His ECG looked like

Ventricular ectopic recorded in bi-geminal rhythm

His  echocardiogram showed

 

His echo showed randomly timed mitral regurgitation was detected .See the Doppler MR jets below.

We know ventricles are integral  part of mitral valve apparatus  .Hence  it  wouldn’t  be a surprise to note  abnormally timed ventricular contraction  can  have a major impact  on mitral valve function.

When ventricles  prematurely begin  to contract  ( As  during  VPDs) it  interferes with  opening of mitral valve. In other words every VPD  technically imparts a  sort of  diastolic dysfunction !

VPDs occur in which part of cardiac cycle ?

VPDs  occur  either in early   or mid  diastole . Thank fully VPDs can not occur in systole . (Refractory period )

What would be the status of mitral valve at times of  VPDs?

Though it depends upon the timing of VPD ,  generally it interrupts the rapid inflow period of diastole .

In fact ,  it converts the cardiac  cycle from diastole to a partial systole or  a combination( fusion ) of diastole   and systole ! *

More MR jets are visualised than LV filling waves . Note the some of the E waves are sandwiched between two MR jets. ECG gating should have made this image more interesting .Any way , we have good MR jets to time systole nicely

* Is that a funny  imagination  ?

During   diastole ,  if  LV suddenly  begins  to contract   instead of  receiving the blood  ,  what will happen ?

VPDs are such a common arrhythmia , we  rarely  wondered  ,  it can have a dramatic  consequence  in a any  given cardiac cycle .While   the cardiologists think too  technically  their  patients observe with  shrewd  sense and tell us clearly  what  they feel  is  actually a   missed beat !

(Yeh  . . .  how simple  they describe the complex  hemo-dynamics  of  missing  diastole !)  .They also tell  us ,  next systole is felt as big thump as palpitation . (Post VPD potentiation )

Just imagine ,  if a patient  has  multiple VPDs  with  different  coupling intervals   that fall in different location of diastole  also  interspersed with sinus beats ,   how chaotic  would be the  the  mitral   filling .

This is what  is recorded in the above patient with multiple random MR jets .

Why all VPDs do  not cause MR ?

The timing is critical .We know all VPDs do  not generate a powerful contraction to cause MR. Atrial fibrillation, Prolonged PR intervals , heart blocks , critically raised LVEDP all can influence the trans mitral gradient . In fact these situation can result in  an  entity called diastolic MR that would be discussed later.

Can  VPD induced MR be  referred to  as diastolic MR ?

When VPDs  occur  in  diastole  , it  interrupts the diastole  and a new systole begins. In any  particular point of time there will be  leak into the LA  if the mitral valve is open .This is technically a new systole but in true sense it is the diastole of  the  previous beat . I wonder , whether   VPD induced MR  may be referred  to as one  form of  diastolic MR.  Of course ,  this MR can spill over to true  systole as well .

This also  makes  sense (Non !) as many of the VPDs do not open the  aortic valve ,   hence technically we can’t call the phase reset  by  all  VPDS   as a true systole !

What is the effect of VPDs  on pulmonary venous flow ?

Left atrial  cannon waves can occur that can elevate PCWP .This is the prime reason for resting or  exertional  dyspnea in these patients. Some may get a paradoxical relief  during exertion   as  exercise  suppress VPDs which are frequent at rest.

If VPDs can seriously interfere with mitral valve function , why  they are  often  considered benign  ?

VPDs are well tolerated* as long as  the  LV function is intact.  If VPDs are associated with  LV dysfunction  it  can initiate a vicious cycle of   hemodynamic deterioration .  Multiple VPDs  if left untreated can lead to progressive LV dilatation  in a  significant population .  Hence patients with  recurrent VPDS need some sort of  follow up. It  makes good medical sense to suppress VPDs in the long run. (Of course the  available anti VPD  drugs  are not very safe  !  The search for non toxic ,  ideal drug should go on !)

*”Well tolerated VPDs”   in no way  means  normal physiology.  Read a related article in my site.  “3 minutes crash course on VPDs”

Final message

VPDs  though considered  largely benign , can lead to dramatic  alterations in the  functions  of mitral valve , especially in diseased hearts.

We  must  realise  when ventricular  ectopic beats occur frequently  , it  interfere with the  both opening and closing of mitral valve.

It is really surprising  ,  the literature is  devoid of  major studies  about the  impact of  VPDs on  mitral valve  physiology . . . rather pathology !

The patient   defied  both  and  somehow landed in my echo lab  .  Looking at the ECG   I also  expected  it to be a  STEMI  evolving into a  Non Q  MI .

