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Incidence of and risk stratification for sudden cardiac death after myocardial infarction

Incidence of and risk stratification for sudden cardiac death after myocardial infarction
Author:
Philip J Podrid, MD, FACC
Section Editors:
Peter J Zimetbaum, MD
Bernard J Gersh, MB, ChB, DPhil, FRCP, MACC
Deputy Editor:
Todd F Dardas, MD, MS
Literature review current through: Jan 2024.
This topic last updated: Jun 13, 2022.

INTRODUCTION — The process of risk stratification in a patient who has had an acute myocardial infarction (MI) has two components:

●Early in-hospital identification of patients at increased risk for recurrent ischemic events

●Identification of patients at increased risk for arrhythmic or nonarrhythmic death

Patients who have had an acute MI are at increased risk for sudden cardiac death (SCD), most often due to a ventricular tachyarrhythmia. However, not all post-MI patients have the same risk of SCD. Thus, the therapeutic approach to the prevention of SCD depends upon the identification of those patients who are most likely to have a ventricular tachyarrhythmia and the effectiveness of the available preventive measures [1,2].

The incidence of SCD after acute MI and identification of patients at increased risk for SCD will be reviewed here. The approach to primary and secondary prevention of SCD post-MI, as well to risk stratification for recurrent ischemic events after ST elevation and non-ST elevation infarctions, are discussed separately. (See "Primary prevention of sudden cardiac death in patients with cardiomyopathy and heart failure with reduced LVEF" and "Secondary prevention of sudden cardiac death in heart failure and cardiomyopathy" and "Risk stratification after acute ST-elevation myocardial infarction" and "Risk stratification after non-ST elevation acute coronary syndrome".)

OUR APPROACH TO RISK STRATIFICATION — Although a large number of risk factors for SCD have been identified, significantly reduced left ventricular ejection fraction (LVEF) is the most widespread clinical identifier of patients at increased risk for SCD. Our approach to risk stratification of SCD post-MI is in general agreement with the recommendations of various professional societies [3-6].

●We recommend evaluation of LV function, including LVEF, prior to discharge post-MI and again at 90 days post-MI. (See 'LV dysfunction' below.)

●While invasive electrophysiology studies (EPS) are not routinely performed post-MI in contemporary practice, EPS can aid in the decision regarding implantable cardioverter-defibrillator (ICD) implantation in patients with nonsustained ventricular tachycardia who do not meet MADIT-2 or SCD-HeFT criteria and in patients with syncope or other symptoms (such as palpitations, lightheadedness or presyncope associated with NSVT) of suspected but not confirmed arrhythmic etiology. (See 'Inducible VT/VF' below.)

INCIDENCE OF SCD — One-year mortality following acute coronary syndrome (ACS) is approximately 5 percent, with three-quarters of the deaths due to a cardiovascular event [7]. Among all deaths in the first year, SCD (36 percent) and recurrent MI (23 percent) are the most commonly reported causes, with the relative contribution of SCD increasing more than 30 days post-ACS.

Mortality after acute MI, including SCD, has declined substantially since the 1970s due primarily to changes in the care of these patients [8-10]. These include:

●The initial treatment of acute MI with dual antiplatelet therapy, beta blockers, statins, and reperfusion using catheter-based treatments (eg, angioplasty and stents) and fibrinolytic agents.

●Secondary prevention measures. (See "Prevention of cardiovascular disease events in those with established disease (secondary prevention) or at very high risk".)

The incidence of ventricular arrhythmias after an MI remains elevated for months to years, if not indefinitely. Ventricular tachycardia (VT) and ventricular fibrillation (VF) are most frequent in the first hours of an infarction, and the incidence then declines in phases during the days, weeks, and months after the event. This pattern reflects the electrophysiologic manifestations of the evolving interactions between ischemia, infarction, reperfusion, and scar formation. A detailed discussion of ventricular arrhythmias in the acute phase of an MI is presented separately. (See "Ventricular arrhythmias during acute myocardial infarction: Incidence, mechanisms, and clinical features".)

For the purposes of long-term risk stratification, the time since an MI is relevant for two reasons:

●The clinical significance of risk factors may vary over time.

●The overall risk of events, regardless of risk profile, varies over time.

