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Posts Tagged ‘lancet’

Why PCI  in   left main CAD is considered  an inferior modality than CABG ?

CABG is superior to PCI for the  simple reason it provides complete revascularisation virtually in all  patients with LMCAD , while PCI is possible only in a fraction of patients with LMCAD.

If  we take 100 patients  with left main  disease may be ten (At best !)   would be  suitable for PCI ! In other words PCI is contraindicated in vast majority of LMCAD  by technical criteria alone , while there can never be a contraindication for CABG in patients with LMCAD.(Except  when , comorbidity precludes surgery )

Why  PCI in  LMCAD difficult ?

It is  dependent on  technicalities

CABG does not tackle a lesion,  it simply avoids it  and by passes it ” No great brains required”

while PCI takes on the plaque frontally ,  in the dangerous  terrain of  left main artery  itself !

so,  much caution,  planing ,  logistics are required . Further ,  if there is a complication there is a potential

for catastrophe  as the only  supply line is cut off . This is the reason , cardiologists were worried to try this on

unprotected left main. (Protected LMCAD refers to left main disease following CABG  wherein atleast   LAD or LCX is  grafted )

Points to ponder in LMCAD

  • PCI is suited for isolated discrete LM disease.In realty  this is seen in less  than 5-8 % CAD.
  • LMCAD is very often associated  with  critical and multivessel distal CAD . So these patients will be candidates for CABG.
  • Left main ostium or LAD ostial  involvement makes PCI a tougher exercise
  • Calcification is more common in LMCAD that  again makes PCI difficult.

The following article in Feb 2009 is a major blow for proponents of  PCI for left main

http://circ.ahajournals.org/cgi/content/extract/119/7/1013

left-main

http://content.onlinejacc.org/cgi/content/abstract/51/5/538?ijkey=84c977d189e84327c3abbd4c1228de17dd99048a&keytype2=tf_ipsecsha

Final message

  • Conquering left main disease is an interventionist’s  ultimate dream.
  • But, before that they have  to tackle the bifurcation lesions .This is of vital importance, because 2/3 rd of left main  patients have  some form of bifurcation lesions. Current techniques , hardware  and outcomes are far below the idealistic solutions in bifurcation lesions.
  • Till that time ,  CABG would  remain the only choice for all , but for  a small fraction of isolated  left main disease where PCI may be possible.

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Drug eluting stents : A slap on the face of Evidence based cardiology . . .

Click the BMJ link or read below

 

venkat-bmj

It is often said science is sacred and unfortunately we forget ,  science is not a heavenly creation and it is the creation of scientist of varying grades of integrity fueled by the vested interest of medical industry . It has been a almost a daily affair , some of the devices and drugs are recalled or found to be unsafe on patients.

Now the big cat has come out .The Drug eluting stent has fallen from Hero to Zero in a short span of 5 years. It was projected to have zero percent restenosis in 2002 . And now we realize it is Zero percent truth.

What has started as anecdotal reports of late stent thrombosis has indeed become an epidemic in all DES patients. The five studies that has been published in the NEJM this month (March 2007) has convincingly proved how unsafe these stents are in most of the coronary population .

Millions of patients in whom this stent was implanted will carry an impending stent thrombosis and possibly an SCD . Who is to take care of them ?

The DES story is a clear cut case of getting premature approval for a dangerous form of treatment inside human coronary arteries.

It is amazing how the scientist’s eyes are shut by the illusion of knowledge and lure of wealth. How foolish they were to think drug which was administered via the stent will selectively prevent vascularisation and leave the normal endothelium intact . Now they realized , one should not suppress the endothelial growth around the stent and got the fundamental point wrong. Which was the key reason for the astonishing episodes of late stent thrombosis. When we play with biology of nature we have to be little more careful .God has created man and his heart for over a million years . One can not alter it by a 6 month follow up study of DES .

When ICDs were exposed last year , of similar disastrous outcome they were recalled and explanted . How are we going to unstent the millions of coronary arteries ?

