Table of Contents
Significant Events in the 1970s:
- 1973: U.S. withdraws from the war in Vietnam.
- 1974: Culmination of the Watergate scandal; Richard Nixon resigns as President.
- 1976: President Gerald Ford signs into law the Medical Device Amendments empowering the Food & Drug Administration (FDA) to regulate medical devices.
- 1977: First report of percutaneous transluminal coronary angioplasty, (Andreas Gruntzig, Zurich, Switzerland).
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Treatment of Supraventricular Tachycardia with Inductive Radiofrequency Pacemaker and Surgical Treatment of Wolff-Parkinson-White Syndrome 
We made two sets of inductive radiofrequency pacemakers for treatment of supraventricular tachycardias and applied them to clinical patients in 1969. (1) The first one was a button type receiver (upper panel) and larger size transmitter. The other set consisted of a disc type receiver attached to venous atrial catheter electrodes and a smaller hand-held transmitter (middle panel). The latter was preferred, and 130 sets were used throughout Japan and a few in Europe. When the supraventrocular tachycardias appear, the patient initiates the transmitter for a few seconds and terminates the tachycardia by himself (lower panel).
Iwa T, Abe H, Sugiki K, Wada J: Treatment of supraventricular tachycardia with inductive radiofrequency atrial stimulation. Progress in Medicine (Igaku no Ayumi, in Japanese), 74: 372-4, 1970.
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The Bilitch Report - Performance of Implantable Cardiac Rhythm Management Devices 
Reports1 and new data gathered2, relative to recalls and safety alerts involving pacemakers and ICDs referenced the now ended Bilitch report which was initiated in 1974 by Michael Bilitch, and two colleagues in response to a Food and Drug Administration RFP. Bilitch had studied pacemakers from the Los Angeles coroner's office to ascertain whether malfunction was related to death. Newark Beth Israel Medical Center and Montefiore Medical Center had independently maintained hospital based computerized patient and device databases including the pulse generators and leads used. It was possible to track and determine the relative quality of the devices and modify usage for patient benefit. The coauthors lectured about the data and practices, frequently sharing the podium and had discussed pooling the data. The RFP provided that opportunity. Data publication had been episodic by competitive manuscripts but continuous publication occurred with the founding of the journal Pacing and Clinical Electrophysiology (PACE), when cumulative longevity of specifically named pulse generators with both numerator and denominator of the sample became possible. The report was eagerly anticipated by physicians and industry, which occasionally contested and inquired about specific data and competitive comparisons. Ten additional centers were added and Susan Song RN, who worked with Bilitch, came to manage the database and coordinate contributions. After Bilitch's 1987 death, the report was renamed in his honor with Song as the first author of each publication. The FDA progressively reduced and then ended its support as it established regulatory authority to compel industry to provide reports on defective devices. The registry continued, supported by the investigators while we unsuccessfully importuned government and industry to provide modest support. By 1993 the unfunded effort was no longer sustainable. Data collection ended December 31, 1993 with a final publication in PACE of the cumulative data in April 19943. Since then all data, during vast device changes has come from industry only. The North American Society of Pacing and Electrophysiology (NASPE) attempted to start a registry, but funding was unavailable. Robert G. Hauser, with funding from the Minneapolis Heart Institute, established an internet based registry deriving data from fifteen institutions and has published valuable data concerning substandard device performance.4 An immensely valuable registry of every pacemaker, ICD and lead implanted in Denmark, with identical internationally available hardware, is now also available.5 Possibly, after an interval of seven years, independent information about device quality has become a reality once again.
1Maisel WH, Sweeney MO, Stevenson WG, Ellison KE, Epstein LM. Recalls and safety alerts involving pacemakers and implantable cardioverter-defibrillator generators. JAMA 2001;286:793-799. 2Eagle KA. Safety Alerts involving device therapy for arrhythmias. JAMA 2001;286:843-844.
3Song SL. The Bilitch Report: Performance of Implantable Cardiac Rhythm Management Devices. PACE 1994;17:692-708.
4Hauser RG, Hayes DL, Almquist AK, Epstein AE, Parsonnet V, Tyers GFO, Vlay SC, Schoenfeld MH. Unexpected ICD Pulse Generator Failure Due to Electronic Circuit Damage Caused by Electrical Overstress. PACE 2001;24:1046-1054.
5Moller M, Arnsbro P. Danish Pacemaker and ICD Register. PACE 2000;23:S2-S92.
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Ventricular Fibrillation: A Possible Mechanism of Sudden Death in Patients with WPW Syndrome 
This series of EKGs was the first demonstration of the onset of ventricular fibrillation in a 63 year old individual with WPW syndrome and atrial fibrillation. The patient had received a large dose of digoxin in an attempt to control the ventricular rate in the presence of atrial fibrillation. The case illustrated ventricular vulnerability associated with a short refractory period of the bypass tract and the danger of digitalis in the presence of WPW syndrome. Histology revealed three discrete bypass tracts. Later research led to ablative techniques to protect these individuals from ventricular fibrillation.
