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Treatment of sinoatrial rhythm disturbances with permanent cardiac pacing
Treatment of Sinoatrial Rhythm Disturbances with Permanent Cardiac Pacing
DEENBANDHU S. CHOKSHI. MD EUGENE MASCARENHAS, MD PHILIP SAMET, MD, FACC SOL CENTER, MD, FACC Miami Beach, Florida Coral Gables, Florida
From the Division of Cardiology, Department of Internal Medicine and Department of Surgery, Mount Sinai Medical Center, Miami Beach, and the University of Miami School of Medicine, Coral Gables, Fla. Manuscript accepted January 24, 1973. Address for reprints: Deenbandhu S. Chokshi, MD, 4300 Alton Rd, Miami Beach, Fla. 33140.
Fifty-two patients with sinoatrial disturbances causing syncope, dizzy spells, heart failure or predisposition to ventricular tachyarrhythmias were treated with permanent cardiac pacing between January 1966 and June 1970. They were followed up from 12 to 60 months. The rhythm disorders treated with permanent pacer implantation were: (1) sinus bradycardia (27 patients); (2) sinoatrial block or arrest (10 patients); (3) brady-tachyarrhythmia syndrome (11 patients); and (4) sinus bradycardia with ventricular tachyarrhythmia (4 patients). Forty-seven patients had ventricular and 5 had coronary sinus pacemakers. Two of the five patients with coronary sinus pacemakers subsequently required ventricular pacing because of failure of the coronary sinus electrode to capture the atrium. One patient died 3 weeks after pacemaker implantation because of renal failure. Eleven others died of natural causes 3 to 38 months after implantation of the pacemaker. Long-term pacemaker complications such as perforation of the right ventricle, dis.placement or fracture of the pacing electrode, infection at the site of the powerpack and raised threshold were observed in nine patients. Syncopal or near syncopal episodes were abolished in 32 of 35 patients, chronic congestive heart failure was alleviated i'n 7 of 12 patients, and recurrent ventricular tachyarrhythmias were controlled in 3 of 4 patients by pacing and antiarrhythmic agents. We conclude that permanent ventricular pacing is an effective therapeutic approach in sinOatrial disturbances causing symptoms such as syncope, dizzy spells, brady-tachyarrhythmia syndrome, heart failure or recurrent ventricular arrhythmias.
Sinoatrial disturbances can give rise to sinus bradycardia, sinoatrial block, brady-tachyarrhythmia syndrome and sinus bradycardia with ventricular arrhythmias. Sinus bradycardia has been considered a benign arrhythmia. However, persistent sinus bradycardia in which the ventricular rate fails to increase during exercise or after administration of atropine or isoproterenol is a potential problem. In recent years several authors 1,2 have reported a significant incidence of syncope and classic Stokes-Adams attacks due to prolonged periods of bradycardia or asystole caused by transient sinoatrial block or sinus' arrest. Fatigue, palpitations and heart failure have also been described. Some patients may exhibit alternating sinus bradycardia and supraventricular tachyarrhythmias. 3 These patients may present with episodes of syncope, light-headedness, increasing heart failure or embolic phenomena. Drug therapy in brady-tachyarrhythmia is often unsatisfacto.ry on a long-term basis. ~ The relative facility and ease of permanent transvenous pacing 5 has now provided an alternate means of treating these dysrhythmias, but there are few published data on the results of long-term pacing. This study reports our experiences with 52 patients with symptomatic sinoatrial disturbances treated by permanent pacemaker implantation. The follow-up period ranged from 1 to 5 years.
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PACING FOR SINOATRIAL RHYTHM DISORDERS--CHOKSHI ET AL.
TABLE I
2,!
Primary Cardiac Diagnoses and Associated Conditions in 52 Patients with Sinoatrial Disturbances
20.
Diagnosis
Patients* (no.)
Arteriosclerotic heart disease Rheumatic valvular heart disease Hypertensive heart disease Digitalis-related disturbances Diabetes mellitus Hyperthyroidism Renal failure Chronic obstructive lung disease Heart disease of unknown origin
38 3 7 7 4 3 2 3 10
rq}
~
16. Mort
"6 ~. 12
I~l Wo,.°.
..Q
E
Z
8
< 50
51-60
61-70 71-80 81-90 • 91 Age in Years FIGURE 1. Age and sex distribution of 52 patients. The majority of the patients, 21 men and 12 women, were in eighth decade.
* Several patients had more than one associated condition.