Somewhere along the line the medical professionals have lost the battle against the Wall street and NASDAQ . Or how else we can explain repetition of similar events.

The wages for the modern technology , the patients have to pay a heavy price.

Let us all hope common man with common sense will reign supreme over the sixth sense of the uncommon man . . .

“Ignorance is better than illusion of knowledge”

Dr Venkatesan Sangareddi MD , Assistant Professor of cardiology , Madras medical college Chennai, India

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Anginal pain is a type of visceral pain.It is carried by type  C  unmylinated  nerve fibres.The perception of angina is a complex process.It is a combination of visceral and cutaneous referral pain.

How often is angina silent in diabetes mellitus ?

Presence of  diabetes per se does not make an angina silent. In fact,  if  one takes 100 patients with diabetes  , if angina occur in them , it is more often  , manifest than silent. So , only few of  the  diabetic patients who develop diabetic autonomic neuropathy fail to have angina.The exact incidence is not known.It could be around 20%.

If angina can be silent in diabteics , can they have anginal equivalents ?

This again is not answered in literature. Among the anginal equivalents , the most common is  dyspnea , which  can occur in diabetics.But now , we know dyspnea also needs thoracic nerve signals  from the intercostal muscle spindle and colgi organs.This can also be impaired in diabetics.

Can silent and mainfest episodes occur in a same  patient  ?

Yes.

Once silent does not mean always silent, and similarly once angina is felt it  does not mean he is going to feel the next episode as well !

This  strongly reminds us medical science  is  much a complex  subject and what we know is very little in pain perception.

How is silent ischmia different from silent angina ?

There is considerable  overlap  between  silent ischemia and silent angina

The questions to be answered are 

Which is silent  ?  Is it the angina or is it the ischemia or both ?

Silent ischemia can occur in any individual ,  this is also called as silent CAD . When  ischemia occurs  but  fails  to generate pain it is silent ischemia .Undiagnosed  CAD in asymptomatic individuals is also called silent ischemia or CAD.In this population  Exercise stress testing detects  CAD which was otherwise silent and masked.These patients may develop angina during EST.

During exercise stress testing many times patient has significant ST depression  more than 2mm but still chest pain may not occur.These episodes may either be silent ischemia or  ngina. Many times the EST is terminated before angina is manifest .( Chest pain is the last to occur in the chain of events following ischemia- Concept of ischemic cascade )

What are the other situations where angina can be silent ?

  • Pain perception  and threshold  level is  high ,  so patient indeed has anginal  signals but fails to feel it .
  • Patients on  antianginal medication , fail to feel the angina.
  • Chronic betablocker therapy can exactly mimic  autonomic neuropathy

Is it a blessing for the patient  to have painless episodes of angina ? 

When their  ischemic colleagues , suffer a lot with chest pain it is tempting to think these diabetic patients  are blessed!

Scientifically , this could be true in at least in  some  especially in a patients  who’s coronary anatomy is known  and devoid of any critical proximal lesions. For example a small PDA  lesion can produce  severe angina  , but may be silent  in diabetic and be comfortable .This lesion is  insignificant other wise * !

It should  also be recalled , pain relief has been an important goal for treatment  of CAD .In olden days,  thoracic sympathectomy was done for angina . In fact ,  even in  CABG  , one of the the  mechanisms  for  angina  relief  is attributed  to cardiac denervation.

Caution: Even a small  episode of ischemia can trigger an electrical event .But it is rare.

 How common is silent infarct (STEMI) in diabetic patients ?

In a simple questionnaire we asked the diabetic patients in our CCU how they felt their pain during MI.Most felt it normally as do other non diabetic .  Diabetes  does not make  all anginal episodes  silent. Severe episodes of ischemia may be painful while less severe episodes may be painless. Diabetic autonomic neuropathy  is a  least recognized and  poorly understood complication of diabetes.Diabetes , involves  the vasanervorum of the autonomic nerves.

