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Extensive clinical experience has demonstrated that implantable cardiac pacemakers are safe and effective mechanisms for controlling symptoms and preventing the hazards of third degree heart block with Stokes-Adams syncope. Medical management of this disease does not provide reliable protection and life expectancy averages about two years after diagnosis. Hence the negligible surgical morbidity and mortality associated with pacemaker implantation justifies broad indications to implant one of the four commercially available battery-powered units.

Elective implantation of a pacemaker should be considered in patients with persistent third degree heart block who have had: One or more episodes of Stokes-Adams syncope; surgical injury to the conduction system, regardless of syncopal attacks; evidence of low cardiac output with cardiomegaly secondary to bradycardia. Few if any other cardiac arrythmias are satisfactorily controlled by an electrical pacemaker.

Emergency pacemaker control is obviously necessary for patients developing intractable or recurrent bouts of asystole. During the interval until an implantable unit can be obtained and sterilized, the patient may be controlled by intravenous isoproterenol or by an external pacemaker attached to a transvenous catheter electrode, a precordial skin electrode or a percutaneous myocardial wire electrode.

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Ten patients, between the ages of 39 and 75 years, underwent subcutaneous implantation of an electrode pacemaker for relief of recurrent syncopal episodes of Stokes-Adams disease. Their prolonged course of severe disability on medical therapy is in marked contrast to their new life, free of syncopal attacks, on pacemaker therapy. Experience in the management of these patients has shown that the electrode catheter, introduced intravenously to stimulate the right ventricular endocardium, is the best temporary therapy in a patient with uncontrollable syncopal attacks, and it should be used in all patients undergoing the surgical procedure of implantation. Pacemaker therapy is applicable to patients in sinus rhythm as well as to those in complete heart block. Observations on the effect of heart rate on cardiac output have shown the need of a faster rate in the presence of congestive failure for the maintenance of an adequate cardiac output. The favourable course of patients after implantation of a pacemaker indicates that this is the treatment of choice in Stokes-Adams disease.

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Background

Due to lack of efficacy in recent trials, current guidelines for the treatment of neurally-mediated (vasovagal) syncope do not promote cardiac pacemaker implantation. However, the finding of asystole during head-up tilt –induced (pre)syncope may lead to excessive cardioinhibitory syncope diagnosis and treatment with cardiac pacemakers as blood pressure is often discontinuously measured. Furthermore, physicians may be more inclined to implant cardiac pacemakers in older patients. We hypothesized that true cardioinhibitory syncope in which the decrease in heart rate precedes the fall in blood pressure is a very rare finding which might explain the lack of efficacy of pacemakers in neurally-mediated syncope.

Methods

We studied 173 consecutive patients referred for unexplained syncope (114 women, 59 men, 42±1 years, 17±2 syncopal episodes). All had experienced (pre)syncope during head-up tilt testing followed by additional lower body negative suction. We classified hemodynamic responses according to the modified Vasovagal Syncope International Study (VASIS) classification as mixed response (VASIS I), cardioinhibitory without (VASIS IIa) or with asystole (VASIS IIb), and vasodepressor (VASIS III). Then, we defined the exact temporal relationship between hypotension and bradycardia to identify patients with true cardioinhibitory syncope.

Results

Of the (pre)syncopal events during tilt testing, 63% were classified as VASIS I, 6% as VASIS IIb, 2% as VASIS IIa, and 29% as VASIS III. Cardioinhibitory responses (VASIS class II) progressively decreased from the youngest to the oldest age quartile. With more detailed temporal analysis, blood pressure reduction preceded the heart-rate decrease in all but six individuals (97%) overall and in 10 out of 11 patients with asystole (VASIS IIb).

Conclusions

Hypotension precedes bradycardia onset during head-up tilt-induced (pre)syncope in the vast majority of patients, even in those classified as cardioinhibitory syncope according to the modified VASIS classification. Furthermore, cardioinhibitory syncope becomes less frequent with increasing age.

