Salivary steroid hormone response to whole-body cryotherapy in elite rugby players.

Saliva represents a low stress, not-invasively collected matrix that allows steroid hormone monitoring in athletes by reflecting type, intensity and duration of exercise. Whole body cryotherapy (WBC) consists of short whole-body exposures to extremely cold air (-110° to -140°C) which, despite being initially used to treat inflammatory diseases, is currently acquiring increasing popularity in sports medicine. Cryostimulation practice is now widely accepted as an effective treatment to accelerate muscle recovery in rugby players. The aim of this work was to study the changes of steroid hormones in saliva of rugby players after both 2 and 14 consecutive WBC sessions, in order to investigate the effects of the treatment on their salivary steroid hormonal profile. Twenty-five professional rugby players, belonging to the Italian National Team, underwent a 7-day cryotherapy protocol consisting of 2 daily sessions. Saliva samples were taken in the morning prior to the start of the WBC, in the evening after the end of the second WBC, and in the morning of the day after the last WBC session. The samples were analyzed for cortisol, DHEA, testosterone and estradiol using competitive enzyme-linked immunosorbent assays. Cortisol and DHEA showed a reduction already after the 2 WBC sessions of the first day; after 14 consecutive WBC sessions cortisol, DHEA, and estradiol levels decreased, while testosterone increased as did the testosterone to cortisol ratio. These results were confirmed by the fact that the majority of subjects showed variations exceeding the critical difference (CD). In conclusion, we found that WBC acutely affects the salivary steroid hormone profile, and the results are evident already after only one twice-daily session. Most significantly, after one-week of consecutive twice-daily WBC sessions, all the hormones were modified. This is the first experimental report that links changes in the hormonal asset to WBC.

[Ventricular tachycardia induced by a bent catheter electrode migrated to the pulmonary artery]. / Tachicardia ventricolare indotta da catetere elettrodo incuneato "ad ansa" in arteria polmonare.

The possibility of migration of a transvenous electrode bend in the infundibulum of the pulmonary artery is a very rare complication of permanent pacing. The Authors describe the case of a patient whose transvenous electrode, positioned in the pulmonary artery 5 years after implantation, was presumably the cause of a ventricular hyperkinetic arrhythmia (VT) and of cerebral disturbances (sublipothymia, syncope). The re-position of the electrode removed the arrhythmia thus considerably improving the symptoms of the patient.

[Hemodynamic and neuroendocrine profile of 2 different cardiovascular responses in vasodepressor syncope induced by the head-up tilt test]. / Profilo emodinamico e neuroendocrino di due distinte risposte cardiovascolari nella sincope vasodepressiva indotta da head-up tilt test.

BACKGROUND: Syncope in apparently healthy subjects is usually attributed to a vasovagal reaction. However, a vagal cardio-inhibitory component is not always associated with a vasodepressor component in causing syncope: in fact, increases in heart rate, arterial pressure and plasmatic levels of catecholamines frequently precede loss of consciousness. METHODS: Prolonged 60 degrees head-up tilt table test (HUTT) was performed in 50 healthy subjects (27 male, 23 female - mean age 37.2 years) with recurrent syncope of vasodepressor or unknown origin. The upright-tilt test lasted 45 minutes: every minute of HUTT we measured heart rate (HR) and systolic (SBP) and diastolic blood pressure (DBP); at set intervals we took a blood sample to determine epinephrine (EP) and norepinephrine (NEP) levels. RESULTS: In patients with positive HUTT (42%) we observed a vaso-vagal response (10 patients) characterized by a sharp drop in SBP and DBP (> 50% of the basal values) and bradycardia (< 40 bpm) and/or sinus node arrests, and a hyperchronotropic-vasodepressor response (11 patients) characterized by a considerable increase in HR (> 60%) and simultaneous drop in SBP and DBP (> 30% of the basal values), and a large increase in plasmal EP (+881.9%). CONCLUSIONS: According to the Authors, vasovagal response is mainly due to a reflex reaction originating from the cardiac stretch-receptors, whereas hyperchronotropic-vasodepressor response is mainly due to psychic stress and anxiety provoked by prolonged and forced posture during HUTT. The high levels of adrenergic activity and plasmal EP cause the excessive chronotropic response and the vasal effects of the syndrome. Due to the induction of a state of anxiety and its postural effects, HUTT is a useful provocative tool for complete evaluation of young patients with syncope of vasodepressor origin. We treated the patients differently, depending on how they responded to HUTT. Those with a vaso-vagal response were treated with alpha-sympathomimetic agents (ethylephrine or mydodrine) and those with a hyperchronotropic-vasodepressor response received non-selective beta-blockers. None of our patients had syncope recurrences during a mean follow-up of 12.3 months. Only two patients complained of dizziness; in one of them, symptomatology was abolished by an alpha-sympathomimetic beta-blocker association.

Effects of acute hypoxia on the normal and diseased sinus node.

We have studied the effects of breathing 12% oxygen in three groups of patients with sinus bradycardia: 11 with intrinsic sick sinus syndrome, 11 with extrinsic sick sinus syndrome and 11 without any evidence of sinus dysfunction. During hypoxia, the heart rate increased by an average of 6.7 beats/min in the patients with intrinsic sick sinus syndrome, 15.7 beats/min in the patients with extrinsic sick sinus syndrome and 14.3 beats/min in those with normal sinus node function. The difference in response of the heart rate between the two groups with sick sinus syndrome was highly significant (P less than 0.001). There was no difference between the three groups in the response of the blood pressure, ventilation, and partial pressures of oxygen and carbon dioxide. The increased heart rate which accompanies hypoxia is thought to be mediated through sympathetic mechanisms consequent on hyperventilation. In the intrinsic sick sinus syndrome, there is evidence that the sympathetic tone is already increased and this may limit the extent of the tachycardia due to hypoxia. Hypoxia may be a useful clinical test to distinguish between the two forms of sick sinus syndrome.

