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In one of  our patients  who had a recent STEMI , CAG revealed  70% LAD  lesion  with   TIMI 1  flow .The distal run off was slow .He had moderate LV dysfunction with no major symptoms. The angiogram was done routinely .( Yes . . . routine CAG- the term I do not relish ,  while it is becoming a way of  life for all learned cardiologists !)

I  was discussing   this case with my fellows and  about medical management of CAD. I  told them  Aspirin will help prevent ACS, statins will stabilise the plaques , beta blocker would prevent cardiac  events by blunting adrenergic surges and Nitrates is a powerful coronary vasodilator that  will improve the  coronary blood flow

A final year MD fellow  threw a  direct  question at me .

Sir,  do you mean  Nitrates  would increase the  TIMI  flow from 1 to 3  in the long term in this patient ?

I was taken-aback  for a moment . . .   and thanked my student for a valid question .

Nitroglycerine is  a powerful coronary vasodilator  we are taught for nearly  half a century . Oral nitrates are used  liberally in the chronic management of  angina. It is a multi billion  dollar market.

Has it been documented to improve coronary blood flow in the long term ?

No

Why then it is  used long term ?

It is a clear case  of  inappropriate medical therapeutics .

* The confusion is partly due to our mix up the mechanism of  relief of angina from coronary vasodilataion. Realistically , NTG should me known  more as a powerful venodilator reducing the preload . It  dramatically reduces the LV filing pressure  and relieves sub-endocardial stress  .This is the major determinant for angina relief .(Of course after-load reduction also helps)

Final message

Nitrates  should be used only for relief of an episode of angina or just to prevent It .This may surprise you  , Nitrates has no documented  efficacy  in the long term management  of angina.

Anatomically ventricles are separated by a single muscular wall namely inter ventricular septum.But physiologically it has to contribute to both ventricular function.

How does IVS  is able to achieve this ?

For the naked eye both ventricles appear to contract almost simultaneously , but there is an intrinsic delay , first the LV contracts , followed by about 70 milliseconds right ventricle generates the peak pressure. So the IVS is able to help in a sequential, & coordinated contractions.This is called ventricular interdependence. Please note pericardium also contributes to this  .

Final message

The mechanical function of  IVS is effectively  and intelligently shared by both chambers. The electrical  delay even in milliseconds is enough to facilitate this sharing .Such is the power of nature. From this concept it is obvious LV dysfunction can have an adverse effect on RV function & vice versa.Similarly any electrical delay( LBBB, RBBB  ) can impact the septal function. Fortunately the myocardium has much reserve function , bundle branch blocks in isolation rarely result in serious consequences unless there is loss of associated muscle mass.

hypokalemia U wave ECGhypokalemia U wave ECG 2

characters of normal U waves

It is usually recorded in the same direction as that of T waves

If it is opposite  it should be given significance .(Ischemic U waves ?)

More prominent in bradycardia

Mechanism of U waves

There are Three hypothesis

  1. Repolarization of papillary muscle
  2. Late repolarization of M cells in Mid myocardium
  3. After potential  to QRS  ie a  form of depolarization

Currently  the third option appears  closer to truth

How hypokalemia  result in tall U waves ?

If Hyperkalemia elevates T waves  it is natural  to expect  hypokalemia  to blunt , flatten or Invert the T waves .Of course , this happens in many . In others with severe hypokalemia an intact  T  is accompanied by a tall upright U  as well .This adds a mystery twist* to the exact genesis of this wave .

* During diastole cell membrane is closer to k +  if K + is deficient it tends to drift . (Some where i heard this   . . . but I do not understand it fully !)

.

ECG U waves 2

Reference

Both  entities   refer  to contraction of vascular smooth muscle.Vascular smooth muscle tone  is under the control of autonomic neuro and humoral system.

Local mechanical , stretch  receptors also  play a role .( local temperature -Cold vasoconstriction  , warmth relieves it ) Abnormal elevated  vascular  tone occur in pathological situations ( Vascular interventions, surgery , drugs, extreme cold ,   )

Both terms are closely related often used interchangeably .There are some subtle differences though , mainly in the usage pattern.

