CLINICAL RESEARCH
Europace (2016) 18, 1273–1279
doi:10.1093/europace/euv283
Syncope and event loop recorders
Diagnostic role of head-up tilt test in patients
with cough syncope
Roberto Mereu1, Patricia Taraborrelli 2, Arunashis Sau 3, Alessandro Di Toro4,
Sandra Halim 2, Sajad Hayat 2, Luciano Bernardi 4, Darrel P. Francis 2, Richard Sutton 2,
and Phang Boon Lim 2*
1
Emergency Department, G. Brotzu Hospital, Cagliari, Italy; 2Department of Cardiology, Imperial College Healthcare NHS Trust, Hammersmith Hospital, Du Cane Road,
London W12 0HS, UK; 3Imperial College London, London, UK; and 4Department of Internal Medicine, University of Pavia, Pavia, Italy
Received 8 April 2015; accepted after revision 11 June 2015; online publish-ahead-of-print 18 January 2016
Aims
The aim of this study was to describe the head-up tilt (HUT) test and carotid sinus massage (CSM) responses, and the
occurrence of syncope with coughing during HUT in a large cohort of patients.
.....................................................................................................................................................................................
Methods
A total of 5133 HUT were retrospectively analysed to identify patients with cough syncope. Head-up tilt followed by
and results
CSM were performed. Patients were made to cough on two separate occasions in an attempt to reproduce typical
clinical symptoms on HUT. Patients with cough syncope were compared with 29 age-matched control patients with
syncope unrelated to coughing. A total of 29 patients (26 male, age 49 + 14 years) with cough syncope were identified.
Coughing during HUT reproduced typical prodromal symptoms of syncope in 16 (55%) patients and complete loss of
consciousness in 2 (7%) patients, with a mean systolic blood pressure reduction of 45 + 26 mmHg, and a mean increase
in heart rate of 13 + 8 b.p.m. No syncope or symptoms after coughing were observed in the control group. The HUT
result was positive in 13 (48%) patients with the majority of positive HUT responses being vasodepressor (70% of positive HUT). Carotid sinus massage was performed in 18 patients being positive with a vasodepressor response causing
mild pre-syncopal symptoms in only 1 patient.
.....................................................................................................................................................................................
Conclusion
Syncope during coughing is a result of hypotension, rather than bradycardia. Coughing during HUT is a useful test in
patients suspected to have cough syncope but in whom the history is not conclusive.
----------------------------------------------------------------------------------------------------------------------------------------------------------Keywords
Cough syncope † Head-up tilt test † Situational syncope † Loss of consciousness † Carotid sinus massage †
Sensitivity
Introduction
Cough syncope is a very rare cause of situational syncope characterized by a transient loss of consciousness following a single cough or a
coughing fit. When the history is clear, the initial clinical evaluation is
sufficient to make diagnosis.1 However, when the clinical history is
unclear or inconclusive, patients are often referred for a tilt test together with carotid sinus massage (CSM) where indicated. The diagnostic role of head-up tilt (HUT) has not been studied in a large
cohort of patients with cough syncope. The aim of this study was
to investigate haemodynamic and clinical response to coughing, together with the circulatory response to HUT in patients with clear
history of cough syncope. We also investigated the reproducibility
of pre-syncopal symptoms with coughing in the laboratory and its
utility as a diagnostic test for this uncommon condition.
Methods
Patient recruitment
A total of 5133 patients were referred for HUT between 1998 and
2012. From these records, a total of 29 patients presenting with cough
syncope were retrospectively identified. Clinical details including
past medical history, smoking history, and lifestyle information were
documented. In addition, a total of 29 age, sex, and body mass
index-matched control patients with history of loss of consciousness
suspected to be vasovagal syncope but unrelated to cough were identified. These patients were asked to cough as vigorously as they could on
at least two occasions during HUT to characterize the blood pressure
(BP) and heart rate (HR) responses to coughing. Local research ethics
committee approval was granted for the study and all patients gave informed consent.
