A-V Conduction Disturbances in Reiter’s Syndrome

RONALD M. ROSSEN, M.D.

DANIEL J. GOODMAN, M.D.’

DONALD C. HARRISON, M.D.

Palo Alto, California

From the Cardiology Division, Stanford Universi- ty School of Medicine, Palo Alto, California 94305. This work was supported in part by Grant No. HL-5709 and HL-5886 from the Na- tional Institutes of Health, and in part by grants from the Bay Area Heart Research Association (R.M.R. and D.J.G.). Requests for reprints should be addressed to Dr. Donald C. Harrison, Cardiology Division, Stanford University School of Medicine, Stanford, California 94305. Manu- script accepted March 12, 1974.

‘Present address: 15 Anderson Street, Hackensack, New Jersey 07601.

High grade atrioventricular (A-V) block is a rarely described complication of Reiter’s syndrome. This 65 year old man had re- current episodes of arthritis, conjunctivitis and urethritis begin- ning at age 16. A prolonged P-R interval was first noted at age 32. The conduction disturbance progressed to intermittent epi- sodes of high grade and complete heart block by age 65. His bundle electrograms located the site of block above the level of the bundle of His. Atrial pacing to rates of lSO/min produced 51 A-V block, whereas exercise and atropine administration resulted in 1:l A-V conduction. In view of these results, artificial pace- maker therapy is not indicated. The association of conduction disorders and Reiter’s syndrome is reviewed.

Reiter’s syndrome is usually a self-limited illness of unknown etiolo-

gy that is characterized by a triad consisting of urethritis, conjuncti-

vitis and arthritis. The eponym is derived from the report of several

cases by Hans Reiter in 1916 [l]. The venereal form of the dis-

ease is well known, and a similar symptom complex has been re-

ported to follow dysentery [2]. Acute arthritis or conjunctivitis is

usually the initial manifestation, followed by an asymmetrical po-

lyarthritis. Associated manifestations include a circinate balanitis

and a peculiar skin eruption known as keratodermia blennorrhagi-

ca. Recurrent episodes occur in a small number of patients, and in

a few these progress to clinical and roentgenographic changes of

spondylitis [ 2-41.

Cardiovascular manifestations of Reiter’s syndrome have been

infrequently reported [5-151. In general, two clinical forms of heart

disease may be manifest: aortitis and atrioventricular (A-V) conduc-

tion abnormalities. Our purpose is to describe a case of recurrent

Reiter’s syndrome of long duration, complicated by high grade A-V block. The nature of the conduction disturbance was determined by

His bundle recording technics in conjunction with atrial pacing and

pharmacologic maneuvers. We review the reported conduction dis-

turbances in this syndrome with emphasis on therapeutic implica-

tions.

CASE REPORT

A 65 year old man was admitted to Stanford University Medical Center for

evaluation of A-V block. In 1924, at the age of 16, he experienced pain

and swelling in both knees, redness and swelling of the eyes, dysuria and a urethral discharge, attributed at the time to acute rheumatic fever. Re-

peated episodes of arthritis involving the knees, feet and lower back oc-

curred between the ages of 24 and 32. On two occasions, conjunctivitis recurred and was attributed to “eye infections.”

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In 1940, during an acute episode of arthritis and con- junctivitis, a prolonged P-R interval was noted on routine electrocardiogram. The patient had no cardiac symptoms, and denied dizziness or syncope. In 1971, intermittent 2: 1 A-V block was documented. Again, he denied syncope, and no cardiac murmurs were reported. In June 1973, a resting electrocardiogram demonstrated sinus rhythm at a rate of 75, first degree A-V block (P-R interval 0.46 set) and episodes of second degree A-V block (Figure IA), which reverted to 1: 1 A-V conduction with exercise (Figure 1B). Atropine administration similarly produced 1: 1 A-V conduction. A 24 hour electrocardiographic recording re- vealed intermittent episodes of second degree A-V block and one episode of complete heart block lasting 90 sec- onds (with an atrial rate of 76 and a ventricular rate of 5 1). The patient denied cardiac symptoms throughout the course of his illness but admitted to intermittent episodes of low back pain and decreased range of motion of the lumbar spine for over 30 years.

Physical examination revealed a blood pressure of 104/100 mm Hg and a pulse rate of 45/min and irregular. There was no evidence of iritis and no skin eruptions were noted. Chest expansion was 5 cm. There was loss of lum- bar lordosis and decreased range of motion of the lumbar spine. The heart was not enlarged and no murmurs were noted.

The erythrocyte sedimentation rate was 11 mm/hour (Wintrobe method). The serologic test for syphilis (VDRL), fluorescent antinuclear antibody test and latex fixation test for rheumatoid factor were negative. HL-A type was W 27. The remainder of the laboratory examination was unre- markable.