Vasospasm

Is generally a   regional   phenomenon implying central mechanisms  are less  operative.

A local  trigger mechanical or biochemical .( Even a mechanical drag can cause a spasm

It is often transient .

Occurs primarily in small , medium blood vessels .(I  wonder whether  Aorta can go for  spasm !)

Clinical examples

  • Catheter induced vasomotor in cath lab (Radial spasm)
  • Spasm associated with plaque  Prinzmetal angina
  • Cerebral vessel spasm after sub arachnoid hemorrhage ( Need not be transient )

Vasoconstriction

This is also result in  constriction of blood vessels

But the blood vessels involved  are in  micro circulation like capillaries and arterioles .

Often sustained (If transient does it become vasospasm ?)

Vasoconstriction  often involves wide areas and may result in elevated regional or systemic vascular resistance . Hence  it often  result in elevated  blood pressure.

Clinical example

  • Normal Blod pressure  regulation y autonomic mediated vasoconstriction
  • Arteriolar  constriction with Nor adrenaline , dopamine .
  • Capillary Vasoconstriction  due to cold (Raynaud phenomenon )

* Please note other terms like vascular tone , vasomotion   closely competes with above .

Final message

Most of the confusion in medical terminologies are man-made.Both vasospasm and vasoconstriction are  often used  interchangeably .It  is ideal to use  the former for a transient , localised response  in large caliber vessel , and the latter when it occurs as  a general response to altered autonomic  tone and  involve the micro vasculature.

Rheumatic fever and RHD is still a major cause for  cardio vascular morbidity and mortality in India .It seems , improving quality of life  has little  impact on the incidence .(We could realise  this as  we sit in the cardiology OPD of a 200 year old hospital !) There is no country wide data on the true prevalence .  Our understanding of rheumatic heart disease is based on isolated  studies on localized populations .

Of late , cardiology   resources  in our country is diverted towards  much glamorous CAD the poor continue to  suffer with  RHD.

Just Imagine many   hospitals indulge in 1000s of PTCA every year  but hardly do  a  hand full of PTMCs.

How our cath  lab resources  are used   across the breadth and length of country needs some introspection (Currently , I believe we have about 750   labs ) .I think there should  be a binding legislation  in every cath lab .For every 10 PTCAs done   at least one PTMC must be done to heal the poor .( Like the Air-craft license  .You can’t fly only the lucrative metro sector is given only if IT  services less developed areas )

In this scenario ,  it is a pleasant  surprise  to find a  wonderful review article on RHD from the two pioneers ,  in lesser known medical journal IJMR  .

Review article rheumatic fever  Indian journal of medical researchEspecially heartening  is  the fact ,  it is a collective effort  from two  distant  regions of India ( Kochi from down south and  New Delhi In the north) . While politicians keep the divide , it is a great  work  of the authors , which  would help  youngsters  who  would like  to go on a national mission on eradication of RHD. .

Reference

http://www.icmr.nic.in/ijmr/2013/april/centenary%20review%20article.pdf

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2840767/#CIT12

There is no primary rheumatic myocardial dysfunction .The LV dysfunction is related to the valvular lesion especially mitral regurgitation.While this is 100 % true in chronic RHD ,surprisingly it holds good even in acute rheumatic fever as well .(We have been thinking wrongly that acute myocarditis is responsible for most cases of cardiac failure in Acute rheumatic fever !)

( Incidence of LV dysfunction is still noted in 5% in RHD.This is may be due to chronic underfilling of LV in mitral stenosis, fibrosis secondory to hemodynmic stress as in Aortic stenosis or more commonly associated CAD.)

