Banerjee A, Brook M M, Klautz R J, Teitel D F
Cardiovascular Research Institute, University of California, San Francisco 94143.
J Am Coll Cardiol. 1994 Feb;23(2):514-24. doi: 10.1016/0735-1097(94)90441-3.
We sought to evaluate in the young heart the primary assumptions on which the current use of the mean "velocity of fiber shortening corrected for heart rate" as a noninvasive index of contractility are based.
End-systolic wall stress-velocity of fiber shortening relation has been applied as a single-beat, load-independent index of contractility in children. This use is based on poorly validated assumptions of linearity, parallel shifts with changing contractile state and inotropic sensitivity of the end-systolic wall stress-velocity of fiber shortening relation.
In eight anesthetized young piglets, 5F mciromanometric catheters were placed in the ascending aorta and balloon occlusion catheters in the descending aorta. End-systolic wall stress and velocity of fiber shortening were calculated from aortic pressure and M-mode echocardiography under six conditions: in three contractile states 1) baseline, 2) increased contractility during dobutamine infusion (10 micrograms/kg per min), and 3) decreased contractility after propranolol injection (1 mg/kg), each at two afterload states (normal and increased load by partial aortic occlusion).
Dobutamine increased and propranolol decreased afterload-matched velocity of fiber shortening corrected for heart rate significantly to 140% and 77% of baseline, respectively. However, the slope of end-systolic wall stress-velocity of fiber shortening relation was much greater (251% of baseline) during dobutamine infusion, which also significantly decreased wall stress, and was much less (27% of baseline) after propranolol injection, which increased wall stress.
The velocity of fiber shortening corrected for heart rate did change predictably with changes in contractility and as such can be used noninvasively in the temporal evaluation of individual patients undergoing therapeutic interventions or to define the natural history of a disease process. However, the relation on which it is based is not defined by parallel straight lines across contractile states, so that abnormal single point measurements may reflect only the nonlinearity of the relation rather than abnormalities in contractility. Thus, we recommend that the end-systolic wall stress-velocity of fiber shortening relation should not be used as a single-beat index of contractility.
我们试图在幼小心脏中评估当前将平均“心率校正后的纤维缩短速度”用作收缩性无创指标所依据的主要假设。
收缩末期壁应力-纤维缩短速度关系已被用作儿童收缩性的单搏、负荷独立指标。这种应用基于线性、随收缩状态变化的平行移位以及收缩末期壁应力-纤维缩短速度关系的变力敏感性等未经充分验证的假设。
在八只麻醉的幼猪中，将5F微测压导管置于升主动脉，将球囊阻塞导管置于降主动脉。在六种情况下，根据主动脉压力和M型超声心动图计算收缩末期壁应力和纤维缩短速度：在三种收缩状态下，1）基线，2）多巴酚丁胺输注期间（10微克/千克每分钟）收缩性增加，3）普萘洛尔注射后（1毫克/千克）收缩性降低，每种情况在两种后负荷状态下（正常和部分主动脉阻塞导致负荷增加）。
多巴酚丁胺使心率校正后的后负荷匹配纤维缩短速度显著增加，普萘洛尔使其显著降低，分别达到基线的140%和77%。然而，多巴酚丁胺输注期间收缩末期壁应力-纤维缩短速度关系的斜率大得多（基线的251%），这也显著降低了壁应力，而普萘洛尔注射后斜率小得多（基线的27%），这增加了壁应力。
心率校正后的纤维缩短速度确实会随着收缩性的变化而可预测地改变，因此可用于对接受治疗干预的个体患者进行无创的时间评估或确定疾病过程的自然史。然而，其基于的关系并非由跨收缩状态的平行直线定义，因此异常的单点测量可能仅反映关系的非线性而非收缩性异常。因此，我们建议收缩末期壁应力-纤维缩短速度关系不应用作收缩性的单搏指标。