Roentgenograms of the chest and heart were within

Figure 2. Posterior-anterior (A) and left anterior oblique (B) roentgeno- grams of the lumbosacral spine demon- strating irregularity and sclerosis of the sacroiliac joints (large arrows) and asymmetrical bony bridging (small ar- rows).

r-.--r-“-+-n--M~~~ / / I Figure 1. A, resting electrocardiogram demons:rating sinus rhythm with first degree A-V block (P-R interval = 0.46 set) and episodes of second degree A-V block. B, portion of exercise electrocardiogram demonstrating 1: 1 A-V conduction.

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A-V CONOUCTlON IN REITER’S SYNDROME-ROSSEN ET AL.

normal limits. X-ray films of the spine revealed irregularity and sclerosis along the margins of both sacroiliac joints and asymmetrical bony bridging in the dorsal spine (Figure

2). Electrophysiologlc Studies. His bundle recording studies were performed using routine technics [ 16,171. Briefly, a tripofar catheter was positioned across the tricuspid valve to record the His bundle, atrial and ventricular electro- grams. A quadripolar catheter was placed in the high right atrium for recording of a high atrial electrogram and for atrial pacing. Atrial electrograms, His bundle electrograms and a simultaneous lead II electrocardiogram were record- ed on a multichannel oscilloscopic photographic recorder at paper speeds of 100 and 200 mm/set.

Base line resting measurements of heart rate, P wave- low atrial (P-A) conduction time, atrium-His bundle (A-H) conduction time and His bundle-ventricular (H-V) conduc- tion time were recorded. Normal intervals in our laboratory are: P-A conduction time 25 to 45 msec, A-H conduction time 60 to 130 msec and H-V conduction time 35 to 55 msec. After control recordings were made, atrial pacing, atropine administration and edrophonium administration with carotid sinus massage were accomplished. The re- sults are listed in Table I.

Resting recordings demonstrated predominantly a 3:2 A-V (Wenckebach) rhythm with gradual prolongation of the A-H interval from 260 to 360 msec (Figure 3A). The H-V interval on all conducted beats was normal at 45 msec. Atrial pacing to rates of 150/min produced high grade 5:l A-V block (Figure 3B). The A-H interval on conducted beats was 320 msec, the H-V interval remaining at 45 msec. Administration of atropine produced 1: 1 A-V con- duction with an A-H interval of 310 msec and an H-V inter- val of 45 msec (Figure 3C). The administration of edropho- nium, 10 mg intravenously, with carotid sinus massage produced 2:l A-V block, again with a prolonged A-H inter- val of 320 msec and a normal H-V interval of 45 msec.

COMMENTS

The diagnosis of ReiterIs syndrome was made in this patient on the basis of a typical history of an acute episode of arthritis, urethritis and conjunctivitis. Re- current attacks of urethritis and arthritis occurred at widely spaced intervals. The diagnosis is supported by the evidence of sacroiliitis and spinal bony bridging of the lumbar spine which have been observed in a number of patients with recurrent Reiter’s syndrome [ 12,181. Further confirmation of the diagnosis is pro- vided by the HL-A type W 27. Nine of 10 patients with Reiter’s syndrome were reported to have HL-A type W 27 (C.M. Pearson, personal communication).

Aortic insufficiency and heart block have been documented in chronic rheumatic’ disorders including ankylosing spondylitis, psoriatic arthritis, the arthritis associated with inflammatory bowel disease and Reiter’s syndrome [ 11,l g-221. Patients with Reiter’s syndrome have been recognized to have pericardial friction rubs, tachycardias and heart block which

have been attributed to pericarditis and myocarditis [9, lo]. Previous reports of the cardiovascular mani- festations in Reiter’s syndrome have emphasized the aortitis resulting in aortic insufficiency [ 10,12- 15,231. A-V conduction disturbances have been mentioned, but not stressed [5,7,8,1 l-15211.

