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Quantification of myocardial blood flow will reform the detection of CAD
Juhani Knuuti
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Sami Kajander
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Maija Maki
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Heikki Ukkonen
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Knuuti et al Quantification of myocardial blood flow
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Knuuti et al Quantification of myocardial blood flow
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Knuuti et al Quantification of myocardial blood flow
The detection of functional consequences of epicardial coronary artery disease (CAD) has established role in guiding the therapy of the disease.1 In addition, the assessment of impairment in microcirculatory reactivity has recently gained more interest. Estimates of myocardial perfusion contain independent prognostic information about future major cardiac events and perfusion assessment is also useful in the monitoring of the effectiveness of risk reduction strategies.1 The standard assessment of myocardial perfusion is based on its relative distribution. This approach has obvious limitations since the interpretation is based on the assumption that the best perfused region is normal and can be used as a reference. Using quantification this limitation can be avoided and using absolute parameters instead of relative ones is expected to provide benefits in several clinical scenarios. Despite the recognized potential, the clinical use of absolute quantification has remained scarce. Recently, several imaging techniques have been studied aiming for the quantitative measurement of perfusion. In addition nuclear imaging, magnetic resonance imaging, and echocardiography have been investigated and shown promising preliminary quantitative results.2,3 Currently, the most robust technique to quantify perfusion noninvasively in human heart is positron emission tomography (PET). However, although the use of PET in cardiac imaging is rapidly increasing, the image interpretation has still been chiefly based on relative distribution of perfusion.4 This review is aiming for brief summary of the current knowledge of quantification of myocardial perfusion for the detection of clinical CAD. The aim is to demonstrate the potential of quantification using several real clinical examples where the additional information gained from quantification has significant impact on the clinical findings.
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There are two major determinants that define the
potential of imaging technique for quantification of
myocardial perfusion. The imaging device and its performance
will define how accurate and robust is the measurement of
the signal that need to be quantified. The other main factor
is the nature of the tracer or the contrast agent. The detailed
analysis of different imaging technologies and their
performance is beyond the scope of this review.
PET is by nature a quantitative technique and
currently the most robust technique to measure perfusion
noninvasively in human heart. PET allows very fast and
effective imaging protocols with low radiation burden.5-8
Several tracers have been used for the
measurement of myocardial perfusion with PET, in particular,
15O-water,9] 13N-ammonia,10 the potassium analog
82Rb.11 Recently also new 18Fluoride-labeled12,13 as
well as 68Ga-labeled compounds have been tested.14
Currently, 15O-water and 13N-ammonia are the
tracers most widely used for the quantification of
myocardial perfusion with PET. Tracer kinetic models for
quantification of perfusion have been successfully
validated in animals against the radiolabeled microsphere
method over a wide flow range for both tracers.9,10
Single-tissue compartment models for an inert
freely diffusible tracer are used for calculation of MBF
by use of 15O-water.9 For 13N-ammonia a
three-compartment model taking into account the myocardial
metabolic trapping and whole-body metabolism has
been used for calculation of perfusion.10,15 Typically,
the models also correct for the partial volume effect and
spillover from the left ventricular chamber into the
myocardial regions. These two tracers have been found
to be equivalent for quantifying myocardial perfusion.16
There are, however, some obvious differences
between these two tracers. 13N-ammonia is extracted
from blood with an extraction fraction lower than 100%
and the extraction is inversely related to the perfusion
(Figure 1). When 15O-water is used, perfusion is
estimated from the tracers washout from the
myocardium, whereas with 13N-ammonia, perfusion is
calculated from the tracers uptake by myocardium.
The most important limitation of perfusion tracers
as regard to quantification is the suboptimal myocardial
extraction of the tracer. In addition to suboptimal
extraction level, even more problematic phenomenon is
that the extraction is reduced with increasing perfusion
(Figure 1). When extraction fraction is reduced with
increasing perfusion the uptake of tracer is not linear
with perfusion and higher flows are underestimated. This
must be corrected in the mathematical model by
increasing the higher range perfusion values using
specific equations. However, in the case the extraction is
much blunted very high correction factors need to be
used or the correction may become (...truncated)