Key result
111In-antimyosin imaging detects greater heart-to-lung activity in late experimental AR before functional deterioration.
Why the study?
Does 111In-labeled antimyosin antibody imaging detect myocardial damage before functional deterioration in experimental aortic regurgitation?
Does 111In-labeled antimyosin antibody imaging detect myocardial damage before functional deterioration in experimental aortic regurgitation?
Answers are grounded in this paper and cite their sources.
111In-labeled antimyosin antibody imaging may allow for the noninvasive detection of myocardial damage induced by aortic regurgitation prior to the development of systolic dysfunction.
BACKGROUND: Fiber dropout and myocyte necrosis precede heart failure in experimental aortic regurgitation (AR). The current study aimed to determine whether this process can be detected by noninvasive scintigraphic imaging. METHODS AND RESULTS: 111In-labeled antimyosin antibody Fab fragment (1 to 1.5 mCi) (Myoscint) was administered to each of 34 New Zealand White rabbits: 11 early (3 to 5 weeks) after surgical AR induction; 9 late (98 to 128 weeks) after AR induction; 5 normal and 3 sham-operated age-matched with early AR; and 3 normal and 3 sham-operated age-matched with late AR. Echocardiographic fractional shortening was indistinguishable among control, early AR, and late AR groups. In vivo gamma camera imaging 24 and 48 hours after isotope administration, post-mortem heart activity determination (percentage injected dose per gram), and autoradiography were performed. At 24 and 48 hours, heart-to-lung counts-per-pixel ratios from in vivo images were greater (p < 0.05) in the late AR rabbits than in each of the three other groups. No significant differences were found when early AR and older or younger control rabbits were compared. Heart activity (percentage injected dose per gram) in late AR rabbits trended toward higher values than in age-matched control rabbits (p = 0.057), but in early AR it was indistinguishable from that in the corresponding control (p = 0.413, difference not significant). The autoradiographic endocardial/epicardial activity ratio in late AR rabbits was greater than in control and early AR rabbits (1.27 +/- 0.13 vs 1.06 +/- 0.09 and vs 1.13 +/- 0.10, respectively, p < 0.02). CONCLUSIONS: Whereas isotope uptake in late AR rabbits differed from that in control and early AR rabbits, systolic function was indistinguishable. Thus 111In-labeled antimyosin antibody imaging may permit noninvasive detection of AR-induced myocardial damage before functional deterioration.
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Lu et al. (1997) studied Experimental aortic regurgitation (n=34). 111In-labeled antimyosin antibody Fab fragment imaging vs. Control rabbits and early AR rabbits was evaluated on Heart-to-lung counts-per-pixel ratios from in vivo images at 24 and 48 hours (p=<0.05). 111In-labeled antimyosin antibody imaging detected greater heart-to-lung activity in late experimental aortic regurgitation compared to early AR and controls (p<0.05) before functional deterioration.
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