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Archive for January, 2015

We know,management of STEMI is a race against time.It’s rather a group race run by the patient, his close relatives / associates , the ambulance driver, the ER physician, cath lab staff and finally the  treating cardiologist .While the race is on , continuous monitoring and critical decisions are made.

Every minute gone could be a missed opportunity. While a patient is being moved to the hospital, a decision is to be taken whether its going to be primary PCI or lysis or combination of both.

Now,In India, as we embrace the quirky world of medical insurance  and   glamor based medicine , we have one more participant in this race of human life! The coronary flow dynamics in STEMI  appears  to be determined not only by thrombus load the residual plaque but also by the quantum, type and brand of  insurance the patient is blessed with !

I wish , one could hear the silent howls made by the myocardium under distress even as their loved ones are anxiously waiting for insurance  clearance from the  myocardial reperfusion  centers located in the far away back offices of urban metros !

Things won’t stop with that. Once the  PCI is on,and the cardiac team is confronted with a multi-vessel  CAD ,wondering which is true culprit ?, whether to consider  multi-vessel  stenting or early CABG  . Meanwhile the cath lab  liaison officer would desperately struggle to call the insurance guys again and upgrade the request to a newer therapeutic strategy !

Life was simple for every one till recently ,  when we would treat thousands of MI patients with conventional modality with a well proven reduction in mortality , comparable to the current bests .The concept of primary PCI has made things artificially complex without adding on to significant advantage except in some complicated subsets.

I still keep wondering , achieving a near  TIMI -3  flow in a timely fashion  by thrombolysis  in CCU will far exceed the hype of documented TIMI 3 flow in cath lab in  terms of absolute number and of course favorable outcome .Please realise acute myocardial salvage requires a minimum of  TIMI 2 and not TIMI 3 flow !

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Stent thrombosis is a dreaded complication as the number  of PCIs are increasing in exponential fashion.The key issue is to take care of the stented segment till it gets fully endothleised. We  have excellent , time tested  dual anti-platelet protocol to take care of this . Still , they are  not  infallible . ARC has classified  stent thrombosis with reference to the timing  of implanting the stent .

stent thrombosis

The funny aspect of this classification is , it  hides a fact , whenever a stent concludes suddenly it is acute for that patient and his myocardium . So in a given patient who presents with ACS every stent thrombosis is acute. Of course , chronic thrombotic process can occur in  few  and present as as CTOs within the stent . Generally stent thrombosis is considered resistant to lysis . This  more on our perception than on sound scientific data. Every cardiologist would  have experienced at least few cases of  acute stent occlusion that had been successfully lysed.

Underlying mechanism of acute stent thrombosis.

The single important cause for stent thrombosis is not primarily hemo-rheological  but  related to  the some technical insufficiency at the time of stent deployment (Apart from poor compliance of anti platelet agents )

  • Improper stent placement ( Mal-apposition / Geo Miss / under or oversize)
  • Edge effects
  • Plaque prolapse between struts
  • Fresh lesion eruption  (Another true ACS  is always possible)

FInal message

Though , it is risky to rely on lysis alone it is always worth a try . Lysis is easily available and can be instantly  administered without a need of special expertise . Few lives can be saved  while one ponders over shifting the patient  to a bigger center. Pharmaco-invasive approach  can be perfect for this situation.

And now , a provocative comment

Experience suggest , It may be wise , even if  cath lab is available on site or in the vicinity , the option of thrombolysis  is to be considered first for patients with suspected  acute stent thrombosis , if the patient is otherwise stable .

References thrombolysis for stent thrombosis instent streptokinase tenecteplace http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2722500/

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As I was mulling about  the misplaced  priorities  in modern health delivery  , today’s (25-01-2015) edition  of  “The Hindu” , India’s National newspaper carries an exact article by Dr B.M.Hegde .

No doubt  ,his articles are constantly criticized  by the scientific community for  the simple reason, he is forcibly  trying to add wisdom to science !

 

 

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A patient with near 90% LAD disease who had a significant TMT/EST positivity with no clinical angina  was  subjected to FFR by a scientific  cardiac physician. Since FFR was recorded as  .9 , he was adviced against a stent and sent home with drugs.

Now , in the  physiological assessment of a coronary lesion ,  which one you are going to trust , TMT positivity or FFR ?

