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Archive for the ‘Cardiology -Mechnisms of disease’ Category

This cartoon succinctly  depict all the options we have in our fight against end stage heart failure .We know , a failing heart is often compared to a sick , aged and tired horse.

cardiac failure cartoon tired horse whicpping lionel opie book

Image courtesy Heart Physiology: From Cell to Circulation :Lionel H. Opie Lippincott Williams & Wilkins, 2004

 

1.Don’t whip the horse (Except in emergency)

  • Avoid all Inotropics ( Doubutamine and Milrinone were shown to improve quality of life marginally but  with dramatic reduction in quantity of life ! However , the same thing does not apply for Digoxin as it is the  the only Inotropic with a soothing para-sympathetic comfort  !
  • Please be reminded, CRT wires could act as  “multiple whip equivalents” right inside the heart , especially in advanced class 3 or just recovered class 4 patients. Beware!

2.Unload the horse

Vasodilators

  • ACEI/ARBS

3.Slow the horse

  • Never exert too much (Not more than 70% of capacity)
  • Beta blockers
  • Ivabradine (Slow the sinus node and expect a reduction in MVO2 )

4.Change the horse

  • Heart transplant may be the best solution

5.Switch to an Artificial Horse(Tractor )

  • ie  LV assist device

6.Finally try to heal the horse (Still largely in research labs!)

  • Genetic engineering
  • Tissue repairing
  • Stem cells
  • Holistic and spiritual healing etc (Has really  worked in few )

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When a patient comes with angina at rest , it could mean two things .Either a  STEMI or an NSTEMI .This , we can diagnose only after seeing the ECG .

Can we differentiate these two by the  character of chest pain alone ?

Very  tough task isn’t  ? But there are some definite clues .

Infarct  pain

  • Is mostly sudden .
  • Likely to be crescendo , lasts more than 20-30 minutes .
  • Fails to get relived by rest or even  Nitrites.
  • Sweating due to sympathetic activation is more pronounced.

Unstable angina

  • Is rarely  sudden .Often has a pro-drome.
  • UA is  mostly precipitated by an increased demand situation or a stress.
  • It has  a typical waxing and waning  pattern . Rarely assume a true  crescendo character  as myocytes  does not necrose (Just threaten to die !)
  • The chest pain radiation   to  shoulder is less  conspicuous , instead it  tends to  reach  the  jaw area .(* An observation,Is it something to do with multi-vessel CAD in UA ?)

Mechanism of the difference : Epicardial vs Endocardial angina

The pain of UA is   due to subtotal occlusion and  endocardial ischemia , while STEMI is  sudden total occlusion  and the resultant  transmural  ischemia . In STEMI  epicardial  surface is always involved (Which lifts the ST segment in ECG .).We know epicardium  is same as  visceral layer of pericardium which is well innervated .Hence  pain  of STEMI   acquires  more of somatic character  than a  predominately visceral type pain  that occurs with  UA/NSTEMI where epicardial ischemia is absent.

Clinical importance

The demarcation between unstable angina and Infarct pain becomes vital when we calculate the time window for thrombolysing STEMI .Many of them have a phase of pre infarction angina which is a type of unstable angina. If we mistake it for Infarct pain then one may falsely calculate a prolonged time window and deny re-perfusion therapy.

Post -amble

It is tricky issue  to differentiate the  chest pain of  STEMI and NSTEMI  .A significant overlap can occur  in  real coronary care scenario . We know   chest pain  that occurs in both   pre and post infarct  phase  is considered  as unstable angina .(With infarct pain sandwiched between them!) Hence differentiating  them may even be termed as futile.

Still,clinical cardiology  can be  made  fascinating by indulging in such exercise !

 

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We  traditionally believe  LV enlargement  results in dilatation of mitral annulus  from below  and  result in functional MR.
A lesser known  concept is , LA enlargement dilating the  mitral annulus from above and cause MR   !
Can atrial enlargement per se dilate mitral annulus ?

We often find  some degree of MR   associated with chronic  atrial fibrillation.What is the mechanism ?We also know MR begets MR.Is it because of progressive LV or LA enlargement ?

When the literature is searched  we have convincing proof that  LA enlargement can lead to significant  mitral annular dilatation and MR as well .
left atrial enlargement and mitral annuluseffect of la enlargement on mitral annulus
Reference

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critical decision making cardiology cath lab tricks coronary  angiogram primary angioplasty ptca vs cabg acc aha guidelines esc guidelines

Answer

While our brain perceives  whatever option  we  choose is the best for the patient  , in reality it is rarely true !

The only comment I wish to make,  there is nothing called standard guidelines for complex and unusual problems .We need not be obsessed with protocols  !

Please remember , If you apply standard guidelines  in  non-standard situations  9/10 times we  are going to err !

So my  choice  would be, to  go with your gut feeling , of course  your gut should  be alive ,  up to date and periodically maintained !

