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Archive for the ‘My presentations’ Category

pci  powerpoint presentation ptca follow upFile1-PCI 5

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Note : The contents are prepared in 2006 .Recent input are to be added .

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Is Transient Ischemic attacks (TIAs)  belong to the  exclusive domain of cerebral circulation ?  Can it occur in the coroanry arteries ?  If so what situations ?

This is a presentation in one of the cardiological society of India annual scientific sessions . A pdf download is  provided

transient ischemic attacks attack of heart coronary tia

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Can VF be a non sustained  arrhythmia ?   This question was raised and a single case report was presented

in the annual scientific sessions of  Cardiological society of India Meet in  year 2008 in  Chennai.

I am just reposting it from my archives .

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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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This was presented in the cardiology fellow training course in Chennai – March 2012

(Acknowledgement : Paul wood collection , J.K Perloff , Credit to Images from open source )

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It is well  recognised for STEMI  to get aborted   spontaneously or through intervention.

Can a glamorous procedure like  Primary PCI be redundant ?

Yes of course . This paper,  is about how a planned  Primary PCI  can go awry  . . . Presented in the Annual scientific sessions of cardiological society of India Kolkatta December 2010.

Down load full presentation  in PDF format (primary_pci_)

Summary of the presentation

ABORTED  AND     ABANDONED    PRIMARY PCI

S.Venkatesan  G.Gnanavelu.R.Subramanian .Geetha Subramaninan

Madras Medical College. Chennai

Primary PCI has become the  standard of care  for acute STEMI in all  those eligible patients. Apart from the individual & institutional expertise ,the  key  to success  lies in  expediting   the symptom to balloon time to less than an hour.

Even though  STEMI   is characterized  by  acute total obstruction , it  is also a fact during this critical time window , a less recognised   positive  phenomenon takes place within the  ill fated coronary artery. Intrinsic fibrinolytic activity gets activiated and begins to take on the thrombus head on .It should be recalled this is the  earliest intervention in STEMI by natural forces , with zero time window . The power of this natural lytic process has  never  been easy to predict and quantiate . But  we  have  often realised  such a phenomenon do occur often and  is referred  by  various  terminologies like spontaneuous  thrombolyis, aboted MI etc .The exact incidence  is not estimated .In this era of  primary PCI we have found a new opportunity to confirm  this concept.

It has been  observed during  primary PCI ,  an occasional patient  may  have  either  a totally  patent IRA  or a minimal &  insignificant lesion  like luminal irregularity .This has  subsequently led on to cancellation of the procedure .We report our experience with  two patients with  this particular situation .One patient with IWMI with a time window   of  6hours had a totally patent  RCA.  Even , the luminal irregularities were difficult to locate .The other patient had anterior MI with ongoing ischemic pain.He was taken up for primary PCI.The initial angiogram  showed a total mid LAD  obstruction . As soon as the  guidewire reached the thrombotic lesion the  artery opened up   wth a TIMI  3 flow .There was no residual lesion or thrombus  noted. Both of the above  patients  were  young , smokers . 2b 3a antagonists were not administered. We infered, both had thrombotic STEMI and   presumed  to  had either spontaneous reperfusion , or  reperfusion assisted by dye injection & guidewire manipulation. They were  shifted out of cath lab with a new code of aborted primary PCI and  were discharged with normal LV function .It need  to be  realised here, a   distinction must me made between  aborted PCI  and   abandoned or failed  primary PCI  as  the later  connote a negative outcome. The  causes for abandoning  primary PCI are due to complex  lesions like bifurcation /Trifurcation lesions , triple vessel disease  with difficulty in identifying culprit lesions.A  Primary PCI is  considered failed  when the  IRA patency  is not accomplished or  failure to  sustain myocardial flow inspite of  IRA patency (No-Reflow) . These patients may end up in CABG or occasionally fall back on  thrombolysis  which was considered a inferior modality just few hours earlier !

.                                         We conclude , in the management of STEMI ,  primary PCI once contemplated need not always reach it’s  logical conclusion. There are situations  it can  get  aborted or abandoned  at various levels . Aborted  primary PCI  due to spontaneous  lysis though uncommon ,  can be a therapeutically and financially rewarding concept for the patient  and  physician .

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How will you refer to a ventricle which is not dilated but still has severe global contractile dysfunction ?

Traditionally cardiomyopathy is classified as

  • Dilated (DCM)
  • Hypertrophic(HCM)
  • Restrictive (RCM)

But there is large group of pateints who do not show any of the above features and still have global hypokinesia  contractile dysfunction. this group has been largely ignored .It could constitute up to 25%of all cardiomyopathy.there can be some overlap between non dialted cardiomyopathy and RCM.

We report our experience here with

non dilated cardiomyopathy click to download PPT

non dilated  cardiomyopathy

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