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                                Acute coronary syndrome (ACS) is currently classified as STEMI and NSTEMI.This classification came into vogue  primarily to  triage patients for thrombolysis eligibility , as ST elevation is the  only criteria for thrombolysis.The  earlier term  non q MI  is largely used  to denote the  present day NSTEMI. In the past q  MI was referring to transmural MI non q MI  to non transmural  pathologically.(Of course , now we know  the relationship between q waves and transmurality is not good )

So when can we still use term non q MI ?

These terminologies of STEMI and NSTEMI are made on admission  at the emergency room.  ACS being a dynamic entity these  patients can  have rapidly changing  ST shifts , from depression to elevation and vice versa. Fresh T wave changes can also occur .Q waves  may or may not develop ,  depending upon the damage sustained to the myocardium and the efficacy of thrombolysis / PCI. So it should be emphasised here STEMI,  NSTEMI ,  q  MI ,  non q MI are the  descriptions of the  same group of patients in different time frames. The common mode of  evolution  of  STEMI  is  to q MI and NSTEMI  into non q MI. Cross overs can occur.

 

 

 The problem here is NSTEMI getting converted into STEMI  is quiet common and has no nomenclature issues . But  when   STEMI down grades  into NSTEMI  there is apparent  nomenclature incompatibility .This category of  patients have  no other labelling option other than “A STEMI evolving into non q MI”. Because one can’t label  STEMI  evolving into NSTEMI as  many of  them  will  have a residual ST elevation as well.

What is the final message ?

The term non q MI is still relevant and is used at discharge , in a patient with STEMI when he or she evolves without a q wave .In the setting of unstable angina , NSTEMI has largely replaced  the term  non q MI either on admission or at discharge.

Before I close

                 The important point to remember here  is NSTEMI getting converted into STEMI  is an adverse outcome and  in fact, it is  a complication and the patient should get an immediate  thrombolysis or PCI , while a STEMI getting converted into non Q MI is generally a  major therapeutic success.( Effective salvaging and preventing q waves )

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   Dr. Venkatesan   Sangareddi  

AK 53/1, # 9

Narmada enclave

 7th main road

Anna nagar

Chennai -600 040

Tel:044 26209009

                        

 

Age &  Date of birth

42 ,               25-5 -1964

Experience

1998–2007                  Madras  medical college                      Madras 

Asst. Professor  Of Cardiology

Work involves  intensive coronary care, invasive and non invasive cardiology.  Has special interest in  clinical research in Acute Coronary Syndromes

Has    publications in  various  Journals.

 

1997-1998                   Madras  medical college                       Madras           

Asst. Professor  Of Medicine

Worked  in intensive care medicine and  in

 Medical oncology for 6 months

 

 

1994–1996                    Madras   medical college                        Madras 

Resident   Cardiologist

Selected to resident programme   toping the state   in the super speciality  exam

Presented  papers in national conferences

Experience gained in invasive and non invasive cardiology

 

1991–1994                      Govt.  Health  Centre           Karur.       Tamil nadu

Medical Officer   

Worked in internal medicine  department

Family medicine and community health care.

And   socio economic aspects of health care.

Education

1994–1997              Madras  medical college                               Madras           

Doctorate  in cardiology (DM) 

 

1988-1991              Coimbatore medical college                          Coimbatore

 

Doctor  of Medicine (MD) Dr.M.G.R  Medical university  , Madras

 

Secured  three  gold medals for excellence in cardiology.

 

1987-1988            Coimbatore medical college          Coimbatore  India

 

Junior resident in  Medicine

 

1987                     Coimbatore medical college          Coimbatore

 

House  officer

 

1982-1986            Coimbatore medical college        Coimbatore

 

M B., B S.    Bachelor of Medicine and Bachelor of Surgery

 

                             Madras    University                           Madras     

 

Interests

Electro physiology, expert systems in cardiology., clinical research  in acute coronary  syndromes, preventive cardiology,  bio ethics, outcome analysis ,  logistics in cardiology and publishing  online journals. 

