Determinants of outcome in patients with sustained ventricular tachyarrhythmias: The Antiarrhythmics Versus Implantable Defibrillators (AVID) Study Registry Sergio L. Pinski, MD, Qing Yao, PhD, Andrew E. Epstein, MD, Scott Lancaster, MS, H. Leon Greene, MD, Antonio Pacifico, MD, James R. Cook, MD, Ram Jadonath, MD, Roger A. Marinchak, MD, and the AVID Investigators* Clznkago, I@ Seat&, Wash; L3irmingha~ Ala; Houston, Te.q Sprin@ek& Mass; Manbasset, m and Phihdelphia, Pa

Background The prognosis of patients with sustained ventricular tachyarrhythmias varies according to clinical charac-

teristics. We sought to identify predictors of survival in a large population of patients with documented sustained ventricular

tachyarrhythmias not related to reversible or correctable causes included in the Antiarrhythmics Versus Implantable Defibril-

lators (AVID) Registry.

Methods and Results w e analyzed the impact of 36 demographic, clinical, and discharge treatment variables

on the outcome for 3559 patients. Survival status was assessed with the use of the National Death Index. Multivariate analy-

ses were performed with the use of the Cox proportional hazards model. After a mean follow-up of 17 f 12 months, 63 1

patients died. Actuarial survival was 0.86 (95% confidence interval [Cl] 0.85 to 0.88), 0.79 (95% Cl 0.78 to 0.8 1 ), and

0.72 (95% Cl 0.70 to 0.74) at 1, 2, and 3 years. Multivariate predictors of worse survival included older age, severe left

ventricular dysfunction, lower systolic blood pressure, history of congestive heart failure, diabetes, smoking or atrial fibrilla-

tion, and preexistent pacemaker. The hemodynamic impact of the qualifying arrhythmia was not a predictor of outcome.

Defibrillator implantation and hospital discharge while the patient was taking a (3-bl oc k er or an angiotensin-converting

enzyme inhibitor were associated with better prognosis.

Conclusions Despite therapeutic advances, the mortality rates of patients with sustained ventricular tachyarrhythmias

remain high. Prognosis depends on the severity of underlying heart disease, as reflected by the extent of left ventricular dys-

function and the presence of heart failure. Well-tolerated ventricular tachycardia in patients with structural heart disease

does not carry a significantly better prognosis than ventricular tachyarrhythmia with more severe hemodynamic conse-

quences. (Am Heart J 2000;139:804-13.)

Neither the natural history nor the treatment-modified outcome of patients with sustained ventricular tachy- arrhythmias is well established. Patients with these arrhythmias constitute a heterogeneous population in regard to substrate, clinical manifestations, response to therapy, and prognosis. Prior relatively small studies in selected populations have identified age,‘.’ type of

From Rush-Presbytenon-St Luke’s Medical Center; University of Woshmgton; Unwer. sity of Alabomo; Texas Arrhyfhmm Instrtute; Boystote MedIcal Center; North Shore Unwersity Hospital; and Lonkenou Hosprtol. Supported by o contract (NOI-HC-25 I 17) wth the Notional Heart, Lung, and Blood Institute, Bethesda, Md. Presented in port 01 the 70th Scentrhc Sewons of the Amencon Heart Assoc~ot~on, Orlondo, Ho, November 1997. ‘Institutions and inveshgators portupoting ,n the regatry ore hsted ,n the Appendu

SubmItted June 9, 1999; accepted October 2 1, 1999. Reprint requests: Sergio L. Pmski, MD, Rush-Presbytwan-St luke’s Medical Center, 1750 W Harrison St, JS IO9 I, Chlcogo, It 606 12. E-mail: spinrkiBrush.edu

Copyright 0 2000 by Mosby, Inc. 0002.8703/2000/$12.00 + 0 4/l/103844

doi:lO. 1067/mhj 2000.103844

structural heart disease,? severity of congestive heart failure,+’ hemodynamic consequence of the arrhythmia, severity of left ventricular dysfunction,x,9 and the results of programmed electrical stimulation during treatment with antiarrhythmic drugs as prognostic factors in patients with sustained ventricular tachyarrhythmias.

