Szabó Z, Török T, Rudas L, Fazekas T
Pándy Kálmán Kórház, Gyula, II. Belosztály-Kardiológia.
Orv Hetil. 1998 May 31;139(22):1357-60.
Pacemaker syndrome is caused primarily by the lack of atrial kick and by neurocardiogenic reflex mechanisms due to simultaneous atrial and ventricular contractions. The most common clinical symptoms are dyspnoe, hypotension, dizziness and syncopal attacks. A case report of a patient with pacemaker syndrome is presented, in which the main clinical manifestation was a recurrent chest pain. A VVI demand pacemaker was implanted because of sick sinus syndrome ten years ago and shortly afterwards anginal attacks of rest developed. Coronary angiography revealed a non-significant (25%) narrowing of the right coronary artery (RCA). Casual and long-term ambulatory blood pressure (ABPM) measurements elucidated that the patient occasionally has extremely low diastolic blood pressure. This later phenomenon was confirmed and refined by a "beat-to-beat" blood pressure measuring technique. The elimination of the pronounced "beat-to-beat" variability of arterial blood pressure and transient coronary hypoperfusion due to implantation of an AV sequential bifocal pacemaker resulted in a full disappearance of angina pectoris.
起搏器综合征主要由心房收缩功能丧失以及心房和心室同时收缩引起的神经心源性反射机制所致。最常见的临床症状是呼吸困难、低血压、头晕和晕厥发作。本文报告一例起搏器综合征患者，其主要临床表现为反复胸痛。患者十年前因病态窦房结综合征植入VVI按需起搏器，术后不久即出现静息性心绞痛发作。冠状动脉造影显示右冠状动脉（RCA）有轻度（25%）狭窄。偶然及长期动态血压（ABPM）测量表明，该患者偶尔会出现极低的舒张压。随后通过“逐搏”血压测量技术证实并明确了这一现象。植入房室顺序双焦点起搏器后，消除了动脉血压明显的“逐搏”波动以及短暂性冠状动脉灌注不足，心绞痛完全消失。
