The Extended Role of 24 H Ambulatory Blood Pressure Monitoring for Reflex Syncope

Fabian Leys; Alessandra Fanciulli

Disclosures

Eur Heart J. 2022;43(38):3777-3780. 

Graphical Abstract

Extending the role of ambulatory blood pressure monitoring (ABPM) for reflex syncope. In people with neurogenic orthostatic hypotension, ABPM is combined with a semi-structured protocol, in which night rest, medication intake, meals, physical activities, as well as eventual pre-syncope or syncope events are noted. This enables the detection of nocturnal hypertension and post-prandial, drug- or exercise-induced forms of hypotension, thus guiding individualized treatment strategies. In people with reflex syncope, matching ABPM records with an activity diary may likewise help in linking hypotensive episodes with their potential triggers. Created with Microsoft Office PowerPoint 2016, in part using adapted Servier Medical Art images (https://smart.servier.com/).

Syncope is a transient loss of consciousness due to cerebral hypoperfusion, characterized by rapid onset, short duration, and spontaneous complete recovery.[1] Every third woman and every fifth man experiences at least one syncope episode during their life,[2] with typical peak incidences in early and late adulthood.[3] The causes of syncope can be grouped into three main categories: (i) heart rhythm or structural cardio-pulmonary abnormalities; (ii) orthostatic hypotension, which is a sustained fall in blood pressure (BP) when changing from the supine to the upright position and may be due to BP-lowering drugs, volume depletion, or damage of the cardiovascular autonomic nervous system (i.e. neurogenic orthostatic hypotension); or (iii) most commonly, aberrant activation of the baroreflex arch resulting in the so-called reflex syncope.[1]

Typical triggers of reflex syncope include fear, pain, prolonged standing, micturition, gastrointestinal stimulation, coughing, the recovery phase following physical exertion, or pressure stimuli on the carotid sinus.[1] An aberrant activation of the baroreflex arch may result in an abrupt, excessive cardiovagal activation, a withdrawal of the sympathetic stimulation to the heart and blood vessels, or a mixture of both. Depending on the resulting haemodynamic mechanism, reflex syncopes are classified into a vasodepressive, cardioinhibitory, or mixed type.[1] Non-pharmacological measures, including counselling on the causes and triggers of syncope and ways to prevent its recurrence, represent a pivotal therapeutic step in the management of people with reflex syncope and should be recommended to every patient.[1] Additional therapeutic measures are indicated in the case of recurrent syncope, but require a more detailed knowledge of the underlying haemodynamic mechanisms.[1,4] While people with a documented predominant bradycardic phenotype of reflex syncope may benefit from cardiac pacing, those with a predominant hypotensive phenotype require strategies to minimize falls in BP.[4]

In this issue of the European Heart Journal, Rivasi et al. propose a novel approach to screen for hypotensive susceptibility in people with a history of reflex syncope by means of 24 h ambulatory blood pressure monitoring (ABPM).[5] The retrospective, multicentre, cross-sectional SynABPM 1 study comprised a derivation and a validation cohort of people with reflex syncope matched by sex, age, hypertension, and average 24 h systolic BP, with subjects mainly undergoing ABPM for hypertension management purposes. Episodes of low systolic BP during the daytime were found to occur more frequently in people with reflex syncope than in controls and were interpreted as a marker of hypotensive susceptibility in the former. One or more systolic daytime BP readings ≤90 mmHg or two or more systolic daytime BP readings ≤100 mmHg identified hypotensive susceptibility among people with reflex syncope with high specificity, while sensitivity remained <40%. The authors propose the above cut-off values for, respectively, a likely (≥90% specificity) or at least possible (80–90% specificity) diagnosis of hypotensive susceptibility, and postulate that abolishing hypotensive episodes with tailored vasoactive interventions may allow the prevention of future syncope episodes in affected individuals.