TABLE II Predominant Clinical Indication for Pacemaker Insertion Material
and
Methods
All patients were referred because of syncope, dizziness, heart failure or arrhythmia associated with sinoatrial disturbances. The latter arrhythmias did not respond to appropriate drug therapy. Fifty-two patients were treated with permanent pacemakers between January 1966 and June 1970. Their subsequent clinical course was followed up to June 1971, thus giving a minimal follow-up duration of 12 months for each of the surviving patients. The age and sex distribution is shown in Figure 1. The majority of patients (33 of 52) were in the eighth decade. The youngest patient was 54 years and the oldest 89 years of age. The underlying primary cardiac diagnoses and associated significant medical conditions at the time of pacemaker implantation are shown in Table I. Although 38 of 52 patients suffered from arteriosclerotic heart disease, we do not imply that disorders of the sinoatrial node are caused by atherosclerosis. The predominant clinical indications and sinoatrial rhythm disturbances necessitating pacemaker implantation are summarized in Tables II and Ill. Table IV shows the associated conduction defects and rhythm disorders observed in these subjects. Acute myocardial infarction was ruled out by appropriate studies in each instance. Sinoatrial disturbances were associated with use of digitalis in seven patients. However, since digitalis was needed for treatment of congestive heart failure, both pacemaker and drug therapy were required. Other causes of syncope or dizzy spells such as cerebrovascular insufficiency, neurologic disorders or diseases of the ear were excluded clinically. Atrial pacing is preferred to ventricular pacing to preserve atrial contribution to cardiac output. However, atrial pacing can be carried out only if atrioventricular conduction is intact and if atrial arrhythmias are absent. The state of atrioventricular conduction was, therefore, determined by atrial pacing and His bundle electrograms. 6 Sinus nodal function was also evaluated by determination of sinus nodal recovery time. 7,8 All patients were paced by the pervenous pacing technique. Ventricular pacing was performed with a Cordis standby generator in 12 patients, a Medtronic demand unit in 32 patients and a demand Stanicor unit in 3 patients. Atrial pacing by means of an electrode placed in the coronary sinus was used in five patients. Fixed rate
216
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Indication Syncope Dizziness or near syncope Heart failure Suppression of ventricular tachyarrhythmias Total
Patients (no.) 15 21 12 4 52
TABLE III Rhythm Disorders* Treated by Pacemaker Implantation
Condition Sinus bradycardia Rate <45/rain Rate 45-60/min Sinoatrial block or arrest Brady-tachyarrhyth mia syndrome Drug-resistant ventricular arrhythmias associated with sinus bradycardia Total
Patients (no.) 27 19 8 10 11 4 52
* Since some patients exhibited more than one rhythm disorder only the dominant rhythm disorder is tabulated.
coronary sinus pacing was carried out in two of the latter patients and demand atrial pacing in three. Follow-up studies: A note was made of the generator model and capacity, type of electrode catheter, pacemaker spike interval, threshold measurement and radiologic position of the electrode catheter before patients were discharged from the hospital. Patients were followed up either at the pacemaker clinic or in the physician's office at 6 month intervals to 12 months after implantation, 3 month intervals until 18 months after implantation and at more frequent intervals until the generator was replaced.
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PACING FOR SINOATRIAL RHYTHM DISORDERS--CHOKSHI ET AL.
TABLE IV
,
Conduction and Rhythm Disorders Associated with Sinoatrial Disturbances
Conductionand Rhythm Disorder
Patients* (no.)
Left axis deviation Left bundle branch block (alone) Right bundle branch block (alone) Right bundle branch block with left axis deviation Intraventricular conduction defect First degree atrioventricular block Wenckebach atrioventricular block Nodal escape rhythm Atrial premature beats Ventricular premature beats Supraventricular arrhythmia Ventricular tachycardia
2 12 1 7 4 20 13 4
* Some patients had more than one associated disorder.
One patient (treated for brady-tachyarrhythmia syndrome) died of ventricular fibrillation 3 months after pacemaker implantation. One month before the fatal episode, the pacemaker was working well. Three months after the implantation, the patient had a syncopal attack and repeated attacks of ventricular fibrillation that did not respond to treatment. The transition from pacemaker rhythm to ventricular fibrillation was not documented, and the terminal pacemaker spike interval was unchanged from the initial readings. The pacemaker generator was checked by the manufacturer and functioned according to specifications. Autopsy was not performed. Death in two other patients occurred while they were out of the Miami area. Before pacemaker implantation, one of these patients had arteriosclerotic heart disease and two episodes of myocardial infarction; the other patient had arteriosclerotic heart disease, diabetes mellitus and old hemiplegia. We could not obtain accurate data about the terminal events in these cases.
Symptomatic improvement during follow-up period: The duration of the follow-up period in these
TABLE V Causes of Death in 12 Patients with an Implanted Pacemaker Time of Death Patients AfterPacemaker (no.) Implantation(mo)
Causeof Death Acute myocardial infarction Resistant heart failure Cerebrovascular accident Chronic renal failure Gram-negative septicemia Ventricular fibrillation Undocumented deaths
3 2 2 1 1 1 2
4,5,9 16,37 24,38 3 (wk) 3 3 5,12
TABLE Vl Follow-Up Data on Symptoms SymptomsBefore Pacemaker Implantation
Patients (no.)
Syncope Dizziness Heart failure Recurrent ventricular tachyarrhythmia
15 21 12 4
Condition Improved Unimproved 14 19 7 3
1 2 5 1
Results
Mortality: One patient died 3 weeks after pacemaker implantation because of acute renal failure superimposed on chronic renal failure. Eleven other patients died 3 to 38 months after implantation. The causes of death in these patients are summarized in Table V. One patient died of ventricular fibrillation of uncertain origin, and two deaths were undocumented.
52 patients is summarized in Figure 2. Relief of symptoms was noted in 43 of 52 patients (Table VI). Syncope or dizziness was abolished in most patients (33 of 36) after pacemaker implantation. Two patients continued to have dizzy spells and one patient had continued syncopal attacks although their pacemaker was functioning well. These symptoms were attributed to the presence of coexisting disease. The effects of pacing were not as gratifying in patients with chronic congestive heart failure. Effort tolerance increased and digitalis could be administered more effectively in 7 of 12 patients; in 5 others the condition was unchanged. The addition of pacing to antiarrhythmic drugs effectively controlled recurrent ventricular arrhythmias associated with sinus bradycardia in three of four patients. In each patient, pacing alone was ineffective in controlling arrhythmias. In one patient, multiple premature ventricular contractions recurred despite pacing and adequate treatment with antiarrhythmic drugs. Pacemaker complications: The complications associated with permanent pacing are summarized in Table VII. They occurred in 9 of 52 patients, were recognized promptly and treated by appropriate measures. In two of the three patients with coronary sinus demand pacing, atrial pacing was abandoned after 2 days and 4 weeks, respectively, because of failure of the coronary sinus electrode to sense properly the QRS complex or failure to capture the atrium. The catheter was then introduced into the right ventricular apex for ventricular pacing. Discussion
The effects of pacing in patients wth sinoatrial disturbances causing syncope, congestive heart failure, ventricular tachycardia and brady-tachyarrhythmia
August 1973
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Volume 32
217
PACING FOR SINOATRIAL RHYTHM DISORDERS--CHOKSHI ET AL.