Elevated early risk — The definition of the "early" post-MI period has varied across studies over the years. UpToDate authors consider the "early" acute period as <48 hours post-MI and the "late" acute period as 48 hours to seven days post-MI, although some studies have defined the "early" risk to include as long as 30 days post-MI.

The increased risk of SCD in the first months post-MI was illustrated in reports from the VALIANT trial, from a community-based cohort, and from a pooled analysis:

●In the VALIANT population, which included 14,609 patients with LV dysfunction or heart failure (HF) after acute MI, the rate of SCD or resuscitated cardiac arrest was 1.4 percent in the first month compared with 0.14 percent per month after two years [11]. The event rate in the first month was higher (2.3 percent) in patients with an LVEF <30 percent.

●In a community-based (Olmsted County, MN) cohort of 2997 post-MI patients, which included patients with normal LV function, the 30-day cumulative incidence of SCD was 1.2 percent [10]. Following the first month, the risk of SCD fell to 1.2 percent per year.

●In a pooled analysis of 3104 patients with a recent MI and either an LVEF ≤40 percent or frequent ventricular ectopy, the rate of arrhythmic death during the first six months post-MI was 8 per 100 person years [12]. The rate declined and stabilized in the ensuing 18 months at approximately 4 per 100 person years.

Limitations of early risk stratification — Both risk assessment and treatment decisions during this early stage are complicated for several reasons:

●The arrhythmic substrate evolves as stunned myocardium recovers and scar formation occurs in regions of necrosis [13,14].

●With this physiologic evolution, the findings and implications of risk stratification tests (eg, nonsustained ventricular tachycardia, LV function) also change, leading to uncertainty regarding the prognostic significance of abnormal findings in the early postinfarction period.

Consistent with these concerns, two randomized trials that directly addressed the issue of early ICD placement for primary prevention of SCD (DINAMIT and IRIS) did not show an improvement in survival in patients with LV dysfunction randomly assigned to receive ICD placement within 31 or 40 days after an acute MI [15,16]. At present, ICD therapy for primary prevention is not recommended less than 40 days after MI.

While not standard contemporary practice in all patients, early electrophysiologic (EP) testing (more than 48 hours post-MI) may help stratify patients post-MI for ICD placement with suspected increased risk of SCD but in whom the traditional indications for ICD are not satisfied. In an observational study of 360 patients without sustained ventricular tachyarrhythmia who underwent EP testing with programmed ventricular stimulation on day nine post-MI, 39 percent of early post-MI patients had inducible monomorphic VT (EP positive group, of which 71 percent received an ICD) while 61 percent were noninducible (EP negative group, of which only six percent received an ICD) [17]. After two-year follow-up, the EP negative group had a lower risk of the primary combined endpoint of sudden death and spontaneous ventricular tachyarrhythmia (adjusted hazard ratio 0.46, 95% CI 0.22 to 0.95).

RISK FACTORS FOR CHRONIC PHASE (>7 DAYS) SCD — LV systolic function, evaluated using the LVEF, is the most commonly used marker for assessing the risk of late SCD post-MI. In addition to LVEF, a number of clinical features have been evaluated as possible risk factors for the development of a fatal arrhythmia following an acute MI:

●VT induced by electrophysiologic study (EPS)

●Spontaneous ventricular premature beats (VPBs) and more importantly nonsustained ventricular tachycardia documented on 24-hour ambulatory monitoring

●Late potentials on a signal averaged electrocardiogram (ECG)

●Reduced heart rate variability, assessed by ambulatory monitoring

●T wave (repolarization) alternans, especially seen with exercise testing

Sustained ventricular arrhythmias are not included on this list of risk factors, which may seem counterintuitive. However, sustained arrhythmias that occur in the early post-MI phase (usually defined as the first 48 hours) are generally considered epiphenomena of the MI and are not consistently associated with long-term prognosis. This lack of association with long term prognosis is more clearly established for early ventricular fibrillation (VF) and polymorphic VT. These arrhythmias are the only arrhythmias that are provoked by active ischemia, as occurs with an acute MI. Sustained monomorphic VT, even when it occurs early, may reflect permanent arrhythmic substrate. This substrate is most commonly myocardial fibrosis resulting in reentry. Patients with sustained arrhythmias after the early phase are managed according to secondary prevention strategies, and therefore are not included in primary prevention risk stratification protocols. (See "Ventricular arrhythmias during acute myocardial infarction: Incidence, mechanisms, and clinical features" and "Sustained monomorphic ventricular tachycardia in patients with structural heart disease: Treatment and prognosis" and "Secondary prevention of sudden cardiac death in heart failure and cardiomyopathy".)