 

List Of  publications

Enclosed

Reference

Prof.V.Jaganathan. MD.,DM

Professor  &  Head of  Department

Institute of Cardiology, Madras Medical College  Chennai

   

 

Address  for   communication

 

Spouse

 

 

 

 

 

 

 Dr.Latha  Venkatesan  MD . Gynecologist,

 Sundaram  Medical  Foundation, Chennai  India.

AK 53/1, Flat no A- 9

TAS Narmada enclave

 7th main road

Anna nagar

Chennai -600 040

Tel:        044 6209009

Mobile : 9840059947

E.mail : drvenkatesans@yahoo.co.in>

 

 

 

 

 

 

 

 

 

List of publications by  S.Venkatesan

 

 

 

1.QTc  Interval  in atrial fibrillation.  The Tamilnadu Dr. M.G.R Medical university doctorate thesis 1991

 

2 .Thrombolysis in hyperacute MI.

 Indian Heart Jr  1999:51: 321

 

3. Circadian  Response To  Thrombolysis  In Acute Myocardial Infarction Indian Heart Jr  1999:51:686

 

4. Left Ventricular Mass in Pregnancy Induced Hypertension.

  Indian Heart Jr.  1999:51

 

5. Dissection of  interventricular septum by unruptured  right  sinus of valsalva    aneurysm  resulting in complete heart block.

Indian Heart Jr  1995 Nov-Dec: 605

 

6.Angiosarcoma  of leftventricle presenting as hemopericardium and  cardiac tamponade. Indian Heart Jr  1995 Nov-Dec:636

 

7.Asymtomatic multivessel disease  following  myocardial infarction

 Indian Heart Jr  1999:51: 686

 

8. Transmitral pulse doppler echo correlates of mitral regurgitation severity Indian Heart Jr  1999:51:636

 

9. Safety and efficacy of intravenous nicorandil  in unstable angina. Indian Heart  Jr  1999:51:704

 

10. Efficacy of nicorandil as monotherapy in ischemic heart disease Indian Heart Jr  1999:51:728

 

11. Left ventricuar function by angiogram in significant LAD disease. Indian Heart Jr  1999:51:687

 

12. Aortic root dimension in isolated rheumatic mitral stenosis

Journal of association of physicians of India abst: 1998

 

13. Serum phosphate in acute myocardial infarction

Indian J Physiol  Pharmacol 2000  44(2):225-8

 

14.Differential  Response  to  right  and  left  coronary  artery  thrombolysis   Indian Heart Jr  2000:52:715

 

 

15. Therapeutic  issues  in  Stable Ventricular  tachycardia: A coronary  care  unit  perspective Indian Heart Jr  2000: 52: 808.

 

 

16.Current   cardiology  practice: evidence  or  experience  based ?    An  analysis of  ACC/AHA  guidelines. World congress of cardiology   2002 sydney  Oral  presentation.(Published in Journal of American college of cardiology)JACC :2001.39:9 Sup.B 462B

 

17.Isolated  Diastolic Hypertension .World congress of cardiology  2002 sydney  poster  presentation..

( Published in Journal of American college of cardiology) JACC :2001.39:9 Sup.B 175B

 

18.Rescue thrombolysis in  acute myocardial infarction

Journal of association of physicians of India abst: 2002

 

19.Canadian   cardiovascular  society  classification of  angina:

 An  angiographic  correlation. Indian Heart Jr Abstract issue 2001

 

20.Non invasive management  of high risk unstable angina

Accepted for oral presentation in cardiological society of India annual scientific session Kolkata  Dec2003

 

21.Non dilated cardiomyopathy

Accepted for oral presentation in cardiological society of India annual scientific session  Kolkata  Dec 2003

 

22.Safety and efficacy of angiotensin-converting enzyme inhibitors in symptomatic severe aortic stenosis: Symptomatic Cardiac Obstruction-Pilot Study of Enalapril in Aortic Stenosis (SCOPE-AS).
Am Heart J. 2004 Apr;147(4):E19

 

23.Rheumatic heart disease occurrence, patterns and clinical correlates in children aged less than five years.J Heart Valve Dis. 2004 Jan;13(1):11-4.