20' t-"
[]
Living
[]
Deceased
•.~ 15. o a_ o
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Z I--I 0.6
7.12
13.18
19-24
25.30
31-36
43-48
37-42
r-I 49-54
55-60
Follow-up in Months
syndrome will be discussed, including the possible mechanisms involved. Syncope: Since Muller and Finkelstein 9 reported in 1966 on the successful use of a permanent ventricular pacemaker in treatment of sinoatrial block producing syncope in a 29 year old woman, there has been growing interest in this technique. Syncopal episodes due to sinoatrial block have been successfully treated by permanent pacemaker therapy, lon~ and the follow-up data in these patients have extended from 18 months to 5 years, ix In our experience with a larger series of patients, 14 of 15 patients with syncope and 19 of 21 patients with dizzy spells had complete freedom from these symptoms after pacemaker implantation. One patient with syncope and one with dizzy spells were symptom-free for 50 and 13 months, respectively, after insertion of the pacemaker. Recurrence of symptoms in these patients was attributed to vascular insufficiency secondary to cerebral atherosclerosis. The cause of continued dizzy spells in a third patient, aged 86 years, could not be precisely explained. Inability of pacing to control these symptoms on a long-term basis in some patients, particularly older persons, is to be expected because of coexisting cerebrovascular insufficiency. Congestive h e a r t failure: There is little doubt that a slow ventricular rate may contribute to the
TABLE VII
Long-term Pacemaker Complications Ventricular
Pacing
218
Pacing Complications
(no. of patients)
Electrode displacement Raised threshold Fracture of electrode, proximal Myocardial perforation Infection at site of powerpack
1 1 1 2 2
August 1973
Coronary SinusPacing (no. of
patients) 2 0 0 0 0
The American Journal of CARDIOLOGY
61+
FIGURE 2. Survival and mortality data in 52 cases,
pathogenesis of congestive heart failure in patients with complete heart block. Dogs with experimentally produced complete heart block exhibit a reduction in cardiac output and decrease in myocardial contractility. 12 After ventricular pacing was instituted, cardiac output improved and heart failure lessened. Davidson et al. la reported that the condition of 16 of 20 patients with preexisting congestive heart failure was greatly improved after institution of pacing but that 26 patients (17 percent) first experienced heart failure after pacing had begun. Bernstein et al. 1~ found that pacing effectively controlled acute heart failure due to bradyarrhythmia; the same was not true for chronic congestive heart failure. They postulated that many of their patients with chronic failure had repeated episodes of myocardial damage with secondary fibrosis, leading to a relatively fixed stroke volume. Although the patients' condition improved transiently with temporary pacing, there was no lasting benefit from permanent pacing. Comparable experimental or clinical data are not available for congestive heart failure due to sinoatrial disturbances. Of the 12 patients in our study who had congestive heart failure, 7 had symptomatic improvement after pacemaker implantation. Failure of improvement or deterioration of symptoms occurred in the rest (5 patients). Deterioration of effort tolerance was related to worsening of the intrinsic heart disease due to development of acute myocardial infarction in one patient. In the remaining four patients, progressive deterioration may have been related to the presence of severe arteriosclerotic heart disease before pacemaker implantation (2 patients) or due to loss of atrial contribution to cardiac output (2 patients). Atrial contribution to cardiac output has been well demonstrated by Samet et al. ~5 Furthermore, compared to ventricular pacing, coronary sinus or atrial pacing results in a higher cardiac index. 16 However, before institution of permanent atrial or coronary sinus pacing, the integrity of the conduction system should be checked by His bundle recording and atrial pacing at various heart rates. On the basis of His bundle recordings, a new classification of heart block
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PACING FOR SINOATRIAL RHYTHM DISORDERS--CHOKSHI ET AL.
has been proposed. 17 All three degrees of atrioventricular block seen on~ the surface electrocardiogram may result from block within the atrioventricular node or His-Purkinje system or at multiple sites. If atrioventricular and His-Purkinje conduction are normal, and if atrial arrhythmias are absent, these patients with heart failure preferably should have a coronary sinus or atrial pacemaker. However, atrial pacing has many problems, namely, electrode displacement, high threshold and inadequate sensing. V e n t r i c u l a r t a c h y a r r h y t h m i a : Ventricular tachyarrhythmias not associated with sinus bradycardia but refractory to drug therapy have been successfully treated by the addition of permanent pacing. zs Suppression of these arrhythmias with pacingin patients without heart block z9 and in patients with sinus bradycardia or sinoatrial block 2° has been described. Only patients who had recurrent ventricular arrhythmia associated with sinus bradycardia are included in our report. Permanent pacing in conjunction with antiarrhythmic drugs abolished arrhythmia in three of four patients. Slowing of the heart rate to less than 60 beats/min may predispose to ventricular arrhythmias. 2~ The following mechanisms are proposed for beneficial effects of pacing in prevention of ventricular tachycardia: (1) Pacing produces overdrive suppression of ectopic foci. (2) Shortening of the refractory period and an increase in the vulnerable period threshold for ectopic impulses occur when the heart rate is increased. Han et al. 22 produced ectopic beats in experimental animals by coronary occlusion, sudden increase in aortic blood pressure and hypothermia. Under these conditions, the frequency of ectopic
beats was noted when the basic cycle length was 800 to 1,200 msec. When the basic cycle length was progressively decreased, the average time taken to induce ectopic beats was prolonged and the stimulus threshold increased. (3) Areas of asynchronous r e covery of excitability, and hence, areas of asynchronous conduction, are eliminated and ventricular fibrillation threshold is raised when the basic cycle length is decreased. 2s B r a d y - t a c h y a r r h y t h m i a syndrome: Treatment of the brady-tachyarrhythmia syndrome with drugs may present a difficult problem. Drugs like digitalis used to control supraventricular arrhythmia may cause bradycardia and drugs used to accelerate the heart rate, such as atropine or isoproterenol, may precipitate atrial or ventricular arrhythmias. All 11. patients in our series had marked symptomatic improvement with abolition of syncope (4 patients) or dizziness (4 patients). Alleviation of congestive heart failure was noted in three patients. Similar encouraging results have been noted by others, z°,24"26 Rubenstein et al. 26 noted that although electrical pacing was uniformly successful in treating symptoms of bradycardia, it was often disappointing in preventing tachycardia. In 2 of their 13 patients tachyarrhythmias were abolished with addition of pacing to the drug therapy, and pacing permitted more aggressive administration of antiarrhythmic drugs in 3 others. Tachyarrhythmias were abolished in 7 of our 11 patients; although 4 others continued to have such arrhythmias, digitalis could be administered more safely. All 11 patients in this group were receiving digitalis or antiarrhythmic drugs, or both, in addition to pacing.