Leonard S. Driefus, MD, Robert Haiat, MD, Yoshio Watanabe, MD, Jaime Arriga, MD and Norman Reinman, MD, Circulation 1971; 18:520-527 Back to Top
Bundle Activity During the Spontaneous and Stimulated Onset of SVT His bundle activity during the spontaneous and stimulated onset of SVT.The format is the same as in figure 2.
A. During sinus rhythm, the A-H interval is 90 msec and the H-V interval, 45 msec. A spontaneous APD arises 300 msec after the sinoatrial beat, indicated by the vertical bar. The APD falls within the effective A-V nodal refractory period and fails to conduct to the His bundle or ventricle. Nonetheless, prolonged conduction within the A-V node results in a reentrant atrial beat 440 msec later. Only a single atrial echo results, because the A-H interval of the reentrant beat (95 msec) is not prolonged sufficiently for reentry to continue. Sinus rhythm resumes.
B. A spontaneous APD at a longer interval (340 msec) still falls within the A-V nodal effective refractory period (fails to reach the His bundle). Atrial reentry occurs 350 msec after the APD.The shorter interval between the APD and the first beat of SVT results in prolonged A-V nodal conduction of the atrial reentrant beat (A-H interval, 120 msec). Reentry continues as SVT.
C. During atrial pacing a stimulated APD 285 msec after the atrial paced beat fails to conduct to the His bundle, and SVT is initiated. A stimulus 445 msec after the first reentrant beat depolarizes the atrium 5 to 15 msec earlier than expected, but reentry is maintained, and SVT continues.
Circulation 1971; 43:15-26. BIGGER, JT
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Initiation and Termination of Ventricular Tachycardia 
The figure is from the article in which it was shown that clinically documented ventricular tachycardia could reproducibly be initiated and terminated by appropriately timed stimuli during programmed electrical stimulation of the heart.
This article was the basis for subsequent development like mapping, drug evaluation, surgical treatment and catheter ablation of ventricular tachycardia.
Hein J. Wellens, Reiner M. Schuillenburg, Dirk Durrer: Electrical stimulation of the heart in patients with ventricular tachycardia. Circulation 1972; 46: 216-26
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Automatic Threshold Adaptation 
The conception of a pacing system capable of automatic adaptation of the pacing threshold emanated from an effort to conserve power by keeping the long pulse amplitude at the lowest supraliminal level associated with reliable capture. A fixed rate prototype pulse generator was constructed, capable of delivering various pacing voltages controlled by a logical system based on the sensing of an evoked ventricular response. Automatic activation of the control system caused a stepwise decrease in pulse amplitude until loss of capture, at which point the pacing pulse reset itself above threshold. Short-term studies performed in 23 patients confirmed the safety and efficacy of the system. This was Dr. Mugica’s first publication in the field of cardiac pacing.
Mugica J, Lazarus B, Buffet J, Catte M, Pacemaker with automatic adaptation to the pacing threshold. In "Cardic Pacing", Thalen HJT, Editor. Van Gorcum & Comp. B.V. Assen, The Netherlands, Publisher. 1973: 150-155.
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Re-entry within the HPS and the A-V Node 
The basic ventricular cycle length is 700 msec, panel A to D. In panel A, S2 conducts retrogradely with an S2A2 interval of 270 msec and is followed by a ventricular beat with a normal QRS complex. The ventricular activation is preceded by a normal H-V interval of 40 msec and a low to high sequence of atrial activation which suggest A-V nodal re-entry as the underlying mechanism responsible for the origin of this beat. At a closer coupling interval (panel B), S2 blocks in the A-V node (the retrograde His bundle potential emerges from the ventricular electrogram and is not followed by an atrial electrogram) and A-V node re-entry is abolished. At still closer coupling interval of 270 msec (panelC), S2 continues to block in the A-V node and is followed by another beat of ventricular origin (V3). (D) S2 impulse resumes conduction to the atria and encounters both His-Purkinje and A-V nodal delay and results in both V3 interval of 55 msec. A-V nodal re-entrant beats are indicated by asterisks both in panel A and D. In panel D the QRS complex shows a left bundle branch block pattern and is preceded by an H-V interval of 55. This type of aberrancy can be explained if one assumes that V3 either penetrated the left bundle branch system which was found refractory by the A-V nodal re-entrant impulse, or simply that the left bundle branch system had a longer recovery time.
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Interference Effect of Myopotentials on Function of Unipolar Demand Pacemakers A systematic study of all our patients with unipolar pacemakers and pacemaker rhythm (33 out of 44 patients in 1972) demonstrated pacemaker inhibition in 28 of the 33 patients (85 %). The study was performed by recording electromyograms directly from the pectoralis major muscle underlying the pulse generator and in intercostal muscle simultaneously with an ECG. The patients were examined in the supine position with the arm abducted without underlying support, on the side in which the pulse generator was implanted. By putting weights in the patient's hand, an isometric contraction of the pectoral muscle was achieved. Lifting from 2 to 6 kg was often sufficient to produce pacemaker inhibition (Figs). The highest myopotential recorded was 3.2 mV, which was beyond the R-wave sensitivity of the actual pacemakers used (1.5-2.5 mV).
 |
| Figures 1 + 2 |
This problem can now be overcome by using bipolar leads or decreasing pulse generator sensitivity by non-invasive programming.
