Home SVCC                                                  Area: English - Español - Português

The Non Invasive Assessment
of Risk of Sudden Death

Peter J. Zimetbaum, MD; Allison Richardson, MD

Cardiovascular Division, Beth Israel Deaconess Medical Center,
Harvard Medical School, Boston, MA, USA

   The evaluation of the patient at risk for malignant ventricular arrhythmias remains a complex and ill-defined task. Progress has been made in defining a strategy for the evaluation of patients with coronary artery disease, depressed left ventricular function and non sustained ventricular tachycardia (NSVT). Evidence based guidelines for the evaluation of patients with other types of structural heart disease (e.g. idiopathic dilated cardiomyopathy, hypertrophic obstructive cardiomyopathy) or primary electrical disease (e.g. congenital long QT syndrome, Brugada's syndrome) do not currently exist. This paper will review the technologies available for the noninvasive assessment of sudden death risk as well as an approach to risk assessment in certain high risk populations.

Ambulatory Monitoring
   Ambulatory monitors can be useful for the detection of symptomatic and asymptomatic arrhythmias including nonsustained ventricular tachycardia (NSVT), and therefore may be useful in risk stratification in certain patient populations. The Holter monitor introduced in 1961, was the first ambulatory monitor available for the evaluation of arrhythmias and arrhythmic complaints such as palpitations and syncope (1). Newer types of monitors include long term continuous and intermittent recorders with and without transtelephonic capability. The Holter monitor is the prototype for the continuous recorder. These monitors record a continuous ECG tracing in two or three bipolar leads. Data is usually stored in analog form on a cassette or compact disk, and is then digitized for analysis. New models minimize artifact by acquiring data in a digital format. Recently, monitors have been developed which provide data for up to 12 reconstructed ECG leads. Holter monitors can be worn for 24-48 hours at a time, although the incremental diagnostic yield for a second day of monitoring is minimal (2). These monitors do not require patient activation, thus they may be successful in capturing arrhythmias that cause loss of consciousness, and can be used by patients who might have difficulty activating a monitor. They offer full disclosure, and record asymptomatic as well as symptomatic arrhythmias that occur during the monitoring period. Holters are the preferred monitors for use in screening asymptomatic patients for arrhythmias. Their major disadvantage is the short duration of monitoring, as paroxysmal events are relatively unlikely to occur during this time period. In addition, asymptomatic arrhythmias that are detected may decrease the specificity of the findings of the test. Although patient activated event markers and diaries are used to allow correlation between recorded arrhythmias and symptoms, patients often forget to accurately record the timing of symptoms.

   Intermittent recorders, or event recorders, store a brief ECG tracing when activated by the patient. Some of these devices are applied to the chest wall at the time of symptoms, and record information prospectively for approximately two minutes once activated. Loop recorders are worn continuously and record constantly but only store data when activated . This allows storage of data both before and after device activation. Loop recorders usually consist of two or three chest leads attached to a monitor the size of a beeper that can be worn on the patient's belt. These recorders may be worn for up to a month at a time. Data from these devices can be transmitted over the telephone at the patient's convenience or immediately in the case of an emergency. These devices can be worn for up to a month and therefore provide a greater likelihood of capturing infrequent arrhythmias. The correlation between symptom and rhythm is excellent because the patient must activate the device to record the arrhythmia. This system is obviously not useful in detecting asymptomatic arrhythmias. The main disadvantage of using this system for symptomatic patients is that they may be unable to activate the recorder as a result of loss of consciousness, disorientation, or confusion about the activation process. External loop recorders with automatic triggers that activate for predetermined fast or slow heart rates are currently under development.

   Recently, implantable loop recorders (ILRs) have become available. These monitors can be left in place for up to two years, and are particularly useful in diagnosing very infrequent arrhythmias (3). These devices are approximately the size of pacemakers and are implanted subcutaneously to one side of the sternum. Like external loop recorders, they are patient triggered and store data from both pre and post activation. Recordings are initiated by placement of an activator over the device. The most recent ILRs also contain automatic triggers for prespecified high and low heart rates that will allow storage of data without patient activation. Eventually algorithms will be available that also allow the automatic detection of irregular rhythms such as atrial fibrillation. Unlike external recorders, implantable loop recorders are not currently able to transmit tracings over the telephone, however this is likely to change in the near future. The obvious advantage of these devices is that they can conveniently be used even when symptoms occur rarely (less than once per month).

   Finally, current pacemakers and implantable cardioverter defibrillators (ICDs) have sophisticated monitoring capabilities. Most new devices can be programmed to log atrial and/ or ventricular tachyarrhythmias. ICDs and some pacemakers can store electrograms of tachyarrhythmias as well. Thus when present these implanted devices can be used as ambulatory monitors.

Signal Averaged ECG
   The signal averaged ECG was developed in the early 1980's to identify the existence of substrate for reentrant ventricular tachycardia (VT) associated with coronary artery disease (CAD) (7, 8). The purpose of the SAECG is to detect late potentials, which represent low amplitude, high frequency electrical activity that occurs in the terminal portion of the QRS. Late potentials are felt to be caused by slow conduction and delayed activation of tissue, and thus to identify the presence of substrate which could potentially cause reentrant ventricular arrhythmias. Late potentials are very low amplitude, and thus are obscured by noise on a regular twelve lead ECG. Signal averaging improves the signal to noise ratio by temporal or spatial averaging, allowing the detection of low amplitude electrical activity. Signal averaged measurements commonly used to identify a late potential include 1) filtered QRS duration (QRSd), 2) root mean square voltage of the terminal 40 ms of the QRS (RMS40), and 3) duration of low amplitude signal (<40 ms) in the terminal QRS (LAS) (9). This technique is limited in the presence of bundle branch block or significant intraventricular conduction delay. Atrial fibrillation and flutter have also been shown to decrease the predictive accuracy of the SAECG (10).

   There is good evidence that the SAECG can identify post MI patients who are at risk for ventricular arrhythmias (10-17). There is much less data available as to its use in other populations (17). Based on data compiled from 15 studies, 8-48% of post MI patients who have late potentials detected on SAECG will ultimately have sustained VT or sudden death (17). A positive SAECG in this population has a positive predictive accuracy of 14-29% when used to predict major arrhythmic events, and a normal SAECG has a negative predictive accuracy of 95-99% (17). Recent data from the Multicenter Unsustained Tachycardia Trial There is less information about the use of the SAECG in other disease states.

Heart Rate Variability
   Heart rate variability analysis is the evaluation of beat to beat variability of the R-R interval. Data is obtained from digitized Holter tracings. HRV is thought to be largely a reflection of autonomic tone (20). There is evidence for a correlation between risk for sudden cardiac death and autonomic tone, with diminished vagal activity indicating increased susceptibility to lethal arrhythmias (21). Heart rate variability can be analyzed in the time domain or in the frequency domain. These two methods provide similar information about mortality risk in the post MI population (23). Heart rate variability is decreased early after MI, and begins to recover within several weeks (24, 25). In 1987, Kleiger et al. demonstrated a 34% mortality over four years among post MI patients with depressed HRV, as compared to a 12% mortality among patients with normal HRV (26). This finding has been confirmed in other studies both before and after the advent of the thrombolytic era (20, 27). Decreased HRV post MI has been shown to predict sudden cardiac death and sustained ventricular tachycardia (28). Although diminished HRV post MI is an independent risk factor for ventricular arrhythmias and mortality, its predictive accuracy when used alone is low (20, 22). There is conflicting data as to the relationship between HRV and arrhythmic events in patients with underlying heart disease that is not due to CAD (22). Clinical use of HRV in specific disease states will be discussed below.