• References
1. Rasmussen K: Chronic sinoatrial heart block. Amer Heart J 81:38-47, 1971 2. Eraut D, Shaw DB: Sinus bradycardia. Brit Heart J 33:742749, 1971 3. Birchfield RI, Meneffee EE, Bryants GDB: Disease of the sinoatrial node associated with bradycardia, syncope and paroxysmal atrial fibrillation. Circulation 16:20-26, 1957 4. Sanders CA: Heart block. In, Current Therapy (Conn HF, ed). Philadelphia, WB Saunders, 1971, p 149-151 5. Chardack WM: Heart block treated with an implantable pacemaker. Past experience and current developments. Progr Cardiovasc Dis 6:507-537, 1964 6. Scherlag BJ, Lau SH, Helfant RH, et al: Catheter technique for recording His bundle activity in man. Circulation 39:1318, 1969 7. Narula OS, Samet P, Javier RP: Significance of sinus-node recovery time. Circulation 45:140-158, 1972 8. Mandel W, Hayakawa H, Danzig R, et ah Evaluation of sinoatrial node function in man by overdrive suppression. Circulation 44:59-66, 1971 9. Muller OF, Finkelstein D: Adams-Stokes syndrome due to sinoatrial block. Amer J Cardio117:433-436, 1966 10. Easley RM, Goldstein S: Sinoatrial syncope. Amer J Med 50:166-177, 1971 11. Bayley TJ: Long-term ventricular pacing in treatment of sinoatrial block. Brit Med J 3:456-458, 1971
12. Brockman SK, Stoney WS: Congestive heart failure and cardiac output in heart block and during pacing. Ann NY Acad Sci 167:534-545, 1969 13. Davidson DM, Braak CA, Preston TA, et ah Permanent ventricular pacing. Effect on long-term survival, congestive heart failure, and subsequent myocardial infarction and stroke. Ann Intern Med 77:345-351, 1972 14. Bernstein V, Rotem E, Peretz D: Permanent pacemakers: 8 year follow-up study. Incidence and management of congestive heart failure and perforations. Ann Intern Med 74:361-369, 1971 15. Samet P, Bernstein WH, Nathan DA, et ah Atrial contribution to cardiac output in complete heart block. Amer J Cardio116:1-10, 1965 16. Befeler B, Hildner FJ, Javier RP, et al: Cardiovascular dynamics during coronary sinus, right atrial and right ventricular pacing. Amer Heart J 81:372-360, 1971 17. Narula OS, Scherlag BJ, Samet P, et ah Atrioventricular block. Localization and classification by His bundle recording. AmerJ Meal 50:146-165, 1971 18. Friedberg CK, Lyon W, Denoso E: Suppression of refractory recurrent ventricular tachycardia by transvenous rapid cardiac pacing and antiarrhythmic drugs. Amer Heart J 79:44-50, 1970 19. Sowton E, Leatham A, Carson P: The suppression of arrhythmias by artificial pacemaking. Lancet 2:1098-1100,
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PACING FOR SINOATRIAL RHYTHM DISORDERS--CHOKSHI ET AL.
1964 20. Sand¢e E, Flensted-Jensen E: Adams-Stokes seizures in patients with attacks of both tachy- and bradycardia, a therapeutic challenge. Acta Med Scand 186:111-116, 1969 21. Zoll PM, Linenthal AJ, Zarsky LRN: Ventricular fibrillation. Treatment and prevention by external cardiac currents. New EngJ Med 262:105-112, 1960 22. Han J, DeTraglia J, Millet D, et ah Incidence of ectopic beats as a function of basic rate in the ventricle. Amer Heart J 72:632-639, 1966 23. Han J, Millet D, Chizzonitti B, et ah Temporal dispersion of
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recovery of excitability in atrium and ventricle as a function of heart rate. Amer Heart J 71:481-487, 1966 24. Cheng TO: Transvenous ventricular pacing in the treatment of paroxysmal atrial tachyarrhythmias alternating with sinus bradycardia and standstill. Amer J Cardiol 22:874-879, 1968 25. Escher EJW, Furman S: Pacemaker therapy for chronic rhythm disorders. Progr Cardiovasc Dis 14:459-472, 1972 26. Rubenstein JJ, Schulman CL, Yurchack PM, et ah Clinical spectrum of the sick sinus syndrome. Circulation 46:5-13, 1972
Volume 32
DEENBANDHU S. CHOKSHI. MD EUGENE MASCARENHAS, MD PHILIP SAMET, MD, FACC SOL CENTER, MD, FACC Miami Beach, Florida Coral Gables, Florida
From the Division of Cardiology, Department of Internal Medicine and Department of Surgery, Mount Sinai Medical Center, Miami Beach, and the University of Miami School of Medicine, Coral Gables, Fla. Manuscript accepted January 24, 1973. Address for reprints: Deenbandhu S. Chokshi, MD, 4300 Alton Rd, Miami Beach, Fla. 33140.