* Corresponding author. Tel: +44 2033132115; fax: +44 203 313 4232. E-mail address: [email protected]
Published on behalf of the European Society of Cardiology. All rights reserved. & The Author 2016. For permissions please email: [email protected].
1274
What’s new?
† In patients in whom a diagnosis of cough syncope cannot be
made on history alone, we propose that a modified tilt test
protocol is able to diagnose cough syncope with a sensitivity
of 62% and a specificity of 100%.
† In this study, the largest looking into tilt test responses in patients with cough syncope, there was only a 34% association
of cough syncope with chronic pulmonary diseases, compared to an 87% association reported in previous studies.
† Syncope during coughing is likely a result of hypotension, rather than bradycardia.
Head-up tilt test procedure
All patients with cough syncope and controls underwent HUT using the
Italian protocol with glyceryl trinitrate provocation, which has been previously described.2 Head-up tilt was performed by a trained syncope
specialist nurse, while CSM was done by a cardiologist, typically between 5 and 15 min after the HUT. Performing CSM after tilt and coughing ensures that CSM will have no influence on the autonomic milieu
during the HUT. Briefly, all patients had electrocardiographic monitoring, together with a non-invasive continuous BP recording using a finger
cuff (Finometer Pro, FMS, Amsterdam, Netherlands) that was calibrated
with a conventional sphygmomanometer before and during the HUT.
Following a preparatory phase of 5 min in the supine position, patients
were tilted up to 608 and maintained in that position, supported by belts
at the waist and by a footrest. After 10 min of tilt, patients with a clinical
history consistent with cough syncope and the control patients were
asked to cough as vigorously as possible in an attempt to reproduce clinical symptoms of syncope. The cough was repeated 2 min later. The
cough producing the greater change in BP was used for the study of
haemodynamic changes. If syncope occurred after coughing, the HUT
was stopped. If no syncope occurred in first 20 min, 0.4 mg of sublingual
nitroglycerin was administrated to the patient. The HUT was ended if no
symptoms occurred 15 min following nitroglycerin administration.
Head-up tilt responses were classified according to the new VASIS classification: classic (vasovagal) syncope pattern, dysautonomic (vasovagal)
syncope pattern, and orthostatic intolerance pattern.3 A mixed response was defined as hypotension followed by a decrease in HR that
remained .40 b.p.m., a cardioinhibitory response was defined as an
HR decrease to ,40 b.p.m. for .10 s and/or occurrence of asystole
.3 s, and a vasodepressor response was defined as hypotension without an HR decrease of .10% from the peak HR prior to syncope.
Carotid sinus massage
Patients .40 years of age had right- and left-sided CSM performed with
compression for 10 s, in both the supine and 608 tilt positions in accordance with the European Society of Cardiology guidelines.1 Carotid sinus
massage was considered positive with a pause .3 s or a decrease in BP
.50 mmHg.
Statistics
All data in the text and tables are presented as mean + standard deviation. Comparison between groups was performed using an unpaired
two-tailed Student’s t-test. Comparison between the percentage of
positive and negative responses to HUT of the two groups was
R. Mereu et al.
performed using the two proportion Z-test. A value of P , 0.05 was
considered statistically significant. Sensitivity was calculated as the percentage of cough syncope patients who displayed syncope or presyncopal symptoms during the cough attempt in the cough syncope
group. Specificity was calculated as the percentage of control group patients not displaying syncope or pre-syncopal patients after the cough
attempt.
Results
Demographic data and co-existing
medical conditions
The demographic, anthropometric, and lifestyle characteristics of
the 29 patients with cough syncope and the 29 control patients
are shown in Table 1. Patients with cough syncope were mainly
male (26 males and 3 females), with a mean age of 49.4 + 14 years.
