IMAGING Flashcards
Parameters that reflect cardiac function
LVEF, end-diastolic volume, end-diastolic pressure, exercise capacity
common causes of ischaemic LV dysfunction. what are the difficulties?
full-thickness MI, partial thickness infarction, myocardial stunning or hubernation. difficult to differentiate. differnet states can co-exist in the same patient or even the same myocardial region
viable myocardium - how does it relate to contractility?
viable myocardium may contract normally or it may be dysfunctional.
signals of viability in different modalities
NUCLEAR: 1. thallium - reflects membrane function 2// technetium-99m - membrane and/or mitochondrial function 3. FDG - glucose metabolism 4. fatty acids ECHO or CINE MRI 1. myocardial thickness/motion, thickening (also recruitment and deterioration) CONTRAST MRI 1. absence of late enhancement
what are the subgroups of viable myocardium
normal, reversible ischaemic, partial thickness MI (+/-ischaemia), Hibernating, stunned, myopathic
what is stunning?
is a form of contractile dyfunction of VIABLE myocardium that is caused by a BRIEF period of ischaemia followed by RESTORATION of PERFUSION. may be the result of reperfusion injury whereby restoration of blood flow leads to generation of free radicals and transient Ca overload and thus temporary damage to the contractile mechanism
what is hibernation>
a state of contractile dysfunction in VIABLE myocardium but in the setting of CHRONIC ischaemic heart disease. Requires an intervention such as revascularisation for recovery. Strictly, it is a RETROSPECTIVE diagnosis (by definition you need to demonstrate improved contraction after revasc). there must be inducible ischaemia, thus a surrogate definition: Hibernation is viable and dysfunctional myocardium in ehich IMPAIRED PERFUSION RESERVE LEADS TO INDUCIBLE ISCHAEMIA
in PET, what suggests that myocardium is hibernating:
PET mismatch: decreased ammonia uptake with NORMAL or INCREASED FDG uptake
animal models for MH?
rare, so difficult to determine the underlying pathological mechanisms.
myocardium samples from humans receiving CABG show what<
severe changes of the sarcomeres, intracellular space and organelles, the cardiomyocytes themselves and extracellular matrix
the strengths of PET:
- versatility of positron emitting radionuclides that can be incorporated into important biochemical molecular
- the distribution of these moleculas can be imaged
- uptake can be quantified
- can assess: myocardial perfusion, glucose utilisation, fatty acid uptake and oxidation, oxygen consumption, contractile function
properties of FDG
18F-fluoro-2-deoxy-D-glycose is a glucose analogue taken up by VIABLE myocytes in the same way as glucose but its subsequent metabolism is blocked and it remains within the myocyte.
It’s a tracer of exogenous glucose uptake and thus myocardial VIABILITY
features of 13N-ammonia
it is a perfusion tracer. avidly extracted and retained in viable myocytes by incorporation into glutamine.
ammonia and FDG uptakes in stunned, hybernating and infarcted myocardiums
stunned: normal uptake of both;
hibernating: decreased uptake of ammonia, normal or increased uptake of FDG;
infarcted: concordat decrease of uptake of both
what is the simplification with ammonia >?
ammonia is not a pure perfusion tracer, its similar to technetium based tracers: decresed uptake is seen when PERFUSION is DECREASED, When VIABILITY is DECREASED or with combinations of both. not possible to distinguish from the two by doing a resting ammonia study alone