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The stampede to stimulation—numerators and denominators revisited relative to electrophysiologic study of ventricular arrhythmias
EDITORIALS
The stampede to stimulation-numerators denominators revisited relative to electrophysiologic study of ventricular arrhythmias
and
Thomas B. Graboys, M.D. Boston, Mass. Advances in technology continue to exceed understanding of specific clinical problems. Among persons exhibiting ventricular arrhythmia, there has been an avalanche of interest in the use of electrophysiologic testing to aid the management of patients with a variety of symptoms and degrees of ectopic activity. Indeed, one recent issue of a journal distributed widely to primary care physicians listed centers which are now geared to the “electrophysiologic care” of your patient with ventricular arrhythmia.’ Further, they requested additional listings lest some center had been accidently omitted. The medical literature burgeons with an array of seductive studies espousing this technique. Only a few reports have questioned the significance of evoked responses.*,” We stand both befuddled and bewildered. The implications of this technology are quite simple: the fully trained cardiologist or internist is not equipped to manage his or her patient’s “serious” arrhythmia (? defined). Hence patients should be referred to the major medical center experienced in these procedures. The option, of course, is to develop an electrophysiologic laboratory in one’s own hospital-a present occurrence in several community hospitals throughout New England. The situation becomes increasingly muddled when one considers the issue of third party payment. Once a technology becomes a component of “standard care” in the community, fee for service comes fast and furious with complete procedural decontrol. Years ago, Spodick’s4 plaintive cry of “numerators in search of denominators” in regard to myocardial revascularization went all but unheeded. Likewise, Frcrm the Cardiovascular Laboratory, Harvard School of Public Health and the Cardiovascular Division, Brigham and Women’s Hospital. Received for publication Jan. 18, 19X2; accepted Feb. 12, 1982. Reprint requests: Thomas B. Graboys, M.D., Harvard Medical School, 665 Huntington Ave.. Boston. MA O“115. 0002-8703/82/061089
+ 02$00.20/O
0 1982 The
C. V. Mosby
Co.
Phibbs5 in a 1979 Sounding Board piece raised the specter of performance abuse related to coronary arteriography. Do we face a similar issue again? Irrespective of the fact that those centers engaged primarily in electrophysiologic testing have a strong vested interest (and thus there must be a measure of a prophecy self-fulfilled), a number of legitimate queries (delineated below) are apparent at this juncture. (1) What are the numerators and denominators of patients undergoing programmed stimulation techniques (PST); i.e., in what fraction of asymptomatic normals ot coronary patients (with and without overt arrhythmia) can ventricular tachycardia (VT) be induced? And what is the follow-up of such persons? (2) What should be the endpoints of PST: sustained VT, nonsustained VT, or the repetitive ventricular response (RVR)? (3) Which is the most effective (and least dangerous) stimulation protocol to follow? (4) If PST provokes VT or ventricular fibrillation in an asymptomatic patient with complex ventricular premature beats (VPBs), is chronic antiarrhythmic therapy required? And if so, for how long? (5) What fraction of patients with known lifethreatening arrhythmia require PST, or can an antiarrhythmic drug program be defined by the use of ambulatory ECG recordings and exercise stress testing? (6) What is the significance of inducible sustained (or nonsustained) VT in the patient whose ambient VPBs have been abolished by antiarrhythmic drugs? (7) Among patients with a high density of frequent and repetitive VPBs, does continued induction of VT by PST carry the same risk as for the patient in whom this testing was carried out because of a dearth of ambient ectopy? (8) Finally, how do we fathom from the medical literature the meaning, if any, of the above questions when the centers reporting are tertiary referral institutions whose populations (and thus data) are 1089
June. 1982
Gra boy
skewed, and do not reflect the majority of patients seen by the local practitioner? Before we again become enamored with as yet another technology that is both invasive and costly; before we remove the patient from the core of patient care-the local physician; before pronouncements from the academic centers intimate (and intimidate) that “quality” care mandates electrophysiologic testing for the patient with syncope and manifest or occult dysrhythmia, let us call for a rational systematic approach to this procedure in an attempt to once again answer the numerator-denominator issue.