Microvolt T Wave Alternans
   Electrical alternans is variability of the ECG waveform on alternate beats. Repolarization alternans (ST and T wave alternans) shows promise as a risk stratifier for ventricular arrhythmias associated with various conditions (29). T wave alternans, a marker of heterogeneous electrical repolarization, has been observed on ECG tracings immediately preceding the onset of ventricular fibrillation in acutely ischemic animals (30, 31) and humans (32-35). Recently, techniques have become available to allow visualization of microvolt TWA that would otherwise be undetectable on the surface ECG. The T wave is measured at an identical time relative to the QRS in multiple consecutive complexes. Spectral analysis is then used to calculate the T wave power spectrum in order to differentiate minor alterations in T wave morphology occurring at the alternans frequency (every second beat) from alterations caused by respiration or other background noise (36). TWA is measured during atrial pacing or exercise with a target heart rate of approximately 110 BPM to maximize the sensitivity and specificity of the test (37). Frequent ectopic beats or atrial fibrillation can obscure the detection of alternans (32). In 1994, Rosenbaum et al (38) studied TWA during atrial pacing in 83 patients undergoing EPS for a variety of indications. Alternans was predictive of inducibility of VT at EPS, and was also an independent risk factor for spontaneous VT, VF or sudden cardiac death during 20 months of follow up. Other small studies have similarly demonstrated TWA to be predictive of ventricular arrhythmias (39). The clinical implication of TWA has also been evaluated among groups of patients with some specific underlying conditions. Results of these studies will be discussed later.

QT Dispersion
   QT interval dispersion (QTD) is a measure of variability of the QT interval, which, like T wave alternans, is a marker of heterogeneity of ventricular repolarization. QTD is measured by taking the difference between the longest and shortest QT intervals on a 12 lead ECG. There is evidence that QTD is useful in risk stratification of patients with LQTS (40). Its usefulness in other patient populations is less clear. QTD has been found to be an independent predictor of cardiovascular mortality in two large studies, one looking at an elderly population in Rotterdam (41), and the other looking at middle aged and elderly native Americans (the Strong Heart study) (42). In each study, abnormal QT dispersion was associated with an approximately two fold increase in risk of cardiovascular mortality. These large studies looked at populations in which the majority of patients had no known heart disease. When patients with known cardiac disease placing them at risk for sudden death have been evaluated, the results have been variable. Results of studies looking at use of QTD in specific disease states will be discussed below.

   The noninvasive determination of a patient's risk for developing life threatening ventricular arrhythmias may be approached using ambulatory monitoring and/or some of the newer techniques described above. Holter monitoring for asymptomatic ventricular ectopy has been used in the evaluation of patients with various forms of underlying heart disease including coronary artery disease, dilated cardiomyopathy, hypertrophic cardiomyopathy, congenital heart disease, and primary electrophysiologic abnormalities including congenital heart block and long QT syndrome. The use of ambulatory monitoring in some of these groups is summarized in table 1. An important question that remains unresolved for all patient populations discussed below is when and how often monitoring should be undertaken. Obviously, frequent monitoring will result in a higher likelihood of detection of ventricular arrhythmias than will less frequent monitoring.

Post Myocardial Infarction
   Patients with NSVT and left ventricular left ventricular (LV) dysfunction following MI have an up to 30% two year rate of sudden death (59-62). The Multicenter Automatic Defibrillator Implantation Trial (MADIT) (63) demonstrated significantly improved survival among CAD patients with LV dysfunction, NSVT, and inducible, non drug responsive monomorphic ventricular tachycardia treated with ICDs. More recently, the Multicenter Unsustained Tachycardia Trial (MUSTT) 64 found that a similar group of patients treated with EPS guided therapy (antiarrhythmic medication or ICDs) had decreased mortality as compared to those treated with traditional therapy. This benefit was entirely attributable to the use of ICDs. These studies together demonstrate the importance of identifying NSVT in this patient population. These findings raise the question of whether such patients should undergo routine ambulatory monitoring to screen for NSVT. Such monitoring would pose an enormous burden on the health care system (63, 65). There are not currently guidelines recommending routine ambulatory monitoring in post MI patients (22). As is mentioned above, the optimal timing of initial screening and interval follow up has not been defined. Nonetheless, it is probably reasonable to perform screening Holter monitoring on asymptomatic post MI patients felt likely to be at high risk for ventricular arrhythmias such as those with severe LV dysfunction or history of a large MI. In MUSTT, left bundle branch block (LBBB) and intraventricular conduction delay (IVCD) were independent predictors of sudden death and total mortality raising the possibility that these patients should be closely monitored (66). Future studies will define which patients should undergo surveillance monitoring for NSVT, go directly to electrophysiology study or have routine office based follow up.

   Several of the newer techniques for noninvasive risk stratification have also been studied in the post-MI population. The SAECG has been tested extensively in this group (10-17). Although the presence of late potentials is an independent predictor of major arrhythmic events in the post MI population, the positive predictive accuracy of the SAECG is not high enough that clinical decisions regarding treatment of individual patients should be based on this information alone (17). Recent data suggests that in the MUSTT population the SAECG is a better independent predictor of cardiac arrest or arrhythmic death than EPS (67). The SAECG may be used in conjunction with other information to determine which post MI patients may benefit from invasive evaluation, and may be used together with invasive evaluation to determine which post MI patients are at the highest risk for sudden death. We routinely obtain SAECGs in CAD patients but do not yet use it to make clinical decisions.

   HRV has also been extensively tested in the post MI population. As stated above it is an independent risk factor for sudden cardiac death as well as overall mortality in this group (20, 26-28) but with a low positive predictive accuracy when used alone (20, 22). Because HRV begins to recover within several weeks after MI, the current recommendation is that if the test is used it should be performed 7-10 days after the event.68 There is data, however, that it retains predictive value when measured up to a year after MI (25). Information regarding HRV can be used in conjunction with other tests to increase the accuracy of risk stratification post MI (20). HRV analysis may eventually be incorporated into protocols for risk stratification post MI. Currently, there is insufficient information as to how HRV analysis should be used in directing therapy to justify its routine use in the post MI population (22).

   There is also currently insufficient evidence to justify the routine use of TWA or QTD in the evaluation of post MI patients. A recent study (71) of 102 post MI patients who underwent evaluation of LV function, TWA and SAECG. Each was an independent risk factor for sustained ventricular arrhythmias during 12 months follow up. The positive predictive accuracy of TWA when used alone was only 28%. Use of TWA and SAECG in combination resulted in a positive predictive accuracy of 50%. Like HRV, T wave alternans may eventually be used routinely in conjunction with other noninvasive tests to determine which post MI patients are at the highest risk for sudden death. A multicenter trial is planned in which MUSTT population patients will undergo EPS and TWA (David Rosenbaum, personal communication). Patients with positive EPS and/or positive TWA will be treated with ICDs and outcomes will be followed. Information from this study should help direct our use of TWA in this patient population in the future. There is even less data regarding use of QTD in evaluation of patients with CAD. In 1994, a retrospective case control study of patients with CAD showed an association between an abnormal QTD and sudden death (72). Subsequent prospective studies have differed as to whether QTD is predictive of cardiovascular mortality post MI (73, 74). In the Spargias et al (74) study, although QTD was found to be predictive, it was neither a very sensitive nor specific marker. We do not routinely evaluate either TWA or QTD in our post MI patients.

