CLINICAL APPLICATION OF END SYSTOLIC P-V RELATIONS

本研究的统一假设是，长期MR患者的抗心律失常容量的逐渐增加刺激交感神经系统（SNS）的激活，作为维持有效前向输出、动脉压和组织灌注的代偿机制。 这种代偿机制影响β AR反应性的降低，导致LV收缩功能障碍。 因此，二尖瓣手术治疗将恢复LV收缩功能，达到SNS活性降低和β AR反应性恢复的程度。 对5例患者的初步研究表明，抗心律失常体积与腺苷酸环化酶活性（r=0.86）和收缩功能（r=0.75）之间存在相关性。 同样地，血浆去甲肾上腺素水平和腺苷酸环化酶活性也与收缩功能有关（r=0.91 & 0.65）。 因此，初步数据支持这一假设。

The unifying hypothesis of this investigation is that the progressive increase in regurgitant volume in patients with long-term MR stimulates activation of the sympathetic nervous system (SNS) as a compensatory mechanism to maintain effective forward output, arterial pressure, and tissue perfusion. This compensatory mechanism affects a decrease in beta AR responsiveness resulting in LV contractile dysfunction. It follows, therefore, that treatment with mitral valve surgery will restore LV contractile function to the extent that SNS activity is diminished and beta AR responsiveness is restored. Preliminary studies in five patients have demonstrated a relationship between regurgitant volume and adenylyl cyclase activity (r=0.86) and contractile function (r=0.75). Similarly, correlatal plasma norepinephrine levels and adenylyl cyclase activity reserved with contractile function (r=0.91 & 0.65). Thus, preliminary data support the hypothesis.