Influence of Age on Magnitude and Timing of Vasodepression and Cardioinhibition in Tilt-Induced Vasovagal Syncope.

BACKGROUND: Cardioinhibition may diminish with age, but the changing balance of cardioinhibition and vasodepression with age has not been quantified, leaving the mechanism of vasovagal syncope (VVS) in old age unclear. OBJECTIVES: This study sought to quantify age-related changes of vasodepression and cardioinhibition in tilt-induced VVS. METHODS: We studied 163 cases of tilt-induced VVS, evoked using the Italian protocol with blood pressure, heart rate, and video-electroencephalographic monitoring. Presyncope was excluded. Cardioinhibition was defined as the heart rate decrease before syncope; asystolic pauses (≥3 seconds) were divided into early and late asystole, ie, beginning early enough to or too late to be the major cause of loss of consciousness. The log-ratio method was used to quantify contributions of cardioinhibition and vasodepression, assessed in 2 10-second periods before the onset of cardioinhibition and before syncope. RESULTS: With increasing age, cardioinhibition decreased, ie, heart rate decreased less and more slowly near syncope (P < 0.0001), while vasodepression increased. Asystolic pauses were less frequent in the older one-half of the group than the younger one-half (26% vs 57%; P < 0.00001), but when it did, late asystole occurred more often (58% vs 15%; P < 0.001). CONCLUSIONS: The shift toward less cardioinhibition and more vasodepression with increased age probably reflects a physiological shift in circulatory control. The weakening of cardioinhibition with age may detract from the efficacy of pacing in older patients with VVS. Cardioinhibition-vasodepression balance should be considered in pacing decisions in older subjects with VVS.

Five cases of complete atrioventricular block induced by bending forward: unusual but not unique.

AIMS: We describe five patients with syncope caused by a complete atrioventricular block (AVB) while they were bending forward, not rising after bending, and aim to describe the occurrence and the association between bending forward and AVB. METHODS AND RESULTS: In two patients, bending forward was the exclusive trigger for syncope, while in the remaining three, other postural changes (sitting down, standing up, and exertion) could also provoke syncope. Complete AVB as the cause of syncope was documented using ECG monitoring in two cases and an implantable loop recorder in the other three. Ectopic beats without preceding sinus slowing occurred before syncope in four cases. Two cases had a left bundle branch block. All patients responded favourably to cardiac pacing. CONCLUSION: This is the first case series on complete AVB provoked by bending forward. Syncope during bending forward should suggest a search for an AVB. Arguments in favour of a vagal mechanism were syncope triggered by bending forward, and that other triggers could also evoke syncope. However, the absence of sinus slowing before syncope in some cases and the fact that bending forward did not seem to provoke reflex syncope without AVB, cast doubts on a reflex mechanism. There were also arguments favouring conduction disorder: i.e. ectopic beats before syncope and pre-existing conduction disturbances in two cases. The cases are reminiscent of paroxysmal AVB. Discrimination between paroxysmal AVB and vagal AVB is important because a pacemaker is warranted in arrhythmic complete AVB, while the benefit is limited or absent in reflex AVB.

Novel Methods for Quantification of Vasodepression and Cardioinhibition During Tilt-Induced Vasovagal Syncope.

RATIONALE: Assessing the relative contributions of cardioinhibition and vasodepression to the blood pressure (BP) decrease in tilt-induced vasovagal syncope requires methods that reflect BP physiology accurately. OBJECTIVE: To assess the relative contributions of cardioinhibition and vasodepression to tilt-induced vasovagal syncope using novel methods. METHODS AND RESULTS: We studied the parameters determining BP, that is, stroke volume (SV), heart rate (HR), and total peripheral resistance (TPR), in 163 patients with tilt-induced vasovagal syncope documented by continuous ECG and video EEG monitoring. We defined the beginning of cardioinhibition as the start of an HR decrease (HR) before syncope and used logarithms of SV, HR, and TPR ratios to quantify the multiplicative relation BP=SV·HR·TPR. We defined 3 stages before syncope and 2 after it based on direction changes of these parameters. The earliest BP decrease occurred 9 minutes before syncope. Cardioinhibition was observed in 91% of patients at a median time of 58 seconds before syncope. At that time, SV had a strong negative effect on BP, TPR a lesser negative effect, while HR had increased (all P<0.001). At the onset of cardioinhibition, the median HR was at 98 bpm higher than baseline. Cardioinhibition thus initially only represented a reduction of the corrective HR increase but was nonetheless accompanied by an immediate acceleration of the ongoing BP decrease. At syncope, SV and HR contributed similarly to the BP decrease (P<0.001), while TPR did not affect BP. CONCLUSIONS: The novel methods allowed the relative effects of SV, HR, and TPR on BP to be assessed separately, although all act together. The 2 major factors lowering BP in tilt-induced vasovagal syncope were reduced SV and cardioinhibition. We suggest that the term vasodepression in reflex syncope should not be limited to reduced arterial vasoconstriction, reflected in TPR, but should also encompass venous pooling, reflected in SV.

Abnormal cardiovascular response to nitroglycerin in migraine.