Dilated Cardiomyopathy/Congestive Heart Failure
   Nonsustained VT can be identified by Holter monitoring in over 50% of patients with idiopathic dilated cardiomyopathy (75-78). Reports differ as to whether NSVT has any prognostic implication in these patients (75, 79-82). The presence of congestive heart failure (CHF) clearly increases the risk of sudden death in patients with dilated cardiomyopathy (83-86). There is conflicting evidence as to whether NSVT further increases the mortality risk in this population. In the GESICA study (86) patients with cardiomyopathy, CHF and NSVT had a 24% two year mortality as compared to a 9% two year mortality among patients without NSVT (87). However, in the CHF STAT study (88) 80% of patients with cardiomyopathy and CHF had NSVT, which was not found to be an independent predictor of mortality. There is no clear evidence that the use of antiarrhythmic medication to decrease NSVT in this population leads to improved survival (89). As a result, ambulatory monitoring is not recommended in adults with dilated cardiomyopathy with or without CHF (22). Children with dilated cardiomyopathy are felt to have a higher risk of sudden death than adults, and are often followed by periodic Holter monitoring. Dilated cardiomyopathy is a class I indication for screening Holter monitoring in the pediatric population according to the most recent ACC/ AHA guidelines (22).

   Some of the newer methods of noninvasive risk stratification have been tested in the dilated cardiomyopathy/ CHF population. In a pilot study of 70 patients with CHF, the presence of TWA appeared to be a strong marker for sustained VT, VF arrest or death during a one year follow up (32). Three recent small studies of patients with nonischemic cardiomyopathy and/ or CHF have also found TWA to be an independent predictor of sustained ventricular tachyarrhythmias (90-92). Although the measurement of TWA is a promising technique in this patient population there is not yet sufficient evidence to recommend its routine use in asymptomatic patients.

   Little information is available regarding the use of the SAECG, HRV and QTD in patients with nonischemic cardiomyopathy. One recent study of 131 patients with idiopathic dilated cardiomyopathy found the SAECG to be an independent predictor of both cardiac death and major arrhythmic events (93). A reduced SDNN was also an independent predictor of cardiac death and major arrhythmic events in this study.

   Previous evidence has been conflicting regarding the use of HRV in this patient population (94-98). Studies have also differed as to whether QTD is of prognostic value in patients with CHF. Barr et al (99) showed an association between abnormal QTD and sudden death in patients with CHF. However, a larger study (100) failed to demonstrate an independent relationship between QTD and all cause mortality or sudden death after multivariate analysis. There is currently insufficient information to recommend the routine use of any of these tests in the evaluation of asymptomatic patients with dilated cardiomyopathy with or without CHF. There is an ongoing prospective trial evaluating the use of noninvasive markers including TWA, HRV, SAECG, QTD, NSVT and LVEF to predict cardiac risk in the nonischemic dilated cardiomyopathy population (101).

Hypertrophic Cardiomyopathy
   Established risk factors for sudden death in this population include history of syncope and history of sudden death in a first-degree relative (102). NSVT has previously been thought to be predictive of sudden death in these patients, and guidelines once advocated routine ambulatory monitoring of patients with HOCM (103, 104). Later studies found NSVT not to be an independent predictor of death in this population (105-107). A recent study of 630 HOCM patients (109) found that NSVT alone was not significantly predictive of sudden death, but found that it was predictive when used in combination with other risk factors including syncope, family history of sudden death, LV wall thickness and hypotensive response to exercise. Although there remains some debate as to whether adults with HOCM should undergo screening for NSVT, the most recent ACC/AHA guidelines for ambulatory monitoring do not recommend routine Holter monitoring in this population (22). Hypertrophic cardiomyopathy, like dilated cardiomyopathy, is associated with a higher sudden death rate in children than in adults,110 probably because patients who survive to adulthood are selected survivors. Periodic Holter monitoring of children with HOCM is recommended (22).

   In patients with HOCM, exercise induced TWA has been shown to correlate with the presence of traditional risk factors such as a history of syncope or family history of sudden death (111). There is no information yet as to whether TWA will prove to be an independent predictor for ventricular arrhythmias among these patients. QTD does not seem to correlate with any of the known risk factors for sudden death in HOCM patients (112). HRV has not been found to be an independent predictor of risk in this population (113), and there is little evidence available regarding use of the SAECG. None of these tests are currently recommended for routine use in the evaluation of asymptomatic patients with hypertrophic cardiomyopathy.

   Patients with congenital long QT syndrome, Brugada syndrome and congenital heart block are at increased risk for arrhythmic death. Patients with LQTS may develop polymorphic VT (torsades de pointes), causing syncope or sudden death (119, 120). These patients may benefit from treatment with beta blockers and/ or implantation of pacemakers or ICDs. Patients who have a history of syncope or family history of sudden death are at particularly high risk for sudden cardiac death. Ambulatory monitoring can be used to identify patients with significant bradycardia, periods of QT prolongation or asymptomatic nonsustained polymorphic VT, which may put patients at increased risk for sudden death (121, 122). As a result, many clinicians use Holter monitoring to screen patients with LQTS annually or biannually. There is no available data to support this practice. Evaluation of asymptomatic pediatric patients with known or suspected LQTS is a class I indication for Holter monitoring according to the most recent ACC/AHA guidelines (22). Whether monitoring should be routinely undertaken in asymptomatic adults, who are likely to be selected survivors, is less certain.

   Brugada syndrome is a familial syndrome of ST segment elevation in the right precordial leads, right bundle branch block (RBBB) and sudden death (123). Brugada syndrome is believed to be caused by abnormalities of the sodium channel associated with mutation of the gene SCN5A (129). A typical Brugada ECG pattern has been noted in asymptomatic people who have no family history of syncope or sudden death (127). Some patients with Brugada syndrome have no resting ECG abnormality, or display the ECG abnormality only intermittently. Patients with Brugada syndrome who are at risk for sudden death benefit from ICD placement (128). It is unclear how to determine which asymptomatic patients are at risk. There is no clear role yet for ambulatory monitoring or use of the other risk stratification techniques described above in patients with suspected Brugada syndrome.

   Congenital heart block places patients at risk for LV dysfunction, mitral regurgitation (MR) due to LV dilation, and sudden death (131). The likelihood of these complications is diminished by ventricular pacing (131). One study of 27 asymptomatic patients with congenital heart block followed for 8+/-3 years found that the presence of a daytime heart rate less than 50 beats per minute or evidence of an unstable junctional escape (junctional exit block or ventricular arrhythmias) predicted an increased likelihood of complications (132). A more recent study followed 102 patients for up to 30 years and found that ventricular response rate decreased with age with associated increases in ventricular ectopy and worsening of LV function and MR (131). Only a prolonged corrected QT interval was found to be predictive of syncope. Most patients who had syncope were under 30 years old. Our practice is to screen young patients with congenital heart block yearly by Holter monitor to evaluate their ventricular response, corrected QT interval, and ventricular ectopic activity. Exercise testing can provide additional information as to the hemodynamic consequences of bradycardia during exertion. We recommend placement of a permanent pacemaker when patients develop symptomatic bradycardia, exercise intolerance, QT prolongation (greater than 500 ms), frequent ventricular ectopy or a wide complex escape rhythm, worsening mitral regurgitation and left ventricular dysfunction. This practice differs from that outlined in the recent ACC/AHA pacing guidelines (133) only in that we include QT prolongation among absolute indications for pacing in this population. Holter monitoring is limited by the brief period of time during which the monitor is worn. Consequently, episodic QT prolongation, severe bradycardia, and NSVT may be missed. Patients may develop complications of congenital heart block despite the absence of detectable risk factors, possibly in part because periodic Holter monitoring does not adequately disclose their day to day rhythm. As in patients with structural heart disease, palpitations, presyncope and syncope need to be taken very seriously in patients with the electrophysiologic disorders discussed above, and should be evaluated by event monitor or invasive testing (table 2) depending on the clinical setting.