Parapharyngeal space lesions syncope-syndrome. A newly proposed reflexogenic cardiovascular syndrome.

An intense vaso-vagal reaction characterizes those reflex cardiovascular syncopes in which the glossopharyngeal nerve constitutes the main afferent nerve pathway. In these syndromes, afferent fibres of the glossopharyngeal nerve project from the baroreceptorial area to the medullary cardiac and vasomotor centres, from which efferent fibres descend into the vagus. The most common reflex cardiovascular syndromes linked to the IX nerve are carotid sinus syndrome (CSS) and glossopharyngeal neuralgia-asystole syndrome (GNS). Eleven male patients (mean age 65.4 years) with recurrent and severe vaso-vagal attacks are described. The episodes were characterized by asthenia and general malaise, pallor, sudation, unrecordable or very low (40-60 mmHg) arterial blood pressure, mental disorientation and/or syncope. The admission diagnosis in these patients was CSS, but the clinical picture was quite different from classic CSS: triggering factors were not present, vasovagal episodes were longer, syncopes were more frequent and severe and VVI pacing was ineffective. Further investigation, including computerized tomography, showed in all patients a malignant or benign pathological growth occupying and compressing the parapharyngeal space. The authors think that the symptoms exhibited by their patients may be attributed to parapharyngeal space involvement. The pathogenetic mechanism of syncope in these cases could be similar to that occurring in GNS except for the absence of neuralgia itself. Surgical carotid sinus denervation or A-V sequential DDD pacing were ineffective in completely controlling symptoms. Intracranial section of the IX nerve appears to be the most effective mechanism for controlling the syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)

[Hypersensitivity and carotid sinus syndrome in patients with chronic atrial fibrillation]. / Ipersensibilità e sindrome del seno carotideo in pazienti con fibrillazione atriale cronica.

BACKGROUND: Carotid sinus hypersensitivity (CSH) has always been described in patients in sinus rhythm; we did not find reports of CSH in patients with chronic atrial fibrillation (AF). After the observation of bilateral CSH in a patient with chronic AF admitted to our Division for syncope, we began to systematically study patients with chronic AF and neurological disturbances to evaluate carotid sinus stimulation effects upon cardiac activity and arterial blood pressure in these subjects. METHODS: We studied 28 subjects with chronic AF (mean age 73.3 yrs.; range 60-89): 16 patients had dizziness, fainting or syncope, and formed the study group (A); 12 asymptomatic patients were considered the control group (B). After a careful clinical and instrumental evaluation, all the patients underwent a 24 hour ambulatory (Holter) ECG analysis and right and left carotid sinus massage (CSM). If the latter manoeuvre induced asystolia longer than 3 seconds, CSM was repeated during ventricular pacing to evaluate the vasal component of the carotid sinus reflex. RESULTS: In group A, 24-hour Holter monitoring showed a greater incidence (81.2%) of ventricular standstill (mean duration 2.67 seconds) in comparison to the control group. In group A we found CSH in 75% of the cases, more frequently right CSH (7 subjects with right, 1 with left and 4 with bilateral CSH) with prolonged ventricular asystolia (mean duration 5.3 +/- 1.9 sec. with right CSM; 7.8 +/- 1.4 sec. with left CSM); during CSM, we reproduced spontaneous symptomatology in 9 patients. In 12 patients in group A, diagnosis of carotid sinus syndrome was established; the cardioinhibitory forms were clearly prevalent (91.7%); only one patient presented a cardioinhibitory-vasodepressor form with a predominant vasodepressor component. CONCLUSIONS: The authors believe that CSH is frequent in patients with chronic AF; the vagal hyperactivity due to CSH can induce prolonged ventricular asystole that may be responsible for neurological disturbances such as dizziness, fainting or syncope, as observed in patients in sinus rhythm with carotid sinus syndrome. Abnormal sensitivity of the carotid sinus could thus be one of the causes of increased morbidity and mortality in patients with chronic AF. The majority of these patients may be expected to benefit from permanent pacemaker therapy.

Carotid sinus hypersensitivity and syndrome in patients with chronic atrial fibrillation.

Carotid sinus hypersensitivity (CSH) has been studied in subjects in sinus rhythm, but it has never been studied in patients with chronic atrial fibrillation (AF). After a finding of CSH in a patient with chronic AF and syncope, we studied the effects of carotid sinus stimulation in a group of patients with AF. Ten patients with chronic AF and normal ventricular rates who complained of dizziness or loss of consciousness underwent right and left carotid sinus massage (CSM) during ECG monitoring. A control group of ten patients with AF but without neurological symptoms was likewise investigated. CSH was present in eight symptomatic patients (5 patients presented right CSH, 1 left and 2 bilateral CSH), but only in three of the control patients. The mean duration of asystole induced by right CSM was 5.94 +/- 2.10 seconds; the mean asystolic interval induced by left CSM lasted 8.58 +/- 1.42 seconds. Six patients in the symptomatic group had a recurrence of spontaneous symptomatology during CSM, so that a diagnosis of carotid sinus syndrome was established. All symptomatic patients (8 patients with CSH, 2 patients with ventricular standstills but without CSH) received a permanent ventricular pacemaker. Following pacing, all patients, except for one with a significant drop of systolic blood pressure during CSM, became completely asymptomatic. In elder patients with chronic AF, CSH can induce prolonged ventricular asystole, which may be responsible for neurological symptoms such as dizziness, presyncope, or syncope, as observed in patients in sinus rhythm with carotid sinus syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)