Fifty-two patients with sinoatrial disturbances causing syncope, dizzy spells, heart failure or predisposition to ventricular tachyarrhythmias were treated with permanent cardiac pacing between January 1966 and June 1970. They were followed up from 12 to 60 months. The rhythm disorders treated with permanent pacer implantation were: (1) sinus bradycardia (27 patients); (2) sinoatrial block or arrest (10 patients); (3) brady-tachyarrhythmia syndrome (11 patients); and (4) sinus bradycardia with ventricular tachyarrhythmia (4 patients). Forty-seven patients had ventricular and 5 had coronary sinus pacemakers. Two of the five patients with coronary sinus pacemakers subsequently required ventricular pacing because of failure of the coronary sinus electrode to capture the atrium. One patient died 3 weeks after pacemaker implantation because of renal failure. Eleven others died of natural causes 3 to 38 months after implantation of the pacemaker. Long-term pacemaker complications such as perforation of the right ventricle, dis.placement or fracture of the pacing electrode, infection at the site of the powerpack and raised threshold were observed in nine patients. Syncopal or near syncopal episodes were abolished in 32 of 35 patients, chronic congestive heart failure was alleviated i'n 7 of 12 patients, and recurrent ventricular tachyarrhythmias were controlled in 3 of 4 patients by pacing and antiarrhythmic agents. We conclude that permanent ventricular pacing is an effective therapeutic approach in sinOatrial disturbances causing symptoms such as syncope, dizzy spells, brady-tachyarrhythmia syndrome, heart failure or recurrent ventricular arrhythmias.
Sinoatrial disturbances can give rise to sinus bradycardia, sinoatrial block, brady-tachyarrhythmia syndrome and sinus bradycardia with ventricular arrhythmias. Sinus bradycardia has been considered a benign arrhythmia. However, persistent sinus bradycardia in which the ventricular rate fails to increase during exercise or after administration of atropine or isoproterenol is a potential problem. In recent years several authors 1,2 have reported a significant incidence of syncope and classic Stokes-Adams attacks due to prolonged periods of bradycardia or asystole caused by transient sinoatrial block or sinus' arrest. Fatigue, palpitations and heart failure have also been described. Some patients may exhibit alternating sinus bradycardia and supraventricular tachyarrhythmias. 3 These patients may present with episodes of syncope, light-headedness, increasing heart failure or embolic phenomena. Drug therapy in brady-tachyarrhythmia is often unsatisfacto.ry on a long-term basis. ~ The relative facility and ease of permanent transvenous pacing 5 has now provided an alternate means of treating these dysrhythmias, but there are few published data on the results of long-term pacing. This study reports our experiences with 52 patients with symptomatic sinoatrial disturbances treated by permanent pacemaker implantation. The follow-up period ranged from 1 to 5 years.
August 1973 The American Journal of CARDIOLOGY Volume 32
215
PACING FOR SINOATRIAL RHYTHM DISORDERS--CHOKSHI ET AL.
TABLE I
2,!
Primary Cardiac Diagnoses and Associated Conditions in 52 Patients with Sinoatrial Disturbances
20.
Diagnosis
Patients* (no.)
Arteriosclerotic heart disease Rheumatic valvular heart disease Hypertensive heart disease Digitalis-related disturbances Diabetes mellitus Hyperthyroidism Renal failure Chronic obstructive lung disease Heart disease of unknown origin
38 3 7 7 4 3 2 3 10
rq}
~
16. Mort
"6 ~. 12
I~l Wo,.°.
..Q
E
Z
8
< 50
51-60
61-70 71-80 81-90 • 91 Age in Years FIGURE 1. Age and sex distribution of 52 patients. The majority of the patients, 21 men and 12 women, were in eighth decade.
* Several patients had more than one associated condition.
