PubMed · 16362548
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Peter Flachenecker, Karlheinz Reiners. 2005. Abnormal baroreflex responses in multiple sclerosis.. https://doi.org/10.1007/s10286-005-0315-2
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OBJECTIVES: Impaired arterial baroreflex sensitivity (BRS) has been associated with cardiac mortality and non-fatal cardiac arrests after a myocardial infarction. Patients with chronic renal failure (CRF) have a poor prognosis because of cardiovascular diseases, and sudden death is common. The aim of this study was to assess whether BRS or the baroreflex effectiveness index (BEI), a novel index reflecting the number of times the baroreflex is active in controlling the heart rate in response to blood pressure fluctuations, is associated with prognosis in CRF. METHODS: Hypertensive patients with CRF who were treated conservatively, by haemodialysis or peritoneal dialysis were studied. Electrocardiogram and beat-to-beat blood pressures were recorded continuously and BRS and BEI were calculated. Patients were then followed prospectively for 41 +/- 15 months (range 1-64). RESULTS: During follow-up 69 patients died. Cardiovascular diseases and uraemia accounted for the majority of deaths (60 and 20%, respectively), whereas sudden death occurred in 15 patients. In adjunct with established risk factors such as age, diabetes, congestive heart failure and diastolic blood pressure, reduced BEI was an independent predictor of all-cause mortality among CRF patients [relative risk (RR) 0.50, 95% confidence interval (CI) 0.33-0.71 for an increase of one standard deviation in BEI, P < 0.001]. Diabetes and reduced BRS were independent predictors of sudden death (RR 0.29, 95% CI 0.09-0.86 for an increase of one standard deviation in BRS, P=0.022). CONCLUSIONS: Both BEI and BRS convey prognostic information that may have clinical implications for patients with cardiovascular diseases in general.
Despite extensive research, a link between the assumed mechanisms of death and known risk factors for sudden infant death syndrome (SIDS) has not yet been established. Modifiable risk factors such as prone sleeping position, nicotine exposure and thermal stress and non-avoidable risk factors like male gender and some risky socio-economic conditions could be detected, but the etiology of SIDS remains unknown. In many SIDS cases histopathological findings suggest an involvement of vital autonomic control functions and unidentified trigger factors seem to play a role. From a hypothetical point of view, a developmental sympatheticovagal imbalance of the cardiovascular reflex control could cause a predisposition for SIDS. An assumed gastroesophageal trigger impulse is possibly developed during the first weeks of life and could lead to the infant's vagal reflex death. Air swallowed during feeding escapes through the esophagus while the infant is sleeping. The temporarily bloated esophagus exerts pressure on neighboring mediastinal baroreceptors, which is potentially misinterpreted as a rise in arterial pressure. The following cardiodepressoric baroreceptor reflex could lead to arterial hypotension, bradycardia and cardiac arrest. Sleeping in prone position may create an increased thoracic pressure on mediastinal baroreceptors, causing a more pronounced vagal reflex and an increased likelihood of SIDS. Prone position in connection with soft objects in the infant's sleeping environment potentially generates an increased oculobulbar pressure, resulting in an additional cardiodepressoric condition (Aschner-Dagnini phenomenon). From the sixth month of life onwards the sympatheticovagal balance seems to have matured sufficiently to compensate the life-threatening challenges in most infants. Insufficient postprandial burping could either create another independent modifiable risk factor or present the missing link to a common trigger mechanism for SIDS. Further investigations may possibly lead to the explicit recommendation to burp all infants sufficiently and repeatedly before sleep.
It is still unclear whether the low-frequency oscillation in heart rate is generated by an endogenous neural oscillator or by a baroreflex resonance. Our aim was to investigate this issue by analyzing blood pressure and heart rate variability and the baroreflex function in paraplegic subjects with spinal cord injury below the fourth thoracic vertebra. These subjects were selected because they represent a model of intact central neural drive to the heart, with a partially impaired autonomic control of the vessels. In our study, arterial blood pressure and ECG were recorded in 33 able-bodied controls and in 33 subjects with spinal cord lesions between the fifth thoracic and the fourth lumbar vertebra 1) during supine rest (lowest sympathetic activation), 2) sitting on a wheelchair (light sympathetic activation), and 3) during exercise (moderate sympathetic activation). Blood pressure and heart rate spectra, coherence, and baroreflex function (sequence technique) were estimated in each condition. Compared with controls, paraplegic subjects showed a reduction of the low-frequency power of blood pressure and heart rate, and, unlike controls, a 0.1-Hz peak did not appear in their spectra. Sympathetic activation increased the 0.1-Hz peak of blood pressure and heart rate and the coherence at 0.1 Hz in controls only. Paraplegic subjects also had significantly lower baroreflex effectiveness and greater blood pressure variability. In conclusion, the disappearance of the 10-s oscillation of heart rate and blood pressure in subjects with spinal cord lesion supports the hypothesis of the baroreflex nature of this phenomenon.