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Archive for the ‘Cardiology -Mechnisms of disease’ Category

We know Nitroglycerine(NTG) as a most powerful epicardial coronary dilator  . We use it for instant relief during episodes of coronary arterial spasm in cath lab.

What will happen if we administer NTG over a stented segment ?

Does it dilate it with same vigor ? What will be the consequence  ?

A perfect setting for stent migration isn’t ?

Let us bust the myth around  NTG . NTG  rarely  show  visible coronary dilating effect except in the setting of coronary spasm .

NTG and coronary vasodilatation

Does a LAD with 3 mm diameter become 3.1 or 3.2  and so on with NTG ?

No .It won’t .It is my belief. It is well known , NTG’s action varies significantly in normal and diseased endothelium . Again , there is an irony .It seems , it can act only in normal endothelium , but  we need require it’s therapeutic action only in pathological segments.Further any stented segment would contain   clusters of  both normal and abnormal endothelium .

One more inference is that, stented segment exerts constant pressure on intima making any  pharmacological vasodilatation irrelevant .

Importance of  radial strength of a stent

This issue of vaso-dilator induced  stent migration may not arise in self expanding wall stent with high radial force.But we do not know how long these metals will carry this metallic property .Balloon delivered  stents ( currently used 99% of times ) do not have permanent radial strength .

Final message

I am yet to comprehend what nitrates are expected to do (and what it really does ?)  in a patient post PCI ? (By the way  . . . why we need to prescribe Nitrates it in the first place ? but  In real world most continue to take this for many reasons .)

We need to analyse the micro-vasomotion at the stent -coronary intimal interface.The dynamism in this  narrow space  can be critical  , and may make the difference between life and death !

After thought .

In the hind sight,  this post appears quixotic  for myself . But some one , some where , may generate a great idea  out of it , that will help our patients.

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We know LVH and SHT go together . Mind you , this is not an Intimate relationship.

Widespread utilisation  of echocardiography  has revealed  , definite  LVH occurs only in about 20% (A guess !) of  HT . (Do you know in the Famingham study the incidence of LVH  after 12 year follow up was a paltry 3 % .Will you agree with that ? Mind you , It was in 1969 when Echo was not there )

What determines LVH ?  The clear answer is elusive. It is easy to escape  from the issue by calling it  multi factorial !

Why don’t you try this question .

My guess would be ,  magnitude ( or  even duration of HT !)  is  less important than genetic predisposition  or  associated diabetes ,  renal involvement.Our analysis from  hypertension clinic reveals LVH is many fold common in secondary HT  when compared to primary HT !

I often used to provoke the students by saying if the LVH is gross in HT it can not be primary , 9/10 times  ! Invariably  we find some  other  association or reason for the HT !

Link to related topic in this site

Why-lvh-does-not-occur-in-all-patients-with-systemic-hypertension ?

How-diabetes-modifies-lvh-due-to-hypertension ?

incidence of lV left ventricular hypertrophy framingham study

Next  . . .

How does LVH regress with treatment ?

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Left ventricular  hypertrophy (LVH) is one of the most common  structural heart disease.Systemic hypertension, aortic valve disease are responsible for the bulk of the cases .Some  of the LVH occur due to cardiomyopathy (HCM/Non HCM variants).Athlete’s heart is a physiological response to exercise and  it  is largely a normal entity.

How many patients with SHT develop LVH ?

It is surprising to note , not every patient with SHT develop LVH .In fact estimates suggest only  about 30-40% of chronic  hypertensive individuals develop SHT .

What are the determinants of LVH in SHT ?

  • Magnitude of systolic pressure
  • Magnitude of diastolic pressure
  • Pulse pressure
  • Duration of SHT
  • Age
  • Gender
  • Body  weight/Obesity
  • Effect of treatment

While any of the above factors may operate in determining LVH

none of the above are important than this

“Genetic susceptibility ”

The myosin isoforms are determined by the genes .The re expression of   fetal isoforms in adults is responsible for LVH in many .This is determined by the genetic homogeneity

LVH  in  renal disease

Secondary hypertension due to renal dysfunction is a major determinant of LVH. This is espcially true if the pateints are dialysis dependent.The mechanism are not clear .

Diabetes and SHT :  LVH  friendly forces

When diabetes alone and SHT alone is less likely to result in LVH the combination of these two entities greatly increase the likely hood of LVH.DM induced microangitis amplifies the after load effect of HT and result in early LVH.Further this LVH is different from pure forms of hypertensive LVH  in that the interstitium goes for hypertrophy and in some cases neovascualrisation. In hypertensive LVH it is predominately myocyte hypertrophy  with little interstitial  proliferation. this has important therapeutic implication as any drug which reduce the blood pressure can regress pure myocytic hypertrophy, while in diabetic LVH  regression is difficult to achieve .

Lipid levels inversely related to LVH ?

There is no consistent relation between lipids and LVH .Occasional reports suggest a negative correlation.

Which LVH is associated with diastolic dysfunction ?

It is a well known fact , LVH has major effect on LV diastolic function.But it is also a fact only some forms of LVH develop this. Now it is clear only if the interstitial hypertrophy occur  diastolic dysfunction is manifested.  Even as the as the hypertrophied  myocyte  continue to  relax  the interstitium do not have molecular mechanisms to relax .Hence, as discussed earlier , diabetic hypertensive patient often  develop diastolic dysfunction .

Final message

LVH is not a simple expression of raised after load.It has major  non hemodynamic determinants which if identified , could have important therapeutic implication.

Coming soon . . .

Can  coronary artery  disease induce LVH in the absence of SHT or DM ?

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