FFR  measures trans-lesional pressure drop  by creating a artificial exercise physiology  in a particular coronary bed by injecting just one of coronary vasodilators  namely Adenosine. FFR assessment can never be considered truely  physiological .There has been huge discrepancy in the amount , rate and route of administration and the hyperemic response to Adenosine.

Final message

In a single vessel disease population , if TMT is positive the lesion is to be taken as significant, irrespective of FFR.(Provided Anemia and other systemic factors are excluded )

*Read this and get ready to get  confused further , single vessel disease with TMT positivity  doesn’t mean medical management is never an option .OMT ,(optimal medical therapy ) even though a battered concept is not yet dead for SVD !

 

 

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Traditionally , vegetations are sine qua- non for diagnosing Infective endocarditis.

The following  are major criteria to diagnose IE

  1. Evidence for endocardial involvement in the form of  visible vegetation or New onset regurgitant murmur.
  2. Positive blood culture

There are six minor criteria .

To diagnose IE we need

  • Two major or
  • One major and 3 minor or
  •  5 minor criteria alone

Duke criteria for infective endocarditis

 

duke_ie1

Now ,we realise  IE do  occur in the absence of visible vegetation.This happens because, vegetation can appear late, it is too  small and missed , burroughs inside tissue plane instead of entering cavity , may form  micro abscess or vegetation growth is prevented by prompt empirical antibiotics.

Final message

Vegetation is still a prime sign  to diagnosis of IE. However , please do not insist  on it .There can be significant endocardial infection  without formation of vegetation.The current criteria allows us to make a diagnosis of IE without documenting a clear cut visible vegetation.

 

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The major mechanism of exertional dyspnea in HOCM is due to

  1. Hypercontractile LV
  2. LVOT obstruction
  3. Diastolic dysfunction
  4. Mitral regurgitation
  5. Unrelated to HOCM

Answer : 3*

*This has been proven by a simple fact , dyspnea continues to be  a prime symptom in both obstructive as well as non obstructive HCM

Though LVOT obstruction appears to be the core issue , the myocardial disarray is a global one and lies scattered .That is why , myomectomy , septal reduction , may not reduce the symptoms  grossly as one would expect.

Paradoxically , preload reduction with diuretics  (That works well  for most  dyspnea with  raised LVEDP) ,  is vested with the risk of worsening the symptoms in HOCM . Diuretics underfill the  LV and tend to aggravate dynamic LVOT obstruction.

Probably ,the best way to reduce  symptom of dyspnea is to keep the heart rate low with betablocker.Further, betablockers smoothen the LV wall stress and calm down the LV baroreceptors which  indirectly suppress the  afferent input in  the brainstem dyspnea circuit.

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We know cardiac pain is often  referred to Jaw and neck .

What prevents the neck pain of cervical spinal disease to be referred over the  heart ? Can pure spinal lesions mimic angina ?

The answer seems to be “Yes” . The neuronal  circuit is  there .Only , the traffic has to be reversed. Medical logic is always puzzling. There is indeed an entity called cervical angina.

The cardiac pain  can be  referred any where between  dermatomes  C3 to T 10 It is generally  believed cervical radicular pain  can go only one way . . . ie towards the nape of neck and  arms .Dermatomal overlap ,neural cross talks  thalamic inputs and cortical  reflection and perception always make the subject of referred pain too  complex.

Now,It seems possible ,the neck  pain can  spill over into the anterior chest wall ,mimicking  angina .Imagine the  confusion  if the patient  has both  cardiac and cervical entities ! Does the pain signals from the two sites  collide in the local spinal network ? Does one extinguish or amplify the other ?

 

refered pain

This article which was published  in the Spinal Cord .

cervical angina  reverse referral pain

Read also linked angina

http://www.nature.com/sc/journal/v44/n8/pdf/3101888a.pdf

 1.Guler Net al.Acute ECG changes and chest pain induced by neck motion in patients with cervical hernia: a case report. Angiology 2000; 51:861–865.
2.Wells P. Cervical angina.Am Fam Physician1997;55 2262–2264.
3.Jacobs B. Cervical angina. NY State J Med 1990;90: 8–11.
 4.Baba H et al. Late radiographic findings after anterior cervical fusion for spondylotic myeloradiculopathy. spine 1993;18: 2167–2173.

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