A 29-year-old man was referred to the emergency department with a complaint of abdominal pain and dizziness. He had experienced two previous syncopal episodes. His family history revealed that his mother and his two uncles had received permanent pacemaker implantation. His initial heart rate was 49 beats per minute. The electrocardiography (ECG) showed atrial flutter and right bundle branch block (RBBB) with left anterior fascicular block (LAFB). On admission, 24-hour Holter showed ventricular pause up to 16 seconds during syncope. Radio frequency catheter ablation (RFCA) of atrial flutter was performed. The ECG revealed bifascicular block (RBBB and LAFB) and first-degree atrioventricular block. He received a permanent pacemaker implantation. His brother's and his sister's ECGs also showed trifascicular block and the pedigree showed autosomal dominant inheritance. This patient was diagnosed with a progressive familial heart block (PFHB) type I. This would be the first report of a PFHB type I case documented in Korea.

A 21 year old man presented with multiple, recurrent episodes of complete atrioventricular (AV) block associated with swallowing. Electrophysiological study revealed an AV block with swallowing of carbonated beverages and balloon inflation in the lower oesophagus. Evaluation did not demonstrate any underlying oesophageal or cardiac disease, and the AV block was not induced after intravenous atropine administration. The AV block was probably caused by a hypersensitive vagotonic reflex triggered by mechanical receptors in the lower oesophagus, resulting in suppression of the AV node. Head up tilt test revealed an increase in the high frequency spectrum of heart rate variability before the onset of the syncope. These findings suggest that the amplitude of the continual fluctuations in response to a variety of stimuli and derangement from both intrinsic and extrinsic environments was greater in this patient than in normal subjects. Swallow syncope is an unusual but treatable disorder. These reflexes that become exaggerated to the point of causing illness are poorly understood.


Keywords: swallow syncope; AV block; electrophysiological study; head up tilt test

A 41-year-old man with no relevant cardiac history presented for evaluation of episodic syncope. Electrocardiography showed sinus rhythm with right bundle-branch block and Q waves in leads II, III, and aVF. Subsequent exercise treadmill testing and technetium 99m sestamibi study revealed a reversible posterior defect. Coronary angiography later showed a right coronary artery that arose from the left coronary sinus—an anomaly that has been associated with angina, myocardial infarction, and sudden cardiac death.

After being informed of the potential risks and options associated with this anomaly, the patient chose long-term β-blocker medical therapy. At follow-up, this treatment appeared to have resolved his episodic syncope. (Tex Heart Inst J 2002;29:37–9)

Vasovagal syncope is not a benign condition in the elderly population. In patients not responsive to conservative therapy and whose abrupt faints are associated with serious injuries and seriously affected quality of life, pacemaker therapy was suggested. However, the usefulness of cardiac pacing for the prevention of recurrences of vasovagal syncope remains controversial because of the dominant role of the vasodepressor component during the episode. In the Medical Center Alkmaar, the Head-Up Tilt Test (HUTT) has been used since 1996 during the work-up of patients who present with vasovagal syncope. The HUTT showed a dominant cardioinhibitory response in 4.5% of our patients; in elderly patients with vasovagal syncope without prodromal symptoms and refractory on conservative therapy, pacemaker therapy was very effective in preventing syncope during long-term follow-up. (Neth Heart J 2008;16(Suppl1):S15-S19.)

OBJECTIVE--To evaluate the effect of permanent pacing in cardioinhibitory malignant vasovagal syndrome. PATIENTS AND METHODS--37 patients with permanent pacemakers for cardioinhibitory malignant vasovagal syndrome. All presented with syncope (median six episodes, median frequency two episodes a year) and after conventional investigation and invasive electrophysiological assessment they remained undiagnosed, and without a generally accepted indication for pacemaker implantation. In all vasovagal syncope with cardioinhibition (heart rate at syncope < 60 beats/min) developed during tilt tests performed according to the Westminster protocol (head up tilt at 60 degrees with a footplate support for 45 minutes or until syncope intervenes). Dual chamber pacemakers were implanted in 35 (95%) and VVI pacemakers in the remaining two (5%). RESULTS--Over a mean (SD) follow up since implantation of 50.2 (23.9) months symptomatic improvement occurred in 89%: 62% remained free of syncope and 27% were completely symptom free. The collective syncopal burden of these 37 patients was reduced from 136 to 11 episodes each year. During follow up three patients died from unrelated causes. Patients who become asystolic during the tilt test (sinus pause of at least four seconds) experienced no greater benefit from pacing than those with less extreme cardioinhibition. Patients who remained free of syncope since implantation were younger than those who continued to experience syncope. Patients who remained completely symptom free after implantation were younger, more likely to be male, and had had fewer syncopal episodes before implantation than those who continued to experience syncope or presyncope. No other demographic, clinical, investigative, or pacing variable suggested a more favourable outcome after implant. CONCLUSIONS--This retrospective and uncontrolled experience suggests a possible role for permanent pacing in selected patients with cardioinhibitory malignant vasovagal syndrome. Improved acquisition of tilt test data may enable better selection of patients who are suitable for permanent pacing. A randomised prospective study to compare permanent pacing with no treatment or with medical treatment in cardioinhibitory malignant vasovagal syndrome is indicated.

