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Does diastolic dysfunction vanish during bradycardia ?

May 12, 2011 by dr s venkatesan

Heart is mainly perceived  as  a pumping organ but it need to be realised it  also has a   reservoir function  (Temporarily though , for  about .5 seconds every beat ) . Contrary  to the popular belief heart is not  continuously and tirelessly working  .For every contractile  beat it takes  a brief period of rest .This is called diastole. But , even here it is not a complete rest , as  it has to receive the blood from the atria and get filled and be ready for the next beat.

Many think diastole is an active energy-consuming process . . . but it can be debated still ,  as passive elastic properties may contribute substantially to cardiac relaxation blunting the energy requirement

God is so scientific (Greatest scientist !)  he  made it sure   the resting phase(Diastole)   is slightly more  than the contractile phase (Systole ).

This makes the organ relax a bit more than it stresses  in its entire life time . At  any  given heart rate diastole will be slightly  more than systole  , peculiarly  for the same reason  during tachycardia  diastole suffers more than systole.

What happens in diastolic dysfunction ?

Pathologically the ventricles become stiff  and rigid and the filling of the  ventricle is impaired . The commonest cause for diastolic dysfunction are  hypertension, diabetes, and  ischemic  CAD some forms of myopathies  .In systole ,the calcium  is pumped into actin myosin complex  while in diastole the  same calcium molecules  (Or different !)   are ejected back into the cytosol and sarcoplasmic reticulum. The later process is impaired in many situations of diastolic dysfunction.

It should  also be realised not every one with diastolic dysfunction  has a  calcium release /unloading defect .Many  have structural diastolic dysfunction  like interstitial fibrosis  .Here the mechanism goes beyond  calcium kinetics.These are the patients who get maximum  benefit out of heart rate reduction.

It is all Time  . . . Time as a  lusiotropic  drug !

If the ventricle finds difficult to relax  (or slow /sluggish to relax )  we have  two  options to tackle this .

  • To make relaxation  faster( ie positive lusiotropism )*
  • To  prolong the diastole  itself  .

Prolonging diastole makes it certain , the LV relaxation process is completed   as the excess time compensates for  the slowness of calcium reuptake into the sarcoplasmic reticulum . In fact , we have observed at slow heart rates (<60)  it is very difficult to document diastolic dysfunction  by doppler .

In many of  dilated  cardiomyopathies  the beneficial effect of  beta blockers , could be linked to simple reduction in heart rate and prolongation of diastole .(Note In DCM about 30-40 % have restrictive filling )

Final message

As we have no specific drugs to  augment the  process  of   cardiac diastole,  currently heart rate reduction  could be the simple and best method*  to improve diastolic function  .In many cases  diastolic dysfunction  simply vanishes  at low heart rate.Bradycardia  and  diastolic dysfunction   will remain as foes  forever !  Please give the benefit of this simple concept to all your patients with diastolic dysfunction .Your patients  can breath lot more easier !

*Apart from controlling the underlying cause like DM, SHT and CAD  , anti fibrotic drugs,  interstitial relaxants ,selective cardiac   collagen uncouplers  are the  future areas of research .

Posted in Cardiology - Clinical, echocardiography | Tagged , | Leave a Comment »

When atheroscerosis experiments “chaos theory” destruction is complete !

April 21, 2011 by dr s venkatesan

Coronary atherosclerosis  can  strike  an artery  with  variety  of   lesions.It can be  any of the following.

  • Focal
  • Ostial
  • Eccentric
  • Discrete
  • Diffuse
  • Tandem
  • Ectatic
  • Multiple

  Rarely  a coronary artery  is  blessed with  all  of the  above  characters ,     added  with homo and hetero  collaterals   . . .     resulting  in  Atherosclerotic    chaos  !


What is  chaos ?

 

Note one such vessel inflicted with chaos lesions

How to you report the above angiogram  ? What can be done ?

We  do not treat an angiogram. We need to know the clinical background. (This  is a  50 year old man with chronic stable angina )  He also had a  lesion  in LAD and   was advised CABG with grafts to LAD  and PDA.

Is PCI possible in such a vessel ?

Most would agree , it is a crime to think about  PCI in the above vessel. Still , few hard-core  interventional  cardiologists may vouch   for success  in this vessel !

Is there any alternative management other than CABG in this vessel ?