During the past few years, antiarrhythmic strategies for patients with these arrhythmias have changed dra- matically. Class I antiarrhythmic agentsto and direct arrhythmia surgery’ t have been largely replaced by implantable cardioverterdefibrilillators (ICDs),t2 catheter ablation,t3 amiodarone,ti and sotalokts Patients with heart disease in general have also benefited from wider use of angiotensin-converting enzyme (ACE) inhibitorst” P-blockerst’ aspirin, t* cholesterol-lowering drugs,t” and improved surgical”) and percutaneous2t revascular- ization techniques.

In this registry study, we assessed the intluence of easily obtained baseline clinical variables on outcome in a large prospective cohort of unselected patients under-

Pinski et al 805

Table I. Baseline characteristics OF study patients

All patients (n=3559)

No ICD ICD (n= 1931) (n = 1628) P value

Age iv) Male White race Currentsmakers Heart disease lschemic

Nonischemic cardiomyopathy Hypertrophic cardiomyopathy Valvular Other None

LVEF’ Systolic blood pressure (mm Hg) Diastolic blood pressure (mm Hg) Heart rate (beats/min) Clinical presentation

Cardiac arrest VT with syncope VT with severe symptoms but no syncope Vl with mild or no symptoms

History of hypertension History of diabetes History of congestive heart failure History of atrial fibrillation History of myocordial infarction History of syncope History of VT History of VF History of prior cardiovascular procedures History of prior myocardial revascularization History of prior cardiac valve repair or replacement Antiarrhythmic drugs at time of index arrhyihmia

6Ak 12 2704 (76) 3132 (88)

681 (19)

2704 (76) 479(13)

123 (3) 325 (9) 255 (7) 217(6) 3Ak 15

121 + 18 69+11 73+13

1399 (39) 598 (17)

1065 (30) 497(14)

1747 (49) 740 (21)

1458141) 870 (24)

2091 (59) 378 (1 1) 687(19)

173 (5) 1474 (Al) 1161 (33)

183 (5) 597 (17)

65f12 63f 12 1455 (75) 1249 (77) 1665 (86) 1467(90)

362 (19) 319(20)

1457(75) 243 (13)

77 (41 182 (9) 133 (7) 13917)

3Ak 15 121f19

69+ 11 71f13

1247 (77) 236 (14)

A6 (31 143 (9) 122 (7)

78 (5) 33flA

120+17 68&11 75+13

656 (34) 345 (18) 567 (29) 363 (19) 973 (50) A20 (22) 787 (Al) 505 (26)

1086(56) 220 (11) 380 (20)

79 (4) 772 (40) 596 (31)

106 (5) 334(17)

743 (46) 253 (16) 498131)

134 (8) 774 (48) 320120) 671 (Al) 365 (22)

1005 (62) 158 (10) 307(22)

94 (61 702 (43) 565 (35)

77 (5) 263 (16)

COO1 ,340 ,003 ,522

.A26 ,096 ,059 ,508 .A85 ,003 ,081 .075 ,151

COO1 COO1

,088 ,123 ,781 .OlO ,001 ,102 ,531 ,020 ,058 ,015 ,307 .360

Values are n (%) unless otherwise specified ‘n=2928

going contemporary treatment of life-threatening ven- tricular tachyarrhythmias.

Methods Patient population

The Antiarrhythmics Versus ICDs (AVID) Trial was a multi- center. randomized. controlled trial fhat compared ICDs and the antiarrhythmic drugs amiodarone or sotalol in the treatment of patients with life-threatening ventricular tachyarrhythmias.” In panllel to the main trial, a comprehensive prospective reg- istry of patients with these arrhythmias was mainrAined at par- ticipating clinical sites. The design and main findings of the AVID Registry have been previously described.‘3 Briefly. investigators at participating centers were asked fo screen all patients at or referred to their institutions with ventricular fi- brillation (VF), sustained ventricular tachycardia (VT), or syn- cope with inducible VT at electrophysiologic study. Those patients thought to be candidates for therapy with both antiar- rhythmic drugs and an ICD were included in the registry. Exclu- sion criteria from the registry included index arrhythmia occur- ring within 5 days of a mpocardial infarction, heart surgery or percutaneous revascularization, New York Heart Association