   Emerging technologies will continue to change the way diagnoses are made in electrophysiology. In particular, advances in ambulatory monitoring will facilitate the diagnosis of arrhythmia in the outpatient setting. Implantable loop recorders can now self trigger in the setting of prespecified changes in heart rate, a feature which may improve the diagnostic yield of ILRs used in the evaluation of syncope. Ambulatory monitors capable of recording and transmitting blood pressure and oximetry data in addition to ECG data will eventually become available, and will allow more comprehensive monitoring. These systems may provide physicians with an improved understanding of the clinical significance of detected arrhythmias. Increasing information regarding the clinical utility of currently available technology will also change the evaluation of arrhythmias. Emerging techniques for risk stratification such as heart rate variability, T wave alternans, QT dispersion and the signal averaged ECG may be employed routinely once more information as to their clinical applicability becomes available.


1. Holter NJ. New method for heart studies: Continuous electrocardiography of active subjects over long periods is now practical. Science 1961; 134:1214-1220.

2. McClennen S, Zimetbaum PJ, Ho KK, Goldberger AL. Holter monitoring: are two days better than one? Am J Cardiol 2000 Sep 1; 86:562-4, A9.

3. Krahn AD, Klein GJ, Norris C, Yee R. The etiology of syncope in patients with negative tilt table and electrophysiological testing. Circulation 1995; 92:1819-24.

4. Benditt DG, Ferguson DW, Grubb BP, et al. Tilt table testing for assessing syncope. American College of Cardiology. J Am Coll Cardiol 1996; 28:263-75.

5. Kapoor WN, Brant N. Evaluation of syncope by upright tilt testing with isoproterenol. A nonspecific test. Ann Intern Med 1992; 116:358-63.

6. Kapoor WN, Smith MA, Miller NL. Upright tilt testing in evaluating syncope: a comprehensive literature review [see comments]. Am J Med 1994; 97:78-88.

7. Simson MB. Use of signals in the terminal QRS complex to identify patients with ventricular tachycardia after myocardial infarction. Circulation 1981; 64:235-42.

8. Breithardt G, Becker R, Seipel L, Abendroth RR, Ostermeyer J. Non-invasive detection of late potentials in man--a new marker for ventricular tachycardia. Eur Heart J 1981; 2:1-11.

9. Breithardt G, Cain ME, el-Sherif N, et al. Standards for analysis of ventricular late potentials using high-resolution or signal-averaged electrocardiography. A statement by a Task Force Committee of the European Society of Cardiology, the American Heart Association, and the American College of Cardiology. Circulation 1991; 83:1481-8.

10. Borggrefe M, Fetsch T, Martinez-Rubio A, Makijarvi M, Breithardt G. Prediction of arrhythmia risk based on signal-averaged ECG in postinfarction patients. Pacing Clin Electrophysiol 1997; 20:2566-76.

11. Kanovsky MS, Falcone RA, Dresden CA, Josephson ME, Simson MB. Identification of patients with ventricular tachycardia after myocardial infarction: signal-averaged electrocardiogram, Holter monitoring, and cardiac catheterization. Circulation 1984; 70:264-70.

12. Kuchar DL, Thorburn CW, Sammel NL. Prediction of serious arrhythmic events after myocardial infarction: signal-averaged electrocardiogram, Holter monitoring and radionuclide ventriculography. J Am Coll Cardiol 1987; 9:531-8.

13. Cripps T, Bennett D, Camm J, Ward D. Prospective evaluation of clinical assessment, exercise testing and signal-averaged electrocardiogram in predicting outcome after acute myocardial infarction. Am J Cardiol 1988; 62:995-9.

14. el-Sherif N, Ursell SN, Bekheit S, et al. Prognostic significance of the signal-averaged ECG depends on the time of recording in the postinfarction period. Am Heart J 1989; 118:256-64.

15. Breithardt G, Schwarzmaier J, Borggrefe M, Haerten K, Seipel L. Prognostic significance of late ventricular potentials after acute myocardial infarction. Eur Heart J 1983; 4:487-95.

16. Gomes JA, Winters SL, Stewart D, Horowitz S, Milner M, Barreca P. A new noninvasive index to predict sustained ventricular tachycardia and sudden death in the first year after myocardial infarction: based on signal-averaged electrocardiogram, radionuclide ejection fraction and Holter monitoring. J Am Coll Cardiol 1987; 10:349-57.

17. Cain ME, Anderson JL, Arnsdorf MF, Mason JW, Scheinman MM, Waldo AL. Signal-averaged electrocardiography. J Am Coll Cardiol 1996; 27:238-49.

18. Steinberg JS, Zelenkofske S, Wong SC, Gelernt M, Sciacca R, Menchavez E. Value of the P-wave signal-averaged ECG for predicting atrial fibrillation after cardiac surgery. Circulation 1993; 88:2618-22.

19. Tamis JE, Steinberg JS. Value of the signal-averaged P wave analysis in predicting atrial fibrillation after cardiac surgery. J Electrocardiol 1998; 30 Suppl:36-43.

20. Hohnloser SH, Klingenheben T, Zabel M, Li YG. Heart rate variability used as an arrhythmia risk stratifier after myocardial infarction. Pacing Clin Electrophysiol 1997; 20:2594-601.

21. Schwartz PJ, La Rovere MT, Vanoli E. Autonomic nervous system and sudden cardiac death. Experimental basis and clinical observations for post-myocardial infarction risk stratification. Circulation 1992; 85:I77-91.

22. Crawford MH, Bernstein SJ, Deedwania PC, et al. ACC/AHA Guidelines for Ambulatory Electrocardiography. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Revise the Guidelines for Ambulatory Electrocardiography). Developed in collaboration with the North American Society for Pacing and Electrophysiology. J Am Coll Cardiol 1999; 34:912-48.

23. Bigger JT, Jr., Fleiss JL, Steinman RC, Rolnitzky LM, Kleiger RE, Rottman JN. Correlations among time and frequency domain measures of heart period variability two weeks after acute myocardial infarction. Am J Cardiol 1992; 69:891-8.

24. Bigger JT, Jr., Kleiger RE, Fleiss JL, Rolnitzky LM, Steinman RC, Miller JP. Components of heart rate variability measured during healing of acute myocardial infarction. Am J Cardiol 1988; 61:208-15.

25. Bigger JT, Jr., Fleiss JL, Rolnitzky LM, Steinman RC, Schneider WJ. Time course of recovery of heart period variability after myocardial infarction. J Am Coll Cardiol 1991; 18:1643-9.

26. Kleiger RE, Miller JP, Bigger JT, Jr., Moss AJ. Decreased heart rate variability and its association with increased mortality after acute myocardial infarction. Am J Cardiol 1987; 59:256-62.