The mean body mass index was 29.0 + 5.9 kg/m2 and 34% of patients smoked. Cough syncope and control groups were not different in age (mean age of controls 48.2 + 17, P ¼ 0.6), sex (20 males
and 9 females in control group, P ¼ 0.053), or body mass index
(mean body mass index of controls 27.3 + 2.2, P ¼ 0.09). Coexisting medical conditions and drug treatments are summarized
in Table 2. Pulmonary disease was present in 10 (34%) of patients,
with 5 (17%) patients diagnosed with asthma. Chronic bronchitis
was present in two patients. Eight patients had a chronic cough,
one had a diagnosis of sleep apnoea, and one patient presented
with a single episode of cough syncope during a transient viral
bronchitis. Two rare conditions were present in this population:
Eisenmenger’s syndrome and pulmonary atresia. In the control
group, pulmonary disease was present in 7% of patients, cardiovascular disease in 22% (six patients with arterial hypertension and
three with ischaemic chronic heart disease), and 15% of patients
had diabetes.
Table 1 Demographic data of patients with cough
syncope and control group without cough syncope
Group
Cough
syncope
(n 5 29)
Control
(n 5 29)
P-Value
Age (years)
49.4 + 14
48.2 + 17
n.s.
Sex: male, n
Mean body mass index
(kg/m2)
Lifestyle
26 (90%)
29.0 + 5.9
20 (69%)
27.3 + 2.2
n.s.
n.s.
................................................................................
Smoking, n
10 (34%)
5 (17%)
Mean number of
cigarettes/day
21 + 9.9
15 + 8
Ex-smokers, n
Regular alcohol
consumption, n
Mean alcohol
consumption
(units/week)
1 (3.4%)
10 (34%)
3 (10%)
4 (14%)
8.19 + 8.5
8.8 + 6.4
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Diagnostic role of head-up tilt test
Table 2 Past medical history and drug treatment of
patients
Cough syncope
patients
Controls
10 (34%)
2 (7%)
................................................................................
Pulmonary disease
Asthma
Chronic bronchitis
5
2
Primary ciliary dyskinesia
1
Sleep apnoea syndrome
Bronchiolitis
1
1
Pulmonary hypertension
2 (7%)
0
1
0
1
8 (27%)
0
6 (20%)
Hypertension
8
6
Ischaemic chronic heart
disease
4
3
Heart failure
Diabetes
4
3 (10%)
0
4 (15%)
Depression
2 (7%)
0
Eisenmenger’s
syndrome
Pulmonary atresia
Cardiovascular
Treatment
Beta-blocker
4
2
ACE inhibitors
3
1
ARB
Diuretics
3
1
2
0
Calcium channel blocker
2
1
Nitrates
B2 adrenergic agonists
2
5
0
0
Systemic corticosteroids
1
0
Serotonin reuptake
inhibitor
2
0
Clinical presentation of cough syncope
All syncopal episodes were very brief, with consciousness fully
restored without any confusion afterwards. Twenty of the 29 patients also reported pre-syncopal symptoms with a milder bout
of coughing, and immediately prior to syncope while the remaining 9 (31%) patients presented with syncope without any prodromal symptoms. The mean duration of symptoms prior to
HUT was 26 + 34 months, and the mean number of symptomatic episodes was 8 + 7. Other triggers for syncope in these patients included laughing in 10 (29%), sneezing in 3 (9%),
swallowing in 1 (3%), and after playing a wind instrument (trumpet) in 1 (3%). Only one patient sustained a head injury as a result of syncope and another patient had a road traffic accident
due to loss of consciousness following a coughing fit while
driving.
reproduced with coughing. Pre-syncopal symptoms included, in order of decreasing frequency: dizziness, nausea, sweatiness, darkening
of vision, and feeling a ‘hot and tingling’ sensation everywhere. In 11
(38%) patients, coughing did not reproduce any clinical symptoms at
all (Table 3). The mean decrease in systolic BP (SBP) and diastolic BP
(DBP) after coughing was 45 + 26 and 24 + 14 mmHg, respectively. Following a cough, the mean time to recovery of BP to pre-cough
values was 25 + 19 s (median 21 s). There was an increase in mean
HR by 13 + 8 b.p.m. following a cough. No bradycardic response
was seen during coughing.