(NYH&classfVhear&faihue,needforintravenousormechanical inotropic support, life expectancy <l year, inclusion in a heart transplantation waiting list, and severe neurologic impairment precluding consent for participation. The registry included all main trial patients plus patients eligible for the main trial but who were not randomly assigned, and patients with arrhythmias not eligible for the trial (symptomatic VT with ejection fraction >0.40, asymptomatic or mildly symptomatic VT, out-of-hospital documented sustained VT or cardiac arrest associated with a presumed transient or correctable cause, and outaf-hospital syncope with structural heart disease and inducibility of symp tomatic VT or VF at electrophysiologic study). For the purpose of this study, the analysis was limited to patients with docu- mented sustained ventriculartachyarrhythmias notthoughtto be from reversible causes (regardless of their hemodynamic impact or left ventricular ejection fmction [LVF.F]) entered in the registry before December 3 1, 1996. Information regarding demographicandclinicalvariablesandtreatment at discharge from the index hospitalization was collected in all registry patients. Follow-up of vital status was obtained through peri- odic query of the National Death Index. This analysis is based on the 1997 National Death Index follow-up that covers vital status reports through December 31, 1996. The protocols were

806 Pinski et al Amertcan Heart journol

Mav 2000

Table II. Procedures during index hospitolizotion’and treatments at discharge

All patients No ICD ICD (n = 3559) (n = 1931) (n = 1628) P value

Antiarrhythmic agent 1850(52) 1487(77) 363 (22) -coo1 PBlacker 930(26) 420(22) 510(31) coo1 ACE inhibitor 2018 (57) 1036(54) 982 (60) coo1 Digitalis 1399 (40) 677(35) 722(44) coo1 Diuretics 1653 (47) 892 (46) 761 (47) ,870 Aspirin 1965 (55) 1039(54) 926 (57) .lOO Pacemaker implantation 146 (4) 114 (6) 32 121 coo1 Coronary artery bypass surgery 306 (9) 184(10) 122 (7) .031 Catheter ablation 156(4) 132(7) 24 (11 c.001

V&es are n I"/.).

Table Ill. Univariate predictors of death

Variable Hazard ratio 95%CI P value

Age (~1 Severely depressed LVEF Diastolic blood pressure (mm Hg) Systolic blood pressure (mm Hg) Coronary artery disease History of atrial fibrillation History of myocordial infarction History of congestive heart failure History of diabetes History of pacemaker History of coronary artery bypass surgery

1.05 1.04-1.05 coo1 1.99 1.69-2.33 coo1 0.98 0.97-0.98 c.001 0.99 0.98-0.99 coo1 1.63 1.33-2.01 <.OOl 1.72 1.46-2.03 c.001 1.24 1.06-1.46 ,008 2.67 2.27-3.14 coo1 1.45 1.22-1.74 coo1 1.94 1.48-2.54 c.001 1.27 1.07-1.50 .006

approved by the Institutional review boards at the participating centers. Patients gave informed consent for the participation in the registry.

Statistical analyses A total of 36 variables were analyzed. Demographic vari-

ables analyzed were age, sex, and race. Clinical and historic variables analyzed were baseline heart rate and systolic and diastolic blood pressures; hemodynamic consequence of the index arrhythmia; LVEF; current smoking status; evidence of coronary artery disease, hypertrophic cardiomyopathy, nonis- chemic dilated cardiomyopathy, valvular heart disease, or other type of structural heart disease; a history of hyperten- sion, diabetes mellitus, myocardial infarction, congestive heart failure, syncope, VF or VT before the index event; atrial fibriIIa- tion, prior (remote) cardiovascular procedures, myocardial revascularization, or cardiac valve repair or replacement: and administration of antiarrhythmic drugs at the time of the index arrhythmia. The 10 treatment variables analyzed were treatment with P-blocker, aspirin, digitalis, ACE inhibitor, antiarrhythmic drug or diuretic at discharge, performance of myocardial revascularization or catheter ablation after the index event, and implantation of an ICD or a permanent pace- maker during the index hospitalization. The NYHA functional class was not collected in the registry patients.

Continuous variables are presented as mean f 1 SD. Base- line characteristics, procedures during Index hospitalization,

and treatments at discharge were compared between patients who received and did not receive an ICD during the index hospitalization, with t tests for continuous variables and chi- square tests for discrete variables. Survival curves were gen- erated by the method of Kaplan and Meier. Univariate corre- lates of time to death were screened with the log-rank test (for discrete variables) or the Cox proportional hazards model (for continuous variables). For the purposes of plotting the survival curves, continuous variables were dichotomized at the median value except for age (dichotomized at 65 years) and LVEF (categorized into normal [>0.50] or mildly [0.36 to 0.501, moderately [0.26 to 0.351, or severely [SO.251 abnor- mal). The index arrhythmia was classified into 4 categories: VF, VT with syncope, VT with severe symptoms or systolic blood pressure ~80 mm Hg but no syncope, and stable VT.=

