Postural syncope: mechanisms and management

Vaddadi, Gautam; Lambert, Elisabeth; Corcoran, Susan J.; Esler, Murray

doi:10.5694/j.1326-5377.2007.tb01248.x

Cited by 43 publications

(27 citation statements)

References 51 publications

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“…We measured similar MSNA levels in the two groups at baseline and throughout tilt, therefore, we think TPR was unlikely to be lower in the PPFH group. Therefore, our data do not support the hypothesis that PPFH patients have low resting TPR, nor impaired sympatho-vasoconstriction predisposing them to VVS [8, 28]. …”

Section: Discussioncontrasting

confidence: 92%

“…Although MSNA remained well above baseline during presyncope, we observed a terminal fall-off in MSNA immediately before tilt-back in both groups. This data confirms previous studies showing that provided patients became sufficiently hypotensive, some degree of sympathetic withdrawal usually occurred during the final seconds of presyncope before tilt-back [5, 8, 13, 28]. This is partly because individual bursts of MSNA are gated to the diastolic phase of the cardiac cycle and when heart rate decreases, burst rate follows [32].…”

Section: Discussionsupporting

confidence: 89%

“…Even though MSNA has been studied extensively during tilt and presyncope [5–8, 28, 30], few studies include MSNA during recovery [13, 30]. This is because it is technically very difficult to maintain a satisfactory nerve recording field during the course of presyncope and recovery.…”

Section: Discussionmentioning

confidence: 99%

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MSNA during prolonged post-faint hypotension

et al. 2012

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Background Following tilt-induced syncope, blood pressure usually recovers rapidly after tilt back to the horizontal position. However, in some patients, hemodynamic recovery is delayed, a condition recently termed “prolonged post-faint hypotension” (PPFH). The mechanism is thought to be mediated by increased vagal outflow rather than exaggerated peripheral vasodilatation and sympathetic withdrawal. To date, no muscle sympathetic nerve activity (MSNA) recordings have been reported in this condition, so we aimed to confirm that neither vasodilatation nor MSNA withdrawal was responsible. Objectives To retrospectively select patients with satisfactory recordings of continuous BP and MSNA during tilt-induced syncope. To compare hemodynamic and MSNA profiles in patients with PPFH to patients with normal recovery (NR) after tilt-back. Methods All patients were studied in Christchurch, New Zealand, between 1998 and 2008 using continuous arterial BP monitoring, and microneurographic recordings of MSNA from the right leg. Only patients with satisfactory BP and MSNA data throughout baseline, head-up tilt and presyncope were selected. Stroke volume (SV), cardiac output (CO), and total peripheral resistance (TPR) were derived using Modelflow. After baseline measurements, patients were tilted to the head-up 60° position and given GTN spray if asymptomatic after 20 min. Following the onset of presyncope, patients were tilted slowly back to the horizontal. PPFH was defined as systolic BP <85 mmHg for at least 2 min after tilt-back. Measurements were averaged at baseline, early tilt, presyncope, early and late recovery. Within-group comparisons were made between baseline and all other time points. Between-group comparisons were made over all time points. Results Patients with PPFH (7 males, age 46 ± 5 years, n = 8) and with NR (8 males, age 47 ± 6 years, n = 8) were selected. Presyncope was provoked by GTN in 4/8 patients in each group. In both groups, MAP remained below baseline during early and late recovery: PPFH 84 ± 5 versus 51 ± 5 and 64 ± 5 mmHg ( p = 0.001, p = 0.001); NR 104 ± 5 versus 83 ± 5 and 93 ± 5 mmHg ( p = 0.001, p = 0.03). However, MAP and HR were lower in the PPFH group ( p = 0.004, p = 0.023). During early recovery, CO remained below baseline only in the PPFH group ( p = 0.001), whereas TPR remained constant in both groups. In both groups, all MSNA indices tended to remain above baseline levels during early and late recovery. PPFH 25 ± 2 increased to 31 ± 6 and 29 ± 4 bursts/min ( p = 0.09, 0.02); NR 23 ± 3 increased to 33 ± 3 and 34 ± 3 bursts/min ( p = 0.06, 0.01). Conclusions PPFH doe...

