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Archive for the ‘valvular heart disease’ Category

Regurgitant  lesions of cardiac valves  are often tricky for the heart . Myocardium shows “love- hate” relationship with these  leaky valves.  Some of them are  “sort of”  stress relievers for  LV . A mild MR will make the LV comfortable in terms of wall stress. When the wall stress is reduced the contractility increases and LV EF may raise a little.Hence EF is never going to help us to assess true LV function in MR .

LV end diastolic dimension(LVEDD) is  a preload dependent  parameter .A patient with 6.5cm LV EDD  may still  have good contractility  and he may reach even a  40mm LV ESD, implying an intact LV function.

LV function should be best  assessed  in systole .(After all ,  systole is the prime function of heart) .Further , it should be assessed when the LV is  free from  influence of the all  loading  conditions of heart .  (Note : The initial part of systole  depends on after load. As the systole progresses the influence  of after-load lessens .In the pressure volume loop* , the point at which loading conditions are least operative is end systole.)

* Please realise , heart is a dynamic organ there is no true load independent point in cardiac cycle  as pressure and volume are eternally coupled.

What happens in AR ?

The same rule applies for Aortic regurgitation, but the parameters worsen little later than that of MR. For same degree of regurgitant fraction MR will require early surgery than AR.The reason for better  tolerablity of  AR  is due to largely  intact LA function and compliance till very late stages of AR.(In AR- it’s single chamber volume overload , while in MR  it’s two chambers !)

Final message

LVEDD is not used in assessing MR  as it is a pre-load dependent parameter that will not reflect true myocardial  function /dysfunction. LV ESD is fairly accurate  measure of LV systolic function minus all loading factors .

Watch out  for next topic

Vasodilator therapy in MR and AR : How is it different ?

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I wish to  be in New Zealand , not only because of the stunning  natural beauty but also to pay tribute to one of the great  cardiac surgeons  of our time from Auckland .
An alluring  country side cricket ground  abutting the runway  . . . Queenstown I think !

Sir Brian Gerald Barratt-Boyes (1924-2006), Who pioneered all forms of  heart surgery that  specifically included  complex congenial heart disease . Thousands of Kiwi   children are alive and leading a  magnificent life today  because of this  man from Green lane an alumni of Mayo .

barret boyce tof intra cardiac repair cardiac surgeon

Many heart surgeons from India and Asia pacific have trained under him .

greenlane

Green lane Hospital Auckland.

This is the  hospital where Barrat Boyes worked headed the department of cardiac surgery .He had to over come large bureaucratic hurdles before becoming world ‘s leading cardiac surgery center. And , he lives everyday  in all cardiac units   through this book .

barratt boyce kirklin

Here is a link to pay tribute to this extraordinary man.

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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

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The answer is  simple . 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  .(I have been thinking acute myocarditis is responsible for most cases of cardiac failure in Acute rheumatic fever !)
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 heart  , it  relishes only the valve  tissue and bites it harder ,  while  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

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Why should mitral  annulus gets calcified ? .  Degenerative  calcification can be benign in  elderly .  If it occurs prematurely (say < 55 years )   there is enough reasons to worry .  This may represent a systemic vascular inflammation and  is considered a surrogate marker for athero- vascular -sclerosis .  A study from Cidar Sinai  , Los angels  has well documented the link way back in 2003  !

mitral annular calcification mac cad link

This is a  large study involving  17 735 patients (who were investigated for symptoms of CAD )   were screened.

The incidence  of MAC was high (As expected !)

  • 35% > 65 years
  • 5 %  < 65 years
Angiography  revealed more surprises .
  • The incidence of angiographic  CAD among those who had MAC and no MAC   was  88% v68% respectively ,( p = 0.0004),
  • Left main coronary artery disease  was (14% 4%, p = 0.009)
  • Triple vessel disease  was (54% v33%, p = 0.002).
mitral annular calcification  www_drsvenkatesan_co_in

Image source  S.Atar ,  Heart 2003 : 89, 161-164

Conclusion
This study concluded ,  CAD is more aggressive in patients with MAC. It can  also be  an independent  predictor of  high risk CAD .
Further Implications  of MAC
  1. MAC is more common in women, especially diabetics .
  2. Degenerative Mitral regurgitation  is common ,rarely  mitral stenosis
  3. Recurrent VPDs and even  trouble some mitral annular VT is possible
  4. Extensive calcific lesions in coronary  artery is also reported with MAC.
Link between Stroke and MAC .
This was well proven by this paper  published in  NEJM in 1992.
MITRAL ANNULAR CALCIFICATION AND STROKE NEJM  EMELIA BENJAMIN 1992

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VPDs are such a common cardiac arrhythmia . We also know most are benign .Still modern science demands to rule out structural heart disease in any patient with multiple VPDs.

When ventricles get irritated it reacts with VPDs . ( The irritants  can be anatomical , physiological or primary electrical)

Echo can detect only anatomical irritants .We are recognising  more such focus for VPDs . Hence idiopathic VPDs  may simply reflect our ignorance !  A focused  echocardiogram is  required .

The following conditions are often observed in patients  with recurrent VPDs

  1. Posterior Mitral annular calcification (Especially in women ) –Annular VPDs
  2. Aortic valve degeneration /Bicuspid aortic valve with calcification – Cuspal VPDs
  3. Mitral valve prolapse in young -Stretch induced  Pap muscle VPDs
  4. Minimal  pericardial effusions with adherent epicarditis
  5. LV false tendons-Stretch VPDs
  6. RVOT lipid focus -Subclinical ARVD
  7. LVH and Hypertension –Fibrotic VPDs    
  8. Asymmetric septal hypertrophy
  9. Scars in MI/ DCMs
  10. infiltrations in RCMs (Any Interstitial heart disease )

(Conditions 7 and 8 are  common disorders myocardium  just included to  complete the list )

**Please note ,above mentioned entites are anatomical irritants .There is a whole lot of physiological  irritants

that can induce VPDs .  ( Hypoxia, Excess catecholamines ,  K + fluxes ,  acidotic milieu etc ) .

*** Another group is primary electrical diseases inherited channel disease can induce VPDs

Also read

A crash course on ventricular ectopics

 

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Squatting is a simple physical  maneuver that can  be done in bed side.

  • Squatting  increases  systemic venous return.
  • Raises aortic after load and SVR

It is  ideal to do  “Stand -Squat -Stand” sequence to appreciate the attenuation during squatting and augmentation during standing

squatting dynamic auscultation mvps mitral valve prolapse

Hemodynamics

MVPS-MR is  a pre load (LV volume )  dependent phenomenon.The degree of prolapse is inversely proportional to the LV size.

Squatting increases the venous return and after load both tend to  increase the LV volume. More blood in the LV  , means mitral leaflet floats much closer to the  mitral annulus . Hence the  force of LV contractility is not only  less on the prolapsing  leaflet , it  reaches late ,  hence the click is delayed  and murmur is short (It may be less intense as well * )

(* Squatting increases aortic after load hence the murmur of MR  may  get amplified .)

Reference

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