INTRODUCTION: Migraine and vasovagal syncope are comorbid conditions that may share part of their pathophysiology through autonomic control of the systemic circulation. Nitroglycerin can trigger both syncope and migraine attacks, suggesting enhanced systemic sensitivity in migraine. We aimed to determine the cardiovascular responses to nitroglycerin in migraine. METHODS: In 16 women with migraine without aura and 10 age- and gender-matched controls without headache, intravenous nitroglycerin (0.5 µg·kg-1·min-1) was administered. Finger photoplethysmography continuously assessed cardiovascular parameters (mean arterial pressure, heart rate, cardiac output, stroke volume and total peripheral resistance) before, during and after nitroglycerin infusion. RESULTS: Nitroglycerin provoked a migraine-like attack in 13/16 (81.2%) migraineurs but not in controls (p = .0001). No syncope was provoked. Migraineurs who later developed a migraine-like attack showed different responses in all parameters vs. controls (all p < .001): The decreases in cardiac output and stroke volume were more rapid and longer lasting, heart rate increased, mean arterial pressure and total peripheral resistance were higher and decreased steeply after an initial increase. DISCUSSION: Migraineurs who developed a migraine-like attack in response to nitroglycerin showed stronger systemic cardiovascular responses compared to non-headache controls. The stronger systemic cardiovascular responses in migraine suggest increased systemic sensitivity to vasodilators, possibly due to insufficient autonomic compensatory mechanisms.

Temporal Relationship of Asystole to Onset of Transient Loss of Consciousness in Tilt-Induced Reflex Syncope.

OBJECTIVES: The purpose of this study was to investigate the relationship between the onset of asystole and transient loss of consciousness (TLOC) in tilt-induced reflex syncope and estimate how often asystole was the principal cause of TLOC. BACKGROUND: The presence of asystole in vasovagal syncope (VVS) may prompt physicians to consider pacemaker therapy for syncope prevention, but the benefit of pacing is limited in VVS. METHODS: We evaluated electrocardiography, electroencephalography, blood pressure, and clinical findings during tilt-table tests. Inclusion required TLOC (video), electroencephalographic slowing, accelerating blood pressure decrease, and an RR interval ≥3 s. We excluded cases with nitroglycerin provocation. Asystole after onset of TLOC (group A) or within 3 s before TLOC (group B) was unlikely to cause TLOC, but an earlier start of asystole (group C) could be the cause of TLOC. RESULTS: In one-third of 35 cases (groups A [n = 9] and B [n = 3]), asystole was unlikely to be the primary cause of TLOC. The median of the mean arterial pressure at the onset of asystole was higher when asystole occurred early (45.5 mm Hg, group C) than when it occurred late (32.0 mm Hg, groups A and B), which suggests that vasodepression was not prominent at the start of asystole in early asystole, further suggesting that early asystole was the prime mechanism of syncope. CONCLUSIONS: In one-third of cases of tilt-induced asystolic reflex syncope, asystole occurred too late to have been the primary cause of TLOC. Reliance on electrocardiography data only is likely to overestimate the importance of asystole.

Long-term follow-up of psychogenic pseudosyncope.

OBJECTIVE: To determine the outcome of patients with psychogenic pseudosyncope (PPS) after communication of the diagnosis. METHODS: This was a retrospective cohort study of patients with PPS referred in 2007 to 2015 to a tertiary referral center for syncope. We reviewed patient records and studied attack frequency, factors affecting attack frequency, health care use, and quality of life using a questionnaire. We explored influences on attack freedom and attack frequency in the 6 months before follow-up for age, sex, education level, duration until diagnosis, probability of diagnosis, additional syncope, and acceptance of diagnosis. RESULTS: Forty-seven of 57 patients with PPS could be traced, of whom 35 (74%) participated. Twelve (34%) were attack-free for at least 6 months. The median time from diagnosis to follow-up was 50 months (range 6-103 months). Communicating and explaining the diagnosis resulted in immediate reduction of attack frequency (p = 0.007) from the month before diagnosis (median one attack, range 0-156) to the month after (median one attack, range 0-16). In the 6 months before follow-up, the number of admissions decreased from 19 of 35 to 0 of 35 (p = 0.002). The use of somatic and mental health care shifted toward the latter (p < 0.0001). Quality of life at follow-up (Short Form Health Survey 36) showed lower scores for 7 of 8 domains compared to matched Dutch control values; quality of life was not influenced by attack freedom. CONCLUSIONS: After communication of the diagnosis in PPS, attack frequency decreased and health care use shifted toward mental care. Low quality of life underlines that PPS is a serious condition.

[Unexplained loss of consciousness: the diagnosis is never based on one symptom]. / Onverklaarde wegrakingen: de diagnose berust nooit op één symptoom.

Patients with transient loss of consciousness are often seen by a variety of specialists. Even if typical signs occur, it can be difficult to identify specific causes. We discuss two patients with complex presentations. The first patient was diagnosed with sleep syncope, a relatively unknown type of reflex syncope. The prodromal symptoms of discomfort and the subsequent loss of consciousness occurred while the patient was in bed or got up to go to the toilet due to abdominal symptoms. The onset in supine position was misleading, since this is a well-known alarm symptom of a possible cardiac cause. The second patient had vasovagal syncope followed by a psychogenic pseudosyncope. This resulted in frequent loss of consciousness of long duration with typical and atypical triggers and uncommon syncopal signs, including eye closure. These conflicting symptoms can be a pitfall and clinical expertise is required to identify the type of syncope.

Classifying syncope.

An unambiguous definition of syncope is important for care, research and teaching purposes. Unfortunately, many published definitions described 'syncope' as a broad category of transient loss of consciousness (TLOC) but still appeared to use a much narrower concept, creating confusion. The ESC-classification from 2001 and subsequently distinguished between 'transient loss of consciousness', i.e. disorders sharing unconsciousness of short duration with a rapid and spontaneous recovery and syncope, the form of TLOC that is due to cerebral hypoperfusion. Adding the cerebral hypoperfusion element sets syncope apart from other forms of TLOC, mostly epileptic seizures and psychogenic attacks. We provide short descriptions of different forms of syncope and other forms of TLOC.