American
Heart Journal
REFERENCES
‘raking 1hi guesswork out 01’ ant.iarrhythmics. Emergency hled September, 19X1, p 27. Games ,JA, Kang P, Khan R, Kelen G, El-Sherif N: Repetitive ventricular response. Its incidence, inducibility, reproducibility mechanism and significance. Br Heart J 46:159, 1981. Naccarelli GV, Prystowsky EN, Jackman WM, Heger JJ, Rinkenberger RL, Zipes D: Repetitive ventricular response. Prevalence and prognostic significance. Br Heart J 46:152, 1981. Splldick 1)ti: rie~~lxc,ularization 01’ the heart-~ numerators in hearch of tl~nofnitlatl)rs. AM H-FXR’I,
Ventricular tachycardia inititated by late-coupled ventricular extrasystoles: The concept of longitudinal dissociation in the microreentry pathway §hinji Kinoshita, M.D., Yasumichi Kato, M.D., Takeshi Kawasaki, Katsushi Okimori, M.T. Sapporo, Japan
Since the concept of ventricular vulnerability was first shown in animal models by Wiggers and Wegria,’ the mechanism of close-coupled ventricular extrasystoles (PVCs) interrupting the antecedent T wave (the R-on-T phenomenon) has been considered to initiate ventricular tachycardia (VT) and fibrillation.*-” However, selected recent reports in postacute myocardial infarction patients6m’” have shown that late-coupled PVCs may also initiate VT. In the present communication, we suggest a mechanism by which late-coupled PVCs might produce such VT on the basis of observations in patients of ours and other investigators. Microreentry as a mechanism of VT. Recent investi-
From the Second Department (11’Medicine, Hukkaido University School of Medicine; the Department of Medicine. Sapporo Teishin Hospital; and the Department of Medical Technology. Sapporo District General Hospital. Japan Ground Self-defense Fwce. Received for publication Aug. 24. 1’381; revision received ,lan. 4. 198% accepted Feb. 12. 198’. Reprint requests: Shinji Kimrbhlta. M.D., Second Department of Medicine. Hokkaido University. Schwl <,t’ Medicine. Sapporo, .Japan.
1090
M.D., and
utilizing intracardiac stimulation and recording techniques suggested that most recurrent VT can be reproducibly initiated and/or terminated by programmed electrical stimulation (PES). Thus the mechanism of many episodes of VT is thought to be reentry. Furthermore, studies by Josephson et a1.1g,2”showed that the proximal His-Purkinje system was not required for initiation or maintenance of VT, and that ventricular capture by premature depolarizations or PES frequently failed to terminate the tachycardia. These observations suggest that the reentrant circuit for VT may be localized to a very small area within the ventricles. Fig. 1 shows parts of a continuous recording from a 20-year-old man without organic heart disease. This patient was not undergoing antiarrhythmic therapy during the recording. In Fig. 1, late-coupled PVCs initiate short runs of VT. In a short run of VT initiated by the extrasystole E, (the upper strip), the second ectopic impulse, (E,), fails to become manifest; nevertheless, the tachycardia is maintained. Such failure in occurrence of the ectopic beat without terminating the VT suggests that the site of reentry for the tachycargationsl:.”
000%87o3/82/061090
+ 06$00.60/0
r 1982 The
C.
V. Mosby
Co.
The stampede to stimulation-numerators denominators revisited relative to electrophysiologic study of ventricular arrhythmias
and
Thomas B. Graboys, M.D. Boston, Mass. Advances in technology continue to exceed understanding of specific clinical problems. Among persons exhibiting ventricular arrhythmia, there has been an avalanche of interest in the use of electrophysiologic testing to aid the management of patients with a variety of symptoms and degrees of ectopic activity. Indeed, one recent issue of a journal distributed widely to primary care physicians listed centers which are now geared to the “electrophysiologic care” of your patient with ventricular arrhythmia.’ Further, they requested additional listings lest some center had been accidently omitted. The medical literature burgeons with an array of seductive studies espousing this technique. Only a few reports have questioned the significance of evoked responses.*,” We stand both befuddled and bewildered. The implications of this technology are quite simple: the fully trained cardiologist or internist is not equipped to manage his or her patient’s “serious” arrhythmia (? defined). Hence patients should be referred to the major medical center experienced in these procedures. The option, of course, is to develop an electrophysiologic laboratory in one’s own hospital-a present occurrence in several community hospitals throughout New England. The situation becomes increasingly muddled when one considers the issue of third party payment. Once a technology becomes a component of “standard care” in the community, fee for service comes fast and furious with complete procedural decontrol. Years ago, Spodick’s4 plaintive cry of “numerators in search of denominators” in regard to myocardial revascularization went all but unheeded. Likewise, Frcrm the Cardiovascular Laboratory, Harvard School of Public Health and the Cardiovascular Division, Brigham and Women’s Hospital. Received for publication Jan. 18, 19X2; accepted Feb. 12, 1982. Reprint requests: Thomas B. Graboys, M.D., Harvard Medical School, 665 Huntington Ave.. Boston. MA O“115. 0002-8703/82/061089
+ 02$00.20/O
0 1982 The
C. V. Mosby
Co.
