Mizuno Reiko, Fujimoto Shinichi, Saito Yoshihiko, Okamoto Yasuyuki
Central Clinical Laboratory, Nara Medical University, 840 Shijo, Kashihara, Nara, 634-8522, Japan,
Heart Vessels. 2014 May;29(3):384-9. doi: 10.1007/s00380-013-0375-5. Epub 2013 Jun 19.
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.
尽管心脏毒性是蒽环类药物众所周知的副作用，但在潜伏期检测心肌收缩力的亚临床损害却很困难。左心室收缩末期壁应力（WS）与圆周纤维缩短速度（VCF）的关系反映了与负荷无关的心肌收缩力，并且能够灵敏地检测出心肌收缩力的内在异常。这种关系在检测亚临床蒽环类药物诱导的心脏毒性方面的实用性尚未得到证实。我们研究了在接受蒽环类药物治疗的患者中，使用WS-VCF关系是否能够检测出亚临床状态下潜在的蒽环类药物诱导的心脏毒性。我们研究了45例接受蒽环类药物治疗的患者和40例健康对照者。所有患者的左心室射血分数（LVEF）均保持正常。使用超声心动图测量WS和VCF。VCF通过心率进行校正。通过线性回归得出WS-VCF关系。数据点位于对照组-2标准差以下的患者被视为具有内在心肌收缩力受损。尽管所有患者的VCF均在正常范围内，但与对照组相比，患者组总体上VCF显著降低。另一方面，与对照组相比，患者组总体上WS显著升高。WS-VCF关系显示24例患者（53.3%）存在内在心肌收缩力受损。在超过一半的LVEF保持正常的患者中，使用WS-VCF关系检测到了内在心肌收缩力受损，提示存在潜在的蒽环类药物诱导的心脏毒性。WS-VCF关系可能能够灵敏地检测出亚临床阶段潜在的蒽环类药物诱导的心脏毒性。