27. Zuanetti G, Neilson JM, Latini R, Santoro E, Maggioni AP, Ewing DJ. Prognostic significance of heart rate variability in post-myocardial infarction patients in the fibrinolytic era. The GISSI-2 results. Gruppo Italiano per lo Studio della Sopravvivenza nell' Infarto Miocardico. Circulation 1996; 94:432-6.

28. Odemuyiwa O, Malik M, Farrell T, Bashir Y, Poloniecki J, Camm J. Comparison of the predictive characteristics of heart rate variability index and left ventricular ejection fraction for all-cause mortality, arrhythmic events and sudden death after acute myocardial infarction. Am J Cardiol 1991; 68:434-9.

29. Armoundas AA, Osaka M, Mela T, et al. T-wave alternans and dispersion of the QT interval as risk stratification markers in patients susceptible to sustained ventricular arrhythmias. Am J Cardiol 1998; 82:1127-9, A9.

30. Russell DC, Smith JH, Oliver MF. Transmembrane potential changes and ventricular fibrillation during repetitive myocardial ischaemia in the dog. Br Heart J 1979; 42:88-96.

31. Downar E, Janse MJ, Durrer D. The effect of acute coronary artery occlusion on subepicardial transmembrane potentials in the intact porcine heart. Circulation 1977; 56:217-24.

32. Murda'h MA, McKenna WJ, Camm AJ. Repolarization alternans: techniques, mechanisms, and cardiac vulnerability. Pacing Clin Electrophysiol 1997; 20:2641-57.

33. Salerno JA, Previtali M, Panciroli C, et al. Ventricular arrhythmias during acute myocardial ischaemia in man. The role and significance of R-ST-T alternans and the prevention of ischaemic sudden death by medical treatment. Eur Heart J 1986; 7 Suppl A:63-75.

34. Kleinfeld MJ, Rozanski JJ. Alternans of the ST segment in Prinzmetal's angina. Circulation 1977; 55:574-7.

35. Joyal M, Feldman RL, Pepine CJ. ST-segment alternans during percutaneous transluminal coronary angioplasty. Am J Cardiol 1984; 54:915-6.

36. Smith JM, Clancy EA, Valeri CR, Ruskin JN, Cohen RJ. Electrical alternans and cardiac electrical instability. Circulation 1988; 77:110-21.

37. Hohnloser SH, Klingeheben T, Zabel M. Heart rate threshold is important for detecting T wave alternans (abstract). PACE 1996; 19:II-588.

38. Rosenbaum DS, Jackson LE, Smith JM, Garan H, Ruskin JN, Cohen RJ. Electrical alternans and vulnerability to ventricular arrhythmias. N Engl J Med 1994; 330:235-41.

39. Estes MNA, Zipes DP, el-Sherif N. Electrical alternans during rest and exercise as a predictor of vulnerability to ventricular arrhythmias. J Am Coll Cardiol 1995; Special Issue:409A.

40. Priori SG, Napolitano C, Diehl L, Schwartz PJ. Dispersion of the QT interval. A marker of therapeutic efficacy in the idiopathic long QT syndrome. Circulation 1994; 89:1681-9.

41. de Bruyne MC, Hoes AW, Kors JA, Hofman A, van Bemmel JH, Grobbee DE. QTc dispersion predicts cardiac mortality in the elderly: the Rotterdam Study. Circulation 1998; 97:467-72.

42. Okin PM, Devereux RB, Howard BV, Fabsitz RR, Lee ET, Welty TK. Assessment of QT Interval and QT Dispersion for Prediction of All-Cause and Cardiovascular Mortality in American Indians : The Strong Heart Study. Circulation 2000 Jan 4; 101:61-66.

43. Zimetbaum P, Josephson ME. Evaluation of patients with palpitations. N Engl J Med 1998; 338:1369-73.

44. Varma N, Josephson ME. Therapy of "idiopathic" ventricular tachycardia. J Cardiovasc Electrophysiol 1997; 8:104-16.

45. Zimetbaum PJ, Josephson ME. The evolving role of ambulatory arrhythmia monitoring in general clinical practice. Ann Intern Med 1999; 130:848-56.

46. Zimetbaum PJ, Kim KY, Josephson ME, Goldberger AL, Cohen DJ. Diagnostic yield and optimal duration of continuous-loop event monitoring for the diagnosis of palpitations. A cost-effectiveness analysis. Ann Intern Med 1998; 128:890-5.

47. Reiffel JA, Schulhof E, Joseph B, Severance E, Wyndus P, McNamara A. Optimum duration of transtelephonic ECG monitoring when used for transient symptomatic event detection. J Electrocardiol 1991; 24:165-8.

48. Zimetbaum P, Kim KY, Ho KK, Zebede J, Josephson ME, Goldberger AL. Utility of patient-activated cardiac event recorders in general clinical practice. Am J Cardiol 1997; 79:371-2.

49. Kinlay S, Leitch JW, Neil A, Chapman BL, Hardy DB, Fletcher PJ. Cardiac event recorders yield more diagnoses and are more cost-effective than 48-hour Holter monitoring in patients with palpitations. A controlled clinical trial [see comments]. Ann Intern Med 1996; 124:16-20.

50. Kapoor WN, Karpf M, Wieand S, Peterson JR, Levey GS. A prospective evaluation and follow-up of patients with syncope. N Engl J Med 1983; 309:197-204.

51. Day SC, Cook EF, Funkenstein H, Goldman L. Evaluation and outcome of emergency room patients with transient loss of consciousness. Am J Med 1982; 73:15-23.

52. Fonarow GC, Feliciano Z, Boyle NG, et al. Improved survival in patients with nonischemic advanced heart failure and syncope treated with an implantable cardioverter-defibrillator. Am J Cardiol 2000 Apr 15; 85:981-5.

53. DiMarco JP, Philbrick JT. Use of ambulatory electrocardiographic (Holter) monitoring [see comments]. Ann Intern Med 1990; 113:53-68.

54. Bass EB, Curtiss EI, Arena VC, et al. The duration of Holter monitoring in patients with syncope. Is 24 hours enough? Arch Intern Med 1990; 150:1073-8.

55. Brown AP, Dawkins KD, Davies JG. Detection of arrhythmias: use of a patient-activated ambulatory electrocardiogram device with a solid-state memory loop. Br Heart J 1987; 58:251-3.

56. Linzer M, Pritchett EL, Pontinen M, McCarthy E, Divine GW. Incremental diagnostic yield of loop electrocardiographic recorders in unexplained syncope. Am J Cardiol 1990; 66:214-9.

57. Krahn AD, Klein GJ, Yee R, Takle-Newhouse T, Norris C. Use of an extended monitoring strategy in patients with problematic syncope. Reveal Investigators. Circulation 1999; 99:406-10.

58. Krahn AD, Klein GJ, Yee R, Manda V. The high cost of syncope: cost implications of a new insertable loop recorder in the investigation of recurrent syncope. Am Heart J 1999; 137:870-7.

59. Anderson KP, DeCamilla J, Moss AJ. Clinical significance of ventricular tachycardia (3 beats or longer) detected during ambulatory monitoring after myocardial infarction. Circulation 1978; 57:890-7.

60. Buxton AE, Marchlinski FE, Waxman HL, Flores BT, Cassidy DM, Josephson ME. Prognostic factors in nonsustained ventricular tachycardia. Am J Cardiol 1984; 53:1275-9.

61. Bigger JT, Jr., Fleiss JL, Rolnitzky LM. Prevalence, characteristics and significance of ventricular tachycardia detected by 24-hour continuous electrocardiographic recordings in the late hospital phase of acute myocardial infarction. Am J Cardiol 1986; 58:1151-60.

