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Archive for the ‘cardaic physiology’ Category

How diabetes modifies hypertensive LVH ?

Posted in cardiac physiology, Cardiology - Clinical, Cardiology -unresolved questions, tagged , , , , , , , on September 3, 2011| Leave a Comment »

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.

http://care.diabetesjournals.org/content/28/9/2255.full

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Can edema legs occur in diastolic heart failure ?

Posted in cardiac physiology, Cardiology - Clinical, cardiology -Therapeutics, Cardiology -unresolved questions, tagged , , , , , on August 14, 2011| Leave a Comment »

How common is edema legs in diastolic heart failure ?

  1. Can not occur.
  2. As common as systolic failure
  3. Can occur in significant number.
  4. Rare.

Answer : 4

Response  3  may be  correct as well .

When cardiac failure was originally defined by Framingham criteria many decades ago , the entity of diastolic heart failure was non existent .The classical  triad of edema legs, raised JVP, basal rales invariably meant systolic ,  congestive hart failure. We will , never ever know how many of the Framingham cohort had isolated diastolic  heart failure .

Mechanism

For edema to occur there need to be water and sodium retention .For  sodium and water to accumulate either of the two things should happen (Hypoprotienemia, Lymphatic dysfunction excluded)

  • Increased venous pressure
  • Reduced renal clearing of water and salt.

When both join together edema is classical and full blown.

In isolated LV diastolic  heart failure the raise in systemic venous pressure is less pronounced .So ,  edema legs is less conspicuous. but in any type of failure  the net cardiac index tend to decline at least marginally . Kidneys are the first organ to sense this , and the nephrons  goes for  a huddle and begin to retain sodium and water as if body is going to face severe water and salt scarcity .(It is a false alarm actually ! )

Neuro humoral mechanism is   “Alive and well”   in any heart failure whether it is  systolic diastolic , forward ,backward  etc. so  , edema  can indeed occur  in isolated diastolic heart failure

Please note ,  the classical edema  that occur in restrictive cardiomyopathy , constrictive  pericarditis  are due to severe  impediment  to right sided filling and  elevated the lower limb venous  pressure .

Other important determinants of edema legs.

  1. The baseline renal function.
  2. Intra vascular volume status.
  3. The associated  HT induced vascular  changes.
  4. Serum protein  levels.
  5. Venous tone.(A good venous pump   in conditioned  legs develop edema late )
  6. Integrity of lymphatic circulation.
  7. Subcutaneous fat  density and interstitial tissue resistance.

All can modify the local hydro static pressure .These factors operate in various quantum’s  and for this  reason only selcted few develop  significant  edema in cardiac failure .

Also  read  . Why some patients  with cardiac failure never develops edema legs ?

* Please note , the terms diastolic dysfunction and failure can not be used interchangeably. Dysfunction is often a  echo parameter while   failure is its  clinical counterpart .Both can be dissociated in time ,   failure may never follow dysfunction .Most episodes of diastolic dysfunction is transitory   in nature.

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Land mark reviews in cardiology :Patent foramen ovale.

Posted in cardaic physiology, cardiac surgery, Cardiology - Clinical, cardiology -congenital heart disease, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, tagged , , , , , on August 12, 2011| Leave a Comment »

Patent foramen ovale (PFO) is the new generation hole in the heart for  21st century  cardiologist. Present in about 20% of population  , would correspond to 140 crore  “man holes”  as  on  2012   in this planet. PFOs are embryological remnants across the inter atrial septum.

These minute  holes measuring few mm  are largely a  benign finding .In the recent  decades , it is being increasingly debated these holes  may  not  be innocent after all .Extensive  use of echocardiography in recent times   has contributed to  the awareness  as well as anxiety.

Evidence  is mounting  linking PFO to

  • Migraine,
  • Stroke and
  • Peripheral embolism.

While the above   observation may be true  ,  the  fact that >100 crore people have this entity   , raises  a serious question ,  as labeling  all of  them as heart disease will create chaos among the already health obsessed   population .

So , the main purpose should be ,  to identify the high risk subsets* of PFO population .(This will be a <5 %  at the most). People with PFO may  carry  a mental  stigma because it is referred to as a hole in  the heart by the  general  public .For many  the sense of living with a hole in heart is often more damaging than the hole itself ! (Incidentally , many develop  migraine only after reporting about this hole !)In a strict sense  PFO  is not a hole , rather  it is a communication it may be tunnel  or  slit like .It is argued physician should avoid calling PFO as a hole .

*What is a significant PFO ?

  • Large PFOs >5mm
  • PFOs that shunt blood
  • PFOs with septal aneurysms
  • PFOs with documented stroke or embolism
  • PFOs with atrial chiary network
  • PFO in  persons with systemic pro-coagulant states (Except probably in  pregnancy )

Final message 

PFO is a common residual congenital  atrial septal  anomaly . Usually  benign  . One can  live with it perfect harmony. Only occasional patients  are  at risk.

