<Brief
History>
A 52-year-old man was admitted to our hospital
because of increased frequency of syncope for 3 months.
He suffered from
first attack of syncope about 10 years ago, which was noted by
his family at home. No convulsion or myoclonus was noted and
his consciousness recovered spontaneously about several
minutes later. In the following years, he got syncope attacked
once every year. He did not pay attention to it and did not
take any medications. Unfortunately, the frequency of syncope
attack increased up to twice per week since 3 months ago. He
often experienced palpitation, air hunger, cold sweating and
then awoke from sleep at midnight. He would go to bathroom for
defecation and would have a sudden loss of consciousness if
the duration of defecation was too long. His consciousness
recovered in several minutes without confusion or memory loss.
He visited another hospital, where 24 hours Holter-ECG
revealed frequent VPCs. Amiodarone and beta-blocker were
given, but the patient still had frequent syncope attacks and developed progressive exercise intolerance. So
he visited the clinic and admitted for further evaluation.
He was a
business man and denied smoking or alcohol drinking.
Hypertension was told by the doctor in the local hospital 3
months ago, but he did not receive any medical treatment. He
had no other systemic disease, operation or related family
history. No orthopnea or paroxysmal nocturnal dyspnea was noted. Exercise intolerance developed after taking
amiodarone and beta-blocker, but resolved if discontinued those drugs.
His
consciousness was clear and oriented. The temperature was
36°C, the pulse was 64, the respiratory rate was 20 and the
blood pressure was 130/80 mmHg. The conjunctivae were pink and
the sclerae were anicteric. The neck was supple without
jugular vein engorgement. The chest wall was symmetrical
expansion with clear breath sound. The point of maximal
impulse was localized at fifth intercostal space and left
middle clavicular line. No thrill or heave was noted by
palpation. The auscultation disclosed a grade II/VI
pansystolic murmur over apex area without radiation. No S3, S4
gallop was noted. The abdomen was soft and flat, neither
tenderness nor rebounding pain was complained. The liver and
spleen were impalpable with a liver span of 8 cm along the
right middle clavicular line. The bowel sound was normoactive.
The extremities were freely movable without pitting
edema or cyanosis. The other physical examinations were unremarkable.
<Laboratory
data>
1. CBC
|
WBC |
RBC |
Hb |
HCT |
MCV |
MCHC |
PLT |
Date |
K/μL |
M/μL |
g/dl |
% |
fL |
g/dL |
K/μL |
890314 |
5.56 |
6.03 |
13.2 |
41.1 |
68.2 |
32.1 |
198 |
2. BCS+Electrolyte
|
Alb |
Glo |
T-Bil |
D-Bil |
AST |
ALT |
ALP |
GGT |
LDH |
Date |
g/dl |
g/dl |
mg/dl |
mg/dl |
U/l |
U/l |
U/l |
U/l |
U/l |
890314 |
4.4 |
4.1 |
0.5 |
0.2 |
32 |
41 |
148 |
47 |
229 |
|
BUN |
CRE |
UA |
Na |
K |
Cl |
Ca |
P |
Mg |
Date |
mg/dl |
mg/dl |
mg/dl |
mmol/l |
mmol/l |
mmol/l |
mmol/l |
mg/dl |
mmol/l |
890314 |
13.2 |
1.0 |
5.1 |
138 |
4.4 |
103 |
2.61 |
3.8 |
0.89 |
|
TG |
T-CHO |
LDL |
HDL |
Date |
mg/dl |
mg/dl |
mg/dl |
mg/dl |
890314 |
35 |
135 |
84 |
44 |
3. Coagulation
|
PT |
PTT |
Date |
Sec |
sec |
890314 |
14.5/12.2 |
54.7/37.6 |
4. Urine
|
Outlook |
PH |
Sp Gr |
Pro |
Bil |
Sugar |
OB |
Uro |
K.B. |
WBC |
RBC |
Epith |
Date |
|
|
|
mg/dl |
|
g/dl |
|
EU/dl |
|
|
|
|
890314 |
Y;C |
5.5 |
1.018 |
- |
- |
- |
- |
0.1 |
- |
0-1 |
- |
-
|
5. Stool
Date |
Outlook |
Occult blood |
Pus cell |
890314 |
YB;F |
- |
- |
<CXR>
No cardiomegaly, clear lung field
<ECG>(Figure
1)
NSR Left anterior fascicular
hemiblock
<Echocardiography & color
duplex>
AO |
37mm |
IVS |
11 mm |
LVET |
|
LVEF |
M-mode 70% |
AV |
21 mm |
LVPW |
10 mm |
M-EPSS |
|
|
|
LA |
35 mm |
LVEDD |
50 mm |
|
|
LV mass |
228gm |
RV |
|
LVESD |
30 mm |
EF slope |
59 cm/S |
|
|
Ao flow(peak): 159 cm/S (PG:10mmHg) MV flow-E: 91cm/S,
A-62cm/S TR flow(peak): 213cm/S (PG:18mmHg) PA
flow-peak V: 109cm/S, Acc. T:165mS Mild AR,TR,PR
Normal LA & LV size Good LV contractility
<Exercise
ECG>89/3/16 Am 9:00
Indeterminate Reason for
terminate: dyspnea Exercise
duration: 9min Maximal heart
rate: 131 bpm (78% of predicted)
<Holter
ECG>
- Basically sinus rhythm
- Rare VPCs and SVEs
- Mild chest pain without significant ST depression
<Ventricular late
potential> Total QRS duration: 119ms
(<120ms) Duration of HFLA
signal: 36ms (<37ms) RMS
voltage: 20uV
(>25uV) →Negative
<Carotid
duplex> Mild atherosclerosis
over right bulb
<EEG> Normal chloral hydrate
induced sleep EEG with basal lead study
<Brain
MRI> No structural
lesions
<Electrophysiology
Study>
- SA nodal function
No SNRT
prolongation
- AV nodal function
AVW at
S1S1 520ms VAW at S1S1 650ms
- Carotid sinus massage
Ventricular pause> 2000msec during both carotid
massage Longest
pause: 2999msec
- Ventricular extra-stimulation test
VEST performed at RVOT & RV
apex Single double triple
extra-stimulation Baseline
& Isuprel 3 mg/min
