Posts Tagged ‘wall motion defect’

Regional wall motion defect( WMD) is the hall-mark of myocardial infarction.It can vary between complete akinseia to mild hypokinesia.

The wall motion defect is a gross terminology which is used  to describe any abnormal motion of the ventricular   segments.Technically,  hypo,   hyper , dyskinetic , akinetic  ,  even any vigorous  movement of LV segments will also come under the general category of  wall motion  defects. For example in extensive  anterior MI   the posterior segments show vigorous  contraction.Though . this compensatory motion  benefits many , it has a potential to adversely stretch the  scarred myocardium and promote aneurysm formation

What causes the regional wall motion defect ?

  • Infarcted segment
  • Ischemic segment
  • Adjacent normal segment behavior (Piggy pack effect, )
  • Loading conditions
  • Heart rate

Finally ,  and  most  importantly the timing and arrival electrical signal to these ill-fated segments determine the sequential activation fronts. Wall motion defect is a more complex phenomenon than we would tend to believe.

What are the  the classical examples of electrical wall motion defect ?

  • LBBB
  • Pre excitation
  • Some forms of VPD

*LBBB causes a paradoxical septal motion with  reference to lateral fee wall contraction.It is still a mystery ,  this paradoxical motion does not cause any  mechanical  disadvantage in structurally normal hearts  .

WMD  in combination  of  LBBB  and  STEMI

We know ,   LBBB   due to ischemia or infarct carry a  sinister prognosis .

Here , there  is  “Double wall motion defect”  . One electrical and two ischemic .  We do not know , how LBBB influences the ischemia/Infarct related wall motion defect and vice versa. .  This is the reason ,  there is a large chunk of  poor or non responders  for cardiac resynchronisation therapy.

Can peri infarction  blocks and other non specific   intra  ventricular  conduction defects alter the sequence of  ventricular  contraction ?

We do not know .It is distinctly possible.Tissue doppler studeis have indicated this.

What is the influence  of  heart rate on the  of Wall  motion defect ?

An  otherwise insignificant regional wall motion defect  could be  amplified with tachycardia . Paradoxically , (as in a biphasic response to dobutamine stress test )  a significant WMD may be attenuated at a particular heart rate.  So, the influence of  HR on  WMD is  as simple as  it could be  ! ! !

Which  is the best time to assess  LV  function  after  MI ?

Considering these issues , LV function  assessed  at discharge ,  may not give us the exact quantum of  muscle damage.  4 weeks may a  reasonable  time frame . This is important in the current era  as presence of  significant  LV dysfunction  becomes an indication for revascularisation  .We  can’t be offered,  to err on this vital LV functional parameter.

Final message

WMD  is a combination of  electrical, mechanical , structural,  alteration in response to variety of myocardial insults.It is very hard to assess  individual components contributing to the net WMA. The easiest and surest way to  quantify  WMD  due to  muscle damage is to  do a deferred echocardiography , when all time related WMD ( Ischemic  stunning , perinfacion block )  disappear.

Coming soon

Diastolic wall motion defects .Is wall motion defects exclusive phenomenon of  ventricular systole ?

No , definitely not. Regional relaxation abnormalities are quiet common .it is poorly recognised .

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Myocardial wall motion defects are sine qua non of  coronary artery disease. This occurs as regional wall motion defects following myocardial infarction or during unstable angina.Myocardium is divided into 16 segments  for this purpose. The wall motion defect occurs in the respective segments , depending upon the compromised  coronary arterial  blood supply.

Under physiological conditions myocardial segments contract in a synchronous fashion so that the chambers have a uniform contraction and relaxation. The heart is a complex electromechanical organ. Any thing , that interferes  the sequence of  electrical conduction or mechanical  contraction or  relaxation   can result in WMD.

Apart from this , differential filling of right and left ventricle can make one ventricle bigger or smaller in relation  to other ventricle .This  makes the ventricle to  contract or relax earlier or later (ASD ).This can not produce   WMD  in the  strict sense , but since the IVS is shared between the two ventricles there can be paradoxical septal motion which mimics WMD.

The other major cause for WMD in the absence of CAD is pericardial pathology .we know pericardium limits ventricular dilatation. When there is a defect in pericardium , after pericardiectomy  ( cardiac surgery patients)  part of the myocardium can bulge out  (or tend to bulge  ) .This happens  often ,  anteriorly to produce a WMD.

Similarly a pericardial pathology which constricts can cause a regional compression .This can happen in many of the adhesive pericarditis .They may resolve or end up with progressive constriction.These type of WMD is especially common in the posterior surface of the heart just near the AV groove.

