[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)

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.

[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.

Assessment of myocardial perfusion with thallium-201 scintigraphy in exercise-induced left bundle branch block: diagnostic value and clinical significance.

Myocardial perfusion scintigraphy with thallium-201 was performed in 33 subjects (mean age 45 years, range 28-61) with exercise-induced, rate-dependent left bundle branch block (LBBB) in order to assess both the value of Thallium-201 myocardial imaging for the diagnosis of coronary artery disease (CAD) and the pathogenesis (ischaemic or not) of the conduction defect. Of the 33 patients evaluated, 16 had chest pain suggestive of CAD and 17 were asymptomatic. None had a history of prior myocardial infarction or clinical and echocardiographic signs of heart disease. LBBB appeared at a heart rate ranging from 70 to 160 b.min-1. Eighteen patients showed repolarization abnormalities (ST segment depression with deep inverted T waves) compatible with ischaemia, after QRS normalization. Thallium-201 myocardial uptake was normal in 12 subjects; in the remaining 21, reversible Thallium-201 defects were demonstrated in the septum (18 patients), septum and apex (2), and septum and infero-apical wall (1). No patient had irreversible defects and all had normal coronary angiography, with negative ergonovine tests for coronary artery spasm. The patients were followed up for a mean of 43 months (range 16-80). One patient died from sudden death, but no cardiac event occurred in the other patients. In conclusion, exercise Thallium-201 myocardial scintigraphy showed a high prevalence (64%) of reversible perfusion defects in a group of patients with exercise-induced LBBB without any evidence of CAD at angiography or coronary spasm at ergonovine test. Moreover, follow-up showed a relatively low rate of major cardiac events.

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.

[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.

[Arrhythmia related to a dual chamber DDD pacemaker: a study using intra-atrial dynamic electrocardiographic monitoring]. / Le aritmie da pacemaker bicamerali DDD: studio mediante monitoraggio elettrocardiografico dinamico endoatriale.

The intra-atrial Holter monitoring (IAHM) has been recently suggested to accurately analyze atrial activity in some complex arrhythmias. We have used this new method to examine DDD pacing-related tachyarrhythmias (DDD/TAs). Fifteen patients underwent IAHM (24 hours) early after DDD pacemaker (PM) implantation. The intra-atrial ECGs were obtained through a multipolar electrode catheter; simultaneously a chest wall lead (CM5) was recorded. A standard Holter equipment was used. When DDD/TAs were observed, a second 24-hours recording was performed after a suitable PM re-programming. In 9 patients (60%) 1 or more DDD/TAs were observed, due to the following mechanisms: PM re-entry, oversensing of extra atrial potentials, fast ventricular stimulation triggered by spontaneous atrial tachyarrhythmias. Whereas the diagnostic accuracy of the IAHM was manifest, the DDD/TAs were often misdiagnosed on the basis of the CM5 lead data. At last, a right DDD PM re-programming, based on IAHM results, was able to solve or minimize the referred arrhythmic problems. In conclusion, the IAHM can be an useful method to understand the electrogenetic causes of the DDD/TAs and to optimally program the dual chamber PM. However, on account of the invasivity of the procedure, the IAHM must be used only when the noninvasive techniques fail to detect the mechanisms of the DDD/TAs.

Survival rates after pacemaker implantation: a study of patients paced for sick sinus syndrome and atrioventricular block.

It is still a matter of controversy as to whether the patients paced for atrioventricular block (AVB) have different prognosis and survival rates than those paced for Sick Sinus Syndrome (SSS). We have compared the survival rates of 962 AVB patients (group A) with that of 283 SSS patients (group B) who underwent pacemaker implantation during the period January 1968 to December 1986. The survival rate graphs of the examined groups were calculated using the actuarial method and the differences in the survival rates between the groups were evaluated using the Logrank test. Our results show that SSS patients have a higher survival rate than AV block with a difference on the rate of survival between the two groups reaching the borderline of statistical significance. Multivariate discriminant analysis was then used to assess that of the parameters (i.e., age at the time of implantation, sex, electrophysiological indication to pacing, etiology or pacing mode) could have had the main influence upon mortality and the different pattern of the survival rate graph within the two groups of patients. Our data show that survival is mostly related to age, pacing mode and, although more slightly, to underlying heart disease; the electrophysiological indication to pacing, instead, does not significantly influence it.

[A new reflex cardiovascular syndrome: recurrent vasodepressive syncope caused by lesions or tumors of the parapharyngeal space. Etiopathogenesis, clinical picture, differential diagnosis with carotid sinus syndrome and glossopharyngeal neuralgia-asystole syndrome. Therapy by intracranial resection of the 9th cranial nerve]. / Una nuova sindrome cardiovascolare riflessa: ricorrenti sincopi vasodepressive da lesioni o tumori dello spazio parafaringeo. Etiopatogenesi, quadro clinico, diagnosi differenziale con la sindrome del seno carotideo e la glossopharyngeal neuralgia-asystole syndrome. Terapia con la resezione intracranica del IX nervo.

