Stroke and ventricular arrhythmias.

Electrocardiographic abnormalities and cardiac arrhythmias are commonly noted after acute stroke. Risk of malignant ventricular arrhythmias is increased after a stroke and is associated with sudden cardiac death. Autonomic imbalance modulated by direct injury to neurogenic structures and enhanced by catecholamine storm can lead to myocardial damage and arrhythmogenesis. Experimental and clinical evidence suggests that insular cortex infarcts play a key role in autonomic dysregulation that lead to arrhythmias in the acute setting. Management of ventricular arrhythmias associated with acute stroke should focus on continuous cardiac monitoring, drug therapy, and electrolyte correction. Further research is needed to identify neurological structures involved in autonomic control and risk factors for ventricular arrhythmogenesis after acute stroke.

Central serotoninergic response to orthostatic challenge in patients with neurocardiogenic syncope.

AIMS: To determine whether central serotoninergic system activity is impaired by orthostatic challenge in patients with neurocardiogenic syncope (NCS). METHODS AND RESULTS: Thirty-five [mean age: 24 (SD): 6 years] patients with a clinical history of NCS and positive head-up tilt test and 35 age-matched healthy volunteers (CON = 25+/-5 years) with negative response were studied. Overnight dexamethasone suppression test (DST) (1.5 mg given at 11 p.m.) was performed to assess the sensitivity of the hypothalamic-pituitary-adrenal axis by measuring next day cortisol (microg/dL) at 8 a.m. and 4 p.m. Cardiac autonomic function, cortisol, and prolactin (ng/dL) were also determined at baseline supine (BAS) and after 5, 10, and 15 min of orthostatic stress (OS) at 60 degrees . No significant differences were observed in cortisol plasma levels after the DST: CON = 0.6+/-0.6 microg/dL vs. NCS = 0.6+/-0.5; P = 0.7. Cardiac autonomic function, cortisol, and prolactin responses were similar in both study groups (CON vs. NCS; P > 0.05) during BAS: cortisol = 8.6+/-4 vs.8.7+/-4 microg/dL and prolactin = 16.8+/-9 vs. 16.8+/-9 ng/dL; OS-5: cortisol = 8.7+/-5 vs. 8.5+/-4 microg/dL and prolactin = 16.9+/-9 vs. 15.8+/-9 ng/dL; OS-10: cortisol = 8.5+/-5 vs. 8.1+/-3 microg/dL; prolactin = 16.2+/-9 vs. 15.8+/-9 ng/dL, and OS-15: cortisol = 9.0+/-5 vs. 8.4+/-4 microg/dL; prolactin = 17.1+/-9 vs. 15.5+/-9 ng/dL. CONCLUSION: Central serotoninergic response during orthostatic challenge was not impaired in patients with recurrent NCS. These findings suggest that the activation of the hypothalamic-pituitary-adrenal axis is not altered in patients with recurrent NCS.

Impaired baroreflex gain in patients with inappropriate sinus tachycardia.

INTRODUCTION: The aim of this study was to determine the characteristics of heart rate variability (HRV), blood pressure variability (BPV), and baroreflex gain (BRG) at rest and during orthostatic stress in patients with clinical criteria of inappropriate sinus tachycardia (IST). METHODS AND RESULTS: Beat-to-beat HRV and BPV, measured by time- and frequency-domain methods, and noninvasive BRG, calculated by cross-spectral analysis, were obtained during 10 minutes both at rest and during the stabilization phase (5-15 min) of orthostatic stress at 60 degrees in 8 patients with clinical criteria of IST and 9 healthy volunteers (CON). IST patients had a higher resting mean heart rate (78.8 +/- 5.3 vs 58.5 +/- 4.2 beats/min, P=0.01) and mean blood pressure (90.4 +/- 2.4 vs 72.0 +/- 4.2 mmHg; P=0.002). RMSSD, pNN50m, and BRG were significantly reduced in IST patients at rest. BRG during orthostatic stress (7.2 +/- 0.8 vs 20.3 (2.4 ms/mmHg, P <0.01) was significantly reduced in IST patients. Delta BRG (-16.9%+/- 11 vs -50.1%+/- 5, P=0.02) was markedly blunted during orthostatic stress in IST patients. CONCLUSION: BRG was markedly impaired both at rest and during orthostatic stress in IST patients. This alteration may be responsible for the higher resting heart rate and mean blood pressures seen at rest and may facilitate tachycardia during orthostatic stress. A primary alteration in sinus node automaticity coupled with impaired BRG determines heart rate response to orthostatic stress in patients with IST.

[Autonomic dysfunction syndromes associated with orthostatic intolerance]. / Síndromes de disfunción autonómica asociados con intolerancia ortostática.

In recent years increased interest has focused on the nature and pathophysiology of orthostatic intolerance and syndromes associated with autonomic disorders. Understanding the pathophysiology underlying these syndromes has led to the recognition of several distinct clinical entities with overlapping features and the associated need to reclassify many of the previously unrecognized syndromes. Among the clinical manifestations, syncope and near syncope are frequently associated with orthostatic intolerance. In addition, however, a wide spectrum of symptoms have been described ranging from chronic fatigue to recurrent neurally mediated vasodepressor reactions. The present review focuses on the pathophysiology and classification of syndromes of autonomic dysfunction associated with orthostatic intolerance. Primary and secondary causes of dysautonomia as well as therapeutic approach to these frequently unrecognized syndromes is presented.