I wonder this question is being asked over many generations in medical schools , yet to be answered clearly. The traditional explanation given is ” mitral valve is kept open wide till onset of systole and it closes with a bang due to a long excursion it has to make ” This concept is no longer tenable and acceptable ( For the simple reason if the valve is wide open . . . hemodynamically significant mitral stenosis cease to exist !)
There are two major factors that determine the loudness of S1 in mitral stenosis
- Valve structure and morphology
Mitral valve closes whenever the ventricular pressure curve crosses above the LA mean pressure . This is the pressure crossover point (LV/LA) .
In normal persons it happens very early after the onset of ventricular contraction .(ie the LV pressure has to raise only to about 8-12mmhg . At this point the LV pressure curve has certain force of contraction (Dp/Dt) .Since in mitral stenosis the mean pressure is raised well above normal (Often 20-30mmhg) the LV pressure cross over point is slightly delayed and more importantly occur at a higher slope of LV pressure curve . Even this slight delay adds a punch in the ventricular contractility .The impact of LV contractility on mitral valve closure especially the AML is forceful .
(Imagine the force of impact of a stone hitting you from a distance of 1 meter from above , is different from a stone hitting you from 10 meter above as it gains the momentum )
The second phenomenon is probably more important as it involves acoustics the final step in the genesis of loud S1 .
The mitral valve need to be not only pliable but also the conduction properties should be intact.
Acoustic principles state that even a speck of calcium in the AML can dampen the sound that is generated by leaflet motion.
(Try touching a speaker cone while it is playing .The sound immediately drops and dampens.)
Similarly for S1 to be loud the valve should pliable without any significant calcification or extreme rigidity or subvalvular fusion .)
It is important to realize the PML contributes less to the intensity of S1 . Hence even if some calcium present in PML it won’t affect the intensity of S1
Other important factors that affect the intensity of S1 include
- LV function ( Onset of LV dysfunction elevates LVEDP reduces the net gradient across mitral valve )
- Presence of mitral regurgitation .
- Aortic valve disease (Especially AR )
- Heart rate
- Rarely associated Tricuspid stenosis make T 1 component of S 1 louder
The loud S 1 is due to both physiological and anatomical factors of mitral valve .The condition of valve may be more important for the simple reason , whatever be the hemodynamic predispoistion for loud S1 , the prevailing valve morphology has a potential to nullify it !
The image modified from http://www.texasheart.org