I was surprised  to find  only LVH with absolutely no wall motion defect  . There was no evidence of ASH,  HOCM or apical cardiomyoapthy as one of my fellows initially  suspected . His  EF was 70 %.   Cardiac enzymes were sent by then. When  I spent few minutes  with him ,  listening the history , it was very clear  what  he had was  non cardiac pain . In the anxiety ,  no one  got it right  about the character of pain ,which  was localised , lasted  for few seconds and  least suggesed angina.

The moral of the story is   listen to the patient  however dramatic the ECG may look !

What is special in this ECG ?

It is common for LVH with ST depression to be  mistaken for  ACS/NSTEMI

Here , there were  other  observations that  added  more  complexity .

• Presence  of  ST/T changes in inferior leads(ST elevation in lead 3)
• Bi-phasic  T wave in v1 to v3
• ST elevation  in precardial leads

In LVH  it is usual  to note  ST depresion , how do you explain ST elevation in LVH ?

ST elevation in LVH   may occur in  leads  v1 to v3   . It is very rare  for LVH to inscribe  ST  elevation in   v4 v5 v6  .   Why certain  leads elevate the ST segment while others depress  in LVH  is not clear. It may represent  incomplete LBBB pattern where the ST segment deviates opposite to the  dominant QRS  complex. Septal  hypertrophy often elevate  while free  wall  hypertrophy depress the ST segment . Since V5,V6 leads are free wall oriented , these leads  record  classical  ST depression .

Importance of Bi-Phasic T waves

Please remember  Bi phasic T waves are notorious for it’s  unpredictability. An  innocuous looking bi-phasic T waves  (especially  with dynamic behavior )   is a  harbinger of proximal  LAD or even left main disease.

Finally , what will be ECG  changes if a patient with classical  LVH  who  develops a  real  STEMI ?

• LV strain  pattern normalises ?
• Further ST depression  occurs ?
• No great changes . ECG  Looks near normal ?

Answer : ?

What is the significance  of   Bi-phasic T  waves : A  link to  a related post

It is primarily a  local phenomenon . The calcium channels  are primarily  arteriolar dilators . Since the  venules  lack much muscle they  are not much affected by the Amlodipine   .  This  facilitates flooding of  venules and leaks into the peri venular interstitial space. It may be apt to call Amlodipine induced edema  as a form of   local venous edema .

This results in near permanent  collection of fluid  especially  near  the ankle . Systemic fluid retention has no major role . However few patients may  show an  augmented   RASS  response due to sudden arteriolar dilatation  .  In these patients   addition of ACEI or ARB may help relieve  edema legs .The Amlodipine  induced edema is  dose  and  time dependent .(Cumulative)  . It is mostly benign in nature ,  rarely warrants withdrawal of the drug.  The edema can  occasionally be generalised   and weight  gain is  possible .

Other factors that increase the chance of edema is age , women  , obesity. They have loose  interstitial  tissues.Many especailly women complain tingling feeling in the edematous zone.

The calcium blocker induced edema is  an  exclusive feature of dihydrpyridine group  .(For some reason  , Verapamil and Diltiazem do not  share  this side effect .Are they a balanced Arteriolar and venous dilator  )

Can we use diuretics to treat Amlodipine induced edema legs ?

Hydrochorthiazide  is rarely useful as the primary problem is not in the renal  retention.

How to  treat Amlodipine induced edema ?

Unfortunately the popular combination with diuretics do not work . Angiotensin  inhibitors which has some veno dilatation is shown to reduce this edema  . ( COACH study . Olmesartan / Telmisartan combination  is an option ) .It defies logic ,  to  add  another anti HT drug for the sole  purpose of reducing  the side effect of the initial  anti HT drug . Ideally if  your patient is not tolerating  Amlodipine due to edema ,  switch to  an another group of  anti HT drugs.

Reference

http://www.isdbweb.org/documents/file/1664_2.pdf

Aspirin after all may not be safe as a primary prevention drug against CAD . It  seems ,  it considerably increases  the risk of   bleeding . The  new meta analysis just published in Archives of internal medicine  says so !

Be cautious it concludes  ! Since the   track record of evidence  based  medical science  ( and its reproducibility  )   looks   pathetic  in recent times  ,  we may expect another  stunning  study  very soon , with an exactly opposite conclusion  !

After thought

So , we have a  “vacancy  in  the top slot”  for primary prevention of CAD . Mind you ,  makers of  Prasugrel and  Ticagrelor  are already  fastening their seat belts !