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Section: Discussioncontrasting

confidence: 92%

Section: Discussionsupporting

confidence: 89%

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MSNA during prolonged post-faint hypotension

et al. 2012

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“…Vagal overactivity has been proposed as a possible cause of vasovagal syncopes [3], [4], [5], which remain a challenge in many patients, in particular infants and young athletes, and account for 1-2% of all emergency department visits [6], [7]. Vasovagal syncope has a lifetime cumulative influence of 35% and the frequency of syncope in students ranges from 20 to 50% [8], [9]; it may be involved in sudden death, not only in newborns as stated above, but also in young athletes [10], [11].…”

Section: Introductionmentioning

confidence: 99%

Constitutive Overexpression of Muscarinic Receptors Leads to Vagal Hyperreactivity

et al. 2010

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BackgroundAlterations in muscarinic receptor expression and acetylcholinesterase (AchE) activity have been observed in tissues from Sudden Infant Death Syndrome (SIDS). Vagal overactivity has been proposed as a possible cause of SIDS as well as of vasovagal syncopes. The aim of the present study was to seek whether muscarinic receptor overexpression may be the underlying mechanism of vagal hyperreactivity. Rabbits with marked vagal pauses following injection of phenylephrine were selected and crossed to obtain a vagal hyperreactive strain. The density of cardiac muscarinic receptors and acetylcholinesterase (AchE) gene expression were assessed. Blood markers of the observed cardiac abnormalities were also sought.Methodology/Principal FindingsCardiac muscarinic M2 and M3 receptors were overexpressed in hyperreactive rabbits compared to control animals (2.3-fold and 2.5-fold, respectively) and the severity of the phenylephrine-induced bradycardia was correlated with their densities. A similar overexpression of M2 receptors was observed in peripheral mononuclear white blood cells, suggesting that cardiac M2 receptor expression can be inferred with high confidence from measurements in blood cells. Sequencing of the coding fragment of the M2 receptor gene revealed a single nucleotide mutation in 83% of hyperreactive animals, possibly contributing for the transcript overexpression. Significant increases in AchE expression and activity were also assessed (AchE mRNA amplification ratio of 3.6 versus normal rabbits). This phenomenon might represent a compensatory consequence of muscarinic receptors overexpression. Alterations in M2 receptor and AchE expression occurred between the 5th and the 7th week of age, a critical period also characterized by a higher mortality rate of hyperreactive rabbits (52% in H rabbits versus 13% in normal rabbits) and preceeded the appearance of functional disorders.Conclusions/SignificanceThe results suggest that cardiac muscarinic receptor overexpression plays a critical role in the development of vagal hyperreactivity, whereas AchE hyperactivity appears as a compensatory consequence of it. Since similar vagal disorders were observed recently by us in SIDS, muscarinic receptor overexpression could become a marker of risk of vasovagal syncopes and SIDS.

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“…Clinicians are usually interested in diagnosing OH as it can cause fall-related injuries, 8 substantially limit patients' quality of life, 9 and finally, impede relevant treatment of concomitant diseases as hypertension or heart failure. 10,11 In parallel, relatively little is known about prognostic aspects of OH.…”

Section: Introductionmentioning

confidence: 99%

Orthostatic hypotension predicts all-cause mortality and coronary events in middle-aged individuals (The Malmo Preventive Project)

Fedorowski

Stavenow

Hedblad

et al. 2009

European Heart Journal

303

273

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AimsOrthostatic hypotension (OH) has been linked to increased mortality and incidence of cardiovascular disease in various risk groups, but determinants and consequences of OH in the general population are poorly studied.Methods and resultsProspective data of the Swedish ‘Malmö Preventive Project’ (n = 33 346, 67.3% men, mean age 45.7 ± 7.4 years, mean follow-up 22.7 ± 6.0 years) were analysed. Orthostatic hypotension was found in 6.2% of study participants and was associated with age, female gender, hypertension, antihypertensive treatment, increased heart rate, diabetes, low BMI, and current smoking. In Cox regression analysis, individuals with OH had significantly increased all-cause mortality (in particular those aged less than 42 years) and coronary event (CE) risk. Mortality and CE risk were distinctly higher in those with systolic blood pressure (BP) fall ≥30 mmHg [hazard ratio (HR): 1.6, 95% CI 1.3–1.9, P < 0.0001 and 1.6, 95% CI 1.2–2.1, P = 0.001] and diastolic BP fall ≥15 mmHg (HR: 1.4, 95% CI 1.1–1.9, P = 0.024 and 1.7, 95% CI 1.1–2.5, P = 0.01). In addition, impaired diastolic BP response had relatively greater impact (per mmHg) on CE incidence than systolic reaction.ConclusionOrthostatic hypotension can be detected in ∼6% of middle-aged individuals and is often associated with such comorbidities as hypertension or diabetes. Presence of OH increases mortality and CE risk, independently of traditional risk factors. Although both impaired systolic and diastolic responses predict adverse events, the diastolic impairment shows stronger association with coronary disease.

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Postural syncope: mechanisms and management

Abstract: Postural syncope is a transient loss of consciousness secondary to a reduction in cerebral blood flow and is typically precipitated by standing. It is the commonest cause of recurrent transient loss of consciousness.

Cited by 43 publications

References 51 publications

MSNA during prolonged post-faint hypotension

MSNA during prolonged post-faint hypotension

Constitutive Overexpression of Muscarinic Receptors Leads to Vagal Hyperreactivity

Orthostatic hypotension predicts all-cause mortality and coronary events in middle-aged individuals (The Malmo Preventive Project)

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