Usefulness of indium-111 antimyosin scintigraphy in confirming myocardial injury in patients with anthracycline-associated left ventricular dysfunction.

BACKGROUND

In patients with cardiac dysfunction due to anthracycline-induced myocyte damage, continuation of anthracyclines carries a high risk, and modification of chemotherapy is thus indicated. The condition, however, must be distinguished from other causes of cardiac dysfunction, e.g., the transient negative inotropic effect which may accompany and follow the intravenous administration of anthracyclines. In the present study the efficacy of 111In-antimyosin in confirming myocyte injury and its potential applicability in differentiating causes of cardiac dysfunction during anthracycline therapy are evaluated.

PATIENTS AND METHODS

Twenty-seven patients with asymptomatic left ventricle ejection fraction (LVEF) decrease (median LVEF 47%, range 38%-50%) during chemotherapy with anthracyclines (dose range 100-700 mg/m2 doxorubicin or equivalent) were subsequently studied with 111In-antimyosin cardiac scintigraphy. The degree of myocardial uptake, an indicator of heart muscle cell injury, evaluated both visually and quantitatively by means of heart-to-lung ratios (HLR) obtained from 48-hour planar images, was analyzed in relation to the further clinical and LVEF course. The results were also compared with 111In-antimyosin data from 5 patients who had normal LVEF during chemotherapy and 5 patients who had received no anthracyclines. The distribution pattern of myocardial uptake was assessed by means of single photon emission computed tomography (SPECT).

RESULTS

a) Fourteen patients presented with persistent LVEF decrease (median LVEF 42.5%, range 32%-47%) after discontinuation of anthracycline therapy. In 11 of these patients intense and diffuse, as shown by SPECT, cardiac uptake of 111In-antimyosin (HLR 1.87-2.45) was observed. In two patients with intense antimyosin cardiac uptake, spurious HLR values (1.23-1.55) were found which were caused by unexpected lung uptake and focal heart uptake, respectively. All patients with intense cardiac 111In-antimyosin uptake showed persistently decreased LVEF on follow-up (4-26 weeks) and 4 of them subsequently developed congestive heart failure. In another patient with no intense uptake (HLR 1.15) and persistent decrease in LVEF, metastatic cardiac involvement was found. b) In 13 patients with improvement or normalisation of the LVEF (median LVEF 53%, range 51%-63%), generally less intense or slight cardiac uptake (HLR range: 1.20-1.88) was seen; the HLR in these patients, who continued chemotherapy without complications, was consistently lower (p < 0.01) than in patients with persistently decreased LVEF, and comparable to values of patients who had normal LVEF.

CONCLUSIONS

111In-antimyosin scintigraphy can be useful to differentiate cardiac dysfunction caused by severe myocardial injury from temporary decreases in LVEF, without severe concomitant myocyte damage, which may occur during anthracycline therapy. Intense myocardial uptake of 111In-antimyosin can be used as an important confirmatory criterium for the clinical decision to discontinue anthracycline therapy.