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Posts Tagged ‘cad’

What is a coronary risk factor ?

Right from the days of  Framingham study we have conferred a privileged   place   to  few  cardiac  risk factors.

they are

  • Diabetes mellites
  • Hypertension
  • Hyperlipidemia
  • Smoking
  • Obesity

They are referred to as conventional risk factors .  What is the convention ?  Do they deserve  the  cult  status they enjoy ?

Today we also have a  cluster  of non conventional risk factors like , Lip (a) , low HDL, Homocystenemia , CRP , Apo B etc . Currently ,  in any large cohort of CAD  up to 30 %  do not exhibit even a single conventional risk factor  . This is a huge number .Hence   we tend to give more importance to genetic make up and mental stress etc  .The search is still  on for newer risk factors .

Why some research  findings are difficult to comprehend ?

It is because we are yet to  decode the  intricacies  of  human biology  fully . Our knowledge is so superficial  , as we chase  a pseudo scientific  proofs   for  a  presumed  hypothesis.  The classical example is the concept called good cholesterol (HDL) and reverse cholesterol transport which  is never based on solid scientific foundations.

Take the sorry story of  Torcetrapib

Many consider  low HDL  as an independent CAD risk factor to be a  myth  or else why should we miserably fail  to have any positive effect of  increasing the HDL  levels by pharmacological means . (One argument is physiological  and natural elevation of  HDL  would still be beneficial  . But the issue is still wrapped in a statistical mystery

This  paper from  JAMA   adds further insight into our ignorance about  the  genesis of CAD .

The data is from  NRMI registry.

The statistics  reveal  a stunning fact .In  the overall CAD cohort ,  patients  with no major risk factors  experience  highest mortality and the ones with maximum   risk factors have least mortality ! What a shocker of a study ?

http://jama.ama-assn.org/content/306/19/2120

This  paper  would bring  jitters to the population ,  but in the real sense it sends an important message .

A significant population develop CAD without any  known risk factors.(14.5% in NRMI registry )

If a person develops  a CAD without any major risk factor  ,  it seems  . . . it is not at all a  good news   !  rather we need to introspect , why  without any risk factor he or she has suffered CAD ,

One inference is  their vascular system is more vulnerable ! Some hidden factors are operating . How to manage such  patients  without any target to intervene ?   A diabetic dyslipidemic smoker has a   definite  therapeutic target  .

What about these   lesser  humans  who   develop   CAD without any known risk factors  ? They  tend to suffer more !

Is  CAD  due to DM/SHT  is better than  others  ? This study seems to say so ” Known devils are better than unknown ones ”

Final message

Unlearning is an   “essential and fundamental”  component of   scientific learning .  In this progressive scientific world , this applies  most to   medical profession  than any other field !

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Atherosclerosis follows a general hemodynamic  rule.

It has a predilection for medium and small  sized vessels and love to  home in  on the  branch points .

We know coronary  artery disease  mainly involve the proximal tree. We get occasional patient  with mid or distal CAD.

This again ,  in  combination with atleast one  proximal  lesion. Decision making  is easy if there is critical proximal lesion.

Here is a patient who has isolated  critical distal CAD . He created a heated debate in our cath meet

His LV function  was normal , He had TMT  borderline  positive , but no angina ,

What has to be done for him ?

A fellow suggested  a thallium

It was countered by other  ,  we can take it as granted   there is  cold spot in  thallium in a small  posterior segment , then how will you proceed ?

  • PCI, medical , CABG ?
  • CABG definitely  not ,
  • PCI  . . . may be . . .Medical  may be !

When you are confused about  the choice and outcome  . . .confuse the patient* as well ! And , let him decide after a mini  , (but exhaustive ) lecture on coronary blood flow , risk of heart attacks etc .

So in this modern  era of pseudo   empowerment , it is ironical  patients will prevail over doctors after learning   half or quarter  truths  from their android powered smart phones and i pads  !

By the way finally  what  was decided ?

The patient and overwhelming majority voted for a drug eluting stent for  the OM lesion event  as  it appears technically a bifurcation lesion ! This is how cardiology is practiced.

Reference:

Isolated distal coronary artery disease. Presented in cardiological society of  India meet 2005

A clarification .

** One  definition for “confusion” is  being in a  “unclear”  state of mind !

**The aim of this blog is never to confuse the patient. The  above statement is necessary because many patients do believe(or rather want to)  they  understand every thing about their illness even as doctors are baffling with the  great uncertainties and intricacies of  most medical conditions.

Can medical management convert TMT positive into negative ?

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Very often in clinical  practice  cardiologists are asked to R/O significant coronary artery disease in asymptomatic persons .This population includes  people with multiple risk factors like diabetes, HT dyslipidemia  and non specific ST/T changes in ECG.