In the two patients who lost consciousness following the cough,
the mean SBP and DBP decreases were 102 + 47 and 42 +
2 mmHg, respectively, with a mean HR increase of 24 + 9 b.p.m.
In the subgroup of patients who manifested prodromal symptoms
without loss of consciousness, the mean SBP and DBP decreases
were 43 + 13 and 27 + 11 mmHg, respectively, with a mean HR increase of 11 + 7 b.p.m. The subgroup of patients who did not manifest symptoms after coughing demonstrated mean SBP and DBP
decreases of 27 + 22 and 8 + 5 mmHg, respectively, with a mean
HR increase of 8 + 8 b.p.m. In control patients, coughing led to
mean SBP and DBP decreases of 10 + 9 and 8 + 5 mmHg, respectively. The mean increase of HR was 8 + 8 b.p.m. (Figure 1). None of
the 29 control patients manifested prodromal symptoms or syncope after coughing. The difference in BP drop between the first
and the second attempt to cough in the cough syncope group was
11 + 7 mmHg for SBP and 7 + 4 mmHg for DBP while in the control group was 7 + 2 mmHg for SBP and 5 + 4 mmHg for DBP. The
mean time to recovery of BP to pre-cough values in the control
group was 11 + 5 s.
A statistically significant difference in SBP decrease was found between patients with syncope during coughing vs. symptoms during
coughing (P , 0.01), between patients with symptoms during coughing vs. no symptoms during coughing (P , 0.01) and between patients
with no symptoms during coughing and the control group (P , 0.01).
No statistically significant difference in DBP decrease was found between patients with syncope during coughing vs. symptoms during
coughing (P ¼ 0.057). A statistically significant difference in DBP
decrease was shown between patients with symptoms during
coughing vs. no symptoms during coughing (P , 0.01). Finally, no
statistically significant difference in DBP decrease was found between
patients with no symptoms during coughing and the control group
(P ¼ 0.19) (Figure 1).
Sensitivity and specificity of coughing
as a means to reproduce symptoms
during head-up tilt
The sensitivity of cough attempt reproducing syncope or presyncope was 62% (7% for syncope and 55% for pre-syncope). The
specificity was 100% as no control patients reported symptoms
after coughing during HUT.
Head-up tilt test: outcomes
Head-up tilt testing: response to coughing
It was possible to reproduce full loss of consciousness following
coughing in two (7%) patients. In 16 (55%) patients, typical presyncopal symptoms without complete loss of consciousness were
A total of 27 of 29 HUT were completed. Two patients had syncope reproduced by coughing in the tilted position and the test
was therefore stopped at this point. The HUT was positive in 13
(48%) patients and negative in 14 (52%) patients. In patients with
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R. Mereu et al.
Table 3 Individual patient responses to coughing during HUT, HUT response, CSM response, and combined HUT- and
cough-induced responses
Patient
Symptom reproduction on coughing
HUT
CSM
Combined coughing
response 1 HUT response
...............................................................................................................................................................................
1
Syncope
Stop
NP
+
2
3
Syncope
Symptoms
Stop
Vasodepressor
–
–
+
+
4
Symptoms
Vasodepressor
NP
+
5
6
Symptoms
Symptoms
Vasodepressor
Vasodepressor
NP
–
+
+
7
Symptoms
Vasodepressor
–
+
8
9
Symptoms
Symptoms
Vasodepressor
Vasodepressor
NP
–
+
+
10
Symptoms
Mixed
–
+
11
12
No symptoms
No symptoms
Mixed
Mixed
NP
NP
+
+
13
No symptoms
OI
–
+
14
15
No symptoms
No symptoms
OI
OI
–
NP
+
+
16
Symptoms
–
–
+
17
18
Symptoms
Symptoms
–
–
–
–
+
+
19
Symptoms
–
–
+
20
21
Symptoms
Symptoms
–
–
NP
Vasodepressor
+
+
22
Symptoms
–
–
+
23
24
Symptoms
No symptoms
–
–
NP
–
+
2
25
No symptoms
–
NP
2
26
27
No symptoms
No symptoms
–
–
NP
–
2
2
28
No symptoms
–
NP
2
29
No symptoms
–
NP
2
HUT outcomes are defined as: vasodepressor, mixed, or OH. The + symbol indicates a positive test, 2 indicates a negative test, NP indicates test not performed, and Stop
indicates that the test was stopped before conclusion. Positive symptoms included any of the following: dizziness, light-headedness, sweating, nausea, feeling hot, darkening vision, or
loss of consciousness.
