Posts Tagged ‘dr venkatesan’

Evidence-based medicine (EBM) is being projected as a scientific God’s secret specialty. Physicians who don’t follow EBM are considered unfit non-professionals. Presumably, in pursuit of truth, all those glamorous official bodies in cardiology bring out umpteen number of protocols, guidelines, advisories, and recommendations.

The blueprint for EBM

We have the famous 3 levels of recommendation backed up by different levels of evidence. Many of us trust these as the jury’s final verdict for most illnesses in cardiology. I would like to bring one particular issue about this hugely popular model of EBM. It is about one specific class of Indication referred to as 2b. The other day, there was an intense argument for an ICD in a young HCM patient and CRT in DCM based on this 2b stuff. Kindly request all of you to pause for a moment and introspect. We can realize, class 2b plays a mischievous game in EBM with the English language “may and may not”. It tries to push subconsciously an interventional bias from equipoise, in spite of lack of good evidence and clear divergence of opinion and a possible trend towards harm.

Further, there is widespread reluctance in many cardiac workgroups to refer class 3 recommendations as an absolute (or at least relative contraindication) It was strange to note one of my colleagues argued that,  class 3 is also a fair recommendation, to accept or reject is in our domain. I was initially shocked to hear that but had to agree with him ultimately as we realized a significant chunk of interventions we do, like delayed PCI > 24 hrs, CTOs, and chronic stable belongs to the proud class 3 recommendation. The debate came to a funny end when a senior cardiologist confessed somehow class 3 seemed to be a lesser evil than even class 2B.

Final message

For the sake of our patients, we need to bring an urgent reform in the EBM. Let us merge class 2b with class 3 and put it in a single basket and keep it out of reach to all tempting stakeholders. We shall display only class 1 in our therapeutic showcase.


(*Dynamic recommendations is the norm in science, as we accumulate evidence with time.. Agreed, let us do this silently in research labs. Don’t bring it to practical guidelines. No, can’t agree. Freedom to indulge with an experimental modality in a no-option patient must always be there as we are able to give the benefit of doubt to these helpless patients. This is a valid argument but we must not forget even in dire situations  good option need not be a compulsive action, it can be in action as well)



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world congress cardiology dubai  3  2012

Abstracts  published in Circulation 2012


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

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.


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%).


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

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.

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.

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)


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.

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

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.


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.


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.

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.
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

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.


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.


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.


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.
1. Changes in CAG in young MI patients-Branco LM, Patriciol, Port Cardio 2001 Oct;10(10)

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