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Archive for January, 2013

pericardial fluid in plain xray chest xray chest roentgen

How  did the  pericardial  fluid became radio opaque ?

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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 .

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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 .

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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

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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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We always look at the thickness of  Inter ventricular septum for LVH . The Normal IVS thickness is up to 11 mm in diastole .  LVH is definite if IVS measure > 11 mm .It is  certain if it is > 12mm . But , we need to realise LVH by definition is not simply wall thickness .

It is increased LV  mass .

LV mass can increase without wall thickening . This is  referred to eccentric LVH . For example in chronic  volume overload  states  (or even DCMs )  LV mass may increase without septal thickneing .

Final message

LVH is possible without IVS thickening .

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We know q waves are not synonymous with Infarct . It just represents electrical activity going away from the electrode.This is why it can occur  even in physiologically in many leads.

Non  infarct Q wave can be recorded with

  • LVH
  • Fibrosis
  • Fluid/Air in beneath  the recording lead
  • Thick chest wall/pericardium (More often Poor  R wave )

rv cavity potential in inferior leads mimicking inferior mi q in

When a chamber enlarges (Any chamber )  it is  brought near the chest wall the electrode may pick up the intra cavity potential that is recorded as q waves .

(The q wave in V5-V6 in severe volume overload of LV may represent LV cavity potential )

Similarly qR complex in severe RV  enlargement  in V1 represent RA cavity potential.Right ventricle is anatomically a difficult chamber to understand. It is located anterior below the sternum  the inferior and posterior aspect of the RV  is facing the diapharagmatic  surface

copd ra rv enlargement mimic inferior mi q waves in 2 3 avf differential diagnosis

In huge RV enlargement , RV cavity potential or( even RA )  can be picked up by limb leads . While cavity potential is well picked up by unipolar pre-cadial leads , it is uncommon for limb lead  record  intracavitory  potential. However  this patient , who was diagnosed  as inferior MI by a  resident ,  turned out to be a clear case of severe  pulmonary hypertension due to  COPD .

Final  message

One  more differential diagnosis for  inferior MI in ECG  exists. A grossly dilated RA, RV due to COPD  with  severe  pulmonary hypertension.

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