed with the  team they said they have no power to deviate from  protocol and there is one article , that says  BBs are  beneficial even in COPD !

The patient  continues to be in ICU dependent on oxygen with extreme  ICU fatigue  definitely worsened by the heavy dose of adrenergic blockers which is in my opinion delaying recovery !

Different   organ specialist are prescribing  drugs  according to their level of understanding  (evidence is always available for them  . . . some where )  and radiology fellows  keep taking  snaps of  distressed  organs  in various angles  in HD quality images . Meanwhile , CT scan  seems to have revealed a chronic  interstitial  process   . . . how to diagnose a chronic lung condition  in a man who is  yet to recover from major acute inflammatory lung Injury ! I do not know ? And the current development is they are considering disseminated tuberculosis !

You may a big physician , the patient  may be a very close family member  , modern health care  system makes you watch  helplessly once you hand over  patient to a   complex care  unit .

We hope for the  best .

Final message

               Medical practice  . . . however intensive the care may be  . . .   the bottom line is  . . . it  should be based on  common sense . Modern medicine  tends  to make  this faculty of our brain  blunted .

The  specialty of Intensivist   is largely  misunderstood  . It goes more with  satisfying scientific egos  and public  perceptions  rather than true patient needs .

We need not react to every changing parameter that emanates  from the modern machines  that  keep sending out live  data from a seriously ill patient ,  on a moment  to moment  basis ! (We simply do  not need that ! If only a pilot  reacts with  jitters to every air pocket turbulence ,  he will  not reach the destination safely  ! )

From a cardiologist perspective ,  the humble  request  to all Intensivists   and critical  care physicians   is ,   avoid being  in  “fire fighting mode”   for all  those subtle ECG changes  that occur  in ICUs ,  especially with multi- system disorder (Caution : Acute coronary syndrome in CCU / post PCI  set up   is different story altogether where even a minor ST shift can be significant ! )

Heaven’s  sake  let us  rely more  in  our  brain rather than  the machines and devices !

Above story is not even a tip of an Iceberg . I come across it  every day  in  many ICUs  I visit  . The  most saddening aspect  is ,  we can not point out these mistakes  to our fellow professionals ,  as it  amounts to   hurting academic egos .They are more important  than patient care at any given point of time !

Counter point

For any system to work  , it  needs  a  strict set of guidelines ,  other wise the system of care will fail. This is a  fundamental basis on which modem medical  care works . The only issue is ,  we  should keep checking for any inadequacies in the evidence base and try to correct it. So do not blame the  EBM . It has come to stay .That is the future ! You are very pessimistic towards  modern science !

Rapid response to counter point

But the real issue is  . . . by the time next evidence base finds a major flaw  in the existing system of care ,  damages are already done . So with your clinical acumen  every learned physician is free to create  his own real world  experience .(That is also called Level 3 evidence now ) ** Protocols are not  sacred sermons . It  may  be (rather must be !)   violated if there is a need for the benefit of patient .

Disclaimer

* This is not an  attempt to disgrace the concept  of intensive  medical care . Please remember ,  finding fault  could be same as finding facts .(At least in   medical care )

 

Update ( February 24th, 2013  Sunday , 12.05  AM )

After 25 days of  intensive and aggressive  medical care   we lost one of the great lives

of modern times  which will be celebrated by his  sons and daughters forever !

pericardial fluid in plain xray chest xray chest roentgen

How  did the  pericardial  fluid became radio opaque ?

Add PollGreat journals in cardiology american physiological review heart and circulation

http://ajpheart.physiology.org/

americal  journal of physiology

Many of the wonderful breakthrough articles are totally free . Enjoy and enrich .

Anterior  mitral leaflet (AML)  is an  unique structure  in the heart .It is the fastest moving structure inside the heart . It is the first structure visualised by echocardiogram by  Elder and Hertz in early 1950s .

While AML is known for vigorous motion , the PML motion is subdued . By tradition AML shows a  motion which resembles alphabet M .