 

24. Estimation of subjective stress in acute myocardial infarction.
J Postgrad Med. 2003 Jul-Sep;49(3):207-10.

 

25. Serum phosphate in acute myocardial infarction.
Indian J Physiol Pharmacol. 2000 Apr;44(2):225-8.

 

26. Canadian Cardiovascular Society classification of effort angina: An angiographic correlation.
Coron Artery Dis. 2004 Mar;15(2):111-4.

 

Coming soon :

 

List of  top ten  leading famous  cardiologist  in india

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              Intra coronary thrombosis is the sine qua non of acute coronary syndrome ( Both STEMI and NSTEMI.) But thrombolysis is the specific therapy in STEMI and is contraindicated in NSTEMI/UA.

Why is this apparent paradox ? What is basic differnce between UA and AMI ?

In STEMI there is a sudden & total occlusion of a coronary artery usually by a thrombus with or without a plaque .The immediate aim is to open up the blood vessel . Every minute is important as myocardium undergoes  a continuous process ischemic necrosis. So thrombolysis (or more specifically fibrinolysis should be attempted immediately) .The other option is primary angioplasty,  which will not be discussed here.

The thrombus in STEMI  is RBC &  fibrin rich and often called a red clot. Number of fibrinolytic agents like streptokinase, Tissue palsminogen activator,(TPA) Reteplace, Tenekteplace etc have been tested and  form the cornerstone of STEMI management.The untoward effect of stroke  during  thrombolysis  is well recognised , but usully the risk benefit ratio favors thrombolyis in most situations except in very elderly and previous history of stroke or bleeding disorder.

Unstable angina is a  close companion of STEMI . Many times it precedes STEMI often called preinfarction angina. During this phase blood flow in the coronary artery  becomes sluggish gradually,and patients develop  angina at rest .But unlike STEMI there is never a total occlusion and myocardium  is viable but ischemic,  and emergency salvaging of myocardium is not a therapeutic aim but prevention of MI becomes an aim. It is a paradox of sorts ,  even though thrombus is present in  UA ,  It has been learnt by experience thrombolytic agents are not useful in preventing an MI .

 

Why  thrombolysis is not useful in UA ?

1.In unstable angina  mechanical obstruction in the form of plaque fissure/rupture is more common than completely occluding thrombus. So lysis becomes less important.

2. Even if the thrombus is present , it is often intra plaque  or intra lesional and the  luminal  projection of thrombus is reduced  and hence thromolytic agents have limited area to act.

3.Further in UA/NSTEMI since it is a slow and gradual occlusion (Unlike sudden & total occlusion in STEMI) the platelets  get marginalised and trapped within the plaque .Hence in UA  thrombus is predominantly  white  . Often, a central platelet core  is  seen over which fibrin clot may also be  formed.

4.All available  thrombolytic agents act basically as a fibrinolytic agents,  and   so it finds   difficult to lyse the platelet rich clot.There is also a small risk of these agents lysing the fibrin cap and exposing underlying platelet  core and trigger a fresh thrombus.This has been documented in many trials( TIMI 3b to be specific) So if we thrombolyse in UA , there could be a risk of recurrent ACS episodes in the post thrombolytic phase.

5. UA is a semi emergency where  there is no race against time to salvage myocardium .Administering a  stroke prone thrombolytic agent tilts the risk benefit ratio against it.

6. Among UA, there is a significant group of secondary /perioperative UA   due to increased demand situations. Here there is absolutely no role for any thromolytic agents,  the  simple reason is , there is  no thrombus to get lysed. 