 The other mechanisms postulated in diabetic neuropathy are

  • Reduction in neurotrophic growth factors.
  • deficiency of essential fatty acids .
  • Reduced endoneurial blood flow and
  • Nerve hypoxia .

Is diabetic autonomic neuropathy treatable ?

Very difficult problem indeed.Controlling diabetes may partially correct  the neural dysfunction.Many add on neuro vitamins and aminoacids are having a good market !

If you successfully treat diabetic autonomic neuropathy will my patient  start feeling the  hitherto silent episodes of angina ?

We don’t know.Logic would answer ” YES”

What is the ultimate effect of cardiac autonomic neuropathy.

Cardiac denervation.  The manifestations  are

  • Tachycardia, exercise intolerance
  • Orthostatic hypotension

 

Silent Myocardial Infarction : A complete list

 

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                                            The growth of medical science has been phenomenal .It is estimated , the quantum of break throughs  and development  in the  last  50 years  is   nearly equal  to  2000 years of evolution of our  knowledge  put together.  Along with this growth , came the  unavoidable misuse , and abuse of medical science. This  is mainly due to contamination of medicine with commerce . Federal drug authority (FDA) and it’s variants  were formed in all countries to monitor the proper usage of  these technologies for the benefit of mankind. It has an authority to ban a drug or device  , if it is found to bring more injury or side effects  than benefit !

But , unfortunately there is no legal authority to ban an  an  investigation  which is  potentially  or (really  harmful )

or  used  extensively without any valid purpose .

The list of such investigation is increasing in every speciality 

In  cardiology

  • Doing a Troponin assay in patients wuth classical STEMI
  • MDCT in general population
  • Pro BNP in all suspected cardiac  failure
  • Routine C reactive protein for CAD
  • Central venous catheters for all pateints with shock.

Is there a case for banning an investigation (Like banning a drug) for the benefit of  our patients ?

Looking superficially , it  may seem  ironical. But we realise many seemingly  innocuous investigations are responsible for uncontrolled misery for many patients.

This especially true in people who throng the wellness clinic (Also called master health check up)

A incidentally high C – reactive protein   can lead on to forearm blood flow assessment of endothelial dysfunction and carotid intimal plaque  that could  lead onto carotid stents ! and life long anticoagulation , and an  excess INR and sudden cerebral bleed and death !

This is one sample story  in one particular speciality

There is a definite case for banning ( Either total or partial)  some of the questionable investigations  which are done routinely !

Just because these investigation do not have any  physical , visible , adverse reactions like a drug , it should not be allowed to be abused  .The consequence of  false positive results of these investigations could be terrible and worse than the real disese itself !

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Let us not forget the basics !

  • HT management has been made  easier with the availability of  many  good drugs , at the same time it has become a complex  issue with as many classification and guidelines.
  • The management of HT has evolved over the decades. Now we have realised  HT  is not a simple number game . Reducing the blood pressure to target levels is not  sufficient and is not the primary aim !.
  • In fact we now know controlling the numbers alone is never going to work  , combined risk factor reduction is of paramount importance.
  • HT per se is less lethal but when it combines with hyperlipidemia and diabetes or smoking  it becomes  aggressive.The blood lipids  especially the LDL molecule  enjoy the high pressure environment  ,   penetrate and invade the vascular endothelium.
  • ASCOT  LLA  study has taught us,   for blood pressure reduction to  be effective and reduce CAD  events one has to reduce thier  lipid levels also.So , for every patient with HT there is not only a target BP but also a target LDL level .

picture1

 

Final message

The tip for better vascular  health is  , all  hypertensive patients should keep their lipids to optimal levels and all hyperlipidemia patients should keep their BP as low as possible .

“Keep your LDL  as low as  your diastolic blood pressure  and  let us  keep it around 70 -80

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                                                 It is now mandatory for all  journals  to declare the  conflict  of interest by the authors  who are involved in medical research .The purpose apparently is to make all transactions or links  between the researchers and their funding agencies transparent .Even major journals  do not go beyond this . Some ensure it , to appear in the first page of  the article.

