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Posts Tagged ‘madras medical college’

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.

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Here is a  video recipe  !

Please click here to  see more videos from my you tube site

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A  good collection of resources dedicated to cardiology

http://www.touchcardiology.com/articles/primordial-prevention-cardiovascular-disease-the-role-blood-pressure

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cardiologist Is he a person who puts  a   metal coil  coated with a synthetic fungus   in  a   incidentally  detected  block  inside a  small coronary artery and sends the bill to the Insurance company ?

Is he a person in a  cosmopolitan  hospital  who opens up a    chronically   closed  coronary artery , in an asymptomatic patient  and  live telecasts  his achievement trans continentally ?

Is he a person who   checks in by  the early morning flight and  puts multiple wires in  an  aged   patient   with  class 3 heart failure and  make  him walk  20 meters extra at a cost of  1000$ / Meter ?

Is he a person living in   Wall   street  ,   who   looks  for variety of holes In  the heart and trying to occlude  it  with   exotic   devicespci ptca stent

Is he the unknown   physician   who Intervenes in the natural history of Rheumatic heart disease   and arrests   immune mediated   valve damage by giving the  monthly injections  penicillin in remote parts of our country ?

Is he the person   who   Intervenes to prevent young   persons   from  smoking and help maintain  their  coronary endothelium  enriched with nitric oxide  & arrest  the coronary epidemic ?

cardiologist 2

Is he the small town doctor  who  Intervenes  to treat a breathless cardiac failure patient  with  digoxin and frusemide  and  dramatically alleviate the  symptoms and  prolong the  life of our poor country men?

Is she the village health nurse from an inaccessible health  centre  located in a  hilly terrain ,  Intervening  successfully, by   pulling out  live babies  from  severely anemic pregnant  mothers with failing hearts ?

pci ptca cardiologist coronary angiograms

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Thanks to wordpress.This  blog has caught the attention of some professional sites.

I was interviewed   by Jodie Elrod on behalf  of   EP lab digest July 09 Issue

dr s venkatesan www.drsvenkatesan.com

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                                          CRT , cardiac resynchronisation therapy  is being  projected  as a revolutionary treatment for cardiac failure , where a failing heart is rewired electrically through multiple leads and make it contract  more effectively.The success rate of CRT was highly variable.The basic question here  is,  there should be a  significant  documentation of desynchronisation  prior to CRT , for resynchronisation to be effective. Further , the sites of  myocardial  stimulation ( Coronary sinus/LV epicardial) , dose of electricity and the sequence of stimulation and the  electrical delay  are very  critical. Achieving this into perfection  is not a simple job and is  real rocket science ! ( If we can achieve 5 % of what  the normal purkinje network do within the LV we can term it a huge success.) Let us hope we catch up with nature . Finally , it is ironical  the sites of LV pacing ,  electrophysiologists  select currently  is infact not selected by them but pre selected by the patients coronary venous anatomy ! .So as on date ,  one can imagine how scientific this treatment could be !

                                         Initially it was adviced for patients with only wide qrs later for even normal qrs patients.When people started using it indiscriminately  insurance companies started to rethink and thus came the   RETHINQ study in NEJM  and brought a full stop to CRT in normal qrs CHF.

How to identify who will benefit from  the costly CRT  ?

It is a million dollar question. So millions of dollars were spent to identify the correct tool to identify the true responders to CRT.Echo cardiography with sophisticated methods tissue doppler, tissue tracking and , 3 D echo ,velocity vector imaging were done .These methods are not only costly but also time consuming and  hugely expertise driven.

Does all this  efforts with  advanced echo techniques worthwhile ?

This simple question was addressed in PROSPECT study in circulation

Click to read the article

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                                               The superior aspect of   coronary sinus and a portion of the left atrium share a common wall .Embryological defects in this area result in a communication between left atrium and coronary sinus. This defect  descriptively called as unroofed coronary sinus .This entity is most commonly associated with persistent left SVC. Extreme form of unroofing is some times termed as absent coronary sinus.

How to diagnose it ?

A high degree of anticipation is necessary in all patients with ASD or LSVC. A dilated coronary sinus in routine echocardiography warrants full investigation. A contrast echocardiography with agitated saline injection in left cubital vein will clinch the diagnosis as contrast enters LA after opacifying the dilated coronary sinus. During  right heart catheterisation catheter course entering coronary sinus and  advancing into LA through the fenestrations (Unroofing)  will confirm the defect.

How do you classify unroofed coronary sinus ?

The morphologic type of URCS was classified as Kirklin and Barratt-Boyes

 Type   I, completely unroofed with LSVC;

 Type II, completely unroofed without LSVC;

 Type III, partially unroofed midportion;

 Type IV, partially unroofed terminal portion

What is the clinical relevance of this entity ?

This entity should be suspected in every patient with persistent LSVC, ( and LSVC should be suspected in every patient with ASD). The hemodynamics is that of an ASD but if sufficient mixing of LSVC blood and LA blood takes place the child will have mild cyanosis.Some times when the coronary sinus is totally absent it will present as a typical dusky ASD picture which can closely mimic a TAPVC clinically.

Surgeons have a greater role in recognising and treating this entity. A typical repair will be done like this

 

Links to some of interesting articles on this topic

Raghib circulation 1965

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