infusion →
Only 2 ventricular echo beats inducible
No sustained or non-sustained VT/VF inducible
- Procaimamide test
HV time:
28msec→
51 msec RBBB developed
ST-T
change seemed secondary to RBBB
- Occasional multiform VPCs, during Isuprel infusion
Post-EPS diagnosis
- Hypersensitive carotid sinus
- Normal SA nodal function
- VPCs occasional, multiform
- No inducible VT/VF
<Carotid sinus
massage> Protocol:
Carotid massage for 5 minutes with BP, ECG monitor
Baseline: BP: 130/70, HR=60/min
HR drop to <40/min, BP drop to
70/42 mmHg Longest RR interval=
3540 ms Dizziness during carotid
sinus massage
<Head-up tilt table
test>( Figure
2) Protocol :
Stage I :Upright 70o for 30
minutes
Stage II:IV Isopreterenol 4 μg/min to increase HR 25%
Endpoint: Syncope, Pre-syncope
<Clinical course and
treatment> During
hospitalization, 24-hr Holter ECG was negative.
Echocardiography revealed a normal heart structure and normal
flow of blood through the heart chambers and heart valves. LV
contractility was good with an LVEF of 70%. Exercise ECG was
stopped prematurely because
of dyspnea. Ventricular late potential ECG was
negative. MRI & EEG, which were
arranged to evaluate neurological disease,were both negative. Carotid
duplex disclosed only mild arteriosclerosis. EPS was
performed and hypersensitive carotid sinus was suspected. Carotid sinus massage
was repeated and showed a longest RR
interval of 3540 ms, without associated symptoms. A
head-up tilting table test, which has been reported
to be a promising provovative procedure in evaluatingcardiovascular stability,
was arranged and could induce a near-syncope in this patient.
Vasovagal syncope was impressed and because of
drug intolerance, DDDR pacemaker with rate drop response
mode was implanted. He was discharged and was followed up
at our OPD for 4 months without any more attacks of
syncope.
<Discussion>
Syncope is a sudden transient loss of
consciousness and postural tone with spontaneous recovery.
Loss of consciousness results from a reduction of blood flow
to the reticular activating system located in the brain stem
and does not require electrical or chemical therapy for
reversal. Consequently, cessation of cerebral blood flow leads
to loss of consciousness within approximately 10 seconds.
Syncope is an important clinical problem because it is common,
is costly, is often disabling, may cause injury, and may be
the only warning sign before sudden cardiac death. Elderly
persons have a 6 percent annual incidence of syncope. The
cause of syncope remains unknown in about 50 percent of
patients even after a careful history, physical examination,
and 12-lead ECG are performed. Cardiovascular causes are
associated with a 1-year mortality of 19 to 30 percent as
compared to a 1-year mortality of about 6 percent in those
patients with an unknown cause of syncope. The 1-year
mortality in patients with syncope due to noncardiovascular
causes is 1 to 12 percent. Sinus node dysfunction,
tachyarrhythmias, and AV block are the three most common
arrhythmic causes of syncope.
Two types of carotid sinus hypersensitivity have
been described: cardioinhibitory and vasodepressor. The
mechanism responsible for carotid sinus hypersensitivity is
not known; possibilities include abnormalities of
acetylcholine release or responsiveness, inadequate
cholinesterase activity, high levels of resting vagal tone, or
baroreflex hypersensitivity. In the cardioinhibitory type, a
period of ventricular asystole exceeding 3 seconds is produced
by carotid sinus stimulation. The vasodepressor type is
defined as a decrease in systolic blood pressure of 50 mm Hg
or more without slowing of the heart rate, or a decrease in
systolic blood pressure of 30 mm Hg or more with reproduction
of the patient's symptoms. Acutely, cardioinhibitory carotid
sinus hypersensitivity can be prevented by atropine. Long-term
therapy generally requires placement of a permanent pacemaker.
Because of the associated AV-block in these patients,
ventricular pacing (with or without atrial pacing) is usually
required.
Orthostatic hypotension
is most common in tall, asthenic individuals with poorly
developed musculature. Some patients may prevent orthostatic
hypotension by rising slowly from a recumbent position. Venous
pooling occurs in many situations, some of which are
dehydration, prolonged be rest, and blood loss. Patients with
the idiopathic form of orthostatic hypotension also have a
relatively fixed heart rate, anhidrosis, nocturnal polyuria,
urinary and anal sphincter dysfunction, and impotency. Cardiac
abnormalities, especially tachyarrhythmias and
bradyarrhythmias, represent the second most common causes of
syncope, accounting for 10 to 20 percent of episodes.
Ventricular tachycardia is the rhythm disorder that most
frequently causes loss of consciousness. Bradyarrhythmias such
as sick sinus syndrome and advanced AV blocks can also result
in syncope, but less
commonly.
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