62. Mukharji J, Rude RE, Poole WK, et al. Risk factors for sudden death after acute myocardial infarction: two-year follow-up. Am J Cardiol 1984; 54:31-6.

63. Moss AJ, Hall WJ, Cannom DS, et al. Improved survival with an implanted defibrillator in patients with coronary disease at high risk for ventricular arrhythmia. Multicenter Automatic Defibrillator Implantation Trial Investigators [see comments]. N Engl J Med 1996; 335:1933-40.

64. Buxton AE, Lee KL, Fisher JD, Josephson ME, Prystowsky EN, Hafley G. A randomized study of the prevention of sudden death in patients with coronary artery disease. Multicenter Unsustained Tachycardia Trial Investigators. N Engl J Med 1999; 341:1882-90.

65. Naccarelli GV, Wolbrette DL, Dell'Orfano JT, Patel HM, Luck JC. A decade of clinical trial developments in postmyocardial infarction, congestive heart failure, and sustained ventricular tachyarrhythmia patients: from CAST to AVID and beyond. Cardiac Arrhythmic Suppression Trial. Antiarrhythmic Versus Implantable Defibrillators [see comments]. J Cardiovasc Electrophysiol 1998; 9:864-91.

66. Josephson ME, Buston AE, Lee KL, Hafley GE. Prognostic Value of the ECG in MUSTT Patients. Circulation 2000; 102:II-494.

67. Cain ME, Gomes JA, Lee KL, Buxton AE. Performance of the Signal-Averaged ECG and Electrophysiologic Testing in Identifying Patients Vulnerable to Arrhythmic or Cardiac Death. Circulation 1999; 100:I-244.

68. Heart rate variability. Standards of measurement, physiological interpretation, and clinical use. Task Force of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology. Eur Heart J 1996; 17:354-81.

69. Bigger JT, Jr., Fleiss JL, Steinman RC, Rolnitzky LM, Kleiger RE, Rottman JN. Frequency domain measures of heart period variability and mortality after myocardial infarction. Circulation 1992; 85:164-71.

70. Farrell TG, Bashir Y, Cripps T, et al. Risk stratification for arrhythmic events in postinfarction patients based on heart rate variability, ambulatory electrocardiographic variables and the signal-averaged electrocardiogram [see comments]. J Am Coll Cardiol 1991; 18:687-97.

71. Ikeda T, Sakata T, Takami M, et al. Combined assessment of T-wave alternans and late potentials used to predict arrhythmic events after myocardial infarction. A prospective study. J Am Coll Cardiol 2000 Mar 1; 35:722-30.

72. Zareba W, Moss AJ, le Cessie S. Dispersion of ventricular repolarization and arrhythmic cardiac death in coronary artery disease. Am J Cardiol 1994; 74:550-3.

73. Zabel M, Klingenheben T, Franz MR, Hohnloser SH. Assessment of QT dispersion for prediction of mortality or arrhythmic events after myocardial infarction: results of a prospective, long-term follow-up study [see comments]. Circulation 1998; 97:2543-50.

74. Spargias KS, Lindsay SJ, Kawar GI, et al. QT dispersion as a predictor of long-term mortality in patients with acute myocardial infarction and clinical evidence of heart failure [see comments]. Eur Heart J 1999; 20:1158-65.

75. Huang SK, Messer JV, Denes P. Significance of ventricular tachycardia in idiopathic dilated cardiomyopathy: observations in 35 patients. Am J Cardiol 1983; 51:507-12.

76. Suyama A, Anan T, Araki H, Takeshita A, Nakamura M. Prevalence of ventricular tachycardia in patients with different underlying heart diseases: a study by Holter ECG monitoring. Am Heart J 1986; 112:44-51.

77. Neri R, Mestroni L, Salvi A, Pandullo C, Camerini F. Ventricular arrhythmias in dilated cardiomyopathy: efficacy of amiodarone. Am Heart J 1987; 113:707-15.

78. Meinertz T, Hofmann T, Kasper W, et al. Significance of ventricular arrhythmias in idiopathic dilated cardiomyopathy. Am J Cardiol 1984; 53:902-7.

79. Kron J, Hart M, Schual-Berke S, Niles NR, Hosenpud JD, McAnulty JH. Idiopathic dilated cardiomyopathy. Role of programmed electrical stimulation and Holter monitoring in predicting those at risk of sudden death. Chest 1988; 93:85-90.

80. Unverferth DV, Magorien RD, Moeschberger ML, Baker PB, Fetters JK, Leier CV. Factors influencing the one-year mortality of dilated cardiomyopathy. Am J Cardiol 1984; 54:147-52.

81. Pelliccia F, Gallo P, Cianfrocca C, d'Amati G, Bernucci P, Reale A. Relation of complex ventricular arrhythmias to presenting features and prognosis in dilated cardiomyopathy. Int J Cardiol 1990; 29:47-54.

82. Ikegawa T, Chino M, Hasegawa H, et al. Prognostic significance of 24-hour ambulatory electrocardiographic monitoring in patients with dilative cardiomyopathy: a prospective study. Clin Cardiol 1987; 10:78-82.

83. Singh SN, Fletcher RD, Fisher S, et al. Veterans Affairs congestive heart failure antiarrhythmic trial. CHF STAT Investigators. Am J Cardiol 1993; 72:99F-102F.

84. Massie BM, Fisher SG, Radford M, et al. Effect of amiodarone on clinical status and left ventricular function in patients with congestive heart failure. CHF-STAT Investigators [published erratum appears in Circulation 1996 Nov 15;94(10):2668]. Circulation 1996; 93:2128-34.

85. Cohn JN, Johnson G, Ziesche S, et al. A comparison of enalapril with hydralazine-isosorbide dinitrate in the treatment of chronic congestive heart failure [see comments]. N Engl J Med 1991; 325:303-10.

86. Doval HC, Nul DR, Grancelli HO, Perrone SV, Bortman GR, Curiel R. Randomised trial of low-dose amiodarone in severe congestive heart failure. Grupo de Estudio de la Sobrevida en la Insuficiencia Cardiaca en Argentina (GESICA) [see comments]. Lancet 1994; 344:493-8.

87. Doval HC, Nul DR, Grancelli HO, et al. Nonsustained ventricular tachycardia in severe heart failure. Independent marker of increased mortality due to sudden death. GESICA-GEMA Investigators [see comments]. Circulation 1996; 94:3198-203.

88. Singh SN, Fisher SG, Carson PE, Fletcher RD. Prevalence and significance of nonsustained ventricular tachycardia in patients with premature ventricular contractions and heart failure treated with vasodilator therapy. Department of Veterans Affairs CHF STAT Investigators. J Am Coll Cardiol 1998; 32:942-7.

89. Sim I, McDonald KM, Lavori PW, Norbutas CM, Hlatky MA. Quantitative overview of randomized trials of amiodarone to prevent sudden cardiac death [see comments]. Circulation 1997; 96:2823-9.

90. Klingenheben T, Zabel M, RB DA, Cohen RJ, Hohnloser SH. Predictive value of T-wave alternans for arrhythmic events in patients with congestive heart failure [letter]. Lancet 2000 Aug 19; 356:651-2.

91. Hennersdorf MG, Perings C, Niebch V, Vester EG, Strauer BE. T wave alternans as a risk predictor in patients with cardiomyopathy and mild-to-moderate heart failure [In Process Citation]. Pacing Clin Electrophysiol 2000 Sep; 23:1386-91.