Leaving it alone can be an intelligent strategy . (If  LAD is normal  it  may be the  best possible management)  . But , CABG will remain a default choice. But , when a person is having such a rampant atherosclerosis  he is at high  risk  for pre- mature  graft disease as well. Hence  , intensive medical management will be the key  in  such patients irrespective  of  any revascularization procedure.

Posted in Cardiology - Clinical, cardiology- coronary care | Tagged , , | Leave a Comment »

How do you know your coronary circulation has the blessings of God ?

April 18, 2011 by dr s venkatesan

Coronary collateral circulation can be termed as one of the  mysterious  circulation in our body.Cardiologists generally do not  give much importance to it and some interventionists even ridicule it !  . But  ,  God has given it ,  with  a purpose. He adds a riddle though !  .Collaterals  grow  in  almost  every  individual  when   obstruction occurs gradually ( chronic coronary syndrome ) but only in  a few ,  it  will open up  during a real emergency like ACS !

How and why , only  few of us can  recruit  coronary collaterals   during   acute occlusion ?

God  blesses acute coronary collaterals only in selected few  , who  are on the right side of his good books .This can be  the other name for our  destiny !

Role of coronary collateral circulation  in acute coronary syndrome.

  • Limits  infarct size and volume
  • Promotes salvage
  • Converts q  MI to non q  MI
  • Prevents Unstable angina from becoming MI
  • Prevent primary VT and VF*

All  of the above can be vital  in saving a life  . Even as  we realise 30 % of STEMI do not even reach hospital  , it seems certain men and women with early collateral recruitment  will never  fail to reach the hospital alive

Is there a simple  method to identify  people who are blessed with acutely recruitable   collaterlas ?

I am afraid it is  almost equal to  asking   for a glimpse of GOD   !

Wait . . .  when we were on cath lab  few  days ago a  stunning  phenomenon happened  that could pave way for identifying  potential acute  collaterals  in any human being.  Follow this site  . . .the details will be posted !

Posted in Cardiology - Clinical, cardiology -ECG, Cardiology -unresolved questions, Cardiology-Arrhythmias, Cardiology-Coronary artery disese | Tagged , , , | Leave a Comment »

Hypertensive response to exercise stress test and risk of future stroke !

April 16, 2011 by dr s venkatesan

 Hypertension  ranks  number one  in the risk for future  stroke . Surprisingly this is true  for ischemic  as well as  hemorrhagic strokes.

 What  causes  thrombosis or  rupture of small cerebral arterioles ?

 It is somewhat similar to coronary events . ( With one major exception,  coronary vesels  are   not prone for rupture ) .It is  believed   sudden spikes of   blood pressure  and the resultant endothelial injury are responsible. Atherosclerotic plaque fissure and inflammation  also  contribute. 

Is embolic stroke related to hypertension ?

The vast majority of embolic stroke are believed to  arise from heart .This belief is getting gradually eroded , as we now know aortic arch and carotid arteries vie for this honour . .(This was indirectly proved in AFFIRM trial  when rhythm control failed  to reduce the incidence of  stroke inpateints with AF ,   implying much of the strokes arise  in the upstream rather than within the cardiac chambers )  

Meanwhile , there is no controversy  in  SHT  promoting  both cardiac  and non cardiac embolus to brain

Systolic ,  Diastolic or Mean pressure   which is  important  in the genesis of stroke  ?

All parameters  are  important , but the   systolic blood pressure  is vested with more  vigour  to damage the  cerebral arterioles. The reason  systolic pressure is more important lies  in the  fact ,  it  can  attain  high pressure peaks instantly ,  unlike diastolic or pulse pressure which  slowly builds up. Further , systolic BP  carries  leading edge of the pressure  curve with high Dp/Dt and hits  the target  first !

At what pressure the cerebral artery becomes  uncomfortable ?

We do not know  the answer as yet , but any systolic pressure above 180 mmhg is a huge stress for the cerebral arterioles.The rapidity with which the BP  raises  (Dp/Dt) also becomes  important  . High blood pressure increases the shearing stress .It  interferes with nitric oxide synthesis and promotes endothelin release which precipitates  cerebro vascular event.

How do you identify people who are at risk for stroke ?

While  cardiac physicians are obsessed with exercise stress test to predict CAD  very  few  are worried about  stroke . In fact the same exercise stress test can be used to stratify stroke risk. The exercise induced systolic blood pressure  raise  is a useful risk stratifying  tool. This concept is there for more than a decade without reaching the clinical domain.