Phibbs5 in a 1979 Sounding Board piece raised the specter of performance abuse related to coronary arteriography. Do we face a similar issue again? Irrespective of the fact that those centers engaged primarily in electrophysiologic testing have a strong vested interest (and thus there must be a measure of a prophecy self-fulfilled), a number of legitimate queries (delineated below) are apparent at this juncture. (1) What are the numerators and denominators of patients undergoing programmed stimulation techniques (PST); i.e., in what fraction of asymptomatic normals ot coronary patients (with and without overt arrhythmia) can ventricular tachycardia (VT) be induced? And what is the follow-up of such persons? (2) What should be the endpoints of PST: sustained VT, nonsustained VT, or the repetitive ventricular response (RVR)? (3) Which is the most effective (and least dangerous) stimulation protocol to follow? (4) If PST provokes VT or ventricular fibrillation in an asymptomatic patient with complex ventricular premature beats (VPBs), is chronic antiarrhythmic therapy required? And if so, for how long? (5) What fraction of patients with known lifethreatening arrhythmia require PST, or can an antiarrhythmic drug program be defined by the use of ambulatory ECG recordings and exercise stress testing? (6) What is the significance of inducible sustained (or nonsustained) VT in the patient whose ambient VPBs have been abolished by antiarrhythmic drugs? (7) Among patients with a high density of frequent and repetitive VPBs, does continued induction of VT by PST carry the same risk as for the patient in whom this testing was carried out because of a dearth of ambient ectopy? (8) Finally, how do we fathom from the medical literature the meaning, if any, of the above questions when the centers reporting are tertiary referral institutions whose populations (and thus data) are 1089
June. 1982
Gra boy
skewed, and do not reflect the majority of patients seen by the local practitioner? Before we again become enamored with as yet another technology that is both invasive and costly; before we remove the patient from the core of patient care-the local physician; before pronouncements from the academic centers intimate (and intimidate) that “quality” care mandates electrophysiologic testing for the patient with syncope and manifest or occult dysrhythmia, let us call for a rational systematic approach to this procedure in an attempt to once again answer the numerator-denominator issue.
American
Heart Journal
REFERENCES
‘raking 1hi guesswork out 01’ ant.iarrhythmics. Emergency hled September, 19X1, p 27. Games ,JA, Kang P, Khan R, Kelen G, El-Sherif N: Repetitive ventricular response. Its incidence, inducibility, reproducibility mechanism and significance. Br Heart J 46:159, 1981. Naccarelli GV, Prystowsky EN, Jackman WM, Heger JJ, Rinkenberger RL, Zipes D: Repetitive ventricular response. Prevalence and prognostic significance. Br Heart J 46:152, 1981. Splldick 1)ti: rie~~lxc,ularization 01’ the heart-~ numerators in hearch of tl~nofnitlatl)rs. AM H-FXR’I,
Ventricular tachycardia inititated by late-coupled ventricular extrasystoles: The concept of longitudinal dissociation in the microreentry pathway §hinji Kinoshita, M.D., Yasumichi Kato, M.D., Takeshi Kawasaki, Katsushi Okimori, M.T. Sapporo, Japan
Since the concept of ventricular vulnerability was first shown in animal models by Wiggers and Wegria,’ the mechanism of close-coupled ventricular extrasystoles (PVCs) interrupting the antecedent T wave (the R-on-T phenomenon) has been considered to initiate ventricular tachycardia (VT) and fibrillation.*-” However, selected recent reports in postacute myocardial infarction patients6m’” have shown that late-coupled PVCs may also initiate VT. In the present communication, we suggest a mechanism by which late-coupled PVCs might produce such VT on the basis of observations in patients of ours and other investigators. Microreentry as a mechanism of VT. Recent investi-
From the Second Department (11’Medicine, Hukkaido University School of Medicine; the Department of Medicine. Sapporo Teishin Hospital; and the Department of Medical Technology. Sapporo District General Hospital. Japan Ground Self-defense Fwce. Received for publication Aug. 24. 1’381; revision received ,lan. 4. 198% accepted Feb. 12. 198’. Reprint requests: Shinji Kimrbhlta. M.D., Second Department of Medicine. Hokkaido University. Schwl <,t’ Medicine. Sapporo, .Japan.
1090
M.D., and
utilizing intracardiac stimulation and recording techniques suggested that most recurrent VT can be reproducibly initiated and/or terminated by programmed electrical stimulation (PES). Thus the mechanism of many episodes of VT is thought to be reentry. Furthermore, studies by Josephson et a1.1g,2”showed that the proximal His-Purkinje system was not required for initiation or maintenance of VT, and that ventricular capture by premature depolarizations or PES frequently failed to terminate the tachycardia. These observations suggest that the reentrant circuit for VT may be localized to a very small area within the ventricles. Fig. 1 shows parts of a continuous recording from a 20-year-old man without organic heart disease. This patient was not undergoing antiarrhythmic therapy during the recording. In Fig. 1, late-coupled PVCs initiate short runs of VT. In a short run of VT initiated by the extrasystole E, (the upper strip), the second ectopic impulse, (E,), fails to become manifest; nevertheless, the tachycardia is maintained. Such failure in occurrence of the ectopic beat without terminating the VT suggests that the site of reentry for the tachycargationsl:.”
000%87o3/82/061090
+ 06$00.60/0
r 1982 The
C.
V. Mosby
Co.