Although cardiotoxicity is a well-known side effect of anthracycline, detection of subclinical impairment of myocardial contractility at the latent stage is difficult. The left ventricular end-systolic wall stress (WS)-velocity of circumferential fiber-shortening (VCF) relationship reflects the load-independent myocardial contractility and can detect sensitively intrinsic abnormalities in myocardial contractility. Usefulness of this relationship in detecting subclinical anthracycline-induced cardiotoxicity has not yet been established. We investigated whether latent anthracycline-induced cardiotoxicity at the subclinical state can be detected by using the WS-VCF relationship in patients receiving anthracycline therapy. We studied 45 patients who had received anthracycline therapy and 40 healthy controls. All patients had preserved left ventricular ejection fraction (LVEF). WS and VCF were measured using echocardiography. VCF was corrected by heart rate. The WS-VCF relationship was derived by linear regression. Patients with data points lying below -2 SD derived from controls were regarded as having impaired intrinsic myocardial contractility. Although VCF was within normal limits in all patients, it was significantly reduced in the patient group overall compared with the control group. On the other hand, WS was significantly increased in the patient group overall compared with the control group. The WS-VCF relationship demonstrated impaired intrinsic myocardial contractility in 24 patients (53.3 %). In more than half of patients with preserved LVEF, impairment of intrinsic myocardial contractility was detected using the WS-VCF relationship, suggesting the presence of latent anthracycline-induced cardiotoxicity. The WS-VCF relationship may be able to detect sensitively latent anthracycline-induced cardiotoxicity at the subclinical stage.