An intense vaso-vagal reaction characterizes all the reflex induced cardiovascular syncopes. In these syndromes the vagal cardio-inhibitor effect on heart rate is more evident than the vasodilatation and fall in blood pressure. The vasodepressor mechanism is uncommon even in carotid sinus syndrome. We have studied 6 male patients, age range 56-73 years (mean age: 64) with recurrent vasodepressor syncopes. The following were always present during such episodes: generalized malaise, profound fatigue, pallor, cyanosis, copious sweating, lack of peripheral pulses, severe fall in blood pressure (BP) (systolic BP less than or equal to 50-60 mmHg or unrecordable), mental disorientation and/or syncope. The first diagnosis in our patients was carotid sinus syndrome, but, the clinical picture was quite different from classic carotid sinus syndrome: triggering factors were not present, the vasovagal episodes were longer, the syncopes more frequent and severe, and the VVI pacing uneffective. Further investigations, including computerized axial tomography, showed--in all these patients--a malignant tumour originally localized in or near the parapharyngeal space. We think that the symptoms of our patients can be attributed to parapharyngeal tumour and that the parapharyngeal space lesions are able to cause severe vasovagal attacks and syncope. The pathogenetic mechanism in this syndrome, due to neural irritation of the glossopharyngeal afferent fibres, is similar to the glossopharyngeal neuralgia-asystole syndrome, but it obviously doesn't involve pain-pathways since none of our patients had pain. Therefore, this syndrome differs from glossopharyngeal neuralgia- asystole syndrome in the presence of tumours and in the absence of neuralgia and initiating factors.(ABSTRACT TRUNCATED AT 250 WORDS)

[Study of myocardial perfusion by means of scintigraphy with thallium-210 in left bundle branch block induced by exertion]. / Studio della perfusione miocardica mediante scintigrafia con tallio-201 nel blocco di branca sinistra inducibile dallo sforzo.

Myocardial perfusion scintigraphy with 201-TL was performed in a group of subjects affected by exercise-induced, rate-dependent left bundle branch block (LBBB). The aim of the study was: to define the significance of the exercise-induced conduction abnormality: "primitive" or "ischemic". 14 patients, aging 28-58 years (x = 42), 8 with chest pain (4 typical angina, 4 atypical angina) and 6 without any symptoms were studied. None had history of prior myocardial infarction or clinical and echocardiographic signs of heart disease. LBBB appeared at a heart rate ranging from 70 to 160 beats/min. 6 patients showed repolarization abnormalities (ST changes, deep and negative T wave) suggestive for ischemia, during successive QRS normalization. 201-TL-uptake was normal in 5 subjects; in the remaining 9 ones reversible TL defects were demonstrated in the septum (6), in the septum and apex (2), in the septum and inferior-apical wall (1). No patients had irreversible impaired perfusion. All the patients had normal coronary angiography, with negative ergonovine test for coronary artery spasm. In conclusion, in the majority of our subjects (64%) with exercise-induced LBBB, a reversible TL-uptake defect, usually located in the septum without diagnostic value of obstructive CAD, has been observed. Further studies will establish if the TL-defect is only an "apparent phenomenon" due to contraction abnormality secondary to LBBB, or, on the contrary, an expression of myocardial ischemia with normal coronary vessels as a consequence of the LBBB.

[Hypotension during ventricular pacing. A study of the vagal reflex component]. / Ipotensione durante pacing ventricolare (VVI). Studio della componente riflessa vagale.

It has been suggested that hypotension during ventricular pacing (V) could be caused by a parasympathetic vasodilating reflex. In order to evaluate this hypothesis, we studied 10 patients who had wide fluctuations of arterial pressure during V. Intra-arterial pressure, right atrial pressure, EKG and cardiac index (thermodilution) were determined in the following conditions: basal rhythm (B), V, atrioventricular pacing (A-V) and ventricular-atrial pacing (V-A). The same investigations have been carried out in the same conditions (B,V,A-V,V-A) after atropine 0.03 mg/Kg intravenously. The arterial blood pressure during V decreased markedly simultaneously with the appearance of cannon waves in the right atrial pressure tracing. During A-V the arterial pressure remained stable at the highest level observed during V. The start of V-A pacing induced a marked drop of arterial pressure, which, however, gradually increased to a level slightly lower than during A-V pacing. After atropine the arterial blood pressure during V decreased again in all patients concomitantly to the appearance of cannon waves in the atrium as before atropine. The values of arterial blood pressure during B, A-V and V-A were not different from those measured before atropine. Therefore, an increase of parasympathetic activity during V is not responsible for the wide fluctuation of arterial blood pressure. A possible role of sympathetic failure must be considered.