HUT, head-up tilt; CSM, carotid sinus massage; NP, not performed; OI, orthostatic intolerance.
positive HUT, we observed seven patients with a classical vasovagal pattern, three patients with a dysautonomic vasovagal pattern, and three patients with an orthostatic intolerance pattern.
Of the 10 patients with a vasovagal response, 7 (70%) demonstrated a vasodepressor response and 3 (30%) a mixed response.
No cardioinhibitory responses were observed (Table 3). No complications arose from the HUT. In the control group, 19 of 29 patients (66%) had a negative response and 10 patients (34%) had a
positive response. In the control group patients with positive HUT,
we observed six patients with a classical vasovagal pattern and four
patients with a dysautonomic vasovagal pattern. Of the 10 patients
with a vasovagal response, 4 (40%) demonstrated a mixed
response, 2 (20%) a cardiohinibitory response, and 4 (40%)
a vasodepressor response. There was no difference in HUT outcome between the cough syncope group and the control group
(P ¼ 0.19).
Carotid sinus massage
Carotid sinus massage was carried out in 16 patients. In 13 patients,
CSM was not performed due to the presence of carotid bruits or
previously documented carotid stenosis, or because they were
younger than 40 years old. The CSM was negative in 15 (93%) patients, and positive in 1 with a vasodepressor response (50 mmHg
decrease in BP) without bradycardia, reproducing mild pre-syncopal
symptoms (Table 3). No complications arose from the CSM.
Discussion
Main findings
The coughing attempts during HUT were able to reproduce symptoms of pre-syncope or syncope in 62% of patients with clear history
of cough syncope. Coughing showed a high specificity (100%).
1277
Diagnostic role of head-up tilt test
Decrease in 160
BP (mmHg)
during cough
140
P < 0.01
Decrease in SBP
Decrease in SBP
120
P < 0.01
100
P < 0.01
80
P < 0.01
60
40
20
0
LOC during
coughing
Symptoms during
coughing
No symptoms
during coughing
Patients with cough syncope
No symptoms
Controls
Figure 1 Decrease of SBP and DBP following a cough in cough syncope patients and controls. SBP ¼ turquoise columns and DBP ¼ red columns. A statistically significant difference in SBP decrease was found between patients with syncope during coughing vs. symptoms during coughing, between patients with symptoms during coughing vs. no symptoms during coughing, and between patients with no symptoms during coughing
and the control group. A statistically significant difference in DBP decrease was found between patients with symptoms during coughing vs. no
symptoms during coughing.
Conventional HUT using the Italian protocol produces a positive result in ,50% of patients presenting with cough syncope. The predominant positive response was a classical vasovagal
vasodepressor-type response and CSM, when performed, was almost
always negative.
Clinical characteristics
Our patient cohort consisted mainly of men who were overweight,
consistent with previous reports.4 However, there was a comparatively low prevalence of smoking (34%) and pulmonary disease
(34%) in our cohort of 29 patients compared with the largest previously reported cohort of patients with cough syncope (45 patients, smoking in 82%, chronic obstructive airways disease in
86%) by Bonekat et al.4 The high prevalence of cough syncope
seen in male non-smokers without pre-existing pulmonary disease
is unusual and may suggest that the acute haemodynamic changes
resulting from a coughing fit may occur without chronic pathophysiological changes in the pulmonary system. There were 10
(29%) patients in our cohort with co-existing symptoms of laugh
syncope, compared with only two previously described case reports in the literature to our knowledge.5,6 Cough syncope has
been associated with road accidents.7,8 In our study, one patient
had had a road accident due to cough syncope occurring while
driving.