 What does the the journals tend to  convey to the reader by publishing the conflicts of interest ?

  •  Does it  mean the article in question  may have a bias or indeed have a bias  ?  and readers are warned  hereby !
  •  Do they send across a message  that the  article may not be really a genuine one and the judgement is left to the the consumers of the articles ?

How often a journal article is rejected purely on the basis of  conflicts of interest ?

Most of  journal articles are rejected  for poor methodology, statistical analysis and so forth .We don’t know how often a paper is rejected  due to a conflict issue per se.If this could happen ,bulk  of drug trials would face a torrid time from the editors.

Why , even the leading scientific  journals never indulge in grading the significance of the conflict ?

Here is an example .

accomplish

nejm1

The much hyped drug trial on Hypertension “ACCOMPLISH”  was published in the  world’s most prestigious medical journal recently .It  left  it to the readers to  have their  own assessment  on the conflict issue.

  The consequence of not , grading and investigating  about the conflicts could have  serious  global health  implications both financially and academically .

This study was designed, formulated, completed and published  with a single hidden aim of neutralising the land mark trial  of ALLHAT which recommended diuretics as a first line drug in HT.Apparently diuretics are very  cheap  , effective  generic drugs.

 Is it a scientific rule  that  the  latest evidence  ,  should always prevail over the older evidence ?

No. Science can never have such a rule ! The question is how good and genuine is the evidence.
Just because an evidence is current , it does not  attain a scientific sanctity !

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One of the important principles of medicine  is  “Diagnosis should  always precede treatment”

This quote , though appear reasonable , can not be practiced always especially in emergencies,  where we  have to first stabilise the patient   without a  prior diagnosis  .(Like administering IV fluids in hypotension , acetaminophen for fever , etc)

Modern medicine  considers treating a patient without a diagnosis as unscientific.

But,  it is a well recognised fact ,  millions  of decision in everyday medical practice is not based on scientific diagnosis  but on clinical acumen and empirical therapy . There are many  instances  wherein , we are never near the  diagnosis  even after exhaustive investigations. 

prescription3

                       Ironically , in this era of evidence based medicine , when  we are  unable to  conclude ,  we are forced  to do the most  funniest  thing , namely converting patient’s symptom itself as disease entity and  be happy  in labelling them. Like , Motion sickness ,  poly-arthritis, , chronic fatigue syndrome, adult respiratory distress syndrome ,  pre mature ejaculation, fever of unknown origin  , attention deficit disorder , etc (The list is endless . . .)

               This happens because physicians always feel guilty if they are unable to label a patient with a disease entity.

Is the guilt  justified ?  Not necessarily so !  Symptomatic treatment without  diagnosis  is the most dominant theme even today (Fever, pain etc ).So don’t feel unduly negative* when one is not able to fit a patent’s  symptom into a disease entity  but ensure  he  gets relief from his symptom.

 *Except of course , one has to rule out a serious disorder.

 Comments welcome

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                                Hypertension is the most common clinical  cardiovascular entity.Left ventricular hypertrophy (LVH) is  an important consequence of  HT.In fact, it is considered as a end organ effect or damage. Others being brain, kidney, and peripheral vascular disease.Knowing about LVH is important because it has been linked to increased cardiovascular events.

lvh-4

                              Though LVH is considered  as a close companion of  HT  it is  surprising  only a minority (15-30%)  show evidence of LVH .Some  experienced clinicians (Level C evidence)  quote even lower < 10 %  .Traditionally LVH was detected by ECG and now it is replaced by echocardiography.

What determines the LVH ?

It will be suprising to note , answer to this question  is  still not  clear .

