Conveniently forgotten studies in CRT : The importance of diastolic wall motion defect in cardiac failure !
Posted Sep 08 2009 10:24pm
The failing heart enlarges progressively and attain a globular shape . What looks for the naked eye as a simple global hypokinesia of LV , when analysed , reveal multiple forms regional desynchronisation .This is especially true if the QRS complex is wide.
It is generally divided into three groups
Intraventricular desynchrony (IV)
Atrio ventriculo desynchrony(AV)
In our search for improving CHF mortality and morbidity , we have stumbled upon this concept of restoring the lost synchrony of the heart. Cardiac resynchronisation therapy has become ( Rather projected to become !) a great modality for patients with cardiac failure.It was initially advocated only for severe forms of cardiac failure , now advised even for class 1 CHF. (CRT-MADIT 2009)
Restoring the lost synchrony by rewiring the cardiac conducting system with multiple leads and optimally timed pacing increases the effectiveness of cardiac contractility.It can improve EF, and also regress mitral regurgitation.
The above concept was perfect on paper , but was very difficult to replicate on real patients. CRT was ineffective in 30% of patients. Many had partial effect. Few had adverse effect .
The reason for the poor efficacy is technical in many . Identifying the optimal sites for positioning the leads and the futility of such an exercise as the LV epicardial lead is pre- selected by the patients coronary venous anatomy are the major issues.An electrically ideal site for pacing can contain a mechanically dysfunctional scar. While these technical issues may be addressed in due course what worries us is the conceptual flaws.
Emerging facts indicate timing of asynchrony could be vitally important.
What is the incidence desynchrony with reference to the cardiac cycle ?
One major reason that was overlooked totally was the presumption cardiac dysynchrony occur only during systole. It is a less recognised fact is the ventricular relaxation is not uniform and synchronous.A failing ventricle can not be expected to relax systematically and coherently for the simple reason the myocytic calcium reuptake into the sarcoplasmic reticulum is grossly impaired. This is directly responsible for the diastolic dysfunction observed in dilated cardiomyopathy . If this impairment occur uniformly throughout the left ventricle it can be termed global diastolic dysfunction which is little easier to correct .But what really happens is the defect in calcium reuptake occurs in a random fashion with lot of regional variation. This is called regional diastolic wall motion defect or regional diastolic dysfunction.The above mechanisms result in the typical restrictive filling pattern of many of the advanced patients with DCM . CRT as a concept should need to address this issue.
How to diagnose Diastolic WMD?
The fact is ,we have not mastered the quantification of systolic WMD as yet. It may take years before decoding the nuances of diastolic wall motion defects. At least we need to know such a thing exists.Tissue doppler strain rates , velocity vector imaging could be useful tools. As such they are not clinical tools.
Cardiac resynchronisation as a concept is good on paper . Heart need to be synchronous both during systole and diastole .This becomes especially important in an advanced stages of heart failure. Without proper follow up and potential adverse effects of CRT on diastolic WMD , CRT concept has miles to travel ! . Some pessimistic thinking cardiologists ( Me . . . !) would even argue it as a case of prematurely released device into the patient domain. Of course there is lot of scientifc data that will vouch for its beneficial effects .(The latest being from the prestigious NEJM , CRT-MADIT) but it has to prove it’s worth in individual patients. Physicians must exercise caution before embarking on heroic attempts to provide resynchrony of failing hearts .