The following paper was  published in stroke journal (2001)  from the picturesque university of  Kupio Finland.(See below )  It is a wonderfully done study and throws great insight into the  new  emerging  science of  Intra cerebral hypertension .

 

The following can be summed up as risk factors for stroke during EST  (Derived from   various sources  and  . . .  with   liberal dose of personal  logic !)

  • Raise of 20 mmhg  SBP  at  2  minutes .
  • Increment of >  20mmhg in SBP any subsequent minute.   
  • Any  SBP  above 200mmhg during  EST
  • Failure to  reach baseline SBP  at 6 minutes recovery .
  • SBP  or DBP remaining high  even  after  the heart rate reaches baseline.

 

 Final message

For the kind attention  of all  cardiac physicians . . .  whenever you do an  EST for a cardiac indication ,  please spend the first  few  minutes  carefully ,and   look at the  blood pressure response . It is encouraged ,  to  specifically mention about the  behavior of  SBP  and write a remark about the propensity for  stroke in  every EST/TMT report .   Let us grow our brain  sense as well   . . .  for   the sake of our patients !

Thanks again  to Dr S.Kurl et all from Finland  for their  nice article which  stimulated  me to write  this post .

Reference

http://stroke.ahajournals.org/cgi/reprint/32/9/2036

http://heart.bmj.com/content/95/13/1072.abstract

Further queries

How common is stroke following a EST procedure ?  Can high blood pressure dislodge a carotid plaque during a stress test ?

The answers will be posted soon once I  get it . ( Of course you can do it if you know !)

Posted in Cardiology - Clinical, cardiology -Therapeutics, Cardiology -unresolved questions, cardiology journal club, Cardiology-Land mark studies | Tagged , , , , | Leave a Comment »

Confronting Sgarbossa criteria from chennai !

April 16, 2011 by dr s venkatesan

Left bundle branch block (LBBB)   has a curious but important relationship with  STEMI . LBBB inflicts a dramatic change in qrs morphology   with  a diagonally  opposite   polarity of ventricular activation . This masks    the initial qrs vector  and  makes it a difficult task  to diagnose acute MI in this setting. The ST segment which is of primary importance  in STEMI is   lifted  up due to altered repolarization .

LBBB can be associated  with  STEMI in the following ways

  • Acute necrotic LBBB  with massive myocardial damage – Impending shock
  • Chronic LBBB with acute STEMI
  • Transient ischemic LBBB during STEMI
  • Rate dependent  LBBB (Usually tachycardic  ,  rarely bradycardic  )
  • STEMI in pacemaker rhythms

While every one of the above can be experienced ,  the most common diagnostic conundrum  occurs ,  when a patient   comes with acute  chest pain and LBBB . There has been many criterias  suggested to diagnose STEMI in the presence  of LBBB.

The criteria  proposed  by Sgarbosa  (A  GUSTO   off shoot )  in 1996  caught our imagination .One prime reason for this is ,  it came from the prestigious NEJM and Duke university combine. Suddenly this became the de- facto standard to diagnose  STEMI 

In the  past 15  years  ,  our experience in one of largest coronary  care units in India , we have   found this criteria   to have  little utility value  in STEMI and LBBB  . Most of the time  a correct diagnosis was made  by   simple clinical guessing .

Next to  clinical assessment, we found cardiac enzymes (Troponin and CPK ) were reliable in diagnosing  STEMI with LBBB.

Surprisingly ,echocardiography  was as unreliable as ECG .( The paradoxical  septal motion invariably confuses the already  confused  cardiology fellow who usually does the emergency echo  !) 

Even as our  CCU documentation was  far from satisfactory  , now this article from Mayo exactly reflect  our observation.

Sorry   Sgarbosa . . . the criteria was  based  on  sound observation and a  good  electrical principle  . . . still LBBB is able to beat   it convincingly ! ( Very low sensitivity !)

Posted in cardiology -ECG, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, cardiology- coronary care, Cardiology-Arrhythmias | Tagged , , , , | 1 Comment »

Cardiologists beware . . .Bicycle rides threaten angioplasty procedures !

April 14, 2011 by dr s venkatesan

What do you advice a patient with single vessel  CAD  with milder forms of angina or no angina ?

