Seino Y, Shimai S, Ibuki C, Itoh K, Takano T, Hayakawa H
First Department of Internal Medicine, Nippon Medical School, Tokyo, Japan.
J Am Coll Cardiol. 1991 Aug;18(2):459-63. doi: 10.1016/0735-1097(91)90601-5.
Persistent atrial standstill is a very rare pathophysiologic condition whose diagnosis is established when both electrical and mechanical silence of the atria are confirmed. To test the hypothesis that secretion of atrial natriuretic peptide is disturbed in patients with persistent atrial standstill, the response of atrial natriuretic peptide secretion and other neurohormonal factors during exercise was investigated in three patients with a rate-responsive ventricular demand (VVI) pacemaker implanted for confirmed persistent atrial standstill. The results were compared with those observed in eight normal subjects and patients with a rate-responsive VVI (Group A) or atrial demand (AAI) (Group B) pacemaker implanted for confirmed sick sinus syndrome. Patients in Group A displayed significant elevation of alpha-human atrial natriuretic peptide secretion both before and during exercise (122.5 +/- 14.8 and 207.5 +/- 8.3 pg/ml, respectively) compared with those in Group B (55 +/- 14.1 and 116.4 +/- 51.5 pg/ml, respectively) and the normal subjects (18.9 +/- 9.8 and 30.8 +/- 19.2 pg/ml, respectively). This indicated development of a nonphysiologic increase in atrial volume or pressure overload, or both, in rate-responsive VVI pacing because of lack of atrioventricular synchrony. However, patients with persistent atrial standstill had undetectable (less than 10 pg/ml) or almost undetectable secretion of atrial natriuretic peptide as well as lower levels of cyclic guanosine monophosphate in the circulation both before and during exercise. Changes in plasma catecholamines during exercise were similar in patients with persistent atrial standstill compared with the other groups. This study indicates that "endocrinologic silence" accompanies electrical and mechanical silence of the atria, which may constitute a third diagnostic clue to persistent atrial standstill.
持续性心房静止是一种非常罕见的病理生理状态，当心房的电活动和机械活动均消失得到证实时，即可确立诊断。为了验证持续性心房静止患者心房利钠肽分泌受到干扰这一假说，对3例因确诊为持续性心房静止而植入频率应答式心室按需（VVI）起搏器的患者运动期间心房利钠肽分泌及其他神经激素因子的反应进行了研究。将结果与8例正常受试者以及因确诊病态窦房结综合征而植入频率应答式VVI（A组）或心房按需（AAI）（B组）起搏器的患者所观察到的结果进行比较。与B组患者（分别为55±14.1和116.4±51.5 pg/ml）及正常受试者（分别为18.9±9.8和30.8±19.2 pg/ml）相比，A组患者在运动前和运动期间α-人心房利钠肽分泌均显著升高（分别为122.5±14.8和207.5±8.3 pg/ml）。这表明在频率应答式VVI起搏时，由于缺乏房室同步性，心房容积或压力负荷出现了非生理性增加，或两者兼有。然而，持续性心房静止患者在运动前和运动期间心房利钠肽分泌均检测不到（低于10 pg/ml）或几乎检测不到，且循环中的环磷酸鸟苷水平较低。与其他组相比，持续性心房静止患者运动期间血浆儿茶酚胺的变化相似。本研究表明，心房的“内分泌静止”伴随着电活动和机械活动的静止，这可能构成持续性心房静止的第三条诊断线索。
