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Relationship of the fourth heart sound to atrial systolic transmitral flow deceleration
A M McGuire1, M T Hagley, A F Hall
1Cardiovascular Biophysics Laboratory, Washington University Medical Center, St. Louis, Missouri 63110, USA.
Insights
The fourth heart sound (S4) is an oscillation during atrial contraction. It occurs when blood flow causes high ventricular pressure, but may not be loud enough to be clinically audible.
Area of Science:
- Cardiology
- Biophysics
- Medical Acoustics
Background:
- The fourth heart sound (S4) is linked to cardiohemic vibrations during atrial systole.
- It arises from a rapid increase in ventricular end-diastolic pressure due to factors like reduced ventricular compliance or increased atrial filling volume.
Purpose of the Study:
- To mathematically model and characterize the production of the fourth heart sound (S4).
- To compare model predictions with clinical recordings of S4.
Main Methods:
- Modeled the cardiohemic system as a forced, damped nonlinear harmonic oscillator.
- Utilized a closed-form expression for the Doppler A-wave contour as the forcing term.
- Simultaneously recorded phonocardiograms and Doppler A waves in human subjects.
Main Results:
- The model accurately predicted S4 amplitude, duration, timing, and power spectrum.
- Excellent agreement was found between model predictions and recorded phonocardiographic S4 characteristics.
- Oscillations during A-wave deceleration are always present with a normal mitral valve.
Conclusions:
- The study confirms that cardiohemic oscillations occur during A-wave deceleration.
- Audibility of S4 depends on the amplitude, frequency, and chest wall coupling of these oscillations.
- This provides a biophysical explanation for the presence or absence of S4.
Abstract:
The fourth heart sound (S4) is thought to be due to cardiohemic vibrations, powered by deceleration of transmitral blood flow, that occur when atrial systole leads to a disproportionately high rise in ventricular end-diastolic pressure (relative to diastasis), associated with an enhanced atrial systolic blood filling volume or a stiff ventricular wall. To characterize S4 production, we modeled the cardiohemic system as a forced, damped nonlinear harmonic oscillator. The forcing term used a closed-form expression for the Doppler A-wave contour. We simultaneously recorded transthoracic phonocardiograms and Doppler A waves in subjects with and without audible S4 and compared model predictions for S4 amplitude, frequency, and power spectrum with those of the recorded S4. Excellent agreement was observed between the model-predicted amplitude, duration, timing, and power spectrum and those of the phonocardiographic S4. We conclude that, with a normal mitral valve, there should always be an oscillation of the cardiohemic system during A-wave deceleration. However, oscillations may not have high enough amplitude, frequency, or coupling to the chest wall to be clinically audible as an S4.