Medical management ?  May be you are right . But most of us do not  follow this  correct advice.  Why ?  We have a inherent bias against  medical management  . Cath labs exude  unmatched glamor and  attraction in various forms  to both cardiologists and their patients.   Now , here is a   surprise  finding  , unpalatable though , for many of  us !  Simple jogging or bicycling can have equal if not  more relief  than even a angioplasty . This study which came in 2004  was made sure , not to  gain a prominent place in cardiology literature.

http://circ.ahajournals.org/cgi/content/full/109/11/1371?linkType=FULL&resid=109/11/1371&journalCode=circulationaha

Let me pedal faster . . . cardiologists are after me !

The circulation article

How does exercise help in reversing CAD  ?

We know the prerequisite for plaque formation is the endothelial  injury along with lipid accumulation. Further ,  high local adrenergic(vasomotor) tone ,   growth factors and inflammatory activity would accelerate the plaque formation.

Regular exercise  has been  convincingly  shown to improve  the endothelial function. It  restores  the optimal adrenegric tone in the coronary micro circulation so the blood flow is brisk and pro-coagulant  activity is reduced .

It is easy to accept  the fact ,   exercise  can  prevent   progression of plaque   . . .A question that lingers in many including  many  cardiologists is this   . . .How  is it possible   for exercise to  regress well  established plaques ?

When   exercise  can   dissolve  huge  fat loaded  abdominal  tummy  in matter of weeks ,   there need not be any doubt  about the efficacy  of   exercise  in regressing   minute  lipid laden  coronary tummies (also called as plaques) .

(Of course , the  above statement  is supported by  documented  angiographic evidence  as well !)  Read below and  also the AVERT study .

Final message

Attention  all CAD patients ,  empower yourself , you  can become your own  cardiologist . You can perform angioplasties with bicycle  at zero  cost ,  of course  you have to pay for the bicycle !

This article “hypes up” the importance of physical activity in the management of CAD. But , it has to be  combined with optimal anti anginal drugs, good lipid control , blood pressure and diabetes  control  if present  , stress reduction  and good  sleep  to keep the CAD and cardiologists  at bay !

Posted in cardiac drugs, Cardiology - Clinical, cardiology -ECG, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology-Land mark studies | Tagged , , , | Leave a Comment »

A curious phenomenon called dual acute coronary syndrome !

April 14, 2011 by dr s venkatesan

We know  acute coronary syndrome  presents* with  either  STEMI or NSTEMI. (*It actually doesn’t present , it is our understanding and interpretation ).  Bifurcating  ACS into two is more by convention and convenience .Does  the intra-coronary  plaque  dynamics  really  permit us to divide ACS in to two distinct ECG  entities ?

Are we oversimplifying it ?  Probably yes.

The following paper was presented in the cardiological society annual scientific session in New Delhi few years ago (2006)

It generated an intense debate  , finally the chair person  reluctantly concluded such events are  possible. . .

but need more proof   . What is your take on this issue ?

DUAL   ACUTE   CORONARY SYNDROME

S.Venkatesan ,G.Gnanavelu,V.Jaganathan,

Department of cardiology . Madras Medical College. Chennai

Acute coronary syndrome (ACS)  is  classified into  STEMI  and NSTEMI and has gained universal acceptance. The classification was done by   clinical & electro physiological   findings    with   some   pathological basis. The   classification   came into vogue primarily to simplify the decision making process of thrombolysis. ( STEMI –Thrombolysis eligible .NSTEMI  Thrombolysis ineligible.) The limitation of this classification is well   exposed   as   we   now know,    STEMI can evolve into NSTEMI and NSTEMI can evolve into STEMI .   Identifying the culprit artery in ACS is   not straight forward especially in NSTEMI. Adding further complexity   is   the newer   observations that diffuse vessel inflammation,  and  multiple active plaques(MAP) are responsible for many of the episodes of  ACS.

In this scenario   there   could be two are more pathological processes   one   resulting   in  a total occlusion   and other sub total occlusion resulting in both patterns of ACS simultaneously .(STEMI & NSTEMI  Dual ACS)

We   describe two  patients  who had   presented to our CCU  . Both had STEMI one in  lateral  other in anterior wall . They   were thrombolysed   as per  criteria. Both patients had gross ST depression (>4mm)  elsewhere. In one patient it  corresponded  to the reciprocal  leads .The outcome of  thrombolysis  was turbulent .Both patients worsened and one developed  recurrent VT . Paradoxically the ST elevation   regressed   indicating a successful   thrombolysis  in the STEMI  territory  even as the ST depression  was worsening in the other leads. Angiogram   revealed   multivessel CAD with   recannalised  LAD  lesion with eccentric , thrombus containing  lesion in RCA/LCX. One patient expired and other was referred for revascularisation.