All variables were incorporated into stepwise forward multivariable Cox models. Two regression models were ini- tially constructed: one including only baseline demographic and clinical variables and a second one adding treatment variables. Finally, because of the significant benefit conferred by ICD therapy in the main trial, 2 separate multivariable models were constructed to identify multivariate predictors of survival in patients who received and those who did not receive an ICD during the index hospitalization. A 2-tailed value of P I .05 was considered significant. Analyses were performed with the SPSS 7.5 program (Statistical Product and Service Solutions).

American Heart Journal i/&me 139, Number 5 Pinski et al 807

Figure 1

0.0 1 0 10 20 30 40 sb Bo

MONTHS

Kaplan-Meier survival curves according to age (265 or <65 years); P < .OO 1.

Table IV. Multivariate predictors of death for entire population

Variable Hazard ratio 95% Cl P value

Baseline model

Age Iv) Severely depressed LVEF Systolic blood pressure [mm Hg) History of congestive heart failure History of diabetes History of smoking History of atria1 fibrillation History of pocemoker

Boseline models plus discharge treatments

Age (~1 Severely depressed LVEF Systolic blood pressure (mm Hg) History of congestive heart failure History of diabetes History of smoking History of otriol fibrillation History of pacemaker ICD ACE inhibitor (3.Blocker Diuretic

1.05 1.04-l .06 1 s3 1.29-l .82

0.99 0.98-0.99 1.88 1.57-2.25 1.29 1.07-l .55 1.38 1.10-1.71 1.31 1.10-1.57 1.42 1.06-l .91

1.05 1.04-l .05 1.50 1.25-l .79

0.99 0.98-0.99 1.76 1.46-2.14 1.26 1.04-l .52 1.32 1.06-l .65 1.27 1.06-l .53 1.40 1.04-l .87 0.51 0.42-0.62 0.77 0.65-0.93 0.76 0.6 l-O.96 1.27 1.05-l .53

coo 1 c.00 1 coo 1 coo 1

,009 ,004 .003 ,018

coo 1 coo 1 <.oo 1 coo 1

,018 ,013 ,010 ,026

coo 1 .005 ,024 ,015

Results After a mean follow-up of 16.9 f 11.6 months, 63 1 This study included 3559 patients. Baseline character- patients died. Actuarial survival was 0.86 (95% confi-

istics are presented in Table I. Treatments during index dence interval [CI] 0.85 to O.SS), 0.79 (95% CI 0.78 to hospitalization and at discharge from index hospitaliza- 0.81), and 0.72 (95% CI 0.70 to 0.74) at 1, 2, and 3 years, tion are presented in Table II. respectively.

808 Pinski et al

Figure 2

American Heart Journal May 2000

.2-

.l.

0.0 ~ 0 IO i0 10 40 50 54

MONTHS

Kaplan-Meier survival curves according to presence or absence of severe left ventricular dysfunction (LVEF

e0.25); P<.OOl.

Table V. Multivariate predictors of death in 193 1 patients who did not receive an ICD during index hospitalization

Variable Hazard ratio 95%CI P value

Baseline model Age (~1 Severely depressed LVEF Systolic blood pressure (mm Hg) Diastolic blood (mm Hg) pressure Heart rate (per beat/min) History of congestive heart failure History of atrial fibrillation

Baseline plus discharge treatments model Age 1~1 Severely depressed LVEF Systolic blood pressure (mm Hg)

Heart rate (per beat/min) History of congestive heart failure History of atria1 fibrillation Diuretic

1.04 1.03-l .05 coo 1 1.43 1.16-1.76 coo1 0.99 0.98-1.00 ,004 0.99 0.98-1.00 ,030 1.01 1.01-1.02 coo1 1.98 1.60-2.46 coo 1 1.29 1.05-l .59 .018

1.05 1.03-l .06 coo 1 1.36 1.10-1.67 ,004 0.99 0.98-0.99 coo1 1.01 1.00-l .02 ,001 1.84 1.47-2.30 c.001 1.24 1.01-l .53 ,043 1.30 1.05-l .62 ,018