The advent of reperfusion therapy (thrombolysis and percutaneous coronary intervention [PCI]) reduced the prognostic significance of many of the variables that have been useful for risk stratification in the past. (See 'Our approach to risk stratification' above.)

LV dysfunction — We recommend evaluation of LV function, including LVEF, prior to discharge post-MI and again at 90 days post-MI. Significant LV dysfunction, as measured by an LVEF <35 percent, is one of the most powerful predictors of mortality at six months (figure 1) and one year after MI [18-21]. However, early measurements may be misleading, since improvement in LVEF, beginning within three days and largely complete by 14 days, is common in patients who have been reperfused and can sometimes be seen even in those who are not acutely reperfused. This improvement is presumed to reflect recovery from myocardial stunning [13,14]. (See "Clinical syndromes of stunned or hibernating myocardium", section on 'Acute myocardial infarction'.)

Echocardiography is the most commonly used modality for assessing LV function after an acute MI. Other methods such as radionuclide angiography, computed tomography scans, or magnetic resonance imaging have equivalent prognostic value. (See "Risk factors for adverse outcomes after non-ST elevation acute coronary syndromes", section on 'Heart failure'.)

LV dysfunction was an entry criterion in the major trials that have evaluated the possible efficacy of an ICD for primary prevention of SCD in patients who have had an MI: MUSTT, MADIT I, and MADIT II; in all of these trials, patients with significant LV dysfunction benefited from ICD placement [22-24]. It was also an entry criterion for the SCD-HeFT trial, which included patients with either an ischemic or nonischemic cardiomyopathy and New York Heart Association (NYHA) class II to III HF. Consistent with the results of these trials, LV dysfunction is a component of all current indications for prophylactic ICD implantation for primary prevention of SCD in patients with a prior MI. Thus, an assessment of LV function is among the most important steps in initial risk stratification. (See "Primary prevention of sudden cardiac death in patients with cardiomyopathy and heart failure with reduced LVEF".)

The relationship between LV dysfunction and mortality has been shown in various trials including patients receiving standard medical therapy, such as ACE inhibitors and beta blockers [24-26]. The relationship between LV dysfunction and short-term arrhythmic risk has also been assessed in a post hoc analysis from the VALIANT trial, in which 11,256 patients had an assessment of LV function prior to discharge [11]. In the first 30 days after MI, patients with an LVEF <30 percent had the highest rates of SCD or resuscitated cardiac arrest (2.3 percent/month), and each decrease of 5 percent in LVEF was associated with a 21 percent increase in the risk of SCD or resuscitated cardiac arrest in the first 30 days. (See 'Incidence of SCD' above.)

Inducible VT/VF — Invasive EPS for risk stratification is not routinely performed in contemporary practice; however, the ability to induce ventricular tachyarrhythmias may play a role in the risk stratification for ICD placement in the subset of patients where the role of an ICD is still questionable (ie, LVEF of 35 percent or slightly below or above). Settings in which EPS in post-MI patients can aid in the decision regarding ICD implantation include:

●Patients with nonsustained ventricular tachycardia (NSVT) who do not meet MADIT-2 or SCD-HeFT criteria, including:

•Patients with an LVEF 30-35 percent and NYHA class I HF symptoms

•Patients with an LVEF 36-40 percent and NSVT (MUSTT patients)

•Some patients with an LVEF >40 percent who also have NSVT (typically identified from in-hospital telemetry or outpatient ambulatory ECG monitoring if performed for symptoms suggesting an arrhythmia. In contemporary practice most asymptomatic patients do not have routine outpatient ambulatory ECG monitoring).

Even if EPS is positive for inducible VT/VF (typically with inducible monomorphic VT posing a higher risk than polymorphic VT or VF), no prospective randomized clinical trial data have shown that ICDs improve survival, but this is considered clinically significant VT and an ICD can be placed for secondary prevention.

●Patients with syncope of suspected but not confirmed arrhythmic etiology.