We   believe   both of our   patients  experienced  Dual ACS.

When to suspect dual ACS ?

Dual ACS is likely , when  STEMI is associated with ST depression  in at least 5mm in any two leads  or   when there is disproportionate  reciprocal ST depression ( > 2mm of primary). The reason for the poor outcome could be due to a therapeutic conflict between   STEMI & NSTEMI as the former  is  thrombolysis friendly while the later is not . Role of   thrombolysis in  such situations were ACS wanders between STEMI & NSTEMI is not defined. Another possibility is the concept of reciprocal ST elevation,   where in the index event  could be NSTEMI and STEMI is a secondary response  and  thrombolysis is apparently  contraindicated.

We conclude that in patients with ACS,   two or more   plaques can simultaneously get  activated  and  present  as a combination  of STEMI / NSTEMI   in the same  patient  in two different coronary arteries.(Dual ACS) .We suggest   that in every  patient who present with  STEMI  a possibility of   dual ACS  is to specifically considered,  as  thrombolysis could be disastrous  and  instead  they  should  reach   the  cath  lab directly.  .

Posted in Cardiology - Clinical, cardiology -Therapeutics, cardiology- coronary care, Cardiology-Coronary artery disese | Tagged , , , , | Leave a Comment »

A big set back for low molecular weight heparin . . . but a huge step forward for our patients !

April 7, 2011 by dr s venkatesan

The economics of  parenteral  anti-coagulation  took a paradigm shift more than a decade ago.  That was the arrival of low molecular weight heparin in the early 1990s.  The conventional regular heparin ( so called  unpurified /unfractionated )  was ridiculed   over the years. Lobbying   for LMWH was so strong  no one could  dare – stop this pseudo academic onslaught  flying high  with series of powerful articles  in major journals .

The major plus point  claimed for LMWH was   the convenience of administration  without any monitoring .

This convenience masked  some of the vital  truths  about these drugs

  • First and foremost ,  LMWH never proved it’s cost  effectiveness  and worthiness in a convincing manner.
  • Acute administration  by IV route was rarely practiced globally  which was used in all major trials.
  • The onset of action with subcutaneous route  always lagged behind in real ACS.
  • It would  seem ,  the  greatest advantage claimed by LMWH ( of not requiring monitoring  ) is the biggest suspect ,  as we would not know , whether the drug really reaches the peak action or not.

If  raw economics  brought these futile drug to the fore front  ,  the  only  possible way to stop this  redundant  drug was again by the  same  economics ! This , exactly  is happening  now . Suddenly , many  research  papers  are coming out   claiming  the superiority of good old heparin  over LMWH .

Thanks to recession , new  global health polices and politics .

This week’s NEJM restores  at- least some of the   stolen credit  to the regular  heparin after 10

long years !


http://www.nejm.org/doi/full/10.1056/NEJMoa1014475?query=TOC

Assumptions and bias

The above observation by the author  can be labeled as an  extreme form of bias against a wonder drug called LMWH.

It may be  argued  not all LMWH can be considered equal .Will the  outcome from the above trial  results be extrapolated to  enoxaparine  as well  ?What  is your gut feeling ? Gut is many times right than  hyped up RCTS !

In a large tertiary  hospital  where we work  , we have  never switched to the LMWH   in the  bygone  decade (  Both in critical care unit and post op unit )  .We have to withstand   a big  hue and cry and  were   even  humiliated for using regular heparin in our ICU . Now  . . . we  stand fully vindicated !

There are many such falsehoods  that  need to be  corrected in the medical literature. Sooner it happens , better for the humans  of  this planet . We should be glad  . . .things are moving in that direction.

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New criteria required to define LV dilatation !

April 4, 2011 by dr s venkatesan

Human heart is a compact elastic organ .  We know elasticity is lost when it is stretched beyond a point.This is what happens in dilated  cardiomyopathy .When the heart muscle fibers stretch  too long from the baseline  it loses its ability to contract and relax   efficiently.In fact  , after a cut of point even if it comes the original length the elastic fibers are fractured and suffer from irreversible damage.