It is a paradox to note myocardits being a major component in acute rheumatic fever (ARF) ,still it does not persist long term .It invariably resolves and the injury to the valves goes on to result in progressive valve damage .
It is heartening to note this phenomenon in ARF as myocardial involvement behaves just like joint involvement.
Shall we modify the famous statement of the canadian Pathologist William Boyd Rheumatic fever licks the joint but bites the heart”
Though ARF bites the vlave , it simply licks the myocardium like the joints
Is there a chronic indolent myocarditis ?
It was Initially thought there could be process of chronic myocardial inflammation.But now it is almost proven there is no entity like that .
But , it is not uncommon some patients with RHD present with significant LV dysfunction which in all probability unrelated to rheumatic activity .
Assignment for cardiology fellows .
1.Where in the heart Ascoff bodies are densely found ?
  1. Mainly over the valve leaflets
  2. Atrial muscle
  3. Ventricular myocardium
  4. Pericardium
2.Does Ascoff bodies disappear in Chronic RHD ?
Reference

 

asd-closure-device-www-drsvenkatesan-com

The following  factors are critical determinants of the success of ASD device closure

  1. Location of the defect ( Only ostium secundum )
  2. Size of the defect (<35mm .Never forget  simple truth , larger the defect shorter would be the  rim )
  3. Shape  of the defect (Please note ,none are strictly circular but most devices are ! )
  4. Eccentricity of the defect (RA aspect of ASD need not match LA aspect)
  5. Length of the rim ( 5mm said to be adequate)
  6. Thickness of the rim ( Least respected parameter .Thin filament like rims are notorious  in sagging the device into RA)
  7. Pre and Per- operative TEE (As Vital as the procedure)
  8. Technical expertise . (This includes extreme patience  of the primary operator .Most sub optimal results and complications are related to this.
  9. Good team ( Not every  interventional  cardiologist should  attempt this !)
  10. Courage to abandon the procedure
  11. Device brand (Probably less important )

One of my otherwise  well behaving  patient ,  suddenly asked me this question ,  before leaving my  clinic  after a 15 minute consult .

Doctor  . . . I am taking the clopidgrel and aspirin  for 5 years like a vitamin tablet  . . . is that all right  doctor ?

I just got curious, I checked  the prescription again . Yeh ,  he was right !

I have  been mechanically writing  Tablet Clopitab  A  since 2008 !

Clopidogrel abuse long term

For what ?

Some sort of CAD !   Was it for ACS ?   No , it was for chronic stable angina . No PCI,  . . . no DES !

Why the hell  he is taking dual anti-platelet  therapy for 5 years ?

Some  body  , some  where  , has  prescribed it . This man  is taking it  for years together with absolute sanctity.

I was amused  . . . it is also  my mistake . Why it never struck me  to scrutinize the prescription ?

I thanked him . I  removed clopidogrel  from the list , and asked him to continue tablet Ecosprin 150mg  for some time .

( And  now I  had a genuine doubt  ! Does he have CAD at all ! I browsed his file , I couldn’t  find a true documentation for CAD  as I feared  !)

I asked him to get back with an  exercise test ,  . . .  if it comes negative i  can even stop the aspirin as well  I  explained  him  ! (Now he got amused !)

Final message

Who wants Knowledge ?

It is  dumped every  where , free of cost  . . .  both in real and cyber world .Applying it requires more sense  .  and my patient  taught me that  !

Patients  not only  help us  earn  our  bread  and butter , they  do  enrich  our brain  as well ! Never get humiliated when a patient teaches  you a lesson in medicine !

Hypertension is  probably the most   important clinical entity for physicians
for decades .With the advent of modern interventional cardiology management of HT with  drugs have become a  less glamarous job for us. Still , the quantum of the problem and it’s impact on the  risk of CAD and progression   remain a major issue.
There many  different bodies periodically coughing  up guidelines  to manage HT.
  1. JNC from USA
  2. British Hypertension society from UK
  3. European society of cardiology
  4. World hypertension league
  5. Finally WHO guidelines* ( It is not a regular exercise ,WHO releases it  as and when it feels like !)

The stakes are high for the drug industry .Anti hypertensive drugs are the  major source of revenue  to them . Any dip in per capita consumption will have direct impact on their health ! ( WHO bothers about public health ? )

The so called scientific  guidelines,  are generally made balancing patients health vis a vis drug companies health .I have found more often than not it was tilted towards the industry .

