Cortina Cristina, Bermejo Javier, Yotti Raquel, Desco M Mar, Rodríguez-Pérez Daniel, Antoranz J Carlos, Rojo-Alvarez José Luis, Garcia Damien, García-Fernández Miguel A, Fernández-Avilés Francisco
Department of Cardiology, Hospital General Universitario Gregorio Marañón, Dr Esquerdo 46, 28007 Madrid, Spain.
Circulation. 2007 Aug 28;116(9):1015-23. doi: 10.1161/CIRCULATIONAHA.107.691154. Epub 2007 Aug 7.
The physiological basis of right ventricular (RV) diastolic function remains incompletely studied in humans. The driving force responsible for RV filling, the pressure gradient along the RV inlet from the right atrium to the RV apex, has never been measured in the clinical setting.
We validated a method for measuring the RV filling pressure difference (RVFPD) from color Doppler M-mode recordings in 12 pigs undergoing interventions on RV preload, afterload, and lusitropic states (error, -0.1+/-0.4 mm Hg compared with micromanometers; intraclass correlation coefficient, 0.88). Peak early RVFPD correlated directly with mean right atrial pressure and inversely with the time constant of RV relaxation. In 21 patients with dilated cardiomyopathy, the peak RVFPD was 1.0 mm Hg (95% CI, 0.8 to 1.2), significantly lower than in age-matched control subjects (1.4 mm Hg; 95% CI, 1.2 to 1.6). In another population of 19 young healthy volunteers, the peak RVFPD was 2.3 mm Hg (95% CI, 2.0 to 2.6), which was reduced by nitroglycerine and esmolol and was augmented by volume overload and atropine infusions. RVFPD was generated almost exclusively by inertial forces.
For the first time, the RV driving filling force can be accurately measured noninvasively in the clinical setting, and the method is sensitive to detect the effects of preload, chronotropic, and lusitropic states. In patients with dilated cardiomyopathy, the RV filling force is markedly reduced, indicating severely impaired RV relaxation. These findings suggest that this is a useful tool for improving the clinical assessment of RV diastolic function.
右心室(RV)舒张功能的生理基础在人体中尚未得到充分研究。负责右心室充盈的驱动力,即从右心房到右心室心尖沿右心室入口的压力梯度,在临床环境中从未被测量过。
我们验证了一种通过彩色多普勒M型记录测量右心室充盈压差(RVFPD)的方法,该方法应用于12头接受右心室前负荷、后负荷和舒张功能状态干预的猪(与微压计相比误差为-0.1±0.4 mmHg;组内相关系数为0.88)。右心室早期充盈压差峰值与平均右心房压力直接相关,与右心室舒张时间常数呈负相关。在21例扩张型心肌病患者中,右心室充盈压差峰值为1.0 mmHg(95%CI,0.8至1.2),显著低于年龄匹配的对照组(1.4 mmHg;95%CI,1.2至1.6)。在另一组19名年轻健康志愿者中,右心室充盈压差峰值为2.3 mmHg(95%CI,2.0至2.6),硝酸甘油和艾司洛尔可使其降低,容量负荷和阿托品输注可使其增加。右心室充盈压差几乎完全由惯性力产生。
首次在临床环境中可以无创准确测量右心室驱动充盈力,且该方法对检测前负荷、变时性和舒张功能状态的影响敏感。在扩张型心肌病患者中,右心室充盈力明显降低,表明右心室舒张功能严重受损。这些发现表明这是改善右心室舒张功能临床评估的有用工具。