[Diagnosis and follow-up of 330 patients admitted for syncope in the Department of Cardiology and Neurology. How important is an interdisciplinary study?]. / Diagnosi e follow-up di 330 pazienti ricoverati per sincope in Cardiologia e Neurologia. Quanto è importante uno studio interdisciplinare?

Many mechanisms of different nature-hemodynamic, metabolic and reflex-may cause syncope. We have studied all patients referred for syncope to the Divisions of Cardiology and Neurology of our Hospital, focusing five end-points: standardize a diagnostic protocol; evaluate the diagnostic value of the different tools in the diagnosis of syncope; evaluate the causes of syncope in our patients; value the importance of systematic cardiological-neurological co-operation in these patients; observe the prognosis of patients with syncopal attacks. We have studied 330 patients referred to our Divisions for syncopal attacks (239 in Cardiology and 91 in Neurology) with a protocol organized in 4 steps of increasing levels of complexity: step 1: history, clinical examination, standard electrocardiogram, carotid sinus massage, chest radiography, neurological and cardiological examination; step 2: two-dimensional Doppler echocardiography, dynamic 24-72 hour ECG, standard electroencephalogram (EEG), head-up tilt-table test; step 3: EEG after sleep deprivation, computed tomography, Doppler evaluation of carotid flows, transesophageal electrophysiologic study (EPS); step 4: Oxford test for 24-hour evaluation of arterial blood pressure, intracavitary EPS. We have found in 165 patients (50%) a cardiac syncope, in 78 (23.6%) a reflex syncope, in 43 patients (13%) a syncope of different origin ("non cardiac-non reflex") and in 44 patients (13.4%) we have not been able to find a cause of patient's syncopal attacks. We have established a diagnosis in 148 patients (51.7% of diagnoses) with step 1 examinations, in 98 cases (34.2%) with step 2, in 33 (11.5%) with step 3 and in 7 (2.5%) with step 4 examinations. One hundred-twenty three patients - or relatives of died patients-(37.3%) have answered our follow-up questionnaire (mean follow-up 54.85 +/- 13.73 months, range 36-78 months). Among them, patients with cardiac syncope have had a mortality rate of 18.57%, those with reflex syncope of 7.69%, those with "non cardiac-non reflex" syncope of 7.14%. No patients with syncope of unknown origin died. Our study demonstrates that in the evaluation of patients with syncope, the simplest diagnostic tools are of great value: in fact we have obtained 86% of the diagnoses with the first 2 steps examinations. Furthermore, our study confirms that cardiac syncope has a higher mortality rate compared to other forms of syncope. Co-operation between our Divisions has not been very useful in increasing the number of diagnosed cases, but it has allowed to correctly and rapidly direct our attention toward one form of syncope so that we have been able to speed up the diagnostic process.

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)

[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.

[Anomalous origin of the left coronary artery from the pulmonary artery. A rare case diagnosed in adulthood]. / Origine anomala della coronaria sinistra dall'arteria polmonare. Un raro caso diagnosticato in età adulta.

Anomalous origin of the left coronary artery from the pulmonary artery (Bland-White-Garland syndrome) is a rare but often lethal congenital lesion. Clinical manifestations of this syndrome present, in the large majority of cases, in infancy. The authors describe a case of Bland-White-Garland syndrome diagnosed in adult age.

[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.