Among  the systolic vs diastolic dimension it is the diastolic dimension that becomes important in defining dilatation.

When do you say a ventricle is dilated?

  1. When the EDD (End diastolic dimension) > 60mm
  2. EDD > 56mm
  3. EDD > 10 % from baseline
  4. EDD > 25 %  from baseline

Any of the above can be right.

The normal human ventricle measures  between 35 to 55mm in diastole .

Currently accepted  definition for enlargement of heart is EDD  of 56 mm and above. Some believe  in a more strict criteria of 60mm.

Consider the following situation

A man with 35mm EDD   can increase 20mm ( ie 60 % )  from of his baseline  and still be  labeled as  normal LV  dimension ! . If the above patient  is  destined to develop dilated cardiomyopathy    his  heart  would  begin  its  final  journey  slowly but   surely ( from 35 mm  ! ) . So ,  according to current criteria  we can diagnose  DCM only after it travels the half way towards hell .   What a way to define DCM  ! Be cautious LV dimensions can fool  you  . . .

If the EF is low and symptoms develop early ,  one may recognise  the above  entity ( at least erroneously !) as non dilated cardiomyopathy or RCM.

If  the patient is relatively asymptomatic and   if we   overlook  the  baseline  LV parameters ,  we are likely  to miss  most of the early  DCMs

Final message

We need to stress the importance of baseline LV dimension in defining DCM  . It is proposed  from this  site ,  an increase of 25 %   and above from baseline  can be   included as an   additional  criteria  for  LV dilatation . This  could  help us understand   the early muscle dynamics in DCM.

Un-Answered questions

  1. How to diagnose  early DCM ?
  2. When does the EF begins to decline in DCM ?
  3. What is the relation between EDD and EF %?
  4. Is HF with preserved LV function ( previously called diastolic dysfunction ) is the earliest point in the natural history of  DCM
  5. Is there a overlap  between non dilated cardiomyopathy , RCM and early phase of DCM ?

Posted in Cardiology - Clinical, cardiology -Therapeutics, Cardiology -unresolved questions | Tagged , , , , , , , | Leave a Comment »

Living with a single coronary artery : Let us trust the nature atleast once in a while !

March 26, 2011 by dr s venkatesan

We  are at the mercy  of  the three major coronary arteries (LAD,LCX,RCA) that sustain our life . Their  job is clear cut  .It has to perfuse   about 300 Grams of   live bundle of energy  for  an average of 6-7 decades.

What are the hurdles it  faces ,  how it overcomes these obstacles  forms the fascinating story of   “survival  of  human heart”

When coronary blood supply is confronted with a sudden compromise  as in ACS  ,  often the heart has little  time to respond . Hence the damage  and risk of death is  more. Even here there are lots of safety mechanisms and natural lytic process that limit the loss of life to less than 30 %  of all STEMIs. This implies nature protects against the death in 70 % of individuals and help  them  to reach hospital.*

*Among those  who reach hospital , we  the cardiologists  try to reduce the  mortality to about 6-7 % (20% without treatment ) with all  those hi-tech gadgets .It is a  different story and will be addressed elsewhere .

When it comes to  chronic insults ,  the heart has a unique potential to  stage  long haul battles. It has many tricks  under its  sleeves when challenged in a slow fashion.

The main weapons are two

1. Coronary collateral circulation.

2. Ischemic preconditioning.

Here is a patient who fights his life even after all his  three coronary arteries   totally blocked and surviving with one of the branches of left main -Ramus intermedius .

If you have thought his RCA was the savior  you are  mistaken  .

To every one’s   surprise  his  RCA was awful  as well !

He had angina which was  troublesome  but manageable .Was able to live a life with acceptable standards (Indian standard )  After the angiogram he  received  CABG.  A turbulent post operative course ensued  due to various reasons . He  struggled but   fully recovered  . . .  and  ultimately  reached the  previous  standard  of life !

Final message

Modern cardiology is all about not trusting  powers of nature .

But youngsters should realise the enormous potential of those invisible powers.It may sound philosophical , but please  remember  . . .after all . . .  philosophy  is nothing but  search for truths. Atleast believe in them  once in a while !

Posted in cardiac surgery, Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, cardiology- coronary care, cardiology-ethics | Tagged , , , , , , , , , , , , , , , , , , | Leave a Comment »

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