Heart is mainly perceived as a pumping organ but it need to be realised it also has a reservoir function (Temporarily though , for about .5 seconds every beat ) . Contrary to the popular belief heart is not continuously and tirelessly working .For every contractile beat it takes a brief period of rest .This is called diastole. But , even here it is not a complete rest , as it has to receive the blood from the atria and get filled and be ready for the next beat.
Many think diastole is an active energy-consuming process . . . but it can be debated still , as passive elastic properties may contribute substantially to cardiac relaxation blunting the energy requirement
God is so scientific (Greatest scientist !) he made it sure the resting phase(Diastole) is slightly more than the contractile phase (Systole ).
This makes the organ relax a bit more than it stresses in its entire life time . At any given heart rate diastole will be slightly more than systole , peculiarly for the same reason during tachycardia diastole suffers more than systole.
What happens in diastolic dysfunction ?
Pathologically the ventricles become stiff and rigid and the filling of the ventricle is impaired . The commonest cause for diastolic dysfunction are hypertension, diabetes, and ischemic CAD some forms of myopathies .In systole ,the calcium is pumped into actin myosin complex while in diastole the same calcium molecules (Or different !) are ejected back into the cytosol and sarcoplasmic reticulum. The later process is impaired in many situations of diastolic dysfunction.
It should also be realised not every one with diastolic dysfunction has a calcium release /unloading defect .Many have structural diastolic dysfunction like interstitial fibrosis .Here the mechanism goes beyond calcium kinetics.These are the patients who get maximum benefit out of heart rate reduction.
It is all Time . . . Time as a lusiotropic drug !
If the ventricle finds difficult to relax (or slow /sluggish to relax ) we have two options to tackle this .
- To make relaxation faster( ie positive lusiotropism )*
- To prolong the diastole itself .
Prolonging diastole makes it certain , the LV relaxation process is completed as the excess time compensates for the slowness of calcium reuptake into the sarcoplasmic reticulum . In fact , we have observed at slow heart rates (<60) it is very difficult to document diastolic dysfunction by doppler .
In many of dilated cardiomyopathies the beneficial effect of beta blockers , could be linked to simple reduction in heart rate and prolongation of diastole .(Note In DCM about 30-40 % have restrictive filling )
As we have no specific drugs to augment the process of cardiac diastole, currently heart rate reduction could be the simple and best method* to improve diastolic function .In many cases diastolic dysfunction simply vanishes at low heart rate.Bradycardia and diastolic dysfunction will remain as foes forever ! Please give the benefit of this simple concept to all your patients with diastolic dysfunction .Your patients can breath lot more easier !
*Apart from controlling the underlying cause like DM, SHT and CAD , anti fibrotic drugs, interstitial relaxants ,selective cardiac collagen uncouplers are the future areas of research .