92. Adachi K, Ohnishi Y, Shima T, et al. Determinant of microvolt-level T-wave alternans in patients with dilated cardiomyopathy. J Am Coll Cardiol 1999; 34:374-80.

93. Fauchier L, Babuty D, Cosnay P, Poret P, Rouesnel P, Fauchier JP. Long-term prognostic value of time domain analysis of signal-averaged electrocardiography in idiopathic dilated cardiomyopathy [In Process Citation]. Am J Cardiol 2000 Mar 1; 85:618-23.

94. Hoffmann J, Grimm W, Menz V, Knop U, Maisch B. Heart rate variability and major arrhythmic events in patients with idiopathic dilated cardiomyopathy. Pacing Clin Electrophysiol 1996; 19:1841-4.

95. Fei L, Keeling PJ, Gill JS, et al. Heart rate variability and its relation to ventricular arrhythmias in congestive heart failure. Br Heart J 1994; 71:322-8.

96. Ponikowski P, Anker SD, Chua TP, et al. Depressed heart rate variability as an independent predictor of death in chronic congestive heart failure secondary to ischemic or idiopathic dilated cardiomyopathy. Am J Cardiol 1997; 79:1645-50.

97. Fauchier L, Babuty D, Cosnay P, Autret ML, Fauchier JP. Heart rate variability in idiopathic dilated cardiomyopathy: characteristics and prognostic value. J Am Coll Cardiol 1997; 30:1009-14.

98. Jiang W, Hathaway WR, McNulty S, et al. Ability of heart rate variability to predict prognosis in patients with advanced congestive heart failure. Am J Cardiol 1997; 80:808-11.

99. Barr CS, Naas A, Freeman M, Lang CC, Struthers AD. QT dispersion and sudden unexpected death in chronic heart failure [see comments]. Lancet 1994; 343:327-9.

100. Brooksby P, Batin PD, Nolan J, et al. The relationship between QT intervals and mortality in ambulant patients with chronic heart failure. The united kingdom heart failure evaluation and assessment of risk trial (UK-HEART) [see comments]. Eur Heart J 1999; 20:1335-41.

101. Grimm W, Glaveris C, Hoffmann J, et al. Noninvasive arrhythmia risk stratification in idiopathic dilated cardiomyopathy: design and first results of the Marburg Cardiomyopathy Study. Pacing Clin Electrophysiol 1998; 21:2551-6.

102. Wigle ED, Rakowski H, Kimball BP, Williams WG. Hypertrophic cardiomyopathy. Clinical spectrum and treatment [see comments]. Circulation 1995; 92:1680-92.

103. Maron BJ, Savage DD, Wolfson JK, Epstein SE. Prognostic significance of 24 hour ambulatory electrocardiographic monitoring in patients with hypertrophic cardiomyopathy: a prospective study. Am J Cardiol 1981; 48:252-7.

104. Knoebel SB, Crawford MH, Dunn MI, et al. Guidelines for ambulatory electrocardiography. A report of the American College of Cardiology/American Heart Association Task Force on Assessment of Diagnostic and Therapeutic Cardiovascular Procedures (Subcommittee on Ambulatory Electrocardiography). Circulation 1989; 79:206-15.

105. Spirito P, Rapezzi C, Autore C, et al. Prognosis of asymptomatic patients with hypertrophic cardiomyopathy and nonsustained ventricular tachycardia [see comments]. Circulation 1994; 90:2743-7.

106. Fananapazir L, Chang AC, Epstein SE, McAreavey D. Prognostic determinants in hypertrophic cardiomyopathy. Prospective evaluation of a therapeutic strategy based on clinical, Holter, hemodynamic, and electrophysiological findings. Circulation 1992; 86:730-40.

107. Cecchi F, Olivotto I, Montereggi A, Squillatini G, Dolara A, Maron BJ. Prognostic value of non-sustained ventricular tachycardia and the potential role of amiodarone treatment in hypertrophic cardiomyopathy: assessment in an unselected non-referral based patient population [see comments]. Heart 1998; 79:331-6.

108. Maron BJ, Shen WK, Link MS, et al. Efficacy of Implantable Cardioverter-Defibrillators for the Prevention of Sudden Death in Patients with Hypertrophic Cardiomyopathy. N Engl J Med 2000 Feb 10; 342:365-373.

109. Elliott PM, Poloniecki J, Dickie S, et al. Sudden death in hypertrophic cardiomyopathy: identification of high risk patients.[In Process Citation]. J Am Coll Cardiol 2000 Dec; 36:2212-8.

110. McKenna WJ, Franklin RC, Nihoyannopoulos P, Robinson KC, Deanfield JE. Arrhythmia and prognosis in infants, children and adolescents with hypertrophic cardiomyopathy. J Am Coll Cardiol 1988; 11:147-53.

111. Murda'h M, Nagayoshi H, Albrecht P. T-wave alternans as a predictor of sudden death in hypertrophic cardiomyopathy (abstract). circulation 1996; 94(Suppl.):I-669.

112. Yi G, Elliott P, McKenna WJ, et al. QT dispersion and risk factors for sudden cardiac death in patients with hypertrophic cardiomyopathy. Am J Cardiol 1998; 82:1514-9.

113. Counihan PJ, Fei L, Bashir Y, Farrell TG, Haywood GA, McKenna WJ. Assessment of heart rate variability in hypertrophic cardiomyopathy. Association with clinical and prognostic features. Circulation 1993; 88:1682-90.

114. Pinsky WW, Arciniegas E. Tetralogy of Fallot. Pediatr Clin North Am 1990; 37:179-92.

115. Chandar JS, Wolff GS, Garson A, Jr., et al. Ventricular arrhythmias in postoperative tetralogy of Fallot. Am J Cardiol 1990; 65:655-61.

116. Joffe H, Georgakopoulos D, Celermajer DS, Sullivan ID, Deanfield JE. Late ventricular arrhythmia is rare after early repair of tetralogy of Fallot [see comments]. J Am Coll Cardiol 1994; 23:1146-50.

117. Cullen S, Celermajer DS, Franklin RC, Hallidie-Smith KA, Deanfield JE. Prognostic significance of ventricular arrhythmia after repair of tetralogy of Fallot: a 12-year prospective study. J Am Coll Cardiol 1994; 23:1151-5.

118. Marelli A, Moodie D. Adult congenital heart disease. In: Topol E, ed. Textbook of Cardiovascular Medicine. Philadelphia: Lippincott-Raven, 1998:769-97.

119. Schwartz PJ. The long QT syndrome. Curr Probl Cardiol 1997; 22:297-351.

120. Tan HL, Hou CJ, Lauer MR, Sung RJ. Electrophysiologic mechanisms of the long QT interval syndromes and torsade de pointes. Ann Intern Med 1995; 122:701-14.

121. Eggeling T, Osterhues HH, Hoeher M, Gabrielsen FG, Weismueller P, Hombach V. Value of Holter monitoring in patients with the long QT syndrome. Cardiology 1992; 81:107-14.

122. Locati EH, Maison-Blanche P, Dejode P, Cauchemez B, Coumel P. Spontaneous sequences of onset of torsade de pointes in patients with acquired prolonged repolarization: quantitative analysis of Holter recordings. J Am Coll Cardiol 1995; 25:1564-75.

123. Brugada P, Brugada J. Right bundle branch block, persistent ST segment elevation and sudden cardiac death: a distinct clinical and electrocardiographic syndrome. A multicenter report [see comments]. J Am Coll Cardiol 1992; 20:1391-6.