7.Many of the UA patient have multivessel CAD and might require surgical revascualarisation directly .

 

So fibrinolytic  agents are contraindicated in UA so what is the next step ?

The emergence of  intensive and aggressive platelet-lytic agents.

A combination of aspirin, clopidogrel, heparin, glycoprotien 2b 3a antagonist formed the major therapeutic protocol in these patients.Even though these are called antiplalet agents some of them  like 2b/3a antagonist eptifibatide, tirofiban, and many times even heparin has a potential to dissolve a thrombus. So technically one can call these agents  as thrombolytic agents.

What are the unresolved issues

                                       Even though clinical trials have convincingly shown thrombolytic agents  have no use in UA .There is a nagging belief  THAT  there could  be group of patients  with UA , still might benefit from thrombolysis as total occlusions have been documented  in some cases with UA.This is  especially true in peri-infarction unstable angina (Pre & post) as there is a fluctuation  between total and subtotal occlusions ) .But bed side recognition of this population is very difficult.

Many would consider this issue as redundant now,  since  most of  these patients  are taken up for emergency revascularisations

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Recurrent myocardial infarction following an ACS is a fairly common clinical problem. Many times this is not recognised because it is difficult to establish the diagnosis.

The issues relevant here is

When does the first infarct (Index infact) process end ? and when the second infarct process start ?

Can the first infarct be a STEMI and the reinfarct be NSTEMI ? ( Dual acute coronary syndrome )

The only way to confirm a diagnosis of reinfarction is to document raising titres of cardiac enzymes and second peaking of CPK MB . New fresh ST elevation after a succesful thrombolysis is also a useful sign. But ST elevation in a q lead simply reflects a wall motion defect . So it requires enzymes to confirm it.

When there is tachycardia the ST segments tend to elevate following MI.

Other confounders are Infarct expansion and infarct extension .

These are macropathological entities almost impossible to dignose with surface ECG. What we diagnose as re-infarction could be an infact a infarct expansion.The modern terminology for infarct expansion is ventricle remodeling .The extreme remodeling results in ventricular aneurysm .Adverse acute ventricular remodeling can closely mimic a reinfarction .

What is clinical relevance of diagnosing reinfarction ?

Nothing great !

In modern day cardiology it is not a bother whether the infarct is expanding, extending or reinfarcting !All one has to do in a patient with chest pain ,showing a fresh ST elevation following STEMI is to take him/her to cath lab .

The only issue here one has to remember there are mechanical cause also for ST elevation following STEMI .

Dr.S.Venkatesan,Madras medical college, Chennai.

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LV clot formation is one of the important complications of acute myocardial infarction. Preventing this is difficult and managing this problem is still more difficult.Some of these clots are linear and laminar along the shape of LV apex and carry less risk of dislodging.

 While mobile LV clots , even if it is small can cause a embolic episode. Most of these patients have a significant LV dysfunction and they are candidates for early CAG and revascularisation. Even If the coronary anatomy is very ideal for a PCI these patients are often sent for CABG and physical removal of LV clot . If  only ,we have an option to remove these LV clots by a catheter based modality, we can offer them a totally non surgical cure.

This is not impossible,  considering  we are in the era of percutaneous implantation of prosthetic valve in Aorta ! The only issue is potential embolism into carotids and periphery .A temporary distal protection at the level of aortic root will prevent that .

Device companies shall produce one such exclusive catheter system to remove LV clot.

Dr .S.Venkatesan, Madras medical college, Chennai,India

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Thousands of dissections happen in cath labs  all over the world every day  very rarely it is painful . The answer is not clear. Both have rich vasa nervorum. Aortic dissection  involves media and smooth muscle . Coronary dissection may also be a  equally painful  , probably we are not recognising it ! or we attribute   all  chest pain in ACS  to ischemia .

Deep dissections into the smooth muscle should be painful.  Type c nerve fibers carry pain signals from heart

Answers welcome.

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