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Archive for the ‘Cardiology-Coronary artery disese’ Category

When a culprit thrombus keep the  myocardium as hostage . . . don’t storm the coronary artery  indiscriminately   !

When a single gun men  keeps 100 innocent people as hostages , threatening their  lives, rescue mission should start .No can can afford to wait. But, without knowing  the  culprit’s true nature the process of rescue mission is always going to be tricky .There are so many instances Newton’s third law  was reversed , when reactions  evoke more chaos  than the index action.

In the recent world terrorist events ,  the  rescue missions  were so delicate and  it was very  unfortunate we  lost  many   innocent hostages !  The reasoning is ,there  is no way we can avoid these. I wonder is it really true ? !

rescue missionNot all culprit lesions  are true ones.They simply threaten  our myocardium with  thrombus and plaques  in various forms .Don’t show aggression to pseudo threats  you may  ultimately end up with more damage.(What I call as crazy culprits!)

(  Read here , why unstable angina even though thrombus is sitting right inside the coronary artery attempting to lyse it causes more  damage !)

After thought

Iam sure ,bulk of  the Interventionists wouldn’t agree with this thought . They would decry , watching a person  silently when the myocardium  is on  fire is a serious crime !

But . . . we  need to  remember the process of extinguishing  the fire  with some more fire arms is a delicate game played in undefined  philosophical turf.

The only way to introspect  such events in life is , to accept any eventuality    arising out of “not pursuing”  a  presumed rescue mission with vigor. No need to be guilty about that,after all , it can be a myth !

Modern human cognition , growing with a staple  scientific  feed  on a 24/7  basis  is  unlikely to realise , restraint can be an effective tool  even in critical moments !

Oh,is all that I have  scribbled so far  is just a repetition  of 1000 year concept of  “Primum non nocere”

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This  query often  evokes  confusion  among fellows and General physicians .

              The answer is simple .Yes ,  you can.(With few conditions)

  • Thrombolysis  or PCI  is  done  with reference to  the  presence  or absence of ST elevation and chest pain.
  • If there is ongoing chest pain  and  significant new onset ST elevation  thrombolysis or PCI is indicated whether there is associated q  waves or not.

Clinical situations 

 Ischemic  q waves: Q wave can occur  with transmural ischemia which result in electrical stunning and loss of R waves . (Many of them  regenerate this R within few days after STEMI ,  indicating the q  waves can be  ischemic  in origin)

Reinfarction : Patients with  old  MI can develop fresh ST elevation  in q leads due to tachycardia and dyskinetic infarct segment .This group  of patients  should be carefully evaluated before labeling them as  re-infarction

* q RBBB in early hours of  anterior STEMI is fairly common which  may revert later. qRBBB is not a contraindication for re-perfusion .

Final  message

Presence of q waves does not  imply one should not  entertain  thrombolysis or PCI .The decision  to reperfuse  , rather  goes with  presence of  chest pain , ST elevation and  of course  within the  acceptable   time window!

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  • Diabetes , smoking , hypertension , dyslipidemia are the  leading cause of cardiac morbidity and  mortality .
  • Now air pollution the(  passive atmospheric smoking !) is threatening to be a major risk factor .
  • In fact , it has become the  official  cardiac risk factor nominated by WHO !
  • 40 %  of all deaths due to air pollution is due to cardiac events .
  • The surprise element is indoor air pollution is equally injurious .

WHO bulletin  in March 2014

air pollution and cardivascular health

The WHO assessment found the majority of air pollution deaths were linked with cardiovascular diseases.

For deaths related to outdoor pollution, it found:

  • 40% – heart disease
  • 40% – stroke
  • 11% – chronic obstructive pulmonary disease (COPD)
  • 6% – lung cancer
  • 3% – acute lower respiratory infections in children

For deaths related to Indoor pollution, it found:

  • 34% – stroke
  • 26% – heart disease

 

Related article from this site

A-new-coronary-risk-factor-community-smoking

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Time is muscle. This quote  became  sort of ” cardiology sermon”  in the last  few decades .Cardiologist think  they stand  on a 100 meters sprint track once a patient with STEMI arrives .This is indeed true ,  if we  agree  time is  muscle and  our urge is to reduce the door to balloon time .Please  remember ,  this rush matters  much ,  only if the patient comes through very early  when the muscle is really getting damaged . (No issues  . . . even if the fire engine comes in  slow motion if the  house is burnt fully !)

Time is muscle agreed  . . .  but  muscles are  kept alive by  factors other than time  !  So muscles can  defy time if God  is willing !

Time is one of the important components of management of STEMI.  Other things matter too !  Age , baseline co-morbidity ,  underlying extent of CAD, collateral support of IRA territory , and finally  individual variation in hypoxic damage in myocyte is (Rarely  been studied in detail.)

Door  to balloon time for a patient  who lands up within  1 hour window need  to be  much  different from a patient who comes at 10 th hour .The issue is important  because  we use a procedure which requires delicate decision-making ,(IRA-Non IRA issues etc)  the results can be  sub optimal ,  and even be hazardous in low risk STEMI . So , door to balloon time  may be a less  important  component of  time window in a patient who comes after 6 hours .This is the reason  overall outcomes are not changing in a large cohort  of rapidly performed PCI.