Background

Episodes of bradycardia hypotension (BH) or vasovagal syncope have a reported incidence of 13-29% during arthroscopic shoulder surgery in the sitting position after an interscalene block (ISB). This study was designed to investigate whether intravenous fentanyl during shoulder arthroscopy in the sitting position after ISB would increase or worsen the incidence of BH episodes.

Methods

In this prospective study, 20 minutes after being in a sitting position, 160 patients who underwent ISB were randomized to receive saline (S, n = 40), 50 µg of fentanyl (F-50, n = 40), 100 µg of fentanyl (F-100, n = 40) or 30 mg of ketorolac (K-30, n = 40) randomly. We assessed the incidence of BH episodes during the operation and the degree of maximal reduction (Rmax) of blood pressure (BP) and heart rate (HR).

Results

The incidence of BH episodes was 10%, 15%, 27.5% and 5% in the S, F-50, F-100 and K-30 groups, respectively. Mean Rmax of systolic BP in the F-100 group was significantly decreased as compared to the S group (-20.0 ± 4.5 versus -6.3 ± 1.6%, P = 0.004). Similarly, mean Rmax of diastolic BP in the F-100 group was also significantly decreased (P = 0.008) as compared to the S group.

Conclusions

These results suggest that fentanyl can increase the incidence of BH episodes during shoulder arthroscopic surgery in the sitting position after ISB.

The pathophysiology of neurally mediated syncope is poorly understood. It has been widely assumed that excessive sympathetic activation in a setting of left ventricular hypovolemia stimulates ventricular afferents that trigger hypotension and bradycardia. We tested this hypothesis by determining if excessive sympathetic activation precedes development of neurally mediated syncope, and if this correlates with alterations in baroreflex function. We studied the changes in intraarterial blood pressure (BP), heart rate (HR), central venous pressure (CVP), muscle sympathetic nerve activity (MSNA), and plasma catecholamines evoked by upright tilt in recurrent neurally mediated syncope patients (SYN, 5+/-1 episodes/mo, n = 14), age- and sex-matched controls (CON, n = 23), and in healthy subjects who consistently experienced syncope during tilt (FS+, n = 20). Baroreflex responses were evaluated from changes in HR, BP, and MSNA that were obtained after infusions of phenylephrine and sodium nitroprusside. Compared to CON, patients with SYN had blunted increases in MSNA at low tilt levels, followed by a progressive decrease and ultimately complete disappearance of MSNA with syncope. SYN patients also had attenuation of norepinephrine increases and lower baroreflex slope sensitivity, both during tilt and after pharmacologic testing. FS+ subjects had the largest decrease in CVP with tilt and had significant increases in MSNA and heart rate baroreflex slopes. These data challenge the view that excessive generalized sympathetic activation is the precursor of the hemodynamic abnormality underlying recurrent neurally mediated syncope.

Continuous electrocardiographic (ECG) records were made over 24 hours in 130 ambulant outpatients complaining of syncope, dizzy turns, or palpitation. In all these patients resting ECGs had failed to show significant dysrhythmias. Exercise testing was performed on 64 patients and also failed to reveal any dysrhythmias. Analysis of the tape recordings, however, showed appreciable dysrhythmias in 74% of the group. In most cases the dysrhythmias were complex mixtures of rapid supraventricular and ventricular rhythms. bouts of ventricular tachycardia were seen in seven patients, all of whom were women. Episodic complete heart block was seen in only two patients, but prolonged ventricular gaps (greater than 1-5 s), not associated with ectopic beats, were found in 26. No episodes of ventricular fibrillation were recorded. We conclude that many patients with vague symptoms suggestive of transient cerebral ischaemia or irregular heart action have significant and often dangerous dysrhythmias which can be diagnosed only by long-term recording of the ECG under fully ambulant conditions.

