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Altered ventricular repolarization in central sympathetic dysfunction associated with spinal cord injury.

Abstract

Complete injury to the cervical spinal cord results in total disruption of central sympathetic outflow. Although ventricular repolarization can be significantly influenced by disorders of autonomic function, the effects of cervical sympathectomy are unknown. Therefore, 40 subjects with complete chronic spinal cord injury were prospectively divided into 2 groups, half with total disruption of central sympathetic outflow (level of injury C5 to C8) known as the high level injury group, and half with nearly intact sympathetic innervation (T10 to L1) serving as controls. The completeness of autonomic dysfunction was verified by the cold pressor response. ST-segment analysis of the resting surface electrocardiogram revealed multilead ST elevation in the high level injury group, with maximum ST height significantly higher than the control group (131 +/- 21 [standard error] vs 47 +/- 8 microV; p = 0.0005). Unlike the control subjects, maximal arm ergometry exercise in the high level injury subjects failed to decrease ST-segment height (delta ST = -3 +/- 6 vs -43 +/- 14 microV in controls; p = 0.02). This difference persisted even after matching for exercise capacity. However, during exogenous stimulation with the sympathomimetic amine isoproterenol, ST-segment height in the high level injury group markedly decreased (mean delta ST = -84 +/- 26 vs -17 +/- 18 microV in controls; p = 0.04). Thus, central sympathetic dysfunction regularly results in multilead ST-segment elevation that decreases to or below isoelectric baseline during low dose isoproterenol infusion. Unlike normal subjects and individuals with normal variant ST-segment elevation, ST height is not altered by exercise. These findings document that ST-segment height in man is greatly influenced by central sympathetic nervous activity both at baseline and during physiologic and pharmacologic stress.

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BibTeXRIS

K G Lehmann, A H Shandling, A U Yusi, V F Froelicher. 1989-06-15. Altered ventricular repolarization in central sympathetic dysfunction associated with spinal cord injury.. https://doi.org/10.1016/0002-9149(89)90015-5

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Cardiovascular and cerebrovascular responses to lower body negative pressure in type 2 diabetic patients.

In diabetic patients, vascular disease and autonomic dysfunction might compromise cerebral autoregulation and contribute to orthostatic intolerance. The aim of our study was to determine whether impaired cerebral autoregulation contributes to orthostatic intolerance during lower body negative pressure in diabetic patients. Thirteen patients with early-stage type 2 diabetes were studied. We continuously recorded RR-interval, mean blood pressure and mean middle cerebral artery blood flow velocity at rest and during lower body negative pressure applied at -20 and -40 mm Hg. Spectral powers of RR-interval, blood pressure and cerebral blood flow velocity were analyzed in the sympathetically mediated low (LF: 0.04-0.15 Hz) and the high (HF: 0.15-0.5 Hz) frequency ranges. Cerebral autoregulation was assessed from the transfer function gain and phase shift between LF oscillations of blood pressure and cerebral blood flow velocity. In the diabetic patients, lower body negative pressure decreased the RR-interval, i.e. increased heart rate, while blood pressure and cerebral blood flow velocity decreased. Transfer function gain and phase shift remained stable. Lower body negative pressure did not induce the normal increase in sympathetically mediated LF-powers of blood pressure and cerebral blood flow velocity in our patients indicating sympathetic dysfunction. The stable phase shift, however, suggests intact cerebral autoregulation. The dying back pathology in diabetic neuropathy may explain an earlier and greater impairment of peripheral vasomotor than cerebrovascular control, thus maintaining cerebral blood flow constant and protecting patients from symptoms of presyncope.

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