  • Is it the duration of elevated blood pressure ?
  •  Is it the absolute level of blood pressure ?
  • If so , is it  the systolic BP  , diastolic BP or the mean BP ?
  • Or is it related to the etiology of HT ?
  • There has been no significant correlation between the above parameters

When we don’t know  the answer to a question in medicine , the answer will  generally will be inside the genes !

So in HT also the major determinant of LVH is in the genes that determine the myosin heavy chain  response .

and also ACE gene polymorphism.ACE genes are involved in the expression of growth factors within the myocardium.

An excellent study  on the issue http://www.nature.com/jhh/journal/v17/n3/full/1001523a.html#tbl1

It implicates , gender, age, race etc in the genesis of LVH

Final message

So , the  myocardium does not respond with LVH   in all patients with HT.It happens only in a minority* .Duration of HT can be an important determinant , but  the major factor is  the alteration of genetic switches  within the myocytes How this switches are going to  behave ,  is largely inherited .Regression of LVH is also not uniform again implying lesser role for hemodynamics. (Some studies revealed ACEI have maximum regression  of LVH , later disputed )

*LVH is more consistently seen  in hypertension due to reno vascular  or parenchymal disorders .It is also an observed fact , a  combination of diabetes and HT is more likely to result in  LVH.

The other major issue  that needs explanation in HT/LVH  is   , how much of LVH is due to  myocyte hypertrophy perse  and how much is contributed by interstitial cell hypertrophy(Non myocytic hypertrophy)

This issue will be discussed soon

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                                            The science of medicine has evolved over 2000 years since the stone age days.It has  currently reached  a glorious era with  cutting edge  scientifc  technology .Today  one can map the entire human genetic blue print and intervene in the  disease  even before they manifest .One can   keep dying people alive for years with multi organ transplantation. Modern medicine has taught us  how human sufferings can be prevented and life can be prolonged (with or without purpose !)

The term conservative management  conveys two different

meanings for medical professionals.

conservativ-3

For other group of physicians

 

conservative-4

                         

                             Ever since the days of  application of leech over the  head for treating migraine and a crude knife abdominotomy for emergency exit of babies from  pregnant mothers in distress  , healer’s   mind has always  perceived “something  has to be done  urgently when some body suffers”  this sort of  reaction is probably  inherited  and is related to  the primitive flight or fight response .

This may be true in  some of the emergencies but it is untrue in many of the non emergencies.

                                          Unfortunately ,  our mind  finds it difficult   to differentiate  between these  situations . With constant exposure to dramatic medical breakthroughs , modern day physician is made to believe   “Some thing  is always  better than nothing  when illness strikes. Human body is a wonderful machine which has it’s own service station ! in the form autoregulation  and the meticulous  homeostatic mechanisms. Only if the disease process overwhelms,  it needs intervention.( Typical example:In the routine viral fever , you don’t adminster Acyclovir or other antiviral  for all of them !

                                        The problem with early aggressive approach is,  it fails to give an oppurtunity  for the body’s natural defence forces  to respond. Further , we will  never ever know how the administered treatment is going to fare vis a viz the natural response.( With due respects to RCTs).   While the field of medicine   has  so much  evolved , our thought process,  especially  the  aspect of clinical  reasoning  has always been lagging behind .It is now considered  as inferior or even unscientific  treatment  if  some one follows a conservative approach to a problem even if  it  provides   same outcome of that of an invasive or aggressive approach ( The classical example is PCI for chronic stable angina The COURAGE study).

The other major issue is the hazards of unwarrnted  invesitigations , drugs and procedures

Classical example:No one knows how much morbidity or mortality the routine Swan ganz catheter  caused when it was rampantly used for over two decades to monitor central venous pressure .It is estimated  that in modern medicine  there are at least  few  drugs or devices  in each speciality waiting  for the same fate  as that of  the swan ganz catheter.

No body knows when it will be exposed .Our EBM will take it’s own time . . .Till that time humanity need to suffer.

This thinking is not new  The concept  “First do no harm is over 2000 years old”

hippocrates-primum-non-nocere

Questions in search of answers

 Does law of conservation of energy applicable to human body and medicine  ? 