Univariate predictors of survival are presented in Table Multivariate predictors of survival are displayed in Ill. Older age (Figure l), severe left ventricular dysfunc- Table IV. Eight baseline variables were predictors of tion (Figure 2), lower systolic or diastolic blood pressure worse survival: older age (hazard ratio 1.05/y), severe at baseline, presence of coronary artery disease, a history left ventricular dysfunction (hazard ratio 1.53), lower of atrial fibrillation, prior myocardial infarction, conges- systolic blood pressure (hazard ratio 0.99/mm Hg), his- tive heart failure (Figure 3), diabetes, previous (remote) tory of congestive heart failure (hazard ratio 1 .SS>, his- pacemaker, or previous coronary bypass surgery were tory of diabetes (hazard ratio 1.29), smoking (hazard associated with poorer survival. The hemodynamic cate- ratio 1.38), history of atrial fibrillation (hazard ratio 1.3 1). gory of the index arrhythmia did not influence survival. and prior pacemaker implantation (hazard ratio 1.42).

Amer,con Heart Journal Volume 139. Number 5 Pinski et al 809

Figure 3

0.0 J 0 10 20 30 40 54 Q

MONTHS

Kaplan-Meier survival curves according to presence or absence of history of congestive heart failure (HxCHF) at

time of registry inclusion; P C .OOl .

The type of index arrhythmia was not a multivariate predictor of outcome. Treatment with an ICD (hazard ratio 0.5 1) and hospital discharge while the patient was taking a P-blocker (hazard ratio 0.76) or an ACE inhibitor (hazard ratio 0.77) were associated with better progno- sis, whereas hospital discharge while the patient was taking a diuretic was a significant predictor of worse survival (hazard ratio 1.27).

Older age, severely depressed LWF, lower baseline systolic blood pressure, and a history of congestive heart failure continued to be multivariate predictors of death when analyses were restricted to patients who received or did not receive an ICD during the index hospitalization (Tables V and VI). Again, the type of index arrhythmia was not a predictor of outcome.

Discussion This study reports the outcome of patients with SW

tained ventricular tachyarrhythmias treated with con- temporary treatment strategies. It is the largest reported series of its kind, and despite recent therapeutic advances, short- and medium-term mortality rates for these patients remain high. In contrast to previous series, this study included patients from multiple centers, was not restricted to patients who underwent baseline elec- trophysiologic study (a possible cause of selection bias2s), and represented mostly patients enrolled shortly after the index event*6 (only 22% of patients had prior episodes of VT or VF), avoiding possible prevalence-incidence bias.27

As previously reported, older age and variables

related to the severity of left ventricular dysfunction and heart failure continue to be strong risk factors for death. Their importance was similar regardless of the specific antiarrhythmic treatment given at discharge. The prognostic value of a lower baseline blood pres- sure is of particular interest. It may reflect a lower car- diac output in patients with the more severe degrees of ventricular dysfunction or may identify patients in whom treatment with fulI doses of beneficial afterload- reducing28 and antiadrenergic agents is limited or impossible. One can also speculate that patients with lower baseline blood pressure may have limited capac- ity for compensatory vasoconstriction during ventricu- lar tachyarrhythmias,29,30 increasing the likelihood that arrhythmia recurrences may result in hemodynamic compromise or death.

Smoking before the index event was an independent predictor of death in this population. The exact mecha- nism of the association is not clear because we did not collect information on smoking status after hospital dis- charge. Hallstrom et aI31 found that among 310 sur- vivors of out-of-hospital cardiac arrest who had been habitual cigarette smokers at the time of arrest, smok- ing cessation was an independent short- and long-term predictor of freedom from recurrent cardiac arrest.

The impact of the clinical presentation (eg, cardiac arrest vs better-tolerated sustained monomorphic VT) on the prognosis of patients with ventricular tachy- arrhythmias has been controversial. Studies that emphasized clinical and electrophysiologic differ-

810 Pinski et al Amwcon Heart Journal

May 2000

Table VI. Multivariate predictors of death in 1 d28 patients who received on ICD during index hospitalization

Variable Hazard ratio 95% Cl P value

Baseline model

Age (~1 Severely depressed LVEF Systolic blood pressure (mm Hg) History of congestive heart failure

Baseline plus discharge treotments m

Age (~1 Severely depressed LVEF Systolic blood pressure (mm Hg) History of congestive heart failure Pacemaker at discharge Amiodarone or sotolol ACE inhibitor