This study has great value in enriching the diagnostic work-up of reflex syncope with a cost-effective, broadly available, and easy to perform tool such as ABPM. In parallel to neurogenic orthostatic hypotension, the SynABPM 1 study indicates that systolic rather than diastolic BP falls may represent the haemodynamic culprit ultimately triggering reflex syncope episodes.[6] The limited sensitivity found in the SynABPM 1 study could be attributed to several factors: (i) in most patients, fortunately, reflex syncope does not occur on a daily basis; (ii) individuals may not have been exposed to their 'individual' hypotensive trigger on the ABPM day; or (iii) considering the therapeutic implications, specificity was explicitly favoured over sensitivity in the study design.

Owing to the retrospective study design, unfortunately no information on eventual symptoms or triggers of hypotensive episodes was censored in the SynABPM 1 cohorts. The ESC Guidelines for the diagnosis and management of syncope[1] primarily recommend ABPM for people with syncope and suspected orthostatic hypotension. When undergoing ABPM, patients are instructed to compile semi-structured protocols, including the time, type, and dose of medication intake, meals, time and duration of physical activities, night rest, and the eventual occurrence of (pre-)syncope on the examination day (Figure 1).[7] This enables, first, the recognition of supine hypertension (which develops in every second person with neurogenic orthostatic hypotension and needs to be screened for in advance, when planning vasoactive interventions) and, second, of post-prandial, drug- and exercise-induced forms of hypotension, thus guiding tailored treatment strategies.

Figure 1.

English version of the Innsbruck semi-structured ABPM medication (A) and activity protocol (B) for identifying daily-life triggers of hypotensive episodes in people with orthostatic intolerance and syncope.

In people with reflex syncope, linking hypotensive episodes to, for example, prolonged standing, toilet visits, or post-exertional periods may likewise allow recognition of the individual reflex syncope triggers and raise the patient's awareness for syncope prodromes on such occasions. This may also guide the implementation of personalized biofeedback strategies, such as bolus water drinking or practising physical counter-pressure manoeuvres, when exposed to the identified daily-life hypotensive triggers.[8] Pharmacological measures may be equally adjusted to specific situations. Midodrine[9] and fludrocortisone[10] have both been shown to reduce the likelihood of reflex syncope recurrence in randomized, placebo-controlled trials. While the plasma volume expansion determined by fludrocortisone administration may require several days to achieve a significant symptomatic effect,[10] the direct stimulation of vascular α-adrenoreceptors given by midodrine may be preferred as a 'pill-in-the-pocket' strategy for patients exhibiting hypotensive episodes, when exposed to particular triggers, but overall normotensive BP levels on ABPM. Both regular midodrine and fludrocortisone regimens may ultimately represent suitable options for people with reflex syncope and constitutional hypotension on ABPM.[1,4]

Unlike tilt-table examination, ABPM does not allow the definition of the haemodynamic mechanism underlying reflex syncope, and may not increase the diagnostic accuracy, if the initial assessment does not confirm the diagnostic hypothesis.[1,11] However, ABPM bears the potential of reliably identifying hypotensive susceptibility in people with reflex syncope already in a primary care setting.[12] Normal ABPM findings may eventually pinpoint individuals to be referred for further cardiovascular autonomic function tests under continuous heart rate and BP monitoring to identify alternative causes of syncope and orthostatic intolerance such as transient or delayed orthostatic hypotension.[11,13–15]

It was recently shown that hypotensive mechanisms not only underlie vasodepressive and mixed types of reflex syncope, but also play a role in the pathophysiology of cardioinhibitory reflex syncope, suggesting that ABPM may provide additional therapeutic information also in this setting, especially in the case of syncope recurrence after pacemaker implantation.[16] Future studies should incorporate information on daily activities by means of semi-structured ABPM protocols to link hypotensive episodes with their potential triggers, ultimately boosting the diagnostic yield of ABPM in people with reflex syncope.

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