So the prime job of cardiologists is to not diagnose and create panic about  this entity. rather reassure  them (Is it better do not reveal to them if it is found incidentally ? Patient empowerment group would call  this a  foul !  I do not support blind empowerment  )

At the same time our main  aim is to identify the  high  risk subsets who are prone for events.

Closure of   PFO with device is required in a fraction . (*By the way ,  if   PFO is really dangerous ,  why It is never an indication for surgical closure ?  )

Reference

Your  search for best information  on PFO  would end here .  Here is  a  land mark   article  in JACC  by  Hara   also contributed by  Renu Virmani . A US  Japan  combines initiative  : A must read by every cardiologists

http://content.onlinejacc.org/cgi/reprint/46/9/1768.pdf

http://www.anesthesia-analgesia.org/content/93/5/1137.full

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Is there an entity called borderline positive exercise stress test ?

Posted in cardaic physiology, cardiac physiology, Cardiology - Clinical, cardiology -ECG, Cardiology -Interventional -PCI, tagged , , , , , , , , , , , , on August 7, 2011|

In this politically and scientifically  uncertain world nothing is  in black and white. How can you  expect  EST to behave differently ?

Even as  we  are fully  aware of the  limitations  of EST  ,  it  does not make sense   to categorize  EST result into either positive or negative .

In fact , our  estimate suggests  a significant bulk of the patient would fall in the grey zone  .

It is referred  in various terms by  the reporters of EST .

  • Borderline positive
  • Mildly positive
  • Equivocal
  • Inconclusive

What does all these terms mean to the patient ?

It mans only one thing . . .

Physician  who reports  the  EST    is unable to  conclude whether  his patient has  significant  CAD  or not . It is a dignified way of  expressing  the  limitations .

Many factors may play a role. (See the illustration above )

  • Patient factors : Poor exercise stress levels and conditioning
  • Lesion factors:  Collateralised CAD, treated CAD  can result in partial or mild  changes.
  • Machine factors :Caliberation errors.
  • Interpreter : (Physician ) factors

Error in measurement of ST segment . What is borderline  for  one doctor may indeed be true positive  for the other and vice versa .

How will be the  EST in  a  revascularised  or  medically treated CAD ?

If revascularization is a complete success ,  stress test  would  revert back to normal or it can be a borderline as we have just mentioned.

To our  surprise ,  it may  remain  positive in spite of apparently successful procedure.(Residual wall motion defects , scar mediated  ?)

How to proceed  after this borderline EST/TMT ?

Few options are available for the physician/patient

Talk  with the patient again  , assess the  baseline risk  of CAD   if it is low ignore the TMT result and reassure.

  • Repeat  stress test after  a month.
  • Stress thallium
  • Doubutamine  stress
  • CT angiogram
  • Regular Cath  angiogram* (May be the best , of course it also carries a  risk of labeling  the condition as  mild  CAD / non critical CAD etc )

For the  patient  the  easiest  option  may be ,   self  referral to a different cardiologist .   (Also called second opinion )

Final message

There is indeed an entity called   borderline  EST  . Do not dare to  ignore it  or else  face the consequences .

Read  related articles in this site .

1.Can medical management convert EST positive to negative ?

2. Should every one with positive EST should undergo CAG ?

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Squat Echo : Poor man’s stress echocardiography !

Posted in cardiac physiology, cardiology innovation, echocardiography, tagged , , , , , , , , , on August 4, 2011| 1 Comment »

There are innumerable  stresses  to human beings in daily life .

Heart  experiences a few  either directly or indirectly.

  1. Physical stress
  2. Pharmacological  stress
  3. Mechanical stress
  4. Hemodynamic stress
  5. Mental stress

Squatting is rarely realised as a form of physical   stress to heart .  Rather , squatting can also  be termed as a  good exercise  ( Western toilets sans it !)

Squatting  raises the afterload at the level of aorta due to  increments  in SVR (exact mechanism not clear ,neural reflex ?)  and temporary reduction in venous return.

After load raise is synonymous with increased  ventricular wall stress  . So,  it is logical to expect wall motion defect in  vulnerable hearts* when confronted with sudden increase in afterload .(*Ischemic hearts with delicate coronary blood flow ) .Hence ,  sudden squatting , a seemingly simple  maneuver   ,  can  unmask  silent CAD .It can be aptly be named as poor man’s stress echo.

Of course , it  doesn’t   mean in any way ,  it should not be used in rich ! The  purpose of science  is  to make things simpler and cheaper . If squatting can replace  dobutamine with fair degree of accuracy  atleast in a few ,  it can help  control the escalating  costs of  cardiology triaging   due to   many futile diagnostics !

http://content.onlinejacc.org/cgi/reprint/46/5/931.pdf

When squatting  is a stress in normal persons , paradoxically it gives relief to patients with cyanotic heart disease

Read the related articles in this  site .

How squatting relieves hypoxia in TOF ?

Squat Echocardiography in TOF

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