 Can we defy death with modern medicine ?

Final message

  • Conservative management is still  a great medical concept  in many situations  and one should not allow it to die  by the whims and fancies of the modern scientific forces.
  • Whatever you do on the patent’s body  do it ,  only if it is going to helpful for him /her. If you are unsure  Whether a given  treatment  is going to help or not ask this question to an expert .
  • The widely prevailing  dogma  of aggression is always better than  non aggression  has absolutely no evidence.
  • So approach a clinical issue disease by disease ,  individual by individual.
  • Now , in this era  high tech  medicine  ,  It is lot more tougher to choose a conservative path as the pressure to do more and more  looms  larger ! It is easier to follow the crowd  than a path of your own .
  • Always remember it needs a  stronger  mind to  act according to our conscience !

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                    circulatory                                                                            A normally  functioning  circulatory system is vital for our survival . We have about 6000 ml of  blood, circulating  all over the  body in an  approximate time of 15-20 seconds.The pressure at which this blood moves across the body is called the blood pressure . Hypertension  or simply , high blood pressure is an undesirable  hemodynamic disturbance  in human circulatory system.Systemic hypertension is the most common type of hypertension. The blood pressure is primarily  dependent  on the status of the blood vessel(vascular resistance)  and cardiac contractility. This regulation is under  many neural and hormonal factors.Further  the blood pressure varies depending  upon the blood vessel calibre, and the local milieu.There is a progressive drop in blood pressure from major arteries to the small arteries .The pressure drop is maximum  across the arterioles to reach the venules .The venous circulation has the lowest pressure, it ends up at right atrium with a mean pressure of 0- 5mmhg.

Importance of regional variation of blood pressure.

It should be realised  ,  each organ has it’s own regulated blood pressure.The brain  perfuses by the  intracerebral pressure .The lungs decide how much should be the pulmonary arterial pressure.The kidney not only controls it’s own pressure but also  has a major regulatory role in  systemic pressure by rennin angiotensin system.The examples are numerous, portal system has it’s unique pressure controlling hepatic hemodynamics. The  retinal blood vessels regulate  intra ocular pressure. While the human  circulatory system has a wide variation of blood pressure  across the breadth and length of vascular system,  it is ironical a single snap shot BP with a brachial cuff is used  to define the normality and if it is normal every thing is thought to be  hunky dory !

 

 

It is widely acknowledged now , aging of humanity  is nothing but aging of our vascular system

                                    So we should have new parameters to assess individual organ’s vascular health as well as the currently popular systemic vascular health.The single important factor that determine coronary endothelial damage is the intra coronary pressure.It is never taken into account in any of the cardivascular mortality studies. This is the prime reason for  the widely prevalent conflict in the cardiology literature , namely : Controlling systemic  blood pressure has poor correlation with  cardiovascular outcome. Many of the so called normotensive individuals  have serious hemodynamic injury in their  coronary arteries.This was made apparent in the  ASCOT LLA  study , in which patients with  near normal blood pressure also benefited from statin therapy , implying  endothelial damage could occur at any level of systemic blood pressure.

What is the normal intracoronary pressure  ? When do you diagnose intracoonary hypertension?

The normal intracoronary pressure is around 40mmhg . Intra coronary hypertension as a clinical entity  is yet to be  recognised . There is no defintion available for intracoronary HT  , intracerebral hypertension as well. 

It’s still a  long way to  go , for the cardiology and neurology  community to assess non invasively  intracoronary pressures and  intra cerebral arterial pressure to prevent  coronary events ant strokes.

Final message

Simple risk prediction using brachial cuff blood pressure is a grossly unscientific method (Sorry, i really mean it ) to assess one’s vascular health.There has been  few attempts like vascular endothelial health assessment by fore arm blood  flow , central aortic pressure (Instead of brachial cuff pressure) as an  index for risk predictment and  assessment for hypertension is suggested.

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