The commonest and most important one being the mal-aligned conal septum encroaching the infundibulum .(This anterior migration of conal septum is responsible for the aortic  over ride and  VSD as well) .It is erroneous to  think  the RVH in  TOF is simply an after effect of RVOT obstruction .There  can be  intrinsic defects in the RV trabecuale  that hypertrophies and  traverses the RV cavity  in  randon fashion.

Soto described 6 types of obstruction in TOF in elegant anatomic and pathologic study in 1981. Every cardiology fellow must read this original article before going to the Board examination. http://circ.ahajournals.org/content/64/3/558.full.pdf+html

For some reason  God  has  not  arranged  the   RV inflow , body  and out flow  in a linear  fashion . ( ? Meant  for haemic  acceleration in the low pressure venous circuit  )  .In  TOF this becomes important.  It is curious to note even minor  muscle bundles that  criss cross the RV body  act  as a speed breaker and alter the stream and direction of blood flow  .This  is why ,  TOF  can generate   systolic murmurs in various shapes and  time  over the left para-sternal area .(In TOF one can get a murmur right from left  2nd space to well down the lower sternal area )

What are the fixed obstruction in TOF ?

The  resistance  to  blood flow  within the RV  is often multiple ,  extend  from RV body to  pulmonary arterial branch points. It is important to realise few of the obstructions are fixed in nature.  Differentiation of dynamic vs static obstruction  is important in therapeutic aspect also. The efficacy of beta blockers is directly related to the ratio of dynamic vs fixed resistance .

Hypertrophied  trabecuale sept0 margianlis (TSM) usually offers fixed resistance. The infundiubulm is the only place where one can expect a dynamic component . If the annulus and valvualr PS  caused more of a  fixed obstruction

Final message

So,  fellows beware if some one asks this  question “Where is the site of obstruction in TOF “  .Be ready with an elaborate answer . It is better to classify according to sites  of obstruction   with specific  reference to  dynamic or static nature .

http://circ.ahajournals.org/content/64/3/558.full.pdf+html

William Rashkind a cardiologist from Children’s hospital, Philadelphia in 1966  probably is the first person who thought it was indeed possible to use a wire and balloon as cardiac therapeutic intervention .When surgeons were groping in dark with  sick cyanotic new borns with dTGV , He along with Miller executed their idea.

It was published in JAMA

How the Rashkind  has revolutionized  our approach to congenital  heart disease  is evident from the current guidelines in 2011.

The procedure has since evolved with improving hardware and we are able to ferry a blade into the IAS for cutting .

Current  recommendations for Atrial  septostomy

It is primarily useful

1. Atrial septostomy  to enhance atrial  mixing (eg, transposition of the great vessels with restrictive/intact atrial communication) or to decompress the left atrium
2.During Extra corporeal membrane oxygenation (ECMO)   to decompression   of left atrial hypertension

3.If there is poor cardiac return from ECMO  circuit  low venous saturations  (Class 1 Evidence  C)
It may also be tried in  (Class 2 )
1.  Hypoplastic left heart syndrome  with  restrictive atrial communication.

2.  Static balloon dilation of  l synthetic / bioprosthetic  IAS  (eg, Gore-Tex)

3. Tricuspid atresia with restrictive atrial  communication

4 .Pulmonary atresia with intact IVS

5. TAPVC with  restrictive atrial communication.

6. Primary pulmonary hypertension / Eisenmneger VSD/PDA .(Occasionally useful )

Reference

http://circ.ahajournals.org/content/123/22/2607.full.pdf+html

                              A scene  from  Jaipur’s   main commercial  road

Lame  ducks on the road !

             My all time  favorite  news photograph taken  from a Tamil  daily Dinakaran

An After thought

In this fast and furious world ,  the medical profession  too suffers from the same disarray like  the  Jaipur traffic !

• Let  us prey  for the   Noble professionals  to be  blessed with  more   discipline,  character , conduct  and  knowledge ( yeh . . .knowledge  ranks  last and least !)  .
• Let us be focused on task .
• Let us  also  prey for the strength to differentiate  facts from fiction,  distinguish trivia from  the momentous.
• And finally let us  have the courage to follow the truth !

In this era of explosive information  , we rarely get clear-cut answers to  our  problems.

There are rare  exceptions . Here is an wonderful  review article on the issue of multi-vessel CAD  during STEMI. (http://www.ncbi.nlm.nih.gov/pmc/articles)   Especially  heartening ,   is the way the article concludes . It can not be more crisp than this !

Conclusion (Reproduced from the above article )

•  Single-vessel acute PCI should be the default strategy (to treat only the IRA during the acute phase of STEMI).