The ability to induce ventricular arrhythmias (particularly monomorphic VT with one or two extrastimuli) with programmed electrical stimulation during an invasive electrophysiology study suggests the presence of arrhythmic substrate and an increased risk of malignant arrhythmias. The likelihood of inducible VT/VF varies according to several clinical variables including LVEF and NSVT (with more frequent runs, longer runs, faster ventricular rates, and accelerating ventricular rates all suggesting greater risk of sustained VT and SCD). In general, inducibility has a low positive predictive value, but a higher negative predictive value [22,27-30]. (See "Invasive diagnostic cardiac electrophysiology studies".)

Among several studies prior to the widespread use of primary reperfusion therapies, approximately one-third of post-MI patients had inducible VT or VF [31-35]. At one year follow-up, arrhythmic events were more common in patients with inducible VT/VF (average 18 percent, range 6 to 41 percent) than in those who were not inducible (average 7 percent, range 0 to 14 percent). Inducibility appears to be less common in the primary reperfusion era; however, when present, still predicts an increased risk of SCD [36].

Some clinical equipoise exists regarding the risk of VT and SCD post-MI or patients with an LVEF <40 percent in the first 40 days post-MI. An ongoing study, the PROTECT-ICD study, is evaluating the role of EPS and inducible VT/VF in the risk stratification for ICD placement in this patient population [37].

Other risk modifiers/approaches to risk stratification

●VPBs – Ventricular premature beats (VPBs), particularly if frequent (more than 30 per hour) or complex (eg, multifocal, couplets, or NSVT), appear to be associated with a worse prognosis in patients with a prior MI. Although VPBs are associated with increased mortality, there is no role for chronic antiarrhythmic drug therapy to suppress asymptomatic VPBs. (See "Ventricular arrhythmias during acute myocardial infarction: Prevention and treatment".)

●NSVT – Due to the limited predictive value and reproducibility of NSVT, combined with the evolution of broader ICD indications based upon LVEF and HF alone, the role of NSVT in risk stratification is largely limited. Though not frequently performed in contemporary practice, periodic ambulatory monitoring may be considered for post-MI patients with an LVEF <40 percent or symptoms suggesting arrhythmia, with invasive EP testing to search for inducible VT an option for patients who manifest NSVT. For patients with mild LV dysfunction post-MI (LVEF 40 to 49 percent), no data exist to guide the using of ambulatory monitoring; for these patients, our approach is to optimize medical therapy without any ambulatory monitoring, unless arrhythmic symptoms arise. (See 'Inducible VT/VF' above.)

The significance of NSVT following an MI is dependent upon the proximity of the arrhythmia to the time of the MI. In the first 24 to 48 hours after an infarction, NSVT is usually due to transient abnormalities of automaticity or triggered activity in the region of ischemia or infarction; in comparison, NSVT that occurs later is more often due to reentry and permanent arrhythmic substrate (ie, fibrosis).

In the era prior to reperfusion, NSVT detected post-MI was associated with an increased risk of SCD, in particular in patients with LVEF <40 percent [38,39]. However, NSVT has become less significant in risk stratification algorithms for several reasons:

•The incidence and prognostic significance of NSVT appear lower with contemporary primary reperfusion therapies [40,41].

•NSVT on Holter monitoring has low reproducibility (50 percent overall in one study) [42].

•Primary prevention ICD trials (eg, MADIT II and SCD-HeFT) demonstrated a survival benefit with ICD therapy in selected patients even in the absence of NSVT or an abnormal EP study (LVEF ≤30 percent in patients with a prior MI in MADIT II, and LVEF ≤35 percent in patients with NYHA class II or III HF in SCD-HeFT).

●Sustained ventricular arrhythmias – The importance of sustained ventricular arrhythmias on management after MI depends upon the morphology (eg, monomorphic VT, polymorphic VT, or ventricular fibrillation [VF]) and the temporal relationship to the infarction (eg, early or late, usually defined at a cutoff of 48 hours). Most patients with sustained monomorphic VT are at increased risk for future SCD and therefore warrant further risk stratification (eg, EP study) or placement of an ICD for secondary prevention. (See "Ventricular arrhythmias during acute myocardial infarction: Incidence, mechanisms, and clinical features", section on 'Monomorphic ventricular tachycardia'.)