But AML is not be taken lightly .  It can change it’s  motion  not only  in pathological states but also in health . One such  pattern is trifid   motion of AML . Following is a Echo Image in  a  perfectly  normal Individual .

mitral valve motion trifid m pattern  in m mode echocardiography

mitral valve motion in m mode echocardiography trifid

Possible mechanisms underlying Trifid motion of AML

  •    The plane of  M-mode cut  will change the  mitral valve motion .(May  be this is most common ).M-mode at tip of mitral valve may be trifid  ,however a little beyond may record a  bifid-M pattern .
  • Redundant  mitral valve
  • Mid diastolic AML drag
  • Signs of elevated   LVEDP
  • Finally ,  it could be a   sign of  mitral valve  fatigue after excrcise  . Some of these persons   revert back to M pattern after a brief period of  Trifid motion following exercise .

Does trifid AML motion  result in Tri-phasic doppler  flow as well ?

Mitral valve filling is classical E and A .

This usually correspond to M pattern of anatomical  AML motion .

Do the anatomy goes hand in hand with physiology ? Will the mid diastolic  AML  drag result in augmented flow ?

We are looking  at this phenomenon .

It was in 1984   this paper came from mayo clinic proceedings .

Hagen PT, Scholz DG, Edwards WD. Incidence and size of patent foramen ovale during the first 10 decades of life: an autopsy study of 965 normal hearts. Mayo Clin Proc. 1984;59:17-20.

When interventional   cardiology was not even in infancy . Now it remains the only data base of nearly 100o hearts  studied  after autopsy .

After reading the article  I got  few surprises

  • The mean  incidence  is 27.3 % of general population ( That is  27 crore people with PFO  in India )
  • In first three decades it goes up to 40 % .
  • PFOs size increase with age  due to stretch of inter atrial septum
  • It measures 3.4mm  in the first decade and it can grow up to 5.8 mm in later decades .

http://download.journals.elsevierhealth.com/pdfs/journals/0025-6196/PIIS0025619611632606.pdf

Mayo clinic continues to be pioneers in  providing vital  research about PFO

Following  is another excellent review article  on PFO and stroke

patent foramen ovale and stroke

world congress cardiology dubai  3  2012

Abstracts  published in Circulation 2012

http://circ.ahajournals.org/content/125/19/e741.full.pdf+html?sid=94b7a220-982f-4cfe-9792-8c7087dc046d

Paper 1

Echocardiographic IVC diameter: a simple, bedside guide to monitor fluid therapy in right ventricular infarction

Sangareddi Venkatesan1,*, G Gnanavelu1, M.S Ravi1, V.E Dhandapani1, G Karthikeyan1,D Muthukumar1
, Madras medical college, Chennai, India
Introduction:

Right ventricular infarction (RVMI) is one of the unique subsets of acute coronary syndrome. In RVMI augmentation of RV preload with fluids is considered vital. The seemingly paradox of raising the already raised RVEDP and RAP is often a risky hemodynamic adventure .There is no simple guide to monitor fluid therapy in RVMI.

Objectives:

In this context, we reasoned, a simple estimation of IVC diameter and it’s respiratory variation would give an accurate reflection of volume in the right heart chambers Methods: 12 patients with established RVMI by clinical, ECG criteria were the subjects of the study. 6 had associated posterior MI, 3 had lateral ST elevation. Patients were treated as per STEMI protocol .10 were eligible for thrombolysis.The mean blood pressure on admission was 106(70 -120mmhg)
During thrombolyis the blood pressure fell by 5–10mmhg .All patients were administered IV normal saline to augment the blood pressure. 1000ml were given over 1 hour and if the BP was  not raising another 1000 ml was infused in the next 1 hours . Results: Bedside echocardiography  was done on admission and was repeated during and/or after fluid infusion. The  baseline IVC, RA, RV were dilated in 9/12 patients. The mean RV dimension was 2.8cm (2.4 –3.6) RA -3.9 cm(3.6–4.5) The mean IVC diameter was 2.1cm (1.4 –2.6). On completion  of 1000ml fluid infusion, the mean IVC diameter was 2.5(2.3–3.0) .In terms of absolute size,  IVC increased by 3–5mmin diameter at the end of fluid infusion. It amounted to 20–30%  increase of diameter. There was minor increase in RA and RV dimension also. When there
was  30% increase of IVC diameter, JVP became non pulsatile and four patients showed  signs of lung congestion. There was a new reversal of E:A ratio in the mitral inflow in 2 patients  who had lateral ECG changes .There was no significant increase in RV dp/dt following fluid administration. The TR jet derived peak RV pressure did not show significant difference with  reference to fluid therapy. The mean LVEF was 44%(38–62%).