Swallow syncope (also known as deglutition syncope) is a relatively rare type of syncope that is treatable if diagnosed correctly. We report a case of a 39-year-old man with recurrent swallow syncope. The patient did not have structural heart disease. He developed a complete atrioventricular block upon drinking a cold beverage (Chilsung cider) while undergoing a repeated head-up tilt test. The patient was advised to avoid cold beverages and has been symptom free for 5 months.

The Brugada disease, the last clinico-cardiologic entity described in the 20th century, initially called right bundle branch block syndrome with ST segment elevation from V1 to V2 or V3 and sudden cardiac death, is genetically determined in a dominant autosomal mode, and it affects the alpha subunit of the Na+ channel by alteration of chromosome 3 and mutation in the SCN5A gene.

In clinical diagnosis the mentioned electrocardiographic pattern in a patient without structural heart disease and positivity in pharmacological tests are considered major criteria. As minor criteria, the following are considered: positive family history, presence of syncope with unknown origin, documented episode of VT/VF, inducibility in electrophysiologic study and positivity of genetic study.

The long-standing technology of ECG, with more than a century of existence, remains as the supplementary method with highest value in diagnosis, and currently new electrocardiographic criteria are suggested, which indicate high risk of VF.

Natural history indicates a somber diagnosis in symptomatic patients with a high index of arrhythmic SCD secondary to very fast polymorphic ventricular tachycardia bursts, which degenerate into VF. Asymptomatic individuals with only a Brugada-type electrocardiographic pattern have a low risk. The prognosis seems to depend more on clinical facts, since a positive electrophysiologic study has an accuracy of just around 50%.

We propose that this entity should be promoted to the category of disease, since it has a characteristic set of signs and symptoms, and an identified genetic defect.

Atrial and ventricular pacemaker function was studied in 20 patients with idiopathic chronic complete heart block using the rate response to an intravenous bolus dose of isoprenaline (5 mug/70 kg bodyweight). Pacemaker responses were compared with those of 16 normal control subjects. None of the patients was having syncopal attacks at the time of admission and they were therefore selected in that none required immediate pacing. Ten of the patients had His bundle electrograms; all were shown to have a pre-His type of atrioventricular block. Two major groups emerge from the responses to isoprenaline. (a) High risk group: 11 of the 14 patients with reduced ventricular pacemaker responses had frequent syncopal attacks; 8 of the patients with Adams-Stokes syncope had a bundle-branch block pattern, while 3 had a narrow QRS. These patients require pacing. (b) Low risk group: a low risk asymptomatic group (5 patients) was identified with atrial and ventricular responses to isoprenaline within normal range. One of these patients had a bundle-branch block pattern, while 4 had a narrow QRS. These patients might be managed without pacing. The atrial response to isoprenaline was reduced in 12 of the 20 cases, 10 of whom also had reduced ventricular responses. All 9 patients with bundle-branch block had reduced ventricular responses, while 7 had reduced atrial responses. This evidence indicates that cardiac conducting tissue pathophysiology is widespread in complete heart bolck. The present work suggests that consideration of the ventricular pacemaker function is important in assessing liability to syncope in complete heart block. While patients with Adams-Stokes attacks require pacing it is suggested that all asymptomatic patients with complete heart block and those with minor symptoms are assessed using studies of both ventricular pacemaker function and site. A low risk group not requiring a pacemaker may emerge after sufficient follow-up assessment.

The differential diagnosis of syncope versus seizures represents a daily challenge for cardiologists and neurologists. Long Q-T syndrome and hypertrophic cardiomyopathy (HCM) are two hereditary arrhythmogenic heart conditions causing syncope in early adulthood. We report the cases of two patients who were reassessed for transient loss of consciousness (TLOC) with convulsions despite treatment. The first patient, a 40-year-old woman, had been diagnosed with epilepsy and was given phenytoin. Her episodes took place while swimming or when in emotional distress and were not followed by post-ictal confusion. An electrocardiogram showed a very prolonged Q-Tc interval. The second patient, a 30-year-old man with HCM in whom a defibrillator had been implanted on the assumption that he was having cardiogenic syncopes, was actually found to have epilepsy. Adequate treatment rendered both patients asymptomatic. In conclusion, the clinical history and 12-lead electrocardiography remain crucial in the management of TLOC, ideally involving both cardiologists and neurologists.