Pathophysiological observations
Three main pathophysiological mechanisms have been proposed to
explain cough syncope. The first mechanism relates to an acute increase in cerebrospinal fluid pressure during a cough, transiently reducing cerebral perfusion, leading to syncope. 9,10 The second
mechanism is described as a ‘cough concussion’ due to the sudden
explosive increase in venous, arterial, and cerebrospinal fluid pressure during coughing resulting in a concussive effect on the brain
leading to functional impairment.11 The third, and most widely
accepted and validated mechanism for cough syncope12 – 14 was
initially proposed by Sharpey-Schafer15 based on central and peripheral venous and arterial pressure measurements in 27 patients with
cough syncope. Sharpey-Schafer proposed that two events occurred during a bout of coughing which provoked syncope: first,
the high intrathoracic pressure generated during coughing leads to
a critical decrease in venous return, ventricular filling, and cardiac
output; and secondly, the high intrathoracic pressures are transmitted to the arteries, stimulating the arterial baroreceptors that
provoke peripheral vasodilatation, further reducing BP.
In order to evaluate the cardiovascular response to coughing,
Benditt et al.14 studied 9 patients with cough syncope, 13 patients
without cough syncope but with a positive HUT, and 18 patients
without cough syncope with a negative HUT by asking patients to
cough while standing upright. They found that the most significant
1278
drop in SBP after a cough occurred in patients with a history of
cough syncope (51 + 19 mmHg in patients with a history of cough
syncope vs. 23 + 11 mmHg in HUT positive patients without cough
syncope and 28 + 12 mmHg in HUT negative patients without
cough syncope) together with a longer time before recovery of
BP to baseline values (25 + 9 s in cough syncope patients vs. 8 +
2 in HUT positive and 9 + 6 in HUT negative). Data from our larger
cohort of patients are consistent with Benditt’s data, further supporting the Sharpey-Schafer15 hypothesis that syncope is due to
an acute drop in BP due to acute changes in intrathoracic pressures
elicited by coughing.
The most common HUT response in our study was vasodepressor. Additionally, the absence of a bradycardic response during
coughing supports the idea that a cardiovascular, rather than a cardioinhibitory mechanism (as suggested in isolated case reports of
cough syncope),16 – 19 is usually implicated in the pathogenesis of
cough syncope. The isolated case reports of bradycardia being associated with the vasodepression of cough syncope attest to the rarity
of a typical vasovagal reflex in this phenomenon.
Two patients in our cohort also had structural heart abnormalities: Eisenmenger’s syndrome and pulmonary atresia. In these structural heart abnormalities, cardiac filling, and therefore cardiac
output, is heavily reliant on venous return. In addition, the association of cough syncope, with laugh syncope (29% of cases), sneeze
syncope (6% of cases), and syncope during playing brass instruments
(3% of cases) suggests that it may indeed be an acute increase in intrathoracic pressures causing impaired venous return that causes
syncope in these situations.
Diagnostic role of tilt test and cough
attempt during tilt test
This is the largest study to examine the HUT response in patients
with cough syncope. It demonstrates a similar rate of positive
HUT (48%) to that observed in the study by Benditt et al.,14 who
observed a positive HUT in 44% of the nine patients with cough syncope. We also observed a similar magnitude of decrease in BP (by
50 mmHg) and its duration during coughing associated with typical pre-syncopal or syncopal symptoms on the tilt table. The positive responses to HUT in patients with cough syncope were similar
to those observed in patients with a history of suspected vasovagal
syncope (control group).
We observed the presence of syncope or pre-syncopal symptoms in 62% of the cough syncope group while none of the control
group showed any symptoms during cough attempts. Even though
the sensitivity was relatively low (62%), the specificity was 100%.
