Thread by @mugander

When it comes to LV diastolic (dys)function, let's think of the LV like a spring, which is compressed during systole, and recoils during diastole.

A thread 🧵
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@strain_rate @load_dependent @DrWillWatson @shaunrobinson02 @leoshmu

https://twitter.com/strain_rate/status/1321203458079367170

The physics governing the recoil of a spring are well described as a damped harmonic oscillator, and it is well validated that the Doppler E-wave is governed by these same physics, aka parameterized diastolic filling (PDF) [pubmed.gov/3812709].
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This means that the shape of the E-wave can be excellently curve fit to a function that describes the behavior of a damped harmonic oscillator. Figure from pubmed.gov/33066772
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This mathematical function is uniquely described by three parameters, namely:

1. stiffness (k) - LV myocardial stiffness
2. damping (c) - the relaxation or viscoelastic property of the LV myocardium
3. load (x0) - the volume load, proportional to E-wave VTI
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The key here is the difference between stiffness and damping. These words are sometimes used sloppily in cardiology, but being specific about them is important.
5/n

Stiffness contributes to the force DRIVING the recoil of the LV during diastole.

In contrast, damping contributes to the force OPPOSING the recoil of the LV during diastole.
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This has mechanistic consequences that make it possible to understand that diastolic dysfunction (DD) is different in different disease states.
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For example, DD in ⬇️EF is mostly characterized by ⬆️stiffness but unchanged damping [pubmed.gov/33066772], but DD in hypertensive heart disease is mostly ⬆️damping but unchanged stiffness [pubmed.gov/9336374].
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While it remains to be shown, it is thought that:

Stiffness is related to titin, elastin, collagen, recoil of the great vessels and pericardium

Damping is related to calcium sequestration and cross-bridge uncoupling.
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Note, these are two very different pathophysiological manifestations.

That said, disturbances in both stiffness and damping can occur at the same time, and likely overlap in a number of heart diseases.
10/n

Notably, the PDF method can both describe the E-wave and e'-wave. Using the e'-wave as an example, the PDF method has been shown to be mathematically identical [pubmed.gov/32142380] to the Force Balance Model of DD [pubmed.gov/21317306].
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So, how does one do this PDF method analysis that you speak of?

Fortunately, there's published [pubmed.gov/27784288] and freely available software if you want to curve fit one or more Doppler E-waves from dicom images. echoewaves.org
12/n

But there is an even easier method. If one measures the E-wave deceleration time (DT), acceleration time (AT), and E-wave Vmax (E), then one can simply calculate stiffness, damping and load [pubmed.gov/29340885]. I call this the DTATE method.
13/n

On echoewaves.org there is a link to a free Web App, which let's you enter DTATE measurements, and output stiffness (k), damping (c), etc, and you can compare these to published normal values echoewaves.org/normal-values/
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In closing, our lab's experience w the PDF method:

1. It is more variable to measure than conventional measures of DD, making cutoffs for clinical decision-making challenging.

2. The method provides valuable mechanistic insight on a group level.

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