Electrical disorders

  • LBBB (The classical septal wall motion defect )
  • Pacing rhythm
  • WPW syndrome
  • CRT

The much glamorous entity WPW syndromes and it’s variant can result in WMD due to pure electrical short circuiting hence altering the sequence of ventricular  contraction .In fact one can try to locate the accessory pathway origin and insertion sites depending upon the WMD .The segments abutting the insertion site , that are   innervated by  accessory pathway fibres   contracts prematurely and out of phase.

Rarely primary muscle disease like cardio myopathy can have regional WMD .This is uncommon as global hypokinesia is the hall mark . Regional variation in fibrotic processes can result in WMD.

CRT : Cardiac resynchronisation therapy is supposed to normalise  the pathological WMD sas in ischemic or non ischemic cardiomyopathies. Ironically CRT may induce new wall motion defects if lead position and stimulation protocols are not proper.

Now we have identified regional  diastolic wall motion defects as well .This is made possible by  myocardial  tissue doppler velocity profiles

*Even though it is difficult to explain , isolated electrical  de/ repolarisation defects like long QT, early repolarisation syndromes and brugada syndromes have rarely shown wall motion defects(Class 3 , type C observational evidence )

Non cardiac causes of wall motion defects

  • Abnormal heart position can result in WMD.  Ascites , High pressure pleural effusion /Pneumothorax can cause WMD of heart .
  • Post operative ventricle
  • Pregnant women may show physiological WMD due  to relative shift of  abdomen.
  • Hiatus hernia
  • Mediastinal mass

Final message

Contrary to the popular perception , wall motion defects(WMD)  are not an exclusive  property of CAD.It can occur in varied pathological states both mechanical and electrical .The implication  for not recognizing  this fact can be  enormous  .The “fancy habit”  of diagnosing acute coronary syndrome solely by means of echocardiographic  WMD (With out ECG / Enzyme changes ) is to  be strongly discouraged .


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The right ventricle  is a unique  chamber of the heart . It is the anterior most chamber and  triangular in shape.  Even though  the walls of RV are  not  clearly demarcated ,   it does  have  anterior ,  posterior, and lateral free surfaces   . Anatomically it has a inflow  body, apex and outflow portions . The apex of right ventricle , blends with the lower IVS at an acute angle.

How does RVH occur anatomically ?

The anatomy of RV is such that  it does not allow  it  a concentric  RVH ( like LVH ) . In fact , there is a  disproportionate free wall , anterior  wall   hypertrophy  many  situations  like  PHT/Pulmonary stenosis. The  infero posterior aspect of RV rarely show hypertrophy.

Since RV is the anterior most chamber, located just beneath the left border of sternum   RVH brings the RV  further closer to chest wall .This makes the V1 lead to show  tall R in V1.

What happens in RVMI ?

Unfortunately, when we  refer to RVMI , we generally do not make any efforts to locate or estimate it’s  size.  Since RV has , anterior , lateral and posterior surface  , the site  and  the  extent of the  mI will have a major impact  on the  ECG  features .

Most often  the RVMI occur as a  part of infero posterior MI  .Hence ,  it is uncommon for the anterior surface of RV to get involved.  But ,  it can be involved if  RCA gives of a   large RV branch  that reach the anterior surface of RV.

Anterior RVMI can occur as a part  of LAD MI  , if a large conal branch cross the RV surface.

What prevents the lead V1 from showing the  ST elevation of RVMI ?

  • Most of the RVMI do not involve the anterior surface of the RV so , less chances for ST elevation
  • Further , if a true posterior wall  MI  occur as a part of  RVMI (Which is often the case !)  V1 can never  show ST elevation  as the  posterior MI  tend to have a ST depressing effect in the V1, V2 leads.
  • Extensive IWMI , can have reciprocal ST depression in V1-V2.This again , prevents V1 lead to show the ST elevation

So many times , even though V1 lead is just sitting over the chamber RV it fails  to  pick  the  ST elevation forces of RVMI

Advantage of V4 R ?

V4R records remote RV forces , as these  signals are not contaminated by the inferio posterior ST forces. Hence  a  1mm ST elevation in right sided chest leads have good sensitivity  and specificity to diagnose RVMI .

When can V1 show ST elevation in RVMI ?

If the RV anterior wall is predominantly involved (Ie Anterior RVMI ) ST elevation can occur in V 1 like a anteroseptal MI.

rvmi ecg

Rarely a q RBB can occur in V1 in isolated RVMI.

Final message

V1 lead , though anatomically proximal to RV has less value in diagnosing RVMI since this lead picks up  Infero posterior  negative ST forces  and  the anterior  forces of RVMI get neutralised . So relying on lead V1 to diagnose RVMI is not adviced , except when  the anterior surface of RV is predominatly  involved.

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