Posts Tagged ‘diabetic lvh’

Left ventricular hypertrophy (LVH) is the most common structural abnormality of the heart. Hypertension and LVH are close associates . Still ,not every one with HT develop LVH .  So,  there  obviously  is a missing link . Similarly , diabetes  in the company of   hypertension  love to  target the  heart muscle with more vigour .  The  incidence of LVH  can be near  100%  when DM  join hands with HT.

So, what is the secret ?

Sustained elevation of afterload  due to high BP   inflate the myocyte ,  result  in myocyte hypertrophy , which is more of a physiological response.  The diabetes mellitus  adds some spice to the hypertensive LVH.

Diabetes causes glycation of  myocyte cell membrane  proteins . This  opens the  flood gates  and  the  cell permeability barrier vanishes. Hence there is exudate collect in the  cardiac interstitium. This is  equivalent to diabetic microangiopathy seen in retina and  kidneys.

There is  well established link between diabetic LVH and microalbuminuria  , suggesting  a  protein  leak  equivalent  in   heart  (Myocardial proteinuria)  . The only difference  here  , is the  protein leaks into the interstitium   instead of  renal  tubules  .  As we know interstitial leak is a  powerful  stimulant for   fibrotic reaction and  new cell growth. Fibroblasts in combination with extracellular matrix  and macropahges form  a rigid  and timid myocardium . If the patient is also a dyslipidemic(  which is usually the case !)  the leaked LDL , TGL adds to the chaos .

Pathological  effects of  diabetic LVH

  • Increased LV mass
  • Early LA enlargement
  • Early diastolic dysfunction
  • Prevent regression of LVH  even after good BP control

Can  diabetes per se cause LVH without Hypertension ?

Yes .this is also possible , but it  is less recognised.Diabetic LVH  can be a part of generalised organomegaly seen.(Right from the days of fetus diabetes has a  tendency to increase solid  viscera  size –  Large babies in  diabetic mothers , diabetic kidneys rarely shrink !)

Other factors that are related to LVH in diabetes include

  • Female Gender
  • Insulin resistance
  • The lipid connection – Hypertriglyceridmia is linked to LVH

Can tight blood sugar control reverse diabetic LVH ?

We hope so . It may not happen in real life .it depends upon the extent of interstitial invasion of abnormally glycated proteins.

Can echocardiography identify diabetic LVH from hemodynamic LVH of SHT ?

The diabetic LVH is fundamentally different in that ,  the classical septal hypertrophy is uncommon, instead the overall LV mass is increased .This is logical,  as septal LVH is more often reflect hemodynamic stress .

Diabetes  infested myocardium   bright echoes arise  from within . This is due to reflection from  interstitial  proteins.

The newer modalities of echocardiography  like integrated back scattering  analysis can characterise  tissues.

Tissue doppler  myocardial spectral analysis  can identify LVH contributed by DM..

Final  message.

What we know about LVH ,  is far less than we do not know !  , especially when  a patient has a combination of DM and HT. The interaction between them  is so intimate ,  we fail to recognise individual contribution to the process. If only we decode this  mystery , we can intervene better in the  pathological progress of  LVH.


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Diabetes is a systemic disease affecting  almost every cell  that metabolises  glucose .What begins  as  a minor  functional impairment  ,   worsens gradually and ultimately   end up in severe  structural changes.The basement membrane of  cells  face  the brunt of the attack .  (In the strict sense every cell has a basement  but it is well  developed only in kidneys ) . We also  know , diabetes  is able to inflict universal damage by targeting the vascular endothelial cells.

In the kidneys DM makes the  glomerulus  more porous causing protein leak*  and ultimately damages the tubules and end up in CRF. In the retina it excretes the  proteinaceous  material into the vital layers  and result in  retinopathy and progressive visual loss.

* Micro/Macro albuminuria

In fact , there is  a very close link between eyes  and the kidneys  Nephrologists   hesitate to make a diagnosis  of diabetic nephropathy without ocular  changes. The peripheral vascular disease and diabetic foot are  another expression of this microvascular  dysfunction.

What is the impact on cardiac micro-circulation ?

Whenever significant diabetic nephropathy is present there must be a significant cardiac micro- angiopathy as well.This is now  a fact than an assumption. We are not recognizing it rather  ! (If only we have a cardiac  creatinine we can easily identify diabetic myocardial protein leak !)

When kidneys lose protein , cardiac capillaries  lose proteins to interstitial   space  and result  in progressive  fibrotic reaction . We know  extravasaation   of high osmolar  proteins   can play havoc  in cardiac interstitium  !

Proteins are the particles of life   . . . but in wrong places  it can  transform into deadly  molecules  in a fraction of time !

Hence ,  the cardiac protein leak in diabetes can cause  any of the following clinico -pathologic entities.

  • A mild left ventricular  hypertrophy .
  • Increase global  cardiac  mass (Similar to bulky kidneys  seen in early diabetic nephropathy )
  • Simple diastolic dysfunction.
  • Severe restrictive features
  • NDCM (Non dilated cardiomyopathy )
  • Finally a DCM  like  transformation

How to recognize cardiac protein leak ?

  • Clinically it presents either as  angina or early heart failure symptoms ( not both usually ) .Diastolic dysfunction  in echo,  positive stress test , patchy thallium uptake abnormality  often with  features  of   syndrome X  is also recognised.
  • Many of the low flow or slow flow phenomenon  in coronary angiograms  might reflect micro-circulatory dysfunction .
  • This is recognised by prolonged TIMI frame counts  and  prolonged  coronary sinus filling and emptying time .

What about macro-vascular  complications  in diabetes ?  How is it different from micro-vascular complications ?

Though we expect a direct  link between  micro and macro  vascular complication ,   the later  appears  to a  patho-genetically  independent  process . This will be addressed later.

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