1.05 1.73 0.99 1.79

1.05 1.03-l .07 coo 1 1.80 1.30-2.50 c.00 1

0.99 0.98-l .OO .012 1.87 1.34-2.6 1 coo 1 2.24 1.04-4.82 ,039 1.69 1.16-2.44 ,006

0.71 0.50-0.99 ,041

1.03-l .06 coo1 1.25-2.40 coo 1

0.98-l .OO ,008 1.29-2.48 c.001

ences between the two ends of the symptomatic spectrum 32.33 led to the suggestion that a refined classification would promote better risk stratification and treatment selection.3d The results of follow-up studies have been mixed, in part because of the differ- ent outcomes measured and the treatments evaluated. The Dutch Interuniversity Registry evaluated 333 patients with ventricular tachyarrhythmias after myocardial infarction treated mainly with antiarrhyth- mlc drugs and found that an initial presentation with cardiac arrest found at the initial examination was an independent predictor of poorer prognosis. Other studies suggested a stronger association between resuscitation from cardiac arrest found at initial exami- nation and subsequent sudden death than with overall death.35 In view of the difficulties in determining the mechanism of death in patients with chronic cardio- vascular disease36*37 (even in prospective blinded tri- al@), ascertainment bias may be present in some of those studies. In patients treated with antiarrhythmic drugs enrolled in the Electrophysiologic Study Versus Electrocardiographic Monitoring (ESVEM) Trial, the clinical presentation was not an independent predic- tor of arrhythmic death or cardiac arrest.39 In a single- center study of 369 patients followed up for a mean of 30 months, Gomes et al6 identified congestive heart failure and LVEF as the only baseline independent risk factors for cardiac death. Likewise, Menz et aI@ did not find a significant influence of the arrhythmia pre- sentation ln patients treated with ICDs.40

In our study, patients with VT and mild symptoms did not have a better survival than patients with cardiac arrest or VT with severe symptoms. Patients with VT and mild symptoms were believed to constitute a lower-risk popu- lation at the time of trial design and therefore were not randomly assigned in AVID. In the randomized AVID study, the benefit conferred by defibrillator therapy was not significantly different for patients with cardiac arrest or VT and severe symptoms.

Several factors can help explain the absence of a more favorable outcome in patients with better-tolerated arrhythmias, even after adjusting for other powerful pre- dictors (such as age and severity of left ventricular dys function) in multivarlate analyses. It is interesting that in our study, patients with VT and mild symptoms were less likely to be treated with ICDs than patients with ventrlcu- lar arrhythmias and more severe symptoms (27% vs 49%; P < .OOI). Induction of VT of multiple rates and mor- phologles at electrophysiologic study is very common in patients with stable VT,‘1 and some of these arrhythmias may develop spontaneously during follow-up.32 Bijcker et al”3 reported a 20% incidence of shocks for rapid, life- threatening ventricular arrhythmias in 50 patients with stable VT who had received ICDs3 Among the 507 patients randomly assigned to ICDs in the AVID main trial, the incidence of appropriate shocks for rapid tachy- arrhythmias classified as VF by the device was similar (20%) for those initially examined with VT compared with VF.jj Furthermore, proarrhythmic responses to antiarrhythmic drugs*5 can result in VF in patients with more benign tachyarrhythmias.

A limitation of the study resides in the fact that the mechanisms and cause of death were not available. However, the limitations of the classification of the cause of death, (even in prospective studies) are well established. Indeed, a consensus statement from the North American Society of Pacing and Electrophysiol- ogy recommended the use of total death as the end point in clinical studies of the ICD.46 Information about the NYHA functional class was not available in our patients. Because patients in functional class IV were not included in the registry, we essentially compared the outcome between patients without a history of con- gestive heart failure (ie, class I) and those with a history of congestive heart failure (ie, classes II and III). The predictive value of our regression model may have been refined by incorporation of more detailed func- tional class information.6

Amer,can Heart Journal Volume 139, Number 5 Pinski et al 811

Despite therapeutic advances in the fields of heart fail- ure, myocardial ischemia, and arrhythmia management, the mortality rate of patients with sustained ventricular tachyarrhythmias remains high. Well-tolerated VT in patients with structural heart disease does not appear to carry a signitlcantly better prognosis than ventricular tachyarrhythmia with more severe hemodynamic conse- quences. Therefore, until randomized controlled trials are performed in this population, it appears that ICD implantation can reasonably be offered to these patients. Frequent shocks can be avoided by the use of antitachy- cardia pacing without a high risk of arrhythmia accelera- tion,47 although it may be necessary to add antiarrhyth- mic drug therapy more often than in patients who initially presented with VF.