Therefore, a cough challenge during HUT can be a useful test in patients suspected of cough syncope, but where the diagnosis is uncertain based on the history alone.
Limitations
This is a retrospective study, and patient data were obtained from
archived medical files. In 14 patients, we were unable to define
the total number of lifetime syncopal episodes, as the patients described these episodes as ‘frequent’ or ‘numerous’. These patients
were not taken into account in the evaluation of the number of episodes. Patients were asked to cough as strongly and vigorously as
R. Mereu et al.
possible but the magnitude of cough was not measured. However,
all patients who presented for HUT with a likely diagnosis of cough
syncope had a discussion during the assessment prior to HUT about
the importance of reproducing their clinical symptoms during HUT,
and were, therefore, likely to have complied by performing as vigorous a cough as they could manage.
We could not be certain of accurately quantifying the magnitude
of the acute increase in BP during the cough itself from non-invasive
measurements using the Finometer Pro system as there is a high
likelihood of BP artefact recorded from the Finometer system as a
direct result of coughing. Therefore, we have not considered correlating the magnitude of BP rise from coughing to the subsequent
haemodynamic pattern observed after coughing. Furthermore, the
response to cough in a laboratory setting could be different from
the spontaneous cough response in day-to-day life. Finally, CSM
was only performed in 17 of 29 patients due to the presence of contraindications, or because they were ,40 years old.
Conclusions
Syncope during coughing is likely a result of hypotension, rather than
bradycardia. Coughing during HUT is a useful test in patients suspected of cough syncope, in whom a confident diagnosis cannot
be made on history alone.
Funding
This work was supported by the Imperial BHF Centre of Research
Excellence and NIHR Imperial Biomedical Research Centre.
Conflict of interest: none declared.
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EP CASE EXPRESS
doi:10.1093/europace/euv443
Online publish-ahead-of-print 2 February 2016
.............................................................................................................................................................................
Combining an subcutaneous ICD and a pacemaker with abdominal device
location and bipolar epicardial left ventricular lead: first-in-man approach
Christopher Gemein1*, Morsi Haj2, and Jörn Schmitt1
1
Medizinische Klinik I, Kardiologie und Angiologie, Universitätsklinikum der Justus-Liebig-Universität Giessen, Giessen, Germany and 2Klinik für Herz-, Kinderherz- und
Gefäßchirurgie, Universitätsklinikum der Justus-Liebig-Universität Giessen, Giessen, Germany
* Corresponding author. Tel: +49 641 985 42101; fax: +49 641 985 42109. E-mail address: [email protected]
A 78-year-old man with survived SCD and
ischaemic cardiomyopathy underwent twochamber ICD implantation in 1998 and several
lead and device replacements via the left and right
subclavian veins due to lead malfunction or device infection. Over time, RV pacing requirement
increased due to complete atrio-ventricular (AV)
block and ejection fraction decreased to 35%,
while permanent AF emerged. In 2014, the patient was admitted to hospital with anew right
ventricular (RV) lead fracture. Lead extraction
and another transvenous approach were not successful due to venous occlusion. Therefore, an
subcutaneous ICD (S-ICD) was combined with
an abdominally located pacemaker and a bipolar
epicardial lead positioned on the left ventricle
(Figure). No interaction between the S-ICD and
maximum output bipolar pacing (7.5 V/1.5 ms)
or the pacemaker’s safety programme (unipolar;
5 V/0.6 ms) occurred, while maximum output
unipolar pacing evoked noise in two of three
S-ICD detection vectors. Defibrillation threshold
tests were performed without pacemaker interactions. Furthermore, in July 2015, it could be
demonstrated in a spontaneous VF episode not
being sensed by the pacemaker that bipolar
pacing due to pacemaker undersensing at
ongoing VF did not affect the sensing capabilities of the S-ICD in our specific case.
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Electrophysiology/EP-Case-Reports.
Published on behalf of the European Society of Cardiology. All rights reserved. & The Author 2016. For permissions please email: [email protected].