The presumed  absolute  relationship  between  “Time  and  muscle”  concept is  always been a suspect . This  is proven by a flawless study from  NEJM .

nejm stemi most important article

http://www.nejm.org/doi/full/10.1056/NEJMoa1208200

This study should infuse more sense to  us ,  time and again, we are  hijacked and sedated by high dose of  pseudo scientific concoction .In fact ,  indiscriminate rapid PCI may not be in  the good interest of  all  patients with STEMI ,  if it is not properly done  .Without realising this fact many developing countries are indulging in extravagance of  costly STEMI programs wasting  the exchequer.

This landmark NEJM  paper convincingly underscores a fact  that  achieving  rapid door to balloon time  is not  going to be the game changer in  conquering  the Global   STEMI  championship  . We have to take the coronary care into the streets  or to their homes as well .This is where the pre-hospital thrombolysis will  emerge in a big way in the future .

A slow and steady thrombolysis beats a fast and furious primary PCI on any given day in all uncomplicated STEMI .This we have proven for over three decades in  one of the India’s largest coronary care unit .( Where is the data man ?  Genuine experience is data . Why  we require , the act of publication to convert an experience into evidence . Often times ,  I  would feel , data is the most unscientific word in medicine . Many Truths  lack evidence , false hoods come with plenty !  For all those  scientific  homo sapiens  , please recall  70 % of ACC/AHA class 1 recommendations are backed by level C evidence ie simple opinion from  perceived experts! )

Final message

A fast and furious primary PCI may not be  the answer in all STEMI population

Thrombolysis  can be  done  with near  zero time delay , it does not require special expertise where an ambulance driver can reperfuse   a myocardium without much fuss and glamor ! He does not have to  split his hair to identify which is the IRA in a complex multivessel STEMI as well ! The streptokinase and TPA will home in  to the target site  smoothly and swiftly .

If indeed ,  time is the major factor in STEMI , we have many other ways to tame  the time . If muscle is more important than time ,  pPCI is  rarely  the answer !

Some India specific  thoughts

Is it not a shame  , we talk about primary PCI  for all  our patients  who do not even get timely Aspirin* after a STEMI! .It is something akin to what we witness every day ,  as our country folks  wield touch screen  Androids  . . . conversing  in open air toilets !

* While the importance of  Aspirin is undermined , It is different story altogether , these patients  get sorbitarate promptly whenever they get chest pain  (mis-placed and  dangerous priority ! )  prescribed by the  roaring  GPs ,  who suffer from discontinuous medical education ,  propelled  by the deeply penetrated 1000 crore oral Nitrate market .

And STEMI workshops are conducted by self-proclaimed experts  every few months in posh  7 star hotels all over India .

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Even though multiple mechanisms operate  the major mechanism is due to augmentation and  diversion of blood flow towards sub endocardial region* which is  main area of ischemia in most patients with Angina .
subendocardial-blood-flow
*Beta blockers  does this by smoothing   the  myocardial contractility there by  reducing  trans-myocardial gradient. The coronary arterial perforators which traverse from epicardium to endocardium gets less squeezed and promotes sub endocardial perfusion. 
Link to  a related article from this site

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ST segment elevation is the key parameter on which the fate of millions of infarct patients are recognised and managed. It is ironical we do not have standardised reference point for measuring the quantum of SR elevation .

This is especially difficult when ST segment blends with forward limb of T waves.

While we have reference point for measuring  ST depression  (Like during EST ). . . why we do not have one for ST elevation ?

Now we have adopted a rough criteria .Read below .

where will you measure st segment

How to measure ST elevation in ECG
How to measure ?
Measure The ST segment 40 ms from J point.
how to measure ST  elevation in STEMI 2
                        I lost track the source of this Image .(STEMI hand book 2012 ?)
Final message
ST segment  elevation  is  the key parameter in ACS.  Quantifying  it becomes  important in  assessing  the efficacy of reperfusion strategies and risk stratification. Fresh ST elevation can represent pericarditis, reinfarction or an early dyskinetic  segment . Unless we have  proper reference point there is  a room  for  error in this simple parameter.

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Why should mitral  annulus gets calcified ? .  Degenerative  calcification can be benign in  elderly .  If it occurs prematurely (say < 55 years )   there is enough reasons to worry .  This may represent a systemic vascular inflammation and  is considered a surrogate marker for athero- vascular -sclerosis .  A study from Cidar Sinai  , Los angels  has well documented the link way back in 2003  !

mitral annular calcification mac cad link

This is a  large study involving  17 735 patients (who were investigated for symptoms of CAD )   were screened.

The incidence  of MAC was high (As expected !)

  • 35% > 65 years
  • 5 %  < 65 years
Angiography  revealed more surprises .
  • The incidence of angiographic  CAD among those who had MAC and no MAC   was  88% v68% respectively ,( p = 0.0004),
  • Left main coronary artery disease  was (14% 4%, p = 0.009)
  • Triple vessel disease  was (54% v33%, p = 0.002).
mitral annular calcification  www_drsvenkatesan_co_in

Image source  S.Atar ,  Heart 2003 : 89, 161-164

Conclusion
This study concluded ,  CAD is more aggressive in patients with MAC. It can  also be  an independent  predictor of  high risk CAD .
Further Implications  of MAC
  1. MAC is more common in women, especially diabetics .
  2. Degenerative Mitral regurgitation  is common ,rarely  mitral stenosis
  3. Recurrent VPDs and even  trouble some mitral annular VT is possible
  4. Extensive calcific lesions in coronary  artery is also reported with MAC.
Link between Stroke and MAC .
This was well proven by this paper  published in  NEJM in 1992.
MITRAL ANNULAR CALCIFICATION AND STROKE NEJM  EMELIA BENJAMIN 1992

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