The fact that there are multiple guideline with varying impact factors makes sure the confusion among the global physician intact . This is one of the aims of the pharma companies as they influence heavily  when to initiate the treatment ,  and what we are  supposed to prescribe.
Some of the guideline are notorious for insinuations . One example was about the definition of pre hypertension  few years ago .It has since been removed  from the literature after a critical debate .

* One may wonder why I’m focusing always  on non scientific  issues more than academics .(I some how feel non scientific factors are going to impact our health more than any other factor in the coming  generations  )

Now is the beginning of a balance .

European society of cardiology 2013 guidelines for hypertension
Among these guidelines  I would  think  ESC is close to reality and fairness.
Even    it was carrying dubious advices till recently .Now they have come out with new one in 2013.Most changes are  welcome.
  1. It is essentially about cleansing the contaminated guidelines
  2. Removing unnecessary medications
  3. Unified definition.
  4. More efforts to identify true secondary HT
The salient  points
There are  18 point update in the ESC 2013 . All of them are great . Essentially they are about the basics we have been  taught as we learnt in our final year MBBS. (The rest of our life we have to unlearn  the junk we have accrued over the years  from various CMEs )
I can modify it and  short list
  1. Do not start too early .Have universal definition (Now 140mmhg)
  2. Respect non drug treatment ,( However attractive the  gold tipped pen the  representative leaves  in your consulting suit !)
  3. Avoid using multiple drugs
  4. Never miss a secondary HT .( If  diastolic BP> 110mmh almost always a renal component would be there .Remember Conn syndrome (Primary aldosteronism )  is 10 times more common than much hyped pheochromocytoma ! Just do K+ levels to detect this )
  5. In CAD patients never treat HT in isolation .( Measure blood pressure with sugar and  lipid 120 /70 mg of LDL )
ESC 2013 is a commendable Initiative . It has  tried to remove most errors of the past .obviously  the pharma industry will be unhappy as it will definitely bring down  total drug consumption the  population.
Final message
HT  is an important target  for prevention and management of CAD
Thanks to the much maligned pharma industry  .
We have good drugs.Use it judiciously . Try to reduce the number of drugs .
If possible make them drug free.
If a patients taking   beta  blocker for associated  cardiac condition do not add another anti HT drug . (Recall  from your distant memory , beta blocker is a anti HT drug too !)
Simply follow common sense . (* If you think you  lack  it  ,  get  it from your learnt patients .Many  of them have in plenty . I often do that . One  question they keep asking  “Should I take this drug  life long doctor ?”  is a definite common sense booster!  )

A Cardiologist will never accept  the diagnosis ,  if a technician reports   a  ECG as normal in a  patient with chest  pain   . . .

While , the same cardiologist  gleefully  accepts  an  echocardiogram   done by a technician  and  treats  the patient without  verifying the veracity of the finding !

Why ?

Some where along the cardiology training  , we have been made to believe Interpreting  Echo Images does not require serious medical knowledge . . . but we strongly believe  ECG  cannot be read by technicians however well they are trained .(In-spite of the fact , Echo images are highly dependent on the person who does it , while ECG wave forms are  totally independent of the person who record it ! )

ECG, still has a  prestigious place  in cardiologist’s mind ,  while Echo is often considered  an inferior  Investigation.  Many of us consider ECG interpretation  as a  brainy work while Echo image acquisition and  interpretation is perceived a dumb job* !

Lastly , probably most importantly ,  performing  Echo  is   a time intensive process for the  present day cardiologist  who’s hands are tied with  catheters and  guide-wires  .He has little time for  the meanly echo . .  . hence  ready to compromise on the quality .

* With due respects to all non invasive cardiologists (That includes the author !)

Final  message

I would think it is  fundamentally inappropriate  for technician  to  report Echocardiogram (Of-course they may record it  ) . Unfortunately , for some reason this practice is continued  in many  parts of world .