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 ?
- 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.
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.
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 .