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Appendix The following participated in the AVID Registry. Uni-

versity of Alabama, Birmingham: A.E. Epstein, R.A.S. Cooper, S.M. Dailey, G.N. Kay, V.J. Plumb, R.S. Bubien, S.M. Knotts, P.T. McKenna; Arkansas Cardiology Clinic: G.S. Greer, I.H. Santoro, J. Swaim, S. Whittle; Baylor College of Medicine: C. Rizo-Patron, K.M. Belco, P.

Amerlcon Heart Journal Moy 2000

Payne, D.J. Arnold, W.X. Zhu, C.M. Pratt; Baystate Med- ical Center, Springfield, Mass: J.R. Cook, G. Kabell, J.B. Kirchhoffer, D. Warwick, B. Burkott, D. Tomaszewski; Boston (Mass) University Medical Center Hospital: P.J. Podrid, T.T. Fuchs, M. IMazur; Brigham and Women’s Hospital, Boston, Mass: P.L. Friedman, W.G. Stevenson, M.M. Swat, L.I. Ganz, M.O. Sweeney, J.B. Shea; Univer- sity of California, Irvine: M.A. Brodsky, BJ. Allen, S.S. Ehrlich, LJ. Wolff, M.M. Macari-Hinson; University of Calgary (UK): G. Wise, H. Duff, A. Gillis, B. Mitchell, J. Rothschild, R. Sheldon, P. Cassidy; University of Califor- nia, San Francisco: M. Scheinman, S. Eisenberg, L. Epstein, A. Fitzpatrick, G. Griffin, R. Lee, M. Lesh, M. Namekawa-Wang, M. Wang; Cleveland (Ohio) Clinic Foundation: B.L. Wilkoff, S.L. Pinski, J.A. Cross, J.M. Shewchik; University Hospitals of Cleveland (Ohio): M.D. Carlson, D.S. Rosenbaum, W.R. Lewis, L.A. Biblo, J.A. Mackall, A.L. Waldo; Columbia-Presbyterian Med- ical Center, New York, NY: J. Coromilas, J.T. Bigger, Jr, F.D. Livelli, Jr, J.A. Reiffel, K. Hickey; University of Con- necticut Health Center: E. Berns, N. Lippman, M.B. Barry, H.M. Carney; Cooper Hospital/University Med- ical Center: A.M. Russo, H.L. Waxman, C.A. Stubin, J.M. Morrissey, D.H. Raspa; Deaconess/Sacred Heart Medical Centers: D.A. Chilson, T.J. Lessmeier, W.T. Pochis, J.M. Baxter; Florida Arrhythmia Consultants: R.M. Luceri, P. Zilo, D.N. Weiss, A. Jonas, L. Vardeman; Florida Heart Group: K.M. Schwartz, C. Asbell; University of Florida, Gainesville: A.B. Curtis, J.B. Conti, C. Nelson; Good Samaritan Hospital: D.S. Cannom, A.K. Bhandari, R.D. Lerman, B.R. Firth; Indiana University Medical Center: D.P. Zipes, E.D. Engelstein, W.M. Miles, L. Foreman; University of Iowa Hospitals: J.B. Martins, H.C. Lee, J.R. Hopson, R. Hopson; Lankenau Hospital/Medical Research Center, Philadelphia, Pa: R.A. Marinchak, S.J. Rials, P.R. Kowey, R.A. Filart, M. Hernandez, D.L. Scher, L.S. Zukerman, S. Farrell, D. Kolk, H. Criner, B. Tait; Likoff Cardiovascular Institute/Hahnemann Univer- sity: S.P. Kutalek, S.E. Hessen, C. Movsowitz, F. Samuels, S. Wilber, C. Baessler, D. Soto, M. Schuster, G. Scott, R. Covelasky-Robinson, S. Fletcher, K. Siegl, L.S. Finn, C. Saari; Loma Linda (Calit) University Medical Center: V.I. Torres, S. Pai, M.L. Platt, P.C.R. Timothy, V.L. Bishop; Maine Medical Center: J.C. Love, J.E. Cut- ler, S. Bosworth-Farrell; University of Maryland Medical Center: M.R. Gold, S. Shorofsky, R. Peters, N. Kavesh, D. Froman, H. Scott; Medical College of Wisconsin: J.A. Roth, A.M. Gadhoke, S.K. Mauermann; Methodist Hos- pital, Houston, Tex: A. Pacifico, N. Nasir, Jr, K. Trainor; Methodist Hospital, Ind: P. Foster, B. Crevey, H. Gen- ovely, J. Schutzman, K. Viater, C. Coyle; Midwest Heart Research Foundation: M.O. Nora, M.F. O’Toole, R. Col- lura, E.L. Enger; Minneapolis (Minn) Heart Institute: A. Almquist, P. Baldwin, R. Hauser, S. Milstein, M. Pritzker, V. Schreiber; Montefiore Medical Center, Bronx, NY: S.G. Kim, J.D. Fisher, K.J. Ferrick, J.N. Gross, U. Ben-