Ohm OJ, Bruland H, Pedersen OM, Waerness E. Interference Effect of Myopotentials on Function of Unipolar Demand Pacemakers. Brit Heart J, 1974;36:77-84.
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Electrophysiologic and Pathologic Correlations of Chronic Second Degree Atrioventricular Block with Left Bundle Branch Block
A 78 year old male with a history of hypertension and congestive heart failure had type II 2:1 2 AV block with left bundle branch lock. Electrophysiologically the site of block was distal to the His bundle recording site and there was a prolonged A-H interval (145 msec) (fig. 1). Pathologically, there was marked fibrosis of the AV node and severe involvement of both bundle branches (fig. 2a and 2b). The changes distal to the His bundle were more severe than the changes proximal to the His bundle. This study demonstrates that the electrophysiologic data more closely approximated the pathologic findings than did the surface electrocardiographic data alone. It also emphasizes that there may be multiple sites of disease in chronic 2 block with left bundle branch block.  |  |
| Figure 2a. | Figure 2b. |
Bharati S, Lev M, Dhingra RC, Chuquimia R, Towne WD, Rosen KM: Electrophysiologic and Pathologic Correlations in Two Cases of Chronic Second Degree Atrioventricular Block with Left Bundle Branch Block. Circulation 52 (2): 221-229, 1975.
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Epicardial Mapping in Ventricular Tachycardia 
Epsilon wave is the ECG expression of delayed potentials (post-excitation) originally observed on the epicardium of patients with resistant VT. It is the result of a parietal block which could be independent but sometimes combined with a various degree of RBBB. In that case, prolongation of QRS complex in the leads VI to V3 is wider than in V6.The tracing was recorded in a would be pilot, age 27, who experienced some episodes of palpitations.
(Referred by Dr Faouzi Touil, Paris) I. Fontaine G, Guiraudon G, Frank R,Vedel J, Grosgogeat Y, Cabrol C,Facquet J,: Stimulation Studies and Epicardial Mapping in Ventricular Tachycardia: Study of Mechanisms and Selection for Surgery. In- Reentrant Arrhythmias - Kulbertus H.E. Ed MTP Pub. Lancaster 1977:P.334-350
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Overdrive pacing in the WPW syndrome 
In all patients with either spontaneous or induced SVT every episode could be rapidly (<60 seconds) terminated by high right atrial, coronary sinus or right ventricular overdrive pacing. The overdrive rate was > 10% above the basal tachycardia rate. Implantable. The above results prompted the design of an implantable pacemaker for use in WPW patients with medically uncontrollable SVT. A bipolar J-shaped electrode is implanted in the right atrial appendage by the transvenous route. The unit, magnetically activated by the patient during a tachycardia, delivers stimuli at a progressively increasing frequency (150-300 beats/min) over a maximum period of 2 minutes. It can be prematurely deactivated by removing the magnet. This unit has been implanted in a 25-year-old female WPW patient with intractable SVT. The unit has functioned successfully over a 9-month period and has been used as many as 5 times/day. The presence of recurrent SVT in the WPW syndrome unresponsive to medical management has, in the recent past, been managed only by surgical approaches. The ability to rapidly terminate SVT with overdrive, utilize permanent transvenous atrial pacing and design new pacemaker circuitry has led to the development of the implantable unit described in this report. The potential benefits of this method are clear in that a limited surgical procedure with low morbidity may be realized for successful management of a previously unmanageable patient. A noncontinuous record showing the onset of supraventricular tachycardia and its termination by the implanted atrial scanning pacemaker unit. In the first strip, sinus rhythm with prominent delta waves is noted. Subsequently, supraventricular tachycardia is initiated by a premature atrial systole. The second strip shows the initiation of artificial atrial pacing at progressively increasing heart rates.The third strip shows the termination of the tachycardia followed by 1:1 anterograde conduction across the bypass tract. With termination of the atrial pacing, restoration of sinus rhythm is observed.
Mandel WJ,Yamaguchi I, Laks M, Berkovits B. The use of overdrive pacing for termination of tachycardia episodes in the Wolff-Parkinson-White (WPW) syndrome. Cardiac Pacing:ProcV International Symposium.Tokyo,1976.YoshioWatanabe,Ed.Excerpta Medica, 1977; 162-165.
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Tachycardia Terminated by bursts of Rapid Ventricular Pacing 
Recurrent ventricular tachycardia can be terminated by bursts of rapid ventricular pacing. This patient sustained ventricular tachycardia, briefly hemodynamicallywell tolerated. She was managed with an implanted burst pacemaker activated by application of a magnet always available, carried and supported by a necklace, so that it was instantly accessible. During preliminary evaluation different rates and duration of pacing bursts were tested for effectiveness. Above-The burst converts, but does not terminate the tachycardia. Middle-The burst converts the tachycardia to a conducted rhythm.Below-The tachycardia is terminated. Fisher JD et al.Termination of ventricular tachycardia with bursts of rapid ventricular pacing.
Fisher JD, et al. Am J Cardiol 1978;41:94-102
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