If you don’t have the guts  . . . don’t worry  you have plenty of other options !

 

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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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  • Diabetes mellitus is a pro-coagulant state,especially so in severe uncontrolled states.(1)
  • This is mediated by increased  levels of   plasminogen  activator Inhibitor.(PAI 1 and 2
  • This tilts  anti-fibrinolytic  forces towards thrombosis.
  • High PAI-1 is an Independent risk factor for MI in young individuals (3)
  • During STEMI the success rate of  fibrinolysis is significantly lower in diabetic population because high levels of PAI 1 .
  • The triad of DM,Obesity, Insulin resistance is a powerful predictor of  poor  response to thrombolysis.

 

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Is “Non-flow limiting coronary  lesions  more prone for ACS ?

  • If  your  answer  is “No”, you can skip this article.
  • If your  answer is “Yes” , you need to read this article.

ACS is the commonest cardiac emergency .Thousands of patients are treated every day.Millions of dollars are spent.Bulk of the cardiologist’s life revolves around this entity.

Scattered atherosclerotic plaques in coronary artery lead to ACS either in a random fashion or in a predictable manner .

Still, we are  highly  uncertain about  which lesions are likely to result in ACS ! Some time in the beginning of  21st century, the main stream cardiology media were abuzz with the concept, that non obstructive , non-flow limiting lesions are more prone for ACS rather than more tight  stenosis.

atherosclerosis  flow limiting lesion  glagov  plaque rupture vulnerable erosion fissure vs dissection

I fail to understand how a tight lesion is less  prone for ACS. Tighter lesions are  bigger and must be  prone for more complications . Image courtesy :http://upload.wikimedia.org/wikipedia/commons/9/9a/Endo_dysfunction_Athero.PNG

This reasoning was based on few studies, that lacked  solid scientific proof . In fact the initial  observation was  not made in living coronary arteries rather by autopsy observations .(Later live virtual histological studies came ,  but didn’t confirm this !)

Surprisingly the degree of  anatomical narrowing was conferred  vulnerability  , when we know plaque compositions , morphology and hemo-rheological  factors are many fold important in precipitating ACS . (Lipid content , fibrin cap  thickness, eccentricity , etc)

So where is the truth hidden?

Is it really possible, lesser the stenosis more  is the propensity for rupture ?

 We need to introspect .

“In all probability,  it is a meager statistical illusion”

For every tight lesion there are as many minor lesions scattered around in a given a coronary artery. These can progress into ACS  later.

It is basically wrong to assume non-flow limiting lesions are more prone for ACS than non-flow limiting lesions.To believe so , seriously underestimates  the  culpability of big lesions .It appears a coronary mockery to me  !

At best , we can conclude  non-flow limiting lesions  are not benign and can be an important source of ACS.

An unscientific chain reaction !

If we start believing non flow limiting (say  30%  stenosis ) is more prone for ACS , why we are not stenting all  those lesions ?

If the above concept  is  is applied in cath lab  routinely , the principle of  FFR   which relies solely on hemodynamic impact  will  crash into the dustbin !

Some  more truths

However , It is indeed true  when a plaque is hardened by severe sclerotic process or calcification it is less prone for  rupture and clinical ACS  but can be a source for stable angina.

Is it  justified to assume , larger the plaque the harder  would be it’s content  that  resists ACS ?

Meanwhile , we also know there need not be any lesion at all to cause an ACS.( In a young  smoker ,  100 % thrombotic STEMI  is possible  over an area of coronary erosion caused by endothelial dysfunction ! So , where do we go from here !)

Let us be clear

Are you confused more !   . . . after  reading this article, let us clear it by two-line summary !

As on 2014 ,

  • Symptomatic flow limiting lesion   are tackled by stents.
  • All non-flow limiting lesions  are treated by  high dose Statins  and vigorous medical management.

Final message

Contrary to popular  perception, tight lesions are  more complex, eccentric , soft and are at immediate risk of ACS.

Non flow limiting lesions remain static in most,  regress in many , still  carries  distinct  risk of progression into full blown ACS , at any time if conditions are favorable.

Fixed concepts and ideas in medical science do not help us  taking medicine forward. Especially so, when these are based on assumptions and approximations. If only we redo these studies with the currently available technology (FFR/OCT/NIR the conclusions would be dramatically different !

Caution : There is no scientific proof  for the above discussion,  of course . . . we lack evidence against it as well !

Reference

2.Glagov S, Weisenberg E, Zarins C, Stankunavicius R, Kolletis G. Compensatory enlargement of human atherosclerotic coronary arteries. N Engl J Med. 1987; 316: 371–375.

3.Fuster V, Lewis A. Conner Memorial Lecture. Mechanisms leading to myocardial infarction: insights from studies of vascular biology. Circulation 1994;90:2126-2146.

4.Ambrose JA, Weinrauch M. Thrombosis in ischemic heart disease. Arch Int Med 1996;156:1382-1394

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