Many of us have lost the confidence of   ruling out CAD   in these population without looking at their  coronary angiogram.

Is it a right way of practicing cardiology ?

What we need to realise is,  we are asked  to rule out any critical lesions that are going to make a impact on these  other wise comfortable patients.  Nothing wrong if you miss a 30% lesion in PDA or OMs or diagonals !

Can we do this without doing coronary angiogram ?

Yes ,  we can .

Step by step  Ask these questions

  1. Ask the patient , if  he /she   can climb three  flight of  stairs  without any difficulty or
  2. Walk briskly for  20 minutes (5km/hr)

If yes , give  a   certificate   that he  has no critical  left main or proximal LAD  disease.

If you do not believe in his words , put him on a tread mill ,  if he crosses   stage  3   Bruce in TMT ( 9 mts)

give the above certificate  “with a frame”  now .

For still suspicious  physicians ,  We have  one more  investigation called  echocardiography !

Echo : The forgotten tool  for screening left main lesion.

Modern day echo machines have a  3mm resolution power (Many have 2mm ) .While ,  we are expected to look for 3mm vegetation to R/O Infective endocarditis , rarely is  a  cardiologist ,  tuned to  look for the left main ostium  in routine echocardiography  which averages 4-5mm is size. (Left main by echo link to another article)

In short axis  view just tilt at the level of pulmonary valves  (Atrio- pulmonary sulcus) one can visualise the left main ostium and the proximal left main emerging from the 4 o clock position. If you are lucky you can see the entire left main.

If nothing satisfies the physician (Or the patient)  ,Refer him for sliced CT scan , catheter coronary angiogram , or a  nuclear Imaging .Be ready for the attendant anxiety, interpretation errors, corporate  pressures , urge to  balloon ,  kick backs etc etc

By the way , how can  one  be happy by ruling out only left main disease ?  Is it not other lesions possible ?

Experience (Not science) has taught us  no  critical coronary obstruction is  possible ,  if  a patient walks for  9 minutes  in treadmill (10METS).

Even if it is there (A remote chance)  there is little documented benefit of any revascularisation procedure.

Counter point ?

Is it not a “crazy idea  to rely on patients history in ruling out  CAD   in these era , where   angiograms relayed  live  into   cardiologists  ipad  ?

Science has no value if it is not applied  for the patients welfare. Meticulous clinical  examination (And application of mind)  is the foundation stone on which  any medical investigation and therapy  should be based  upon. Most of the inappropriate coronary revascularisation are due to  neglect   of  this vital  component of clinical examination.

(I wonder ,  is it  really possible  these ” acts of omission”   be  deliberate some times  ! )

Final message

Clinical interrogation  may  miss an insignificant  CAD  ,  but it can never miss a critical CAD* .

 

Do not do coronary angiogram routinely to R/O  CAD.

It is not the way cardiology is to be practiced !

If only we apply  those  simple,  time tested concepts in every day practice we not only  save millions of  Rupees ,   but also thousands of futile   diagnostic tests and associated untoward effects can be avoided.

* Senstivity of  ruling out any CAD is about 70% , but it’s capcity to R/O critical CAD approaches 100%.

Reference:

Please refer your own Brain.

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Coronary  atherosclerosis is the number one killer of mankind. Many would consider it as an  essential  process of aging .Modern  life styles and habits make this appear  very early in life . There is currently an endemic (or even  a pandemic ) of   CAD due to premature  atherosclerosis. We need to recognise CAD is not a  primary heart disease  .It is an irony, heart is an  innocent bystander  to the  biological derangement  of coronary  vascular system  when  it is infested with atherosclerotic plaques .

So , when we  are confronted  with  serious atherosclerotic lesions in a coronary artery   what shall we do ?

We have three options

  1. Take on the enemy in a direct confrontation (Like war on terror ) : This is  some times called as Interventional cardiology .Caution is required as the battle  is within the human coronary artery ,  cross fires and collateral  damage  are unavoidable.

2 .Next  method  is to  find the basic cause  of  terrorism , identify  the perpetuates, facilitators    and try to correct the   root cause of it (CAD ) .This approach  also refered to as medical management  in cardiology community*  . It  aims  at regression of plaque  by statins, and life style modification and preventive cardiology. This modality is most ridiculed and  insulted by the main stream cardiologists.

*Comparable to  bilateral peace talks for a political solution to terror

3. And third option is a  real  surprise !   This  neither  confronts   the lesion   nor does it  address the initiating factors . It   just ignores  the lesion and by pass it with a LIMA /SVG  fly over ,  as if  nothing has happened in this vital high way leaving the culprit scot-free  .This option is  executed by surgeons as  CABG surgery . . . and  for mysterious reasons  this is a  well accepted one .

