Spring is here again, and although it is difficult to go up
in the mountains these days, I'm sure the cranes have returned
just as last year.
Vector flow imaging. High frame rate. Image
courtesy of Annichen S Daae.
Added several paragraphs on integration
flow vector imaging data in the basic
, the paragraphs are placed under the
relevant paragrphs on the phases of the heart cycle.
Added a discussion on regional
based on strain-pressure loops. The method
is based on a standardised pressure loop calibrated for actual HR
and BP. This loop will then be the same for all segments, and the
differences in the strain pressure loops will be due to the
differences in strain only. Thus, this is the emperor's new
clothes again, and the concept of wasted work in dyssynchrony, can
be demonstrated without strain pressure loops. Also the method
applied to global
. A new method for estimating myocardial
work, based on strain pressure loops, has aroused interest lately.
Probably because regional strain pressure is just as noise
susceptible as regional strain (and gives no more information),
transition to global myocardial work (GMW) parallels transition
from regional to GLS some years ago. But as the method is
based on a standard pressure loop calibrated by arm cuff BP, it do
not confer more information than SV × SBP. And SV × SBP is
sensitive to both increased cardiac ouptput, and increased load.
But is it useful? It is not a measure of contractility, being the
product of SV and BP, while contractility is the ratio of BP and
SV. In my opinion, this is similar to a business, instead of
considering supply (SV) vs demand (BP) ratio, considering supply ×
demand. So while SV is a result of supply (contractility) and
demand (load), myocardial work is the product of load and SV.
Which kind of business has a use for that? In clinical studies,
GMW seems to decine (with GLS) in heart failure, but increase with
increasing BP in hypertensives, despite decreasing GLS..........
Also added some results
from the HUNT study, where measures are entered into an
ellipsoid model of the LV
showing that MAPSE
contributes about 75%
to the total SV (although this is not
normative as the geometrical model has limitations. However, while
MAPSE decreases with age, there is no compensatory increase in
short axis function (which actually also declines), to explain
maintained EF. EF is maintained with increasing age by the
simultaneous decrease in LVEDV and SV, keeping the ratio constant.
Also, MAPSE remains a constant percentage of the decreasing SV.
The notion that circumferential function is the main contributor
to SV, is bases on the lack of understanding that circumferential
strain (except external CS) is partly due to wall thickening,
which again is mainly due to longitudinal shortening.
myocardial volume do not increase with age
. Due to the
simultaneous increase in wall thickness and decrease in length,
there is no increase in LV myocardial volume by age, when the age
dependent increase in BP is taken into account.
Added a chapter on why
there isn't, and can't be a gold standard for strain
this rests on the choice of basic assumptions. As
there is no universal algorithm for global strain
, of course
the concept of global strain as a universal measure of ventricular
function has no exact meaning. It is only a theoretical
concept.The problem goes beyond the inter vendor differences in
speckle tracking. This is also discussed in the Global
section. There is no universal global strain and
thus no reference, they are method dependent. This means that
strain values cannot be validated, and different methods cannot be
compared in terms of validity, and finally, normal values do only
have validity within the method used.
Added a discussion of why speckle
tracking strain will overestimate true wall shortening
tracking the inward motion due to wall thickening (which is
already accounted for as wall thickening is a function of wall
shortening). This is probably the explanation also for the finding
of a gradient of longitudinal
, not the absurd notion of differential layer
Also added a discussion of why the strain product of the three
do not, in real life Correspond to the
volume ratio VS
, and cannot be used for
determination of the (possible) systolic myocardial compression.
: I've revised and extended the chapters
about the inter relations between the principal strains
(longitudinal, transmural and circumferential). I've added the
relations to the myocardial volumes, and extended the discussion
about myocardial compressibility. As there is no
gold standard for strain
, and different sets of assumptions
as well as specific methods will give different values. This also
means that both the inter relations of strains, as well as the
relations to the myocardial volumes and incompressibility
calculations will vary, and at the present level of technology,
strains cannot be used to decide if the myocardium is
I've added a more extensive explanation of the
relation between strain and MAPSE, and strain rate and velocity to
the paragraph on measures
of global long axis function
in the Basic
physiological concepts in strain and strain rate section
Likewise, in the same section, the paragraph explaining diastolic
, and relation to diastolic velocity, has been
extended, with emphasis on the point that added value of diastolic
strain rate to diastolic velocity is dubious.
This section has been completely rewritten, taking
into account a lot more of the early fundamental physiological
research which still holds true, and which is important in
understanding strain and strain rate imaging. The basic
relations to the phases of the heart cycle have been moved from
the sections on global and regional systolic and diastolic
function, while the clinical relations remains in the respective
sections. This to present a more fully integrated physiology
concept in this section,and an easier access to the clinical parts
in the other sections.