Assessment of anthracycline-induced myocardial damage by quantitative indium 111 myosin-specific monoclonal antibody studies

Abstract

To assess chemotherapeutically induced myocardial damage, myosin-specific antibody scans and ejection fraction measurements were performed in 32 patients with breast cancer and in 9 patients with other tumours. All patients had received chemotherapy including anthracyclines. The ejection fraction decreased by less than or equal to 10% in 14 of 41 (34%) patients after chemotherapy. Antimyosin uptake in the myocardium was observed in 38 of 41 (92%) patients after chemotherapy. Antimyosin uptake was quantified by means of a heart-to-lung ratio, revealing a correlation between the degree of antimyosin uptake in the myocardium and the cumulative dose of anthracycline. Patients with a decreased ejection fraction showed more intense antimyosin uptake, indicating more severe myocardial damage. A higher degree of antimyosin uptake was found in 17 breast cancer patients treated with doxorubicin compared with 15 patients treated with mitoxantrone. We conclude that antimyosin studies provide a sensitive, non-invasive method to monitor myocardial damage in patients treated with anthracyclines. Antimyosin uptake in the myocardium precedes ejection fraction deterioration. This technique may be helpful in the early identification of patients at risk of congestive heart failure during chemotherapy including anthracyclines.

Scintigraphic Techniques for Early Detection of Cancer Treatment–Induced Cardiotoxicity

“…It has been studied in conditions such as myocardial infarction, myocarditis, cardiac transplant rejection, and doxorubicin cardiotoxicity (98). Binding of this antibody to Behave identically to endogenous neurotransmitters 18 F-6-fluorodopamine 11 C-epinephrine Catecholamine analogs…”

Early postoperative reduction of monoclonal antimyosin antibody uptake is associated with absent rejection-related complications after heart transplantation.

“…Studies performed at 1-3 (n=97), [4][5][6][7][8][9][10][11] (n=39), [12][13][14][15][16][17][18][19][20][21][22][23] (n=46), and more than 24 months (n=65) showed a prevalence of abnormal antimyosin studies in each of the four periods of 95%, 77%, 65%, and 46%, respectively (p<0.0001) (Figure 2). In these periods, mean visual estimations were 1.95±0.7, 1.33±0.7, 1.15±0.7, and 0.9±0.7, and mean heart-tolung ratios were 1.93 +0.30, 1 In the 33 patients who were prospectively studied since transplantation, 170 antimyosin scans were sequentially performed (mean, 4.8±+ 1.9 scans per patient; range, 1-10 scans), and follow-up extended from 5 to 37 months (mean, 6 months).…”

“…In these periods, mean visual estimations were 1.95±0.7, 1.33±0.7, 1.15±0.7, and 0.9±0.7, and mean heart-tolung ratios were 1.93 +0.30, 1 In the 33 patients who were prospectively studied since transplantation, 170 antimyosin scans were sequentially performed (mean, 4.8±+ 1.9 scans per patient; range, 1-10 scans), and follow-up extended from 5 to 37 months (mean, 6 months). At 1-3 (n=96), [4][5][6][7][8][9][10][11] (n=38), [12][13][14][15][16][17][18][19][20][21][22][23] (n=24), and more than 24 months (n=12), prevalence of abnormal scans in each of the intervals was 95%, 76%, 58%, and 58%, respectively (p<0.0001). Mean values for visual estimation and heart-to-lung ratios in each of the intervals also decreased, to 1.95+0.7, 1.31+0.7, 1.08+0.8, and 0.9±0.9 and to 1.92+0.3, 1.72+0.23, 1.63+0.25, and 1.64+0.3, respectively (p<0.001).…”

Decreased Myocardial Tl-201 Uptake in Rats: Early Sign of Doxorubicin Induced Myocardial Damage and the Relation to Inflammation

“…DOX-induced cardiac injury presents classical findings such as vacuolization in the cytoplasm, myofibrillar degeneration and necrosis under the light microscopy, as well as myocardial inflammation which is another pathological finding that shows inflammatory cell infiltration itself under the light microscopy and is associated with the injury, but can be seen in isolation (4,(10)(11)(12). There were various scintigraphic evidences associated with it and support this finding which develops secondary to DOX injury (13)(14)(15)(16).…”