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
- Hemodynamic
- 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
Final message
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 !
Acknowledement
The image modified from http://www.texasheart.org
Dr.S.Venkatesan MD 
memorised those lines “closes with a bang due a long excursion it has to make”during exams… so long they taught us.. i learnt it even without trying to understand the meaning… that is why i am still reading articles written by others…when great men like you sir are writing articles…..
Thank you!
Legendary Answer! Thanks!
Thanks a lot our great doctor
Thank you very much sir!
Hi!
I’m having a hard time with this and I’m hoping you won’t mind a question. Why does the absolute pressure that the mitral valve closes at make a difference? I would have thought it would be the difference between the pressure inside the ventricle and the atrium that would make the valve closer more or less forcefully (sort of like a minor breeze closing a door vs a gust of wind slamming it).
(I’m not sure if this is what you were touching on with dP/dT.) For all three curves in the graph the rate of pressure change in the ventricle seems to be constant. Could it be instead the pressure in the ventricle is first slow to increase and then the rate picks up (like the upward stroke of a parabola, for example)? So in a normal heart, the valve would start to close at a pressure gradient of 0mmHg and finish at a gradient of say 5mmHg but in a mitral stenosis it would start closing after the heart was well into it’s contraction, at an initial gradient of 0mmHg but finishing at 10mmHg (thus slamming the ‘door’ more loudly).
It’s unclear to me because the slope of the pressure change appears linear rather than exponential, and the pressure gradient experienced by the mitral valve during closure in all three scenarios seems to be essentially the same (even if the absolute pressure is different).
Thanks for the blog post! It helped a lot
Hi
I agree with you the acoustics of first heart sound is complex both in physiology and pathology. The dynamic pressure gradients are one of the determinants.
You may be right , its the instantaneous slope rather than absolute gradient matters.
Thank you for your input.
Dr Venkatesan
Hello Dr Venkatesan, thank you for you thorough explanation.
May I side-track a bit on aortic stenosis? I have long been feeling confused when trying to compare the underlying mechanism for “loud S1 for mitral stenosis” and “soft A2 for aortic stenosis”. I know both aortic and mitral stenosis got high transvalvular pressure gradient, so shouldn’t both condition resulted in loud heart sound? Or is the soft A2 for aortic stenosis mainly contributed by the calcified aortic valve, which offset the pressure gradient effect, thus resulting a soft A2 instead of a loud A2?