The most common electrocardiographic finding during an acute attack is a prolonged P-R interval with T wave flattening [8]. Paronen [3], in an exten- sive review of Reiter’s syndrome, noted prolonged P-R intervals in 9 of 309 patients studied by electro- cardiography. Fiering [5], in 1946, and Trier [6], in 1950, described a total of four patients with first de- gree A-V block during acute episodes. Neu et al. [ 91, in describing another patient with first degree block, stated that electrocardiographic changes were usual- ly transient but may persist in a small number of pa- tients. Higher degrees of A-V block usually occur in the recurrent form and are reportedly quite rare. Warthin [24] described a patient with second degree heart block of a Wenckebach type, and left bundle branch block and right bundle branch block have been reported on one occasion each [20,25]. Com- plete heart block has been noted on four occasions, but no further electrophysiologic studies were re- ported, and in no case was the electrocardiogram published [4,12,14,23]. The patient described by Collins [14] had episodes of first degree A-V block, second degree A-V block and complete heart block. Cliff [12] suggests that there may be long intervals of time with no electrocardiographic change, after which there is slow progression to more advanced degrees of A-V block. Several investigators have commented on the frequency of aortic root and val- vular disease, which is often preceded by cardiac conduction disturbances [ 12-l 5,211. Paulus, in re- porting on five patients with Reiter’s syndrome and aortic insufficiency, noted that prolonged A-V con- duction had preceded the recognition of valvular dis- ease in three of the patients, by 3 years in one case. Apparently a long latent period between the first epi- sode of Reiter’s syndrome and the appearance of conduction disturbances and aortic root disease is characteristic. Pathologic examination of three pa- tients with Reiter’s syndrome and aortitis revealed focal destruction of the aortic media, myocardial fi- bers and the conduction bundle with replacement by fibrous tissue and accumulations of lymphocytes, monocytes and plasma cells [ 12,13,23]. The aortic valve ring and cardiac conduction tissue are in prox- imity, and it would be expected that processes af- fecting the ring would similarly involve the conduction system. Indistinguishable pathologic findings have been observed in patients with ankylosing spondylitis and aortitis.

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TABLE I His Bundle Recording Results

Time of Recording Atrial Rate Ventricular Rate R-R Interval P-A Interval A-H Interval H-V Interval

(beats/min) (beats/min) (msec) (msec) (msec) (msec)

Resting 80 4%72* 830-1,340* 30 260-360* 45 Pacing 150 30 2,000 40 320 45 After atropine

administration 93 93 640 40 310 45

After edrophonium administration with CSM 60 38 1,650 50 340 45

_____- NOTE: R-R = ventricular cycle length; P-A = P wave-atria1 electrogram interval; A-H = atrial-His electrogram interval; H-V = His-ventricular electrogram interval; CSM = carotid sinus massage. * Wenckebach periods, with 3:2 A-V conduction.

Figure 3. Intracardiac electrograms demonstrating (A) 3:2 Wenckebach rhythm with a prolonged A-H interval (3 10 to 440 msec) and normal H-V in- terval (45 msec); (B) high grade 5: I A-V block with atrial pacing; (C) 1: 1 A-V conduction with a prolonged A-H in- terval (340 msec) and normal H-V inter- val (45 msec) after atropine. L2 = lead 2 electrocardiogram; AE = atrial elec- trogram tracing; HBE = His butidle electrogram tracing; P = P wave; A = atrial electrogram; H = His bundle elec- trogram; V = ventricular electrogram; S = pacemaker spike. See text for dis- cussion. 0

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The use of His bundle recording technics has al- lowed for the precise localization of the site of heart block [ 16,171. The electrocardiographic criteria for determining the site of block may be of limited value in the diagnosis and therapy of conduction system disease [ 171. The prolonged A-H interval and normal H-V interval at rest, during atrial pacing, and with var- ious pharmacologic maneuvers clearly locaiize the site of block in our patient to the region above the bundle of His. This might be suspected by the narrow QRS complex recorded in the electrocardiogram. It is important to note that with atropine administration or with exercise and presumably sympathetic stimula- tion, 1: 1 A-V conduction resulted. The fact that our patient was in a lower degree of A-V block at the time of the His bundle recording study (3:2 A-V Wenckebach) compared to his resting electrocardio- gram (predominantly 2:l A-V block) is probably a re- flection of his anxiety and high sympathetic tone. These findings demonstrate an important functional component of the patient’s A-V block. In addition, during the episode of complete heart block, the ven- tricular rate was 50, which is indicative of a junction- al pacemaker. In view of his asymptomatic state and his 1: 1 conduction response to exercise and atropine

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(and presumably to sympathetic stimulation), we sug- gested that artificial pacemaker therapy was indeed not indicated. Drug therapy, if necessary, would probably be effective. Electrocardiograms of the four patients described with Reiter’s syndrome and com- plete heart block are not available for comparison [4,12,14,23]. One patient had a pacemaker inserted because of a slow rate and congestive heart failure, and apparently did well [4]. Of interest is that aortic insufficiency developed in three of these four pa- tients. In view of the long latent period between the appearance of conduction disturbances and aortic in- sufficiency, our patient will be closely observed. It is recommended that patients with rheumatic disorders complicated by higher grade cardiac conduction dis- orders undergo electrophysiologic study for more precise diagnosis and assessment of possible thera-

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ACKNOWLEDGMENT

We would like to thank Mrs. Jerry Derby and-Mr. Carl Simpson for their valuable technical assistance, and Ms. Pam McCoy and Mrs. Dorothy McCain for their able secretarial help.

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