A case of Prinzmetal variant angina with transient complete atrioventricular block and syncopal episodes following an anteroseptal myocardial infarction is described. The syncopal attacks were not prevented by demand cardiac pacing and were presumably caused by transient severe ischaemia of the left ventricle, with a consequent reduction in cardiac output. The left ventriculogram showed a large anterior dyskinetic area corresponding to the high grade proximal obstruction in the left anterior descending artery demonstrated by coronary angiography. All other coronary vessels appeared free of disease and it is suggested that the anginal episodes were caused by transient proximal segmental spasm of the right coronary artery. The anginal episodes were successfully prevented by a regimen of two-hourly coronary arterial vasodilator therapy.

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Background: Patients with multiple system atrophy (MSA) occasionally have episodes of syncope or pre-syncope after micturition.

Objective: To clarify the mechanism of these episodes by investigating the haemodynamic changes associated with micturition.

Methods: 25 patients with probable MSA and 16 age matched normal controls were studied. Continuous records of blood pressure and heart rate were made during water cystometry, along with the Valsalva manoeuvre, head up tilt testing, measurement of plasma noradrenaline, and calculation of coefficient of variance of RR intervals.

Results: Compared with normal controls, MSA patients had a lower baseline blood pressure, smaller blood pressure and heart rate increases during bladder filling, and an abnormal fall in blood pressure for a longer duration after voiding, resulting in significantly lower blood pressure than at baseline (mean systolic blood pressure reduction –15.2 mm Hg), and hypotension compared with control blood pressure (–29.0 mm Hg). The blood pressure fall was greater in patients with micturition syncope/pre-syncope than in those without. It was also greater in patients with abdominal straining resulting from difficulty in voiding. Other cardiovascular indices did not correlate with the fall in blood pressure.

Conclusions: Hypotension after voiding in MSA patients may result from generalised autonomic dysfunction and abnormal abdominal straining, resulting in micturition syncope.

Twenty-seven patients with complete right bundle-branch block as the only abnormal finding were studied using high speed M-mode echocardiography to determine the effect of the electrical delay on the mechanical events of right ventricular systole. Pulmonary valve opening (PVOm) was delayed in all cases. In some the delay was mainly between mitral valve closure (MVC) and tricuspid valve closure (TVC), and this was designated proximal block. In the others the main delay was between tricuspid valve closure and pulmonary valve opening and this was designated distal block. The patients were divided into those with proximal and those with distal block by calculating the ratio TVC-PVOm/MVC-TVC. Twelve out of 13 of those with distal delay but only one out of 14 of those with proximal delay had episodes of syncope or near syncope. These results are consistent with previous theories about the pathophysiology of right bundle-branch block. Echocardiography may offer a non-invasive method to estimate the prognosis in isolated right bundle-branch block.

We report our experience of 20 patients who have had permanent pacemakers implanted for the first time after the age of 90. The main indications were syncope or presyncope which occurred in 15 patients. Complete heart block was present in 14 patients. Syncopal and presyncopal symptoms were cured in 73%. Nonagenarians paced for complete heart block can expect to survive for as long as others of the same age without heart block. Permanent pacing is an effective and appropriate treatment in the very old.

A 16-year-old male with a prior history of recurrent syncope was referred to our hospital after being resuscitated from cardiac arrest developed while playing volleyball. His electrocardiogram (ECG) demonstrated ventricular fibrillation at a local emergency department. After referral, an ECG showed bidirectional ventricular tachycardia (VT) and nonsustained Torsade de Pointes. Two days later, his heart rate became regular, and no additional episodes of VT were observed. His ECG showed sinus rhythm with a corrected QT interval of 423 msec, and two-dimensional echocardiography was unremarkable. We made the diagnosis of a catecholaminergic polymorphic VT. However, only premature ventricular complex bigeminy was induced on exercise ECG and epinephrine infusion tests, and the patient showed no episodes of syncope. His father and mother had different missense mutations in the cardiac ryanodine receptor on genetic testing. The proband had both mutations in different alleles and was symptomatic. It was recommended that the patient avoid competitive physical activities, and a β-blocker was prescribed.

A 41-year-old woman with metastatic melanoma was admitted to the hospital because of syncopal episodes, which had developed after the administration of an experimental chemotherapy agent that targeted Notch signaling, as part of a phase I clinical trial. Cardiac monitoring revealed recurrent episodes of polymorphic ventricular tachycardia correlating with the patient's syncope. Investigations into the cause of the arrhythmia led to the discovery of metastatic lesions within the left ventricular myocardium. In presenting this case of polymorphic ventricular tachycardia as the antemortem clinical manifestation of metastatic melanoma involving the heart, we discuss the importance of recognizing that cardiac metastases can manifest themselves as arrhythmias in patients with malignant melanoma who are undergoing active anticancer treatment.