CABG :Here the atherosclerotic  burden is untouched by surgery . The graft can get diseased  sooner or later , native vessel disease  shall  progress some times encroaching  the ostia of distal graft site . Incidence of acute coronary syndrome following CABG is not greatly reduced for the simple reason we are not doing anything primarily to the inflamed plaques .These issues  are left ,  to be  taken care by the  medical  management .

* This article  does not want to defame these great development in cardiology(PCI/CABG) . They have a  specific role to play. CABG AND PCI remain the only option for critical  lesions with limiting angina .But please remember without  proper  medical management  ( ie Targeting  the perpetuates of  crime )  both  PCI and CABG will be a big sham !

Final  message

Avoiding   the  lesion  or  attacking the lesion  is a  primitive  method to tackle CAD  . Passifying   the lesions  in a slow and gentle manner,   preventing  further progression  or regression  of lesions is the only  “sane” method for combating CAD   . PCI and by pass surgeries  can be termed  as  21st century’s   medical  adventure sports  which  has  limited role ,  in the overall control  of CAD  for the human kind .

And  now  answer this question . . .

Cardiologists attack the lesion and  surgeon avoids the lesion ?  Who is the winner in our fight against CAD  ?

Both of them are  clear losers .The winners are  all those  humble physicians and parmedical workers (or even the responsible lay public ) who  help recognise  the early forms  of  CAD  and  counsel properly to prevent it .

This is  what  Dean Ornish   in 1991  documented in  Lancet  which was never considered scientific   for the simple reason it has no commercial value !

Reference:

http://www.thelancet.it/journals/lancet/article/PII0140-6736(90)92230-F/fulltext

http://en.wikipedia.org/wiki/Dean_Ornish

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Acute coronary syndrome  is primarily a disease of blood vessel , which perfuses  the heart.  It can even be a disorder of blood, often called vulnerable blood which predispose  for intra- coronary thrombus .

Mind you  , heart is an innocent bystander ! to the onslaught of  coronary atherosclerosis !

Hence , we  often use two terminologies .

CAD : Pure vascular (Coronary )  disease without  any structural and functional impairment of heart  ( No Angina, No myocardial damage ) Most of the asymptomatic plaques  , non flow limiting  lesions, incidentally detected by the modern coronary imaging gadgets  fall in this category.

When does  CAD becomes CAHD ?

CAHD : Coronary artery heart disease .Here not only the coronary artery is diseased , but it has it’s mission fulfilled   ie target organ either damaged structurally (STEMI, NSTEMI ) or functionally (EST positive , Chronic stable angina CSA )

Does the heart does any wrong to suffer from Acute coronary  syndrome  ?

No, it is simply not .The fault lies in one or more  of the following   .Generally at-least two these factors are enough to impede blood flow )  . They  combine to produce an ACS.

  • Blood defect
  • Vessel wall defect
  • Slowing of flow (Stasis)

This is called as Virchow’s triad   suggested over 100 years ago . Still valid in the era of per cutaneous  aortic valve implantation.

* The concept of de-linking  disorders of  coronary  vascular disease  from myocardial disease  is vital  in understanding the implications of current modalities of treatment. 

Even though we PCIs target the culprit ie blood vessel , it need to  realised , we  always fall short of real target . . .namely the heart . In coronary interventions  the catheters and wires roam around superficially over the heart  and they never even touch the heart .This is the reason PCIs are struggling to prove it’s  worthiness over medical therapy in many CAHD patients , which can reach deep  into the vessel, heart  and even every individual cells of heart.

Many (or . . . is it most ?)  Interventional  cardiologists have a bad  reputation for ” failing to look  look beyond the lesion” .  It is estimated  a vast  number  of cathlabs  and CABG theaters worldwide  are engaged in futile  attempt to restore coronary artery patency after a target organ damage is done .This is akin to building flyovers  to dead and closed highways .

Salvaging a coronary  artery and reliving a coronary obstruction is an entirely unrelated and futile  exercise to  a patient who has a problem  primarily in  musculature .

The much debated concept of  documenting  myocardial viability  , before revascularisation  died a premature death as the concept  by itself , was not viable commercially . (Viability studies   , tend to tie down the hands of device industry further , some  interventional   cardiologists began to see this concept  as an  interference to their freedom to adventure  )

Of-course , now  we have  other parameters  phenomenon  like  FFR estimation by Doppler , epicardial  -myocardial dissociation, slow  flow , no re-flow are  gaining importance.

Final message

ACS is primarily a disease of blood vessel but it’s impact is huge on heart. We need to look beyond the lesion .Restoring  a blood vessel  patency  to an ailing organ (Heart ) is not synonymous with total  cardiac intervention  and protection . There is lot more to cardiac physiology other than it’s blood flow. Heart muscle is a too complex organ to be controlled by few balloons and wires  which beat around the bush.