Conclusion:

Simple bedside estimation of IVC dimension by 2D echocardiography, can provide a fairly accurate estimate of  volume status of right heart chambers .Careful monitoring of IVC size help us, in the fluid  management of RVMI. One rule of thumb is an increase of IVC diameter by 30% from its basal  value could be a cut of point for termination of fluid infusion.

world congress cardiology dubai  5  2012 world congress cardiology dubai 2012

Paper 2

Circulation. 2012 125 e741e925  venkatesan  sangareddi madras medical college

Echocardiographic evaluation of papillary muscle function in ischemic mitral regurgitation
Muralidharan Azhakesan1, Venkatesan Sangareddi1, Jai Shankar1, Rudrappa Arunagiri1, Kalyanaraman Kannan1,* and Prof R. Alagesan,Prof P. Arunachalam, Prof V.E. Dhandapani, Prof M.S. Ravi.
1Cardiology, Madras Medical College, Chennai, India
Introduction:

Ischemic MR has been attributed to dysfunction of papillary muscle .The  experimental and clinical data emphasize the importance of changes in the geometry of the LV.
Objectives:

To assess the mechanisms of ischemic mitral regurgitation in patients with old  myocardial infarction Methods: The study cohort comprises 30 consecutive patients with old  myocardial infarction and Mitral regurgitation. Group 1 has old inferior wall myocardial  infarction and Group 2 has old anterior wall myocardial infarction. Patients with increased left
ventricular sphericity belong to Group Ia and with normal left ventricular sphericity belongs to  Group Ib.Echocardiographic evaluation of all patients was done using Philips iE33 machine.
Results:

The incidence of moderate to severe mitral regurgitation is high in group Ia and II  compared to Ib(50%and 40%vs. 20% p0.01). The average left ventricular sphericity is high in group Ia compared to group Ib & groupII (66%VS 49.1%&58.2) .Mitral annular area is  increased in patients with moderate to severe mitral regurgitation than patients with mild mitral
regurgitation (46.8mm vs. 41.2mm, p0.01). The incidence of MR in patients with increased  LV sphericity to normal LV is 50% vs. 20% p0.01. In all groups of patients, the leaflet  tethering distance with moderate to severe MR compared to mild MR is 24.09 mm Vs. 17.84 mm [P0.01]. The papillary muscle systolic peak velocity does not have consistent
correlation with ischemic mitral regurgitation in all groups. In group Ia papillary muscle systolic  peak velocity has linear correlation between mild and moderate to severe ischemic mitral regurgitation(5.98m/s vs 7.9 m/s.p0.05)

Conclusion:

1. Mitral leaflet tethering distance is consistently directly proportional to severity of Ischemic mitral regurgitation. 2. Papillary muscle  dysfunction is not an independent determinant of ischemic MR in all cases.

References:
Burch GE, De Pasquale NP, Phillips JH. The syndrome of papillary muscle dysfunction. Am Heart J 1968;75:399–415.
Kaul S, Spotnitz WD, Glasheen WP, Touchstone DA. Mechanism of ischemic mitral regurgitation. An experimental evaluation. Circulation 1991;84:2167– 80.
Matsuzaki M, Yonezawa F, Toma Y, et al. Experimental mitral regurgitation in ischemiainduced papillary muscle dysfunction. J Cardiol 1988;18 Suppl:121– 6. Kono T, Sabbah HN, Rosman H, et al. Mechanism of functional mitral regurgitation during acute myocardial ischemia. J Am Coll Cardiol 1992; 19:1101–5.

world congress cardiology dubai 2  2012

Cardiac failure following VVI pacemaker, a myth or reality: an echocardiographic study and an indian perspective
Arun Ranganathan1,* Venkatesan Sangareddi, Gnanavelu G, Dhandapani V.E., Ravi M.S. 1Cardiology,

Madras Medical College,Chennai,Tamil Nadu,India, Chennai, India
Introduction:

Permanent pacemakers has revolutionized the management of symptomatic bradyarrhythmias. In India, about 10000 pacemakers are implanted every year. There is a huge  cost variation between modern day pacemakers and conventional pacemakers. The apparent  advantages of newer generation pacemakers over conventional pacemakers are not  clear.There has been some concern about development of cardiac failure with VVI pacemaker1. We have already reported the incidence of cardiac failure with VVI pacemaker from our registry  which was surprisingly negligible. In this context, we studied bi-atrial and left ventricular function in patients following VVI pacing.