Amer~con Heart Jovrm volume 139, Number 5 Pinski et al 813

Zur, J. Durkin, A. Ferrick; Mount Sinai Medical Center: J. Zebede, P. Same& A.O. Tolentino, S. Rubin; Sentara Norfolk (Va) General Hospital: J.M. Herre, R.C. Bernstein, L.R. Klevan; North Shore University Hospital, Manhas- set, NY: R.L. Jadonath, B. Goldner, K. Merkatz, L. Chep- urko; University of Oklahoma, Norman: K.J. Beckman, J.H. McClelland, M.D. Gonzalez, L.E. Widman, R. Lane; Oregon Health Sciences University and Collaborating Medical Centers: J.H. McAnulty, B.D. Halperin, J. Kron, G.C. Larsen, M.H. Raitt, R.D. Swenson, R.C. Florek, C. Marchant, M. Hamlin, G. Heywood; University of Rochester (NY) and Collaborating Hospitals: T. Akiyama, J.P. Daubert, C. Kim, D. Switzer, P. Pande, D. Flynn, M. Keller, C.M. Ocampo, K. Wahl, J. Vogt; St Joseph’s Hos- pital: N.G. Tullo, C.A. Irmiere, A. Henry; St Luke’s-Roo- sevelt Hospital Center and Collaborating Institutions: J.S. Steinberg, F. Ehlert, S. Zelenkofske, E. Menchavez- Tan, M. DeStefano, G. Brown; Stanford University Med- ical Center and Collaborating Medical Centers: R.J. Sung, L.B. Liem, C. Young, M.R. Lauer, J. Peterson, L. Ottoboni, P. Goold; Tacoma (Wash) General Hospital: M. Rome, K. Kresge; Temple University School of Medicine: A.E. Buxton, H.H. Hsia, J.M. Miller, S.A. Rothman, N. Adelizzi,

M.E. Gastineau, L.M. Thome, D.M. Whitley; University of Texas Medical School Houston/Baylor College of Medicine: H.T. Shih, A.H. Dougherty, S. Jalal, G.V. Naccarrelli, D. Wolbrette, D. Wilson; University of Texas Southwestern Medical Center: R.L. Page, M. Jessen, R.C. Canby, G. Erwin; University of Utah Med- ical School/LDS Hospital: J.L. Anderson, B.G. Crandall, L.A. Karagounis, J.S. Osbom, D.A. Rawling, K. Summers, M. Biggins; University of Utah/VA Medical Center: R.C. Klein, R. Freedman, M. Marks; Valley Heart Associates: W. Chien, R. Stevenot, J. Merlllat, M. McPherson; Van- derbilt University Medical Center, Nashville, Term: D.S. Echt, D.M. Roden, MS. Wathen, J.T. Lee, K.T. Murray, J.H. Baker, D.M. Crawford; University of Virginia Med- ical Center, Charlottesville: S. Nath, D. Haines, S. Ack- erman, L. Bowman; Wilson Regional Medical Center: N.J. Stamato, D. Whiting; Clinical Trial Center, Univer- sity of Washington: A.P. Hallstrom, H.L. Greene, Q. Yao, M. Scholz, J.L. Powell, E. Graham-Renfroe, S. Sullivan, R.B. Ledingham, M. Flewelling-Morris, S.E. Lancaster, R. Moore, A. Olarte; Clinical Trials Branch/National Heart, Lung, and Blood Institute, Bethesda, Md: E.B. Schron, M.J. Domanski, D. Follmann, Y. Rosenberg, C.A. Jennings.