TABLE II Predominant Clinical Indication for Pacemaker Insertion Material
and
Methods
All patients were referred because of syncope, dizziness, heart failure or arrhythmia associated with sinoatrial disturbances. The latter arrhythmias did not respond to appropriate drug therapy. Fifty-two patients were treated with permanent pacemakers between January 1966 and June 1970. Their subsequent clinical course was followed up to June 1971, thus giving a minimal follow-up duration of 12 months for each of the surviving patients. The age and sex distribution is shown in Figure 1. The majority of patients (33 of 52) were in the eighth decade. The youngest patient was 54 years and the oldest 89 years of age. The underlying primary cardiac diagnoses and associated significant medical conditions at the time of pacemaker implantation are shown in Table I. Although 38 of 52 patients suffered from arteriosclerotic heart disease, we do not imply that disorders of the sinoatrial node are caused by atherosclerosis. The predominant clinical indications and sinoatrial rhythm disturbances necessitating pacemaker implantation are summarized in Tables II and Ill. Table IV shows the associated conduction defects and rhythm disorders observed in these subjects. Acute myocardial infarction was ruled out by appropriate studies in each instance. Sinoatrial disturbances were associated with use of digitalis in seven patients. However, since digitalis was needed for treatment of congestive heart failure, both pacemaker and drug therapy were required. Other causes of syncope or dizzy spells such as cerebrovascular insufficiency, neurologic disorders or diseases of the ear were excluded clinically. Atrial pacing is preferred to ventricular pacing to preserve atrial contribution to cardiac output. However, atrial pacing can be carried out only if atrioventricular conduction is intact and if atrial arrhythmias are absent. The state of atrioventricular conduction was, therefore, determined by atrial pacing and His bundle electrograms. 6 Sinus nodal function was also evaluated by determination of sinus nodal recovery time. 7,8 All patients were paced by the pervenous pacing technique. Ventricular pacing was performed with a Cordis standby generator in 12 patients, a Medtronic demand unit in 32 patients and a demand Stanicor unit in 3 patients. Atrial pacing by means of an electrode placed in the coronary sinus was used in five patients. Fixed rate
216
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Indication Syncope Dizziness or near syncope Heart failure Suppression of ventricular tachyarrhythmias Total
Patients (no.) 15 21 12 4 52
TABLE III Rhythm Disorders* Treated by Pacemaker Implantation
Condition Sinus bradycardia Rate <45/rain Rate 45-60/min Sinoatrial block or arrest Brady-tachyarrhyth mia syndrome Drug-resistant ventricular arrhythmias associated with sinus bradycardia Total
Patients (no.) 27 19 8 10 11 4 52
* Since some patients exhibited more than one rhythm disorder only the dominant rhythm disorder is tabulated.
coronary sinus pacing was carried out in two of the latter patients and demand atrial pacing in three. Follow-up studies: A note was made of the generator model and capacity, type of electrode catheter, pacemaker spike interval, threshold measurement and radiologic position of the electrode catheter before patients were discharged from the hospital. Patients were followed up either at the pacemaker clinic or in the physician's office at 6 month intervals to 12 months after implantation, 3 month intervals until 18 months after implantation and at more frequent intervals until the generator was replaced.
Volume 32
PACING FOR SINOATRIAL RHYTHM DISORDERS--CHOKSHI ET AL.
TABLE IV
,
Conduction and Rhythm Disorders Associated with Sinoatrial Disturbances
Conductionand Rhythm Disorder
Patients* (no.)
Left axis deviation Left bundle branch block (alone) Right bundle branch block (alone) Right bundle branch block with left axis deviation Intraventricular conduction defect First degree atrioventricular block Wenckebach atrioventricular block Nodal escape rhythm Atrial premature beats Ventricular premature beats Supraventricular arrhythmia Ventricular tachycardia
2 12 1 7 4 20 13 4
* Some patients had more than one associated disorder.
One patient (treated for brady-tachyarrhythmia syndrome) died of ventricular fibrillation 3 months after pacemaker implantation. One month before the fatal episode, the pacemaker was working well. Three months after the implantation, the patient had a syncopal attack and repeated attacks of ventricular fibrillation that did not respond to treatment. The transition from pacemaker rhythm to ventricular fibrillation was not documented, and the terminal pacemaker spike interval was unchanged from the initial readings. The pacemaker generator was checked by the manufacturer and functioned according to specifications. Autopsy was not performed. Death in two other patients occurred while they were out of the Miami area. Before pacemaker implantation, one of these patients had arteriosclerotic heart disease and two episodes of myocardial infarction; the other patient had arteriosclerotic heart disease, diabetes mellitus and old hemiplegia. We could not obtain accurate data about the terminal events in these cases.
Symptomatic improvement during follow-up period: The duration of the follow-up period in these
TABLE V Causes of Death in 12 Patients with an Implanted Pacemaker Time of Death Patients AfterPacemaker (no.) Implantation(mo)
Causeof Death Acute myocardial infarction Resistant heart failure Cerebrovascular accident Chronic renal failure Gram-negative septicemia Ventricular fibrillation Undocumented deaths
3 2 2 1 1 1 2
4,5,9 16,37 24,38 3 (wk) 3 3 5,12
TABLE Vl Follow-Up Data on Symptoms SymptomsBefore Pacemaker Implantation
Patients (no.)
Syncope Dizziness Heart failure Recurrent ventricular tachyarrhythmia
15 21 12 4
Condition Improved Unimproved 14 19 7 3
1 2 5 1
Results
Mortality: One patient died 3 weeks after pacemaker implantation because of acute renal failure superimposed on chronic renal failure. Eleven other patients died 3 to 38 months after implantation. The causes of death in these patients are summarized in Table V. One patient died of ventricular fibrillation of uncertain origin, and two deaths were undocumented.
52 patients is summarized in Figure 2. Relief of symptoms was noted in 43 of 52 patients (Table VI). Syncope or dizziness was abolished in most patients (33 of 36) after pacemaker implantation. Two patients continued to have dizzy spells and one patient had continued syncopal attacks although their pacemaker was functioning well. These symptoms were attributed to the presence of coexisting disease. The effects of pacing were not as gratifying in patients with chronic congestive heart failure. Effort tolerance increased and digitalis could be administered more effectively in 7 of 12 patients; in 5 others the condition was unchanged. The addition of pacing to antiarrhythmic drugs effectively controlled recurrent ventricular arrhythmias associated with sinus bradycardia in three of four patients. In each patient, pacing alone was ineffective in controlling arrhythmias. In one patient, multiple premature ventricular contractions recurred despite pacing and adequate treatment with antiarrhythmic drugs. Pacemaker complications: The complications associated with permanent pacing are summarized in Table VII. They occurred in 9 of 52 patients, were recognized promptly and treated by appropriate measures. In two of the three patients with coronary sinus demand pacing, atrial pacing was abandoned after 2 days and 4 weeks, respectively, because of failure of the coronary sinus electrode to sense properly the QRS complex or failure to capture the atrium. The catheter was then introduced into the right ventricular apex for ventricular pacing. Discussion
The effects of pacing in patients wth sinoatrial disturbances causing syncope, congestive heart failure, ventricular tachycardia and brady-tachyarrhythmia
August 1973
The American Journal of CARDIOLOGY
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217
PACING FOR SINOATRIAL RHYTHM DISORDERS--CHOKSHI ET AL.
