Department of Internal and Specialty Medicine, Chair of Clinical Pathophysiology, University of Palermo, Italy.
Am Heart J. 2012 Sep;164(3):351-7. doi: 10.1016/j.ahj.2012.05.025. Epub 2012 Aug 17.
High values of cardiac troponin in acute decompensated congestive heart failure (ADHF) identify patients at higher risk and worsened prognosis. A cardiac troponin increase during therapy indicates the need for more appropriate intervention, aimed at compensating cardiac disease and effectively minimizing myocardial wall stress and subsequent cytolysis. This study evaluated the effects of an intravenous high dose of furosemide with (group A) or without small volume hypertonic saline solution (HSS) (group B) on myocardial cytolysis in patients with ADHF.
A total of 248 consecutive patients with ADHF (148 men, mean age 74.9 ± 10.9 years) were randomly assigned to group A or B. Plasma levels of cardiac troponin-I, brain natriuretic peptide, glomerular filtration rate by Modification of Diet in Renal Disease formula, bioelectrical impedance analysis measurements, and delta pressure/delta time (dP/dt) rate were observed on admission and discharge for all patients.
We observed a significant reduction of cardiac troponin in both groups and a significant improvement in renal function, hydration state, pulmonary capillary wedge pressure (P < .0001), end diastolic volume (P < .01), ejection fraction (P < .01), and dP/dt (P < .004) in group A. We also observed a significant reduction in body weight (64.4 vs 75.8 kg) (P < .001), cardiac troponin I (0.02 vs 0.31 ng/mL) (P < .0001) and brain natriuretic peptide (542 vs 1,284 pg/mL) (P < .0001), and hospitalization time (6.25 vs 10.2 days) (P < .0001) in the HSS group.
These data demonstrate that intravenous high doses of furosemide do not increase myocardial injury and, in addition, when associated to HSS, significantly reduce cardiac troponin I release. This behavior is mirrored by the achievement of improved hemodynamic compensation at echocardiography and body hydration normalization.
在急性失代偿性充血性心力衰竭（ADHF）中，高值的心肌肌钙蛋白可识别出风险更高和预后更差的患者。治疗过程中心肌肌钙蛋白升高表明需要更适当的干预，旨在代偿心脏疾病，并有效最小化心肌壁压力和随后的细胞溶解。本研究评估了静脉注射大剂量呋塞米联合（A 组）或不联合小容量高渗盐水溶液（HSS）（B 组）对 ADHF 患者心肌溶解的影响。
共有 248 例连续 ADHF 患者（男 148 例，平均年龄 74.9 ± 10.9 岁）被随机分配到 A 组或 B 组。所有患者入院和出院时均观察心肌肌钙蛋白 I、脑利钠肽、改良肾脏病饮食公式计算的肾小球滤过率、生物电阻抗分析测量值和压力/时间变化率（dP/dt）。
我们观察到两组患者的心肌肌钙蛋白均显著降低，肾功能、水合状态、肺毛细血管楔压（P <.0001）、舒张末期容积（P <.01）、射血分数（P <.01）和 dP/dt（P <.004）均显著改善。我们还观察到 A 组患者的体重显著降低（64.4 与 75.8kg）（P <.001）、心肌肌钙蛋白 I（0.02 与 0.31ng/mL）（P <.0001）和脑利钠肽（542 与 1284pg/mL）（P <.0001）以及住院时间（6.25 与 10.2 天）（P <.0001）显著降低。
这些数据表明，静脉注射大剂量呋塞米不会增加心肌损伤，并且当与 HSS 联合使用时，可显著减少心肌肌钙蛋白 I 的释放。这种行为反映在超声心动图和身体水合作用正常化时实现的更好的血液动力学代偿。
