The Bradycardia-Tachycardia Syndrome Treatment with Cardiac Drugs and Adrenal Corticosteroid Junichi FUJII, M.D., Nobumitsu TAKAHASHI,M.D., and Kazuzo KATO, M.D. Seven patients of S-A block complicated by tachycardic paroxysms of atrial fibrillation or flutter were described and the medical treatment in this syndrome was reappraised. Damage to S-A node and adjacent atrial tissue was assumed in all patients. All the patients had syncopal attacks associated with cardiac arrest occurring especially at the termina- tion of tachycardia. Overdrive suppression of diseased S-A node and lower automatic pacemakers was demonstrated by ECG recordings. The term "bradycardia-tachycardia syndrome" or "syndrome of alternating bradycardia and tachycardia" seemed appropriate. In spite of difficulty of medical treatment reiterated by previous de- scriptions, 6 of 7 patients were improved with drug therapy, including adrenal corticosteroid. Adrenal corticosteroid in combination with or- ciprenaline or belladonna alkaloids was most helpful among the drugs used. Obviously, pacemaker implantation should be performed without delay in patients with frequent and prolonged attacks of syncope. But not all patients have need of pacemaker implantation. A trial of drug therapy may be permitted in many patients of this syndrome before in- troduction of pacemaker. Additional Indexing Words: Sick sinus syndrome S-A block Atrial tachyarrhythmias Syn- cope Overdrive suppression ECENTLY there have been some reports concerning the patients with S-A block or sinus bradycardia accompanied by paroxysmal atrial tachy- arrhythmias such as fibrillation, flutter and paroxysmal tachycardia. As pointed out by several authors, these patients repeatedly exhibited syncopal attacks associated with asystole following termination of the tachycardia. Short1) in 1954 advocated the term "the syndrome of alternating bradycardia and tachycardia" to distinguish these patients from those with bradycardia or tachyarrhythmia alone. Subsequently Ferrer2) described "the sick sinus syndrome" with wide clinical spectrum, ranging from sinus bradycardia with- From the CardiovascularInstitute, 8-1-22 Akasaka,Minatoku, Tokyo. Receivedfor publicationJune 14, 1973. 414 Vol.14 No.5 BRADYCARDIA-TACHYCARDIA SYNDROME 415 out distressing symptoms to recurrent attacks of syncope. "Sluggish sinus node syndrome"3) and "sino-atrial syncope"4) also were applied to much the same group of patients. Though they were all characterized by depressed sinus node function, episodes of cardiac arrest associated with syncope seem to develop more frequently when tachyarrhythmias are complicated. Frequent mention has been made of a great difficulty in medical treat- ment of this group of patients. Antiarrhythmic drugs eliminating tachyar- rhythmias are prone to develop more marked bradycardia or asystole, whereas cardio-accelerators, favorable to bradycardia, may precipitate tachycardia attacks. In 1966 Muller et al.5) reported a case treated successfully with the use of artificial pacemaker, which has thereafter been increased perceptibly. At present many investigators believe the application of pacemaker to be the most efficacious method of therapy in this group of patients. Nevertheless its use is not likely to be indicated to all patients. Although patients having grave syncopal attacks of prolonged duration should unquestionably be aided by pacemaker without delay, treatment may be started with drugs in the others. As for the genesis of this syndrome, damage to the S-A node and the adjacent atrial tissue around it was supposed to be responsible for both the development of sinoatrial block or sinus bradycardia and the occurrence of tachyarrhythmia attack. Yet neither clinical nor pathological data have been available enough to explain the special features of the syndrome. It may be said that its genesis still remains to be investigated. We have experienced 7 cases of this syndrome for the last 7 years. An attempt was made to treat them mainly with drugs including adrenal cor- ticosteroid with good success. Then the purpose of this paper is to reappraise the effect of medical treatment on this syndrome and to review the discussion on its clinical features. MATERIAL Seven patients having tachyarrhythmia attacks were selected from 62 cases of sinoatrial block who were seen in the Cardiovascular Institute Hospital from 1964 to 1971. Cases of sinoatrial block caused by drugs such as digitalis , quinidine, ƒÀ-blocker and the like were not included . RESULTS Table I shows the clinical data on 7 patients . The patients of this series, 4 men and 3 women , were admitted to this 416 FUJII, TAKAHASHI, AND KATO ap. Heart J. Table hospital, complaining of syncopal episodes with palpitations or arrhythmias, which