PubMed · 7928319
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P Cortelli. 1994. Autonomic function in migraine.. https://doi.org/10.1111/j.1526-4610.1994.hed3406375_1.x
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BACKGROUND: Analysis of heart rate variability (HRV) is a valuable noninvasive method for quantifying autonomic cardiac control in humans and has been utilized during dipyridamole echocardiographic test to differentiate positive from negative test results. HYPOTHESIS: We aimed to evaluate, by means of HRV analysis, the influence of the angiographic severity of coronary artery disease on cardiac autonomic control during dipyridamole-induced myocardial ischemia. METHODS: We analyzed RR interval variability changes during dipyridamole-induced myocardial ischemia in 31 selected patients (mean age 54 +/- 9 years) with available coronary angiography and positive dipyridamole echocardiographic test. Spectral components of HRV were assessed by means of wavelet transform analysis for the last 5 min before the beginning of the test (baseline) and for 5 min after the onset of ischemia-related events (peak dipyridamole effect). RESULTS: Patients were divided into three groups according to the number of coronary diseased vessels (Group A, single-vessel disease; Group B, double-vessel disease; Group C, triple-vessel disease). No difference was detectable at baseline among the three groups. After dipyridamole, low-frequency power, a measure of sympathetic modulation of heart rate, increased and echocardiographic wall motion score index worsened in all groups (p < 0.001). The increase in low-frequency power was more evident in Group C patients than in the other two groups (p < 0.005). Furthermore, after dipyridamole, a direct correlation was found between low-frequency power and wall motion score index (r = 0.59; p < 0.001). CONCLUSIONS: These data suggest that HRV analysis performed during dipyridamole echocardiographic test provides useful information to assess the severity of coronary artery disease.
About 20% of all GBS patients have symptoms of dysautonomia: labile hypertension, orthostatic hypotension, sinustachycardia or sinus arrest. This rate rises to 75% in patients with tetraplegia. Proprioceptive loss predicts dysautonomia independently from the severity of weakness. It is frequently responsible for dysautonomia. The afferent limb of cardiovascular regulation contains more myelinated fibers than the sympathetic and parasympathetic efferences, which determine the common classification of dysautonomia. The frequence of mixed sympathetic and parasympathetic hyperactivity is hard to explain by efferent lesions. Afferent conduction block releases the sympathetic efference of the baroreceptor reflex. The resulting catecholamine excess explains hypertension, tachycardia, ECG-changes and hyperglycemia. Norepinephrine sensitizes left ventricular stretch receptors. They induce cardiovascular depression and neurocardiogenic syncope which has a temporal behaviour similar to the blood pressure variations of GBS. Conduction block of sinoatrial stretch receptors causes inappropriate secretion of ADH and renin. Dysbalance between myelinated and unmyelinated afferents which decrease and increase heart rate may cause parasympathetic hyperactivity, as exemplified by pulmonary stretch receptors that are stimulated by artificial ventilation. Wrong afferent feedback is responsible for many cardiovascular instabilities in GBS. Blockade of misguided efferent reactions is an attractive therapeutical approach.
Upright posture imposes a substantial gravitational stress on the body, for which we are able to compensate, in large part because of the autonomic nervous system. Alteration in autonomic function, therefore, may lead to orthostatic intolerance. On one extreme, patients with autonomic failure caused by degenerative loss of autonomic function are severely disabled by orthostatic hypotension and may faint whenever they stand up. Fortunately, such patients are relatively rare. On the other hand, disabling orthostatic intolerance can develop in otherwise normal young people. These patients can be severely impaired by symptoms of fatigue, tachycardia, and shortness of breath when they stand up. The actual incidence of this disorder is unknown, but these patients make up the largest group of patients referred to centers that specialize in autonomic disorders. We will review recent advances made in the understanding of this condition, potential pathophysiological mechanisms that contribute to orthostatic intolerance, therapeutic alternatives currently available for the management of these patients, and areas in which more research is needed.