20' t-"
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Living
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Deceased
•.~ 15. o a_ o
lO,
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Z I--I 0.6
7.12
13.18
19-24
25.30
31-36
43-48
37-42
r-I 49-54
55-60
Follow-up in Months
syndrome will be discussed, including the possible mechanisms involved. Syncope: Since Muller and Finkelstein 9 reported in 1966 on the successful use of a permanent ventricular pacemaker in treatment of sinoatrial block producing syncope in a 29 year old woman, there has been growing interest in this technique. Syncopal episodes due to sinoatrial block have been successfully treated by permanent pacemaker therapy, lon~ and the follow-up data in these patients have extended from 18 months to 5 years, ix In our experience with a larger series of patients, 14 of 15 patients with syncope and 19 of 21 patients with dizzy spells had complete freedom from these symptoms after pacemaker implantation. One patient with syncope and one with dizzy spells were symptom-free for 50 and 13 months, respectively, after insertion of the pacemaker. Recurrence of symptoms in these patients was attributed to vascular insufficiency secondary to cerebral atherosclerosis. The cause of continued dizzy spells in a third patient, aged 86 years, could not be precisely explained. Inability of pacing to control these symptoms on a long-term basis in some patients, particularly older persons, is to be expected because of coexisting cerebrovascular insufficiency. Congestive h e a r t failure: There is little doubt that a slow ventricular rate may contribute to the
TABLE VII
Long-term Pacemaker Complications Ventricular
Pacing
218
Pacing Complications
(no. of patients)
Electrode displacement Raised threshold Fracture of electrode, proximal Myocardial perforation Infection at site of powerpack
1 1 1 2 2
August 1973
Coronary SinusPacing (no. of
patients) 2 0 0 0 0
The American Journal of CARDIOLOGY
61+
FIGURE 2. Survival and mortality data in 52 cases,
pathogenesis of congestive heart failure in patients with complete heart block. Dogs with experimentally produced complete heart block exhibit a reduction in cardiac output and decrease in myocardial contractility. 12 After ventricular pacing was instituted, cardiac output improved and heart failure lessened. Davidson et al. la reported that the condition of 16 of 20 patients with preexisting congestive heart failure was greatly improved after institution of pacing but that 26 patients (17 percent) first experienced heart failure after pacing had begun. Bernstein et al. 1~ found that pacing effectively controlled acute heart failure due to bradyarrhythmia; the same was not true for chronic congestive heart failure. They postulated that many of their patients with chronic failure had repeated episodes of myocardial damage with secondary fibrosis, leading to a relatively fixed stroke volume. Although the patients' condition improved transiently with temporary pacing, there was no lasting benefit from permanent pacing. Comparable experimental or clinical data are not available for congestive heart failure due to sinoatrial disturbances. Of the 12 patients in our study who had congestive heart failure, 7 had symptomatic improvement after pacemaker implantation. Failure of improvement or deterioration of symptoms occurred in the rest (5 patients). Deterioration of effort tolerance was related to worsening of the intrinsic heart disease due to development of acute myocardial infarction in one patient. In the remaining four patients, progressive deterioration may have been related to the presence of severe arteriosclerotic heart disease before pacemaker implantation (2 patients) or due to loss of atrial contribution to cardiac output (2 patients). Atrial contribution to cardiac output has been well demonstrated by Samet et al. ~5 Furthermore, compared to ventricular pacing, coronary sinus or atrial pacing results in a higher cardiac index. 16 However, before institution of permanent atrial or coronary sinus pacing, the integrity of the conduction system should be checked by His bundle recording and atrial pacing at various heart rates. On the basis of His bundle recordings, a new classification of heart block
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PACING FOR SINOATRIAL RHYTHM DISORDERS--CHOKSHI ET AL.
has been proposed. 17 All three degrees of atrioventricular block seen on~ the surface electrocardiogram may result from block within the atrioventricular node or His-Purkinje system or at multiple sites. If atrioventricular and His-Purkinje conduction are normal, and if atrial arrhythmias are absent, these patients with heart failure preferably should have a coronary sinus or atrial pacemaker. However, atrial pacing has many problems, namely, electrode displacement, high threshold and inadequate sensing. V e n t r i c u l a r t a c h y a r r h y t h m i a : Ventricular tachyarrhythmias not associated with sinus bradycardia but refractory to drug therapy have been successfully treated by the addition of permanent pacing. zs Suppression of these arrhythmias with pacingin patients without heart block z9 and in patients with sinus bradycardia or sinoatrial block 2° has been described. Only patients who had recurrent ventricular arrhythmia associated with sinus bradycardia are included in our report. Permanent pacing in conjunction with antiarrhythmic drugs abolished arrhythmia in three of four patients. Slowing of the heart rate to less than 60 beats/min may predispose to ventricular arrhythmias. 2~ The following mechanisms are proposed for beneficial effects of pacing in prevention of ventricular tachycardia: (1) Pacing produces overdrive suppression of ectopic foci. (2) Shortening of the refractory period and an increase in the vulnerable period threshold for ectopic impulses occur when the heart rate is increased. Han et al. 22 produced ectopic beats in experimental animals by coronary occlusion, sudden increase in aortic blood pressure and hypothermia. Under these conditions, the frequency of ectopic
beats was noted when the basic cycle length was 800 to 1,200 msec. When the basic cycle length was progressively decreased, the average time taken to induce ectopic beats was prolonged and the stimulus threshold increased. (3) Areas of asynchronous r e covery of excitability, and hence, areas of asynchronous conduction, are eliminated and ventricular fibrillation threshold is raised when the basic cycle length is decreased. 2s B r a d y - t a c h y a r r h y t h m i a syndrome: Treatment of the brady-tachyarrhythmia syndrome with drugs may present a difficult problem. Drugs like digitalis used to control supraventricular arrhythmia may cause bradycardia and drugs used to accelerate the heart rate, such as atropine or isoproterenol, may precipitate atrial or ventricular arrhythmias. All 11. patients in our series had marked symptomatic improvement with abolition of syncope (4 patients) or dizziness (4 patients). Alleviation of congestive heart failure was noted in three patients. Similar encouraging results have been noted by others, z°,24"26 Rubenstein et al. 26 noted that although electrical pacing was uniformly successful in treating symptoms of bradycardia, it was often disappointing in preventing tachycardia. In 2 of their 13 patients tachyarrhythmias were abolished with addition of pacing to the drug therapy, and pacing permitted more aggressive administration of antiarrhythmic drugs in 3 others. Tachyarrhythmias were abolished in 7 of our 11 patients; although 4 others continued to have such arrhythmias, digitalis could be administered more safely. All 11 patients in this group were receiving digitalis or antiarrhythmic drugs, or both, in addition to pacing.