• Acute multi-vessel PCI can be justified only in haemo-dynamically  unstable patients with multiple truly critical (90%) lesions.

• Significant lesions of the non-culprit arteries should be treated either medically or by staged revascularization procedures— both options are currently acceptable.

In-spite of the clearest possible guidelines   there  are frequent   debates  going on  for aggressive approach  to non IRA  lesions in hemo-dynamically  stable patients  as well  !  Many of the  learned cardiologists are calling for a  a  “legal violation”  of above guidelines !

The term staged primary PCI (Non IRA)  is often misused  . One such strategy is  rescheduling the non IRA PCI by 24 to 48 hours  later  than  the primary  ira PCI.  This  enables  us to violate the guidelines silently   . Please mind , the excess morbidity of non IRA PCI is due to the altered hemo -rheology which is expected to persist for at least few weeks !

I have recently come across a  cardiologist performing RCA PCI on Monday and LAD PCI (A 70 % lesion )  on Wednesday in a hemo-dynamically stable inferior STEMI ( Incidentally , he  felt  no guilt  , as  he was   ignorant about  existence of such  guidelines . In fact ,  he wanted to finish both angioplasties  on the same sitting  . It seems  he had to defer  the LAD  PCI   to Wednesday as the initial insurance  limit was exceeded   .

I do not want to dwell into another  unfortunate story  , as  this   patient had  to borrow  Rs 1.25lakh for  his life saving second stent  !

Final message

Come on   . . . let us violate the primary PCI guidelines . . . after all , our patients do not know the reality !

Reference:

The moment  we  saw the angiogram,   we knew ,  we had a real problem on hand !  . First of all ,  It looked a complex lesion for  a pPCI .(A brief  thought about an emergency CABG  creeped in,  but was dropped  with   enthusiastic residents voted unequivocally in favor of  PCI . Of course , to be frank  we didn’t have a  CABG team ready either ! )

So the plan  was : To open the IRA  . . .  &   forget the non IRA (  for the time being )  which  is the current management mantra as on 2012 !

Trouble from unusual  quarters !  By the way   . . . which is the IRA  ?

Even as the consultant  was  initiating  the rituals with wires and balloons  to tackle the LCX , some one behind the consultant  mumbled  “why can’t the LAD be  the IRA “  After all  , it  also has  a critical lesion  and  mind you  we are dealing a case of   anterior MI  !) . That mumble  was  loud enough to create buzz of confusion in cath lab .

Now everyone quipped  , ” IRA is  what ?

Is that  the critical mid LAD lesion ?

(or ) Is it the total LCX   (or ) Both ?

Logic would suggest in the setting of STEMI   any  total occlusion should be considered as IRA  . Of course  , one can not be dogmatic about it.  When a patient is having   anterolateal MI  both LAD  and  LCX can contribute to the MI .

What about  proposing a new  concept  of  “Double IRA” ?

When  multiple  plaques  are  activated suddenly in unstable angina ,  it is  possible  for multiple IRAs  to occur  in STEMI as well . But this issue is rarely discussed in literature .

Other  possibilities

The 100 %  lesion  in LCX  could  still be the primary culprit  and  a  thrombus migration into LAD   might have  resulted  in  infarct  extension into anterior wall .

Further ,  confounding may occur if a patient with chronic total occlusion  develop a  SEMI  . It  makes it really difficult to identify the  IRA.

When  the supposedly gold standard coronary angiogram   fails to identify the IRA ,  what shall  we do ?

Go to the basics . The good old ECG might help .

(Please beware in a patient  with pre- existing  multi-vesel CAD  , none of  the ECG algorithms work  to localise  IRA !(Especially   the famous Wellen’s miserably fails ! )

Still unclear ?  Look for the wall  motion defects  in echo . An echo cardiogram (Need to be meticulous )   will help match the  dysfunctional segment with IRA.

Wall  motion defects are notoriously  error prone in ACS  for  two reasons.

• We do not have easy and accurate  methods to differentiate ischemic wall motion defect from infarct related wall motion defects.
• Tethering artifacts  ,  differential behavior  epicardial  vs endocardial ischema on contractility   will confound  the issue .

So what is left ?

One  need to  go back  to the CAG again  . Have  a critical  look  at the lesion once more. Look for thrombus or eccentric /unstable lesions . If  present it is  going  to be the IRA in 90 % of times. Let it be a  wild guess in the remaining 10 % .

There is also a  practical solution . Poke the lesions  with your favorite  guidewire ! . The one that  gives way easily  is likely to be the  IRA !