Objectives:

To Assess Biatrial And Left Ventricular Function In Vvi Pacemaker Implanted Patients. Methods: 31 patients were randomly selected from a group of 526 VVI pacemaker implanted patients of duration more than 6 months with
mean 50 40 months.The shortest duration was 6 months and longest was 185 months. Of the 31 patients,17 were males and 14 were females. The indications for VVI Pacemakers were complete heart block (22 patients) and sick sinus syndrome(9 patients). Patients who sustained MI, valvular heart diseases, cardiomyopathies and who had RWMA were excluded from the study. 31 persons of similar age and sex distribution without pacemaker were included in the
study as controls. All selected patients including controls underwent ECHO, ECG.

Results:

In VVI  group there was no significant reduction in EF and LA volume index,but mitral E/E’& RA volume index were reduced significantly. Paradoxical septal motion(PSM) did not influence any parameter.
Conclusion:

Contrary to the popular belief, VVI pacemaker was not associated with worsening LV function and left atrial dimension in our study. But there was a marginal deterioration in LV diastolic functional parameter.There was no significant impact on the quality of life indices, and no adverse outcome observed.We believe VVI pacemaker would continue to be safe and effective for our population.The usage of dual chamber pacemaker may be selectively used and need not be recommended routinely.
Reference:
1. Nathan AW, Davies DW. Is VVI pacing outmoded? Br Heart J 1992; 67: 285–8.

world congress cardiology dubai  4  2012

Changing angiographic CAD profile in young STEMI population
Venkatesan S. Sangareddi1, Pattanam S. Chakkaravarthi1, Srikumar Swaminathan1,* 1Department of Cardiology,

Madras Medical College, Chennai, India
Introduction:

Previous data on young patients with acute myocardial infarction have indicated  higher rates of normal CAG. Incidence of normal CAG in young STEMI is reported to be between 40–50%. There was a suggestion of decline in normal CAG in young STEMI .In this context, this study was planned.

Objectives:

The present study was conducted at madras medical college, Department of Cardiology, Chennai to assess the incidence of CAD in young diabetic post myocardial infarction patients in the urban and suburban populations of Chennai.
Methods: Angiographic data of 80 consecutive young patients with MI were studied Patients  who were nondiabetic,more than 40 years old and not thrombolysed were excluded.

Results:

out of 80 patients 74 were males and 6were females.25% of patients had normal LV function and75% had mild LV dysfunction. All are having DM and 30% are having HT and 40% are smokers In our study 20%of patients with inferior wall MI and 80%had anterior wall MI. CAG was performed on a mean average of 4 weeks after the index myocardial infarction and optimal medical treatment. Of the 80 patients 75%(60) had coronary artery disease and the remaining
25 %( 20) had normal coronaries .Of the 60 patients with CAD, 52(65%) patients had single vessel disease, 4(5%) had double vessel disease and 4(5%) had triple vessel disease.LAD lesion was present in 46patients and RCA lesions found in 16 patients. This made us to think why there is a higher incidence of CAD in these group of patient’s .Physical inactivity has become rampant due to high degree of automation. Diabetes added to this physical inactivity accelerates atherosclerotic process. So these patients might have had CAD already and myocardial infarction might have occurred as an acute insult .More lesions were found in atherosclerotic prone LAD than RCA.

Conclusion:

According to our observation, it seems, CAD in young is taking a different avatar compared to what we have witnessed few decades ago. The incidence of normal coronary arteries following a STEMI is distinctly reduced. While most
have critical SVD, significant subset do have extensive mutivessel disease. We suggest this changing angiographic profile need to recognized and looked for in different geographical locations of our country. It would have major management implication.
Reference:
1. Changes in CAG in young MI patients-Branco LM, Patriciol, Port Cardio 2001 Oct;10(10)
749–55.