PubMed · 831979
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1977-01-01. Sick sinus syndrome.. https://pubmed.ncbi.nlm.nih.gov/831979/
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The functional anatomy of the sinoatrial node (SAN) in man is first reviewed, together with its possible anatomical substructure. The true group pacemaker (PM) shift under autonomic drive is then related to a continuous competition between the intrinsic auto-firing period hierarchy and the autonomic topological susceptibility hierarchy. Accordingly, the PM 'skip' to both lower and higher periods following an abrupt and consistent acetylcholine (ACh) release at the SAN periphery, and the PM 'slip' towards a relocation of the next period, as a possible response to a slower and smaller ACh release, are considered. The PM 'skip' and 'slip' as boundaries of the true PM excursion within the SAN during the respiratory cycle, and their statistical properties, are then examined. Under current heart rate control menus in normals, the PM skip appears to follow central influence, whereas the conservative or slipping PMs suggest peripheral control. Finally, interpretation of the PM skip as a salutary sign of functional reserve is proposed, and a method of alleviating the PM skip which confounds electrophysiological testing of the SAN function in patients is devised.
Fetal heart rate (FHR) monitoring forms the basis of routine fetal assessment, particularly short-term variability in the interbeat interval which can be difficult to interpret. Respiratory sinus arrhythmia (RSA), the change in heart rate in response to breathing, contributes to short-term variability, and the presence of RSA in utero may reflect the functional integrity of the central nervous system. This paper describes the use of Doppler ultrasound to derive the required measures of fetal heart rate and fetal breathing movements and spectral analysis to identify RSA. Cases are presented to illustrate the results obtained both in the presence and absence of RSA.
A retrospective study of 252 patients who received a DDD pacemaker between October 1982 and December 1990 was performed. During a mean follow-up of 30 months, reprogramming to the VVI mode was necessary in 39 patients (15.5%). Technical problems causing downgrading occurred 15 times, of which 13 problems became permanent. A total number of 24 patients had sustained atrial arrhythmias, including 14 with atrial fibrillation and 10 with atrial flutter. In this group, conversion to sinus rhythm could be obtained in 38%. After 2 years, reliable DDD pacing was maintained in 86% of the surviving patients. The survival after 1 and 2 years was 94% and 89%, respectively, and was not influenced by arrhythmias or technical problems. We conclude that atrial arrhythmias including flutter are the most important reasons for reprogramming to the VVI mode, although in an important number of patients, predominantly those with flutter, restoration of AV synchrony can be obtained. The high number of patients with atrial flutter could imply some role for DDD devices offering the option of antitachycardia pacing. Reprogramming of the pacing mode did not influence mortality.