began to develop an average of 1.7 years before admission. Ages varied from 18 to 79 years (average 61 years). All 7 patients exhibited documented episodes of sinoatrial block or sinus arrest with A-V junctional escape beats. The basic heart rate usually was between 32 and 54per minute with an average of 34per minute. In addition, 6 patients had paroxysms of atrial fibrillation, and 5 of atrial flutter, both lasting a few seconds to a few hours. The ventricular rate during these paroxysms was between 120 to 170per minute in all but 1 patient (Case 4), who showed paroxysms of atrial flutter with a ventricular rate of 66per minute. In 4 patients asystoles of 3.6 to 12.8sec duration were demonstrated at the termination of tachycardic paroxysms by long-term ECG recording, causing syncope and/or dizziness. Prolonged periods of asystole frequently Table J Vol.14 No.5 BRADYCARDIA-TACHYCARDIA SYNDROME 417 I observed during the basic rhythm in another patient (Case 4) were also as- sociated with syncopal episodes. Other abnormalities than the rhythm en- countered in the routine electrocardiograms were slight depression of S-T segments of I, II (III) and left precordial leads in 5 patients and incomplete right bundle branch block with left axis deviation in 1. On X-ray 6 patients showed cardiomegaly. Though a few of these com- plained of short breathness on exertion, otherwise no signs of congestive heart failure were noted. Laboratory examinations revealed increased sedimenta- tion rate, positive C-reactive protein and positive RA-test in 2 cases, respec- tively, and positive Wassermann reaction in 1 case (Table II). Serum potassium level was normal in all patients. Hypercholesterolemia was found in 1 patient. From these laboratory, electrocardiographic and historical evidences, the diagnosis of coronary artery disease was made in 4 patients, 1 of whom had II Jap. Heart J. 418 FUJII, TAKAHASHI, AND KATO September, 1973 also rheumatoid arthritis and syphilis. Single case of hypertension and aortic regurgitation was also noted. No etiologic basis could be established in the remaining 1 case. Medical treatment including adrenal corticosteroid was successful in 6 out of 7 patients. In 5 cases the treatment was initiated with belladonna alkaloids or orciprenaline, or a combination of both. After the use of or- ciprenaline with or without extractum scopoliae, the atrial rate was increased to some extent but paroxysms of atrial fibrillation or flutter occurred more frequently in 4 patients. However, 1 patient (Case 7) was improved from oral administration of orciprenaline and extractum scopoliae without adverse effects. Extractum scopoliae alone employed in 1 patient was of little help in increasing the atrial rate. Oral therapy with a combination of prednisolone together with orciprenaline and/or extractum scopoliae was then instituted in 3 patients and from start of the treatment in 2 patients. In 4 of these, episodes of both sinoatrial block or asystole and tachycardia were practically abolished, the patients being essentially symptom-free. A sinus rhythm was maintained without recurrence of atrial tachycardia after gradual decrease in prednisolone dose to 5-10mg every other day. One of 2 additional patients who received prednisolone alone had abbreviated asystole following tachy- cardic paroxysms, being asymptomatic. Quinidine and digitalis glycosides benefited 1 and 3 patients, respectively, by either decreasing the frequency of tachyarrhythmic paroxysm or controlling the ventricular response. However these drugs caused a deterioration of symptoms related to bradycardia, to sinus arrest, or to depression of the A-V junctional escape beats. None of this series of patients was given pacemaker therapy. All patients had been asymptomatic at follow-ups for 3 months to 7 years after discharge from hospital. Four patients showed sinus rhythm throughout the follow-up, while 2 had intermittent sinoatrial block or sinus arrest with A-V junctional escape rhythm. In another patient persistent atrial fibrilla- tion developed after 4 months. Only 1 patient died of cerebral thrombosis about 3 years later. CASEREPORTS Case 1. A 71-year-old female admitted to this hospital on February 24, 1970, had experienced several episodes of arrhythmias, vertigo and syncope for 2 years. A recent increase in their frequency had been noted. She had sometimes showed signs of CHF also for the last 6 months. One of her sisters was treated of bradycardia of unknown etiology, but her own past history was non-contributory. On admission no abnormal physical findings were noted except for bradyarrhythmia of 36 beats per minute. Laboratory findings were shown in Table II. Ophthalmoscopic Vol.14 BRADYCARDIA-TACHYCARDIA SYNDROME 419 No.5 Fig. 1. Case 1. examination