124. Kirschner RH, Eckner FA, Baron RC. The cardiac pathology of sudden, unexplained nocturnal death in Southeast Asian refugees. Jama 1986; 256:2700-5.

125. Gotoh K. A histopathological study on the conduction system of the so-called "Pokkuri disease" (sudden unexpected cardiac death of unknown origin in Japan). Jpn Circ J 1976; 40:753-68.

126. Nademanee K, Veerakul G, Nimmannit S, et al. Arrhythmogenic marker for the sudden unexplained death syndrome in Thai men. Circulation 1997; 96:2595-600.

127. Hermida JS, Lemoine JL, Aoun FB, Jarry G, Rey JL, Quiret JC. Prevalence of the brugada syndrome in an apparently healthy population. Am J Cardiol 2000 Jul 1; 86:91-4.

128. Brugada J, Brugada R, Brugada P. Right bundle-branch block and ST-segment elevation in leads V1 through V3: a marker for sudden death in patients without demonstrable structural heart disease. Circulation 1998; 97:457-60.

129. Chen Q, Kirsch GE, Zhang D, et al. Genetic basis and molecular mechanism for idiopathic ventricular fibrillation. Nature 1998; 392:293-6.

130. Brugada R, Brugada J, Antzelevitch C, et al. Sodium channel blockers identify risk for sudden death in patients with ST-segment elevation and right bundle branch block but structurally normal hearts. Circulation 2000 Feb 8; 101:510-5.

131. Michaelsson M, Jonzon A, Riesenfeld T. Isolated congenital complete atrioventricular block in adult life. A prospective study [see comments]. Circulation 1995; 92:442-9.

132. Dewey RC, Capeless MA, Levy AM. Use of ambulatory electrocardiographic monitoring to identify high-risk patients with congenital complete heart block. N Engl J Med 1987; 316:835-9.

133. Gregoratos G, Cheitlin MD, Conill A, et al. ACC/AHA Guidelines for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices: Executive Summary--a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Pacemaker Implantation). Circulation 1998; 97:1325-35.

134. Preliminary report: effect of encainide and flecainide on mortality in a randomized trial of arrhythmia suppression after myocardial infarction. The Cardiac Arrhythmia Suppression Trial (CAST) Investigators [see comments]. N Engl J Med 1989; 321:406-12.

135. Teo KK, Yusuf S, Furberg CD. Effects of prophylactic antiarrhythmic drug therapy in acute myocardial infarction. An overview of results from randomized controlled trials [see comments]. Jama 1993; 270:1589-95.

136. Waldo AL, Camm AJ, deRuyter H, et al. Effect of d-sotalol on mortality in patients with left ventricular dysfunction after recent and remote myocardial infarction. The SWORD Investigators. Survival With Oral d-Sotalol [see comments] [published erratum appears in Lancet 1996 Aug 10;348(9024):416]. Lancet 1996; 348:7-12.

137. Singh SN, Fletcher RD, Fisher SG, et al. Amiodarone in patients with congestive heart failure and asymptomatic ventricular arrhythmia. Survival Trial of Antiarrhythmic Therapy in Congestive Heart Failure [see comments]. N Engl J Med 1995; 333:77-82.

138. Reiter MJ, Karagounis LA, Mann DE, Reiffel JA, Hahn E, Hartz V. Reproducibility of drug efficacy predictions by Holter monitoring in the electrophysiologic study versus electrocardiographic monitoring (ESVEM) trial. ESVEM Investigators. Am J Cardiol 1997; 79:315-22.

139. Biblo LA, Carlson MD, Waldo AL. Insights into the Electrophysiology Study Versus Electrocardiographic Monitoring Trial: its programmed stimulation protocol may introduce bias when assessing long-term antiarrhythmic drug therapy. J Am Coll Cardiol 1995; 25:1601-4.

140. Winters SL, Curwin JH. Sotalol and the management of ventricular arrhythmias: implications of ESVEM [editorial]. Pacing Clin Electrophysiol 1995; 18:377-8.

141. Page RL, Wilkinson WE, Clair WK, McCarthy EA, Pritchett EL. Asymptomatic arrhythmias in patients with symptomatic paroxysmal atrial fibrillation and paroxysmal supraventricular tachycardia. Circulation 1994; 89:224-7.

142. Zimetbaum PJ, Schreckengost VE, Cohen DJ, et al. Evaluation of outpatient initiation of antiarrhythmic drug therapy in patients reverting to sinus rhythm after an episode of atrial fibrillation. Am J Cardiol 1999; 83:450-2, A9.

143. Mandel W, Hayakawa H, Danzig R, Marcus HS. Evaluation of sino-atrial node function in man by overdrive suppression. Circulation 1971; 44:59-66.

144. Strauss HC, Saroff AL, Bigger JT, Jr., Giardina EG. Premature atrial stimulation as a key to the understanding of sinoatrial conduction in man. Presentation of data and critical review of the literature. Circulation 1973; 47:86-93.

145. Strauss HC, Bigger JT, Saroff AL, Giardina EG. Electrophysiologic evaluation of sinus node function in patients with sinus node dysfunction. Circulation 1976; 53:763-76.

146. Scheinman MM, Peters RW, Modin G, Brennan M, Mies C, J OY. Prognostic value of infranodal conduction time in patients with chronic bundle branch block. Circulation 1977; 56:240-4.

147. McAnulty JH, Rahimtoola SH, Murphy E, et al. Natural history of "high-risk" bundle-branch block: final report of a prospective study. N Engl J Med 1982; 307:137-43.

148. Dhingra RC, Palileo E, Strasberg B, et al. Significance of the HV interval in 517 patients with chronic bifascicular block. Circulation 1981; 64:1265-71.

149. Tonkin AM, Heddle WF, Tornos P. Intermittent atrioventricular block: procainamide administration as a provocative test. Aust N Z J Med 1978; 8:594-602.

150. Dhingra RC, Wyndham C, Bauernfeind R, et al. Significance of block distal to the His bundle induced by atrial pacing in patients with chronic bifascicular block. Circulation 1979; 60:1455-64.

151. Myerburg RJ, Castellanos A. Evolution, evaluation, and efficacy of implantable cardioverter-defibrillator technology [editorial; comment]. Circulation 1992; 86:691-3.

152. Josephson ME. Clinical Cardiac Electrophysiology: Techniques and Interpretations. Philadelphia: Lea & Febiger, 1993.

153. ACC/AHA Task Force Report. Guidelines for Clinical Intracardiac Electrophysiological and Catheter Ablation Procedures. A report of the American College of Cardiology/American Heart Association task force on practice guidelines (Committee on Clinical Intracardiac Electrophysiologic and Catheter Ablation Procedures). Developed in collaboration with the North American Society of Pacing and Electrophysiology. J Cardiovasc Electrophysiol 1995; 6:652-79.


Your questions, contributions and commentaries will be answered
by the lecturer or experts on the subject in the Arrhythmia list.
Please fill in the form (in Spanish, Portuguese or English) and press the "Send" button.

or commentary
Name and Surname:
E-Mail address:


2nd Virtual Congress of Cardiology

Dr. Florencio Garófalo
Steering Committee
Dr. Raúl Bretal
Scientific Committee
Dr. Armando Pacher
Technical Committee - CETIFAC

Copyright© 1999-2001 Argentine Federation of Cardiology
All rights reserved


This company contributed to the Congress