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)

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.

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)

No abstract

Summary: The hemodynamic efffects of combined administration of ibopamine (Ib) (150 mg orally) with nitroprusside (NP) (50-150 pg/min intravenously) were compared with those of NP alone in 17 patients with severe congestive heart failure due to coronary artery disease (7 patients) or idiopathic cardiomyopathy (10 patients). Hernodynamic measurements were obtained using a Swan-Ganz thermodilution catheter and a bedside thermodilution cardiac output computer. Nitroprusside alone produced a significant decrease (-12.4%) in mean arterial pressure, mean pulmonary arterial pressure (-28.3%), and systemic vascular resistance (-22.6%), and a significant increase in stroke volume index (23.1 %). The administration of combined NP and Ib produced a further significant increase of stroke volume index (20.1 %) with a concomitant and significant reduction of systemic vascular resistance (-19.4%); heart rate, mean systemic and pulmonary arterial pressures did not change significantly from the values observed with NP alone. Moreover, stroke work index, although not significantly modified with the vasodilator alone, was significantly increased over control values with NP+Ib association. Although NP alone induced similar effects in both the ischemic and idiopathic cardiomyopathies, the association of Ib gave a more favorable, though not significant, hemodynamic response in the subjects with primitive cardiomyopathy than in the ischemic ones. Thus, the association of Ib to NP therapy, in patients with congestive heart failure, further increases stroke volume index and stroke work index with a concomitant reduction of systemic vascular resistance, without any significant change in mean systemic and pulmonary arterial pressures, or hem rate. These results point out the possibility of associating Ib with other orally active vasodilators in the chronic treatment of congestive heart failure.