PubMed Health⌕ Search

PubMed · 1279548

Autonomic nervous system controlled closed loop cardiac pacing.

Abstract

A multicenter clinical study is presented, which focuses on the reestablishment of closed loop cardiac control in patients with chronotropic insufficiency. Using the information about sympathetic tone contained in the myocardial contractility, it is possible to reconnect the heart rate to the physiological control mechanisms. Intracardiac impedance is measured with the ventricular electrode and the ventricular inotropic parameter (VIP) is derived from that. The VIP serves directly as input to the control of heart rate by the pacemaker. Over 200 patients have received autonomic nervous system (ANS) controlled pacemakers. The patient-pacemaker system was investigated in different ways. This included standard exercise tests, long-term studies of every day activities over 24 hours, psychological, and pharmacological challenges. To prove the validity of the approach we specifically looked at (1) the appropriateness of changes in paced heart rate with sympathetic tone during exercise, (2) the correlation between heart rate and sinus rate, if detectable, and (3) the correlation between the echocardiographically determined preejection period (PEP) and the VIP controlled heart rate.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

A M Pichlmaier, D Braile, E Ebner, O T Greco, H Hutten, G H von Knorre, W Niederlag, W Rentsch, H Volkmann, D Weber. 1992. Autonomic nervous system controlled closed loop cardiac pacing.. https://doi.org/10.1111/j.1540-8159.1992.tb02969.x

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

The diagnostic workup of patients with neuropathic pain.

Determining the causes of neuropathic pain is more than an epistemological exercise. At its essence, it is a quest to delineate mechanisms of dysfunction through which treatment strategies can be created that are effective in reducing, ameliorating, or eliminating symptomatology. To date, predictors of which patients will develop neuropathic pain or who will respond to specific therapies are lacking, and present therapies have been developed mainly through trial and error. Our current inability to make therapeutically meaningful decisions based on ancillary test data is illustrated by the following: In a study specifically designed to assess the response of patients with painful distal sensory neuropathies to the 5% lidocaine patch, no relationship between treatment response and distal leg skin biopsy, QST, or sensory nerve conduction study results could be established. From a mechanistic perspective, the hypothesis that the lidocaine patch would be most effective in patients with relatively intact epidermal innervation, whose neuropathic pain is presumed attributable to "irritable nociceptors," and least effective in patients with few surviving epidermal nociceptors, presumably with "deafferentation pain," was unproven. The possible explanations are multiple and outside the scope of this review. However, these findings, coupled with the disparity in C-fiber subtype involvement in diabetic small-fiber neuropathy, and the recently reported inability of enzyme replacement therapy in Fabry disease to influence intraepidermal innervation density, while having mixed effects on cold and warm QST thresholds, and beneficial effects on sudomotor findings, when therapeutic benefit was demonstrated, lead one to conclude that the specificity of ancillary testing in neuropathic pain is inadequate at present, and reinforce the aforementioned caveats about inferential conclusions from indirect data. The diagnosis of neuropathic pain mechanisms is in its nascent stages and ancillary testing remains "subordinate," "subsidiary," and "auxiliary" as defined in Webster's Third New International Dictionary. As a consequence of these difficulties, the recent approach by Bennett and his colleagues may have merit. They have hypothesized (and provide data in support) that chronic pain can be more or less neuropathic on a spectrum between "likely," "possible," and "unlikely," based on patient responses on validated neuropathic pain symptom scales, when compared with specialist pain physician certainty of the presence of neuropathic pain on a 100-mm visual analog scale. The symptoms most associated with neuropathic pain were dysesthesias, evoked pain, paroxysmal pain, thermal pain, autonomic complaints, and descriptions of the pain as being sharp, hot, or cold, with high sensitivity. Higher scores for these symptoms correlated with greater clinician certainty of the presence of neuropathic pain mechanisms. Considering each individual patient's chronic pain as being somewhere on a continuum between "purely nociceptive" and "purely neuropathic" may have diagnostic and therapeutic relevance by enhancing specificity, but this requires clinical confirmation. Thus, symptom assessment remains indispensable in the evaluation of neuropathic pain, ancillary testing notwithstanding

Autonomic Nervous System↗