PulseExploreJournal ClubDebatesTrendingResearchersJournals
Instagram
HomeExploreJournal ClubTrending
Synapse
⌘+K
Synapse
January 11, 2006Magnetic Resonance in Medicine30 citationsOpen Access

Noninvasive measurement of myocardial tissue volume change during systolic contraction and diastolic relaxation in the canine left ventricle

View Full Paper
IRIgnacio RodríguezDEDaniel B. EnnisHWHan Wen

Structured PICO

P
Population
10 closed-chest beagles
I
Intervention
MRI with displacement encoding with stimulated-echo technique
O
Outcome
Intramyocardial tissue volume change between end-systole and end-diastolesurrogate

MRI with displacement encoding can noninvasively measure cyclic intramyocardial tissue volume changes, which correlate with regional perfusion levels in a canine model.

Abstract

In coronary circulation the flow in epicardial arteries and veins is observed to be pulsatile and out of phase with each other. Theoretical considerations predict that this phenomenon extends to all levels of the vascular tree and leads to a cyclic fluctuation of regional tissue volume. Intramyocardial tissue volume change between end-systole and end-diastole was measured noninvasively with MRI in 10 closed-chest beagles. The displacement encoding with stimulated-echo technique was used to obtain pixel-by-pixel tissue displacement field between end-diastole and end-systole and vice versa in the midlevel left ventricle, from which the 3D strain matrix and volume changes were calculated. The volume change was between 0.8+/-0.5% (mean+/-STD) in the epicardial layer and 1.5+/-0.6% in the subendocardial layer of the left ventricle. Tissue volume fluctuation reflects the amount of arterial inflow in a heartbeat under the assumption that regional arterial inflow and venous outflow have little time overlap. The corresponding perfusion level was estimated to be from (1.0+/-0.6) ml/min/g in the epicardial layer to (1.7+/-0.6) ml/min/g in the subendocardial layer, in good agreement with microsphere measurements in the same dog model. The result supports the notion of high arterial resistance at the microvascular level from intramyocardial pressure during systole.

Ask AI
Helpful
Bookmark
Share
View Full Paper

Cite This Study

Rodríguez et al. (2006) studied this question.

synapsesocial.com/papers/6a0762c5fa6637d4ea841ad2https://doi.org/10.1002/mrm.20786
Ask AI
Helpful
Bookmark
Share
View Full Paper