• References
1. Rasmussen K: Chronic sinoatrial heart block. Amer Heart J 81:38-47, 1971 2. Eraut D, Shaw DB: Sinus bradycardia. Brit Heart J 33:742749, 1971 3. Birchfield RI, Meneffee EE, Bryants GDB: Disease of the sinoatrial node associated with bradycardia, syncope and paroxysmal atrial fibrillation. Circulation 16:20-26, 1957 4. Sanders CA: Heart block. In, Current Therapy (Conn HF, ed). Philadelphia, WB Saunders, 1971, p 149-151 5. Chardack WM: Heart block treated with an implantable pacemaker. Past experience and current developments. Progr Cardiovasc Dis 6:507-537, 1964 6. Scherlag BJ, Lau SH, Helfant RH, et al: Catheter technique for recording His bundle activity in man. Circulation 39:1318, 1969 7. Narula OS, Samet P, Javier RP: Significance of sinus-node recovery time. Circulation 45:140-158, 1972 8. Mandel W, Hayakawa H, Danzig R, et ah Evaluation of sinoatrial node function in man by overdrive suppression. Circulation 44:59-66, 1971 9. Muller OF, Finkelstein D: Adams-Stokes syndrome due to sinoatrial block. Amer J Cardio117:433-436, 1966 10. Easley RM, Goldstein S: Sinoatrial syncope. Amer J Med 50:166-177, 1971 11. Bayley TJ: Long-term ventricular pacing in treatment of sinoatrial block. Brit Med J 3:456-458, 1971
12. Brockman SK, Stoney WS: Congestive heart failure and cardiac output in heart block and during pacing. Ann NY Acad Sci 167:534-545, 1969 13. Davidson DM, Braak CA, Preston TA, et ah Permanent ventricular pacing. Effect on long-term survival, congestive heart failure, and subsequent myocardial infarction and stroke. Ann Intern Med 77:345-351, 1972 14. Bernstein V, Rotem E, Peretz D: Permanent pacemakers: 8 year follow-up study. Incidence and management of congestive heart failure and perforations. Ann Intern Med 74:361-369, 1971 15. Samet P, Bernstein WH, Nathan DA, et ah Atrial contribution to cardiac output in complete heart block. Amer J Cardio116:1-10, 1965 16. Befeler B, Hildner FJ, Javier RP, et al: Cardiovascular dynamics during coronary sinus, right atrial and right ventricular pacing. Amer Heart J 81:372-360, 1971 17. Narula OS, Scherlag BJ, Samet P, et ah Atrioventricular block. Localization and classification by His bundle recording. AmerJ Meal 50:146-165, 1971 18. Friedberg CK, Lyon W, Denoso E: Suppression of refractory recurrent ventricular tachycardia by transvenous rapid cardiac pacing and antiarrhythmic drugs. Amer Heart J 79:44-50, 1970 19. Sowton E, Leatham A, Carson P: The suppression of arrhythmias by artificial pacemaking. Lancet 2:1098-1100,
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PACING FOR SINOATRIAL RHYTHM DISORDERS--CHOKSHI ET AL.
1964 20. Sand¢e E, Flensted-Jensen E: Adams-Stokes seizures in patients with attacks of both tachy- and bradycardia, a therapeutic challenge. Acta Med Scand 186:111-116, 1969 21. Zoll PM, Linenthal AJ, Zarsky LRN: Ventricular fibrillation. Treatment and prevention by external cardiac currents. New EngJ Med 262:105-112, 1960 22. Han J, DeTraglia J, Millet D, et ah Incidence of ectopic beats as a function of basic rate in the ventricle. Amer Heart J 72:632-639, 1966 23. Han J, Millet D, Chizzonitti B, et ah Temporal dispersion of
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recovery of excitability in atrium and ventricle as a function of heart rate. Amer Heart J 71:481-487, 1966 24. Cheng TO: Transvenous ventricular pacing in the treatment of paroxysmal atrial tachyarrhythmias alternating with sinus bradycardia and standstill. Amer J Cardiol 22:874-879, 1968 25. Escher EJW, Furman S: Pacemaker therapy for chronic rhythm disorders. Progr Cardiovasc Dis 14:459-472, 1972 26. Rubenstein JJ, Schulman CL, Yurchack PM, et ah Clinical spectrum of the sick sinus syndrome. Circulation 46:5-13, 1972
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