Artikkelit
Noninvasive evaluation of anthracycline-induced cardiotoxicity in man
01.01.1984, Yearbook of Nuclear Medicine 77-78 (& R. Lahtinen, M. Uusitupa, J. Kuikka)
(ei kuvausta)
Noninvasive evaluation of anthracycline-induced cardiotoxicity in man
The potentially fatal cardiotoxicity associated with anthracycline treatment may develop without antecedent evidence of cardiomegaly or early symptoms of congestive heart failure. R. Lahtinen, M. Uusitupa, J. Kuikka, and. E. Länsimies (Univ. Central Hosp. of Kuopio, Finland) used first-pass radiocardiography to evaluate left ventricular (LV) function in 37 patients given doxorubicin or daunorubicin in treatment of various malignancies. The validity of systolic time intervals and of echocardiography (ECHO) in detection of LV failure also was assessed using radionuclide first-pass LV ejection fraction (LVEF) as the reference method. Twenty-three patients had no evidence of previous cardiovascular disease (group A), and 14 had previously diagnosed cardiovascular disease (group B).
Before treatment with anthracyclines, the mean LVEF was 0.71 ± 0.06 in patients in group A and 0.53 ± 0.09 in patients in group B. A significant decrease in LVEF was observed in both groups when measurements at anthracycline dose levels of 0-149 Mg/M2 were compared with measurements at doses of 300-449 Mg/M2 (p < .01). The LVEF was abnormal (< 0.51) in 11 (30%) of the 37 patients, of whom 3 were in group A. These 3 received a cumulative dose of 290-500 Mg/M2, whereas 3 of the 8 group-B patients with an abnormal LVEF received a cumulative dose of 0-149 mg/m2. Multiple regression analysis indicated that an abnormal LVEF was significantly associated with the cumulative anthracycline dose (P < .001), patient's age (P < .01), and previous cardiovascular disease (P < .05). In contrast, an abnormal LVEF was not significantly associated with mediastinal irradiation or simultaneous cyclophosphamide or vincristine therapy. Five patients, including 1 in group A, had to discontinue taking anthracyclines because of signs or symptoms of cardiac dysfunction. Both groups showed a tendency toward an increased preejection period/LV ejection time ratio with increasing cumulative doses of anthracycline, and this ratio was pathologic at least once in 50% of the patients. However, this index had a rather low sensitivity (67%) and specificity (59%) for LV dysfunction compared with radionuclide assessment of LVEF. The corresponding values for ECHO (75% sensitivity; 43% specificity) were also low when compared with radionuclide measurement of LVEF.
In this series, radiocardiographic measurement of LVEF indicated a significant decrease in LV function during anthracycline treatment, even in a low cumulative dose in patients with previous cardiovascular disease and in patients older than 70 years of age.
This study again points out the value of resting left ventricular ejection fraction measurement for evaluating anthracychne-induced cardiotoxicity. Obtaining data only at rest may provide all of the information that is necessary from a clinicai standpoint for adequately evaluating conditions in these patients.
The potentially fatal cardiotoxicity associated with anthracycline treatment may develop without antecedent evidence of cardiomegaly or early symptoms of congestive heart failure. R. Lahtinen, M. Uusitupa, J. Kuikka, and. E. Länsimies (Univ. Central Hosp. of Kuopio, Finland) used first-pass radiocardiography to evaluate left ventricular (LV) function in 37 patients given doxorubicin or daunorubicin in treatment of various malignancies. The validity of systolic time intervals and of echocardiography (ECHO) in detection of LV failure also was assessed using radionuclide first-pass LV ejection fraction (LVEF) as the reference method. Twenty-three patients had no evidence of previous cardiovascular disease (group A), and 14 had previously diagnosed cardiovascular disease (group B).
Before treatment with anthracyclines, the mean LVEF was 0.71 ± 0.06 in patients in group A and 0.53 ± 0.09 in patients in group B. A significant decrease in LVEF was observed in both groups when measurements at anthracycline dose levels of 0-149 Mg/M2 were compared with measurements at doses of 300-449 Mg/M2 (p < .01). The LVEF was abnormal (< 0.51) in 11 (30%) of the 37 patients, of whom 3 were in group A. These 3 received a cumulative dose of 290-500 Mg/M2, whereas 3 of the 8 group-B patients with an abnormal LVEF received a cumulative dose of 0-149 mg/m2. Multiple regression analysis indicated that an abnormal LVEF was significantly associated with the cumulative anthracycline dose (P < .001), patient's age (P < .01), and previous cardiovascular disease (P < .05). In contrast, an abnormal LVEF was not significantly associated with mediastinal irradiation or simultaneous cyclophosphamide or vincristine therapy. Five patients, including 1 in group A, had to discontinue taking anthracyclines because of signs or symptoms of cardiac dysfunction. Both groups showed a tendency toward an increased preejection period/LV ejection time ratio with increasing cumulative doses of anthracycline, and this ratio was pathologic at least once in 50% of the patients. However, this index had a rather low sensitivity (67%) and specificity (59%) for LV dysfunction compared with radionuclide assessment of LVEF. The corresponding values for ECHO (75% sensitivity; 43% specificity) were also low when compared with radionuclide measurement of LVEF.
In this series, radiocardiographic measurement of LVEF indicated a significant decrease in LV function during anthracycline treatment, even in a low cumulative dose in patients with previous cardiovascular disease and in patients older than 70 years of age.
This study again points out the value of resting left ventricular ejection fraction measurement for evaluating anthracychne-induced cardiotoxicity. Obtaining data only at rest may provide all of the information that is necessary from a clinicai standpoint for adequately evaluating conditions in these patients.