Transient atrial standstill may reflect SA nodal ischemia, while persistent atrial standstill can result from a distinct atrial degenerative disease, with His bundle lesion location affecting H-Q interval prolongation.
Distinguishes ischemic from degenerative atrial standstill; extends His bundle lesion insights but leaves open need for prospective validation.
Electrophysiologic studies, including His bundle recording and atrial pacing (AP), were performed in one patient with transient (TAS) and another with persistent atrial standstill (PAS). Both subsequently expired, and postmortem examinations with serial sections of the conduction system were obtained. The patient with TAS had left bundle-branch (LBB) block, a P-H interval of 140 msec (normal, 80-140 msec), an H-Q of 40 msec (normal, 35-55 msec), and an AP threshold of 1.2 ma. Postmortem examination revealed total left circumflex occlusion proximal to the sinoatrial (SA) nodal artery takeoff, SA nodal arteriolosclerosis without infarction, and left-sided cardiac skeletal sclerosis (LSCSS) disrupting the penetrating portion of the His bundle and the LBB. Intracardiac recordings in the patient with PAS showed absent atrial activity and an H-Q of 60 msec. The atria were inexcitable with AP up to 15 ma at multiple sites. Postmortem examination revealed a previously undescribed atrial disease characterized by arteriolosclerosis, fibroelastosis, fatty infiltration, and vacuolar degeneration of muscle cells, with only moderate SA and A-V nodal involvement. LSCSS was present, disrupting the branching portion of the His bundle. Thus, TAS reflected SA nodal ischemia without infarction; PAS reflected a new atrial degenerative disease; H-Q was normal with a lesion in the penetrating portion of the His bundle and was prolonged with a similar lesion in the branching portion.
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Rosen et al. (1971) studied this question.