Finally,  if the confusion still prevails ,

Stent both the  lesions. That’s what , was  done to this patient . Many would have thought ,  this should  have been the default approach instead of scratching  our heads to identify the IRA ,  wasting crucial minutes !

Final message  : 

Current  guidelines do not recommend  pPCI for non -IRA   at the same sitting  of  IRA pPCI . However the issue  of  IRA  “too close to call “ is  rarely addressed.I do not know  how commonly  this issue is encountered  in angiographic  core labs that deal  huge loads  of pPCI world wide .

Our  early  experience  suggest  the problem is   real ,  unique and  definitely not rare  .

What is your take ?  We argue guidelines committee   to  specifically  address  the issue of  uncertain IRA as a  branch point in the pPCI decision making  tree !

                                        “  In most  life instances  the primary determinant  blood pressure  is not the state of cardiac contractility  “

                 For many ,  this  would  appear as  shocker of  a statement !

Fellows  should not be  confused with above inference  . What it means is ,  the  heart initiates  the blood pressure by a brief  period of  systole .The pulse wave attains a peak during ejection phase  . This is the peak systolic blood pressure  . There is nothing called  sustained  systolic  blood pressure .  The quantum and  duration of peak systolic pressure  contributed by the LV contraction  is  far less than we imagine .

If blood pressure is to be controlled   primarily  by  cardiac contractility , how is that ,  a  blood  pressure of   about 80mmhg is maintained throughout diastole when the heart is taking rest and the  aortic  valves  are closed  ?

Image courtesy http://www.mayoclinicproceedings.com/content/85/5/460

The  major elastic blood vessels  aorta and the major branches use the potential  energy gained during systole  (Like a rubber band )  into   kinetic energy as vessels recoil during diastole . This recoil  imparts an   important component  to the  diastolic blood pressure  augmentation  and maintenance.

It is  prudent to note  since  diastole is  much  longer than systole  , integrity of the vascular tree  become  much more important  to maintain the blood  pressure  till the next systole arrives.

Note

*The cardiac contractility  , might  still be  important  in determining systolic BP  in  patients  with  severely compromised  LV function** For example ,  in  dilated cardiomyopathy  with  LV failure ,  systolic blood pressure will  be directly related to LV  function.  When LV function is critically  low , the elastic  blood vessels  fail  to  amplify the blood pressure  beyond  a limit.

**Still it is not  uncommon to find high systolic blood pressure  recorded in the back ground of with severe LV dysfunction especially hypertensive individuals.

What happens during aging ?

The  aorta and it’s major branches  gets thickened , the  vascular collagen  goes  cracking  with wear and tear of  life.  In effect , these vessels become less compliant . So , when blood is rapidly ejected  from the  left ventricle  into aorta  and their branches  it’s  distensibility   is  reduced  .This  fails to dampen the  pressure  wave  and  hence systolic  pressure spiking occurs. This we refer to systolic hypertension of elderly.

It is  important to  emphasise   major elastic arteries  has a big  say in fixing the systolic pressure. For the same cardiac output systolic pressure can surge in elderly this  is why we have kept the normal  in adults as 16o mmhg.

Another key point to be understood  is  ,  Aortic compliance  has an impact on diastole blood  pressure too ! . The  stiff vessels during diastole bring  less diastolic recoil. Diastolic recoil of large elastic arteries  determines the diastolic pressure . Hence there  could be  a mild fall in diastolic pressure with physiological aging when recoil is attenuated .  Since the  reduced diastolic  recoil ensures diastolic pressure from being elevated  the entity is aptly named as isolated systolic hypertension.(ISH)

Image courtesey :Norman M Kaplan, Lionel H Opie Lancet 2006; 367: 168–76

Final message

While the traditional  teaching  ramains  as  systolic blood  pressure  would be determined by cardiac contractility  / cardiac out put , while the   diastolic pressure is determined by peripheral  vascular  resistance .This is not an absolute reality ,  rather it is  too simplistic way of teaching circulatory physiology !

The  peak systolic blood  pressure is more often determined by the integrity of  Aortic  and major arteries   rather than cardiac contractility  and stroke volume. Similarly , aortic properties do have a  say in the diastolic pressure as well !

Further reading and debate

 The net effect of aging  on blood pressure :  Is it  physiological or pathological  ?

  Should we  treat  this  raised  pressure due to aging  related systolic hypertension  ?

There is a huge controversy going around ,  regarding the need  of  treating this mild elevation of systolic  blood pressure due to arterial stiffening .This will be addressed separately in this forum .

Reference

http://www.mayoclinicproceedings.com/content/85/5/460.full.pdf+html