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Stable angina is graded by Canadian cardiovascular society classification ( CCSC ) by 4 grades. Angina at rest  usually  denotes unstable angina. But,  patients with stable angina  may also experience rest angina according to CCSC ,  still this is   not considered as  unstable angina by many . Post prandial angina is one such  example.

Few consider post prandial angina as unstable angina . This sort of reasoning can not be faulted .

In  the logical sense ,  we are dealing with varied  categories of unstable angina.  The importance of diagnosing unstable angina is to intervene early ,  so that we can avoid  major adverse outcome .

The problem in CAD is , often , the plaques and angina do not  obey the conventional  rules  !

.The following permutations and combinations could be  observed in any coronary care unit .

  1. Unstable angina –  stable plaques  – stable ECG – stable patient
  2. Unstable angina – unstable plaques  –  unstable patient
  3. Unstable Angina  – unstable plaque  –  stable patient
  4. Stable Angina –  unstable plaque  –  unstable patient
  5. Stable angina  –  stable plaque  –    stable patient
  6. Stable angina –  unstable  plaque  – stable patient

Among the above 6 categories  2nd  is   probably  the most dangerous group and category 5 is most benign.

Post prandial angina is a serious  form of angina.It implies  , even   diversion of  little blood to GI system immediately after a meal can provoke an episode of  ischemia  .This infers a  very tight  lesion somewhere in the coronary tree,  very often it could be the  left main or proximal LAD.

Of course ,  there is  another mechanism for post prandial angina, namely GI neurotransmitters  like gut peptides acting as a coronary vasoconstrictor.

Snippets on  post prandial angina  .

It is also recognised , post prandial angina occurs more often during dinner, followed by lunch and breakfast. Carbohydrate foods are  more likely to precipitate it .

Does PPA cause ST depression ?

Logically it should .In reality It happens in few .

How to manage it ?

It is very important to recognise , even though this article  argues  for including  PPA  as UA, there is no acute thrombotic process during  an   episode of  post prandial angina . In fact , it is  more of a secondary UA due to altered  blood flow pattern.

So , do not admit these patients  in CCU and administer  heparin or 2a 3b blockers.  (Unless of course ,they have other forms of rest angina )

Link to reference

1 PP angina angiographic correlation

2.Effect of carbohydrate diet on postprandail angina

3.Hemodynamics of eating !

Final message

Post prandial angina has all the characters  of a severe form of angina  .There  is every reason to label it as UA .It is suggested , ACC,ESC, AHA  should consider including  post prandial  angina as  UA or at least  UA equivalent .This would help intervene this entity early.

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Poverty is the number one killer in this world . Malnutrition, infectious diseases  , poor maternal child and health are the leading killers. The life expectancy is short in many underdeveloped countries.

While the scenario  is dismal for most of the poor people in this world.

Can affulence be a risk factor for poor health ?

Yes. This seemingly awkward  answer is  many times true. The disease  acquired by affluence is labeled attractively as life style diseases . They are : Obesity, Diabetes mellitus, cardiovascular diseases, some forms of cancer etc .

coronary angiogram cardiology

How else can affluence affect the health of an individual ?

Apart from affluence being a risk factor ,  it  is a powerful  risk factor for getting  inappropriate  medicines,  procedures  &   surgeries  ,  hence  the resultant  adverse effects.

It is a  non-established fact , in  both  developed  and developing world , the single important  predictor of a given form of treatment  say  revascualrisation or  surgery  for CAD  is affordability to the treatment (Either  by insurance or  self payment) .Financial well being , interferes with applying  valid scientific principles on them . Applying  the  results of  the  land mark trials CAD trials ,   COURAGE  &  BARI 2D  are very difficult  for them , which argues for   simple , less costly , less glamorous medical therapy for CAD.

Example 1

A wealthy adult  male  who  lands  up for master health check up  in a big state of the art  hospital found to have a  borderline stress test , CAG reveals a single vessel distal RCA disease .He was given an  option of PCI , undergoes  it ,  and ends up in a complication and damages his entire  inferior myocardial  territory.

Had he been a poor uninsured  guy , he would have promptly be  labeled as stable CAD and would have been on  good medical therapy*  and his  myocardium could have been saved .

* PCI can never be an option  for him ,  courtesy : His wealth status !

Mind you , this is not an isolated  example, such  affordability  guided treatment modalities  are rampant in the society and has a potential to make  our rich and  affluent a major health risk target !

Final message

Being wealthy and affluent can also be a health risk factor. While the poor suffer from lack of health care the  rich many times suffer because of  too much health care ! (or  Is it care less ,  health care ?)

Coming Soon

How reccession  time  is a  boon  for human health  !

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