Catheterization and Cardiovascular Diagnosis 42:216218 (1997)

Recurrent Syncope Due to Complete Atrioventricular

Block, a Rare Presenting Symptom of Otherwise Silent
Coronary Artery Disease: Successful Treatment By PTCA

Jan D. Kovac,* MD, Francis D. Murgatroyd, MRCP, and J. Douglas Skehan, FRCP

A patient presented with recurrent syncope and episodes of AV block preceded by

asymptomatic ST segment elevation on ambulatory monitoring. Coronary angiography
revealed a severe stenosis in the midsegment of the right coronary artery (RCA).
Successful PTCA and stent insertion abolished further episodes of syncope. Cathet.
Cardiovasc. Diagn. 42:216218, 1997. r 1997 Wiley-Liss, Inc.

Key words: right coronary artery; AV block; coronary angioplasty

CASE REPORT fully with an excellent angiographic result (Fig. 3). No

A 67-year-old female patient with no significant medi-
cal history was treated for hypertension for 6 mo. During
this period she developed several episodes of presyncope
and three episodes of syncope, initially thought to be
related to antihypertensive medication (calcium channel
blockers, beta blockers, finally an ACE inhibitor). These
episodes were not preceeded by chest pain. Further
syncopal episodes occurred after discontinuation of anti-
hypertensive medication. The patient was therefore re-
ferred for ambulatory monitoring.
Ambulatory monitoring of this patient revealed recur-
rent episodes of AV block with ventricular standstill of up
to 4 sec (Fig. 1), at which time the patient reported
lightheadedness. The conduction block was preceded by a
striking level of ST elevation in the monitored lead,
lasting up to 16 min. Urgent coronary angiography
revealed tight stenosis of the midportion of the right
coronary artery (RCA) (Fig. 2). Left coronary and left
ventricular angiography were normal. Coronary angio-
plasty (PTCA) to the RCA lession was advised. Follow-
ing placement of the guiding catheter in the ascending
aorta, right atrial stimulation was carried out via the right
femoral vein monitoring the atrioventricular responses
via His bundle and surface ECG recording. No AV
conduction abnormality and no ischemia were provoked
at stimulation up to 160 bpm. Subsequent PTCA and stent
(3,5 mm 3 20 mm) insertion were performed unevent-
heart block occurred during balloon inflation lasting up to
1 min. Right atrial stimulation immediately post-PTCA
showed 1:1 AV conduction without Wenckebach pattern
up to 160 bpm. At 9 mo after PTCA, the patient is
symptom free on aspirin and amlodipine.
DISCUSSION
Adult patients with presyncope or syncope and docu-
mented high-degree AV block are routinely referred for
permanent pacing [1]. Degenerative disease of the con-
ducting tissue rather than ischemia is usually considered
to be the most likely etiology. This is based on clinical
and autopsy evidence [2]. As earlier detailed anatomical
studies have shown, arterial supply to the AV nodal
territory is usually abundant [3]. Even in the presence of
atheroma in the RCA or left circumflex artery (LCX),
from which AV nodal artery originates, there is alternate
anatomical supply to the AV node from the left anterior
descending artery (LAD) via septal perforators. Postmor-
Cardiology Division, Glenfield General Hospital, Leicester, United
Kingdom
*Correspondence to: Dr. J. Kovac, Cardiology Division, Glenfield
General Hospital, Leicester, LE3 9QP, United Kingdom.
Received 23 December 1996; Revision accepted 4 May 1997

r 1997 Wiley-Liss, Inc.

 Recurrent Syncope Successfully Treated by PTCA 217

Fig. 1. Episodes of ST elevation followed by paroxysmal ventricular standstill on ambulatory

monitoring.

tem studies in elderly patients paced for AV block show
the incidence of coronary artery disease (CAD) in AV
node artery is low [4]. The incidence of CAD is some-
what higher in middle age group patients presenting with
AV block. However, clinical AV block has been observed
only in those patients where the dominant RCA or
circumflex (LCX) artery stenosis coexists with proximal
disease of the LAD [5]. This emphasizes the potential
importance of the collateral supply from this vessel.
Furthermore, the occurrence of complete AV block in the
setting of acute myocardial infarction is rarely a pure
consequence of ischemia. In inferior myocardial infarc-
tion, it is mediated also via changes in the vagal tone,
probably due to afferent impulses from the C receptors of
ventricular muscular fibres by means of the Bezold
Jarisch reflex. Another possible mechanism is the nega-
tive chrono and dromotropic effect of endogenous adeno-
sine [6]. In this circumstance, AV block is usually only
temporary. When AV block complicates anterior myocar-
dial infarction, the mechanism has been postulated to be
the extensive myocardial necrosis and/or potentially
reversible ischemia following vessel closure [7]. Thus
because of this abundance of blood supply to the
AV node, ischemia-induced AV block is rare and appears
to require either extensive ischemia or synergistic cofac-
tors such as augmented vagal tone. This may explain the
218 Kovac et al.
Fig. 2. Tight midportion RCA stenosis.
rarity of AV block in the context of exercise induced
ischemia [8].
Indeed, in the current case, ischemia-induced AV block
occurred at a relatively low heart rate (Fig. 1) and was not
related to the higher heart rate accompanying augmented
sympathetic tone. For this reason, AV block is usually
assumed to be primarily structural conducting tissue
disease. Pacing is, therefore, usually preferred without
prior investigation of coronary anatomy.
In this unusual case, PTCA seems to have provided a
definitive treatment without need for pacing. The absence
of conduction block during balloon inflation is probably
atributable to brief ischemia compared with clinical
episodes (1 min vs. up to 16 min). Reversible ischemia is
probably a rare cause of AV block and may be difficult to
detect if silent. However, the possibility should be borne
in mind as successful revascularization may obviate the
need for pacing in addition to restoring normal blood
flow.
Fig. 3. PTCA and stent result.
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