Syncope associated with the act of swallowing (deglutition syncope) and syncope associated with head and neck cancers have been documented independently. We present a case of syncope precipitated by a combination of both these mechanisms. It is important to recognize the coexistence of different hemodynamically significant mechanisms leading to syncope. A 66-year-old male recently diagnosed with head and neck cancer presented with syncope associated with eating. Diagnosis was complicated because of multiple factors in this patient, which individually could have led to syncope. The patient was on beta-blocker therapy, had a neck mass, and the episodes were associated with swallowing. Our hypothesis is that all these etiologies together led to the events but not in their typical mechanisms and raises the possibility that swallowing can be considered a carotid massage equivalent in patients with neck masses not physically extending to the carotid sinus.

A 41 year old man with incomplete right bundle branch block and persistent coved-type ST elevation in the right precordial leads during sinus rhythm had an episode of syncope while driving. He had never had syncope before and there was no family history of sudden cardiac death. Ventricular fibrillation was induced during electrophysiological study (EPS) by double extrastimuli applied to the right ventricle. Disopyramide was effective in preventing ventricular fibrillation during EPS. β Adrenoceptor stimulation manifested bifid T waves and reduced ST segment elevation in right precordial leads. Simultaneously recorded monophasic action potential (MAP) duration at 90% repolarisation did not change in the right ventricular outflow tract, while it shortened in the left ventricular septum. These findings suggest that right precordial bifid T waves might result from relatively early repolarisation of the left ventricles. Moreover the gradient of action potential duration might explain the mechanism of ST segment abnormalities in a patient with Brugada syndrome.

 Keywords: ventricular fibrillation;  Brugada syndrome;  monophasic action potential;  bifid T waves

A man presented with recurrent syncope, weakness and fatigue. His ECG showed marked QRS widening and he had gross hyponatraemia and hypokalaemia. His medications included bendroflumethiazide (long term) and flecainide (started 2 months previously).

This presentation was consistent with flacainide cardiotoxicity exacerbated by electrolyte disturbance. The syncopal episodes probably represented life‐threatening arrhythmias. The ECG and symptoms resolved completely once the electrolytes were corrected.

Increased cardiotoxicity with hypokalaemia is documented, but not widely recognised. Hyponatraemia‐induced flecainide cardiotoxicity has not been documented. The clinical effects of flecainide are due to use‐dependent block of sodium channels. There are reports that support the use of hypertonic sodium salts to reverse flecainide toxicity via antagonism at the receptor. By this rationale, hyponatraemia would lead to Flecainide toxicity.

Flecainide has been shown to reduce salt absorption in animal bowel. It is possible that in combination with bendroflumethiazide it acted synergistically to produce profound electrolyte disturbance.

Flecainide cardiotoxicity has a significant mortality and can present non‐specifically. Thus, early recognition is essential. This case demonstrates the importance of strict electrolyte control in patients who are on flecainide. We would discourage concomitant use of flecainide and bendroflumethiazide.

A 69 year old man is described with a 12 year history of intermittent syncope associated with ingesting solid food, mainly after having fasted. He was taking enalapril, propranolol, bendrofluazide (bendroflumethiazide), omeprazole, finasteride, and aspirin. Detailed investigations, including gastrointestinal evaluation, measurement of various gut hormones, and autonomic testing, indicated no abnormality. A liquid meal, performed before fasting, failed to elicit an episode. However, a solid meal after an overnight fast provoked near-syncope. Continuous non-invasive haemodynamic monitoring (with a Portapres II) indicated a short lived rise in blood pressure and heart rate, followed by severe hypotension, a fall in stroke volume and cardiac output, and then bradycardia. This favoured an initial increase in sympathetic activity, followed by vasodepression due to sympathetic withdrawal or activation of humoral vasodilatatory mechanisms, with bradycardia secondary to impaired cardiac filling. Withdrawal of enalapril abolished the episodes. The unusual nature of this case, in which haemodynamic recordings continuously were made during and after swallow syncope, induced soon after food ingestion, is discussed.