•Early – Early sustained ventricular tachyarrhythmias are usually considered to be related to transient arrhythmogenic phenomena associated with the evolving infarction. They are associated with increased in-hospital and 30-day mortality, but among patients with early arrhythmias who survive 30 days, long-term SCD risks are unclear and may vary with the type of arrhythmia. Early VF alone does not appear to predict adverse late outcomes, but this may not apply to early sustained monomorphic VT.

•Late – Late sustained arrhythmias, particularly VF, polymorphic VT, and symptomatic monomorphic VT, predict an increased risk of SCD. Patients with these arrhythmias do not require further risk stratification and should be treated with an ICD for secondary prevention. (See "Secondary prevention of sudden cardiac death in heart failure and cardiomyopathy".)

●Late potentials – Late potentials on the signal-averaged ECG (SAECG) are indicative of late and slow impulse conduction through diseased or scarred myocardium. They indicate the potential for reentry, and their presence may identify patients after MI who are at risk for sustained VT and/or SCD [43]. However, the predictive value of SAECG alone is low, and in practice this test is now rarely used for risk stratification.

●Reduced HRV – Heart rate variability (HRV) is related to the balance between sympathetic and parasympathetic neural inputs, and is measured as the beat to beat variation in heart rate, which is attributable to effects of respiration and to normal blood pressure fluctuations. A reduction in HRV post-MI may be due to a decrease in parasympathetic tone and/or an increase in sympathetic neural activity, both of which can facilitate arrhythmia initiation [15,44,45]. However, the predictive value of HRV alone is low, and in practice this test is now rarely used for risk stratification. (See "Evaluation of heart rate variability".)

●T wave alternans – T wave or repolarization alternans (TWA) refers to variability in the timing or morphology of repolarization occurring in alternate beats on the surface ECG [46]. TWA is indicative of repolarization heterogeneity, which increases susceptibility to ventricular tachyarrhythmias. The presence of TWA has high sensitivity and specificity for predicting inducible ventricular arrhythmias on EPS. However, the predictive value of TWA alone is low, and in practice this test is now rarely used for risk stratification. (See "T wave (repolarization) alternans: Overview of technical aspects and clinical applications".)

●Cardiac imaging – Cardiac magnetic resonance (CMR) imaging offers excellent characterization of myocardial function and the extent of scar after an MI. As these features may characterize arrhythmic substrate, efforts are underway to correlate CMR findings with arrhythmic risk. (See "Clinical utility of cardiovascular magnetic resonance imaging", section on 'Prediction of post-MI mortality'.)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

●Basics topics (see "Patient education: What can go wrong after a heart attack? (The Basics)")

SUMMARY AND RECOMMENDATIONS

●With regard to primary prevention of sudden cardiac death (SCD), the most important initial parameter is left ventricular ejection fraction (LVEF). We recommend evaluation of LV function, including LVEF, prior to discharge post-myocardial infarction (MI) and again at 90 days post-MI. (See 'LV dysfunction' above.)

●Invasive electrophysiology study (EPS) for risk stratification is not routinely performed in contemporary practice; however, settings in which EPS in post-MI patients can aid in the decision regarding implantable cardioverter-defibrillator (ICD) implantation include patients with nonsustained ventricular tachycardia who do not meet MADIT-2 or SCD-HeFT criteria (including LVEF ≤40 percent and LVEF >40 percent) and patients with syncope of suspected but not confirmed arrhythmic etiology. (See 'Inducible VT/VF' above.)

●The indications for ICD implantation are discussed in detail elsewhere. (See "Primary prevention of sudden cardiac death in patients with cardiomyopathy and heart failure with reduced LVEF".)

●A number of additional risk factors are associated with the risk of SCD after an acute MI, including microvolt T wave alternans, signal-averaged ECG, and heart rate variability. However, because the results of these studies do not usually affect management decisions, we do not recommend their routine use. Such studies may provide additional insight into a given patient's arrhythmic risk, but data do not support using this information to guide decisions regarding ICD or antiarrhythmic drug therapy. (See 'Risk factors for chronic phase (>7 days) SCD' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Leonard Ganz, MD, FHRS, FACC, who contributed to an earlier version of this topic review.

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  46. Armoundas AA, Tomaselli GF, Esperer HD. Pathophysiological basis and clinical application of T-wave alternans. J Am Coll Cardiol 2002; 40:207.
Topic 1052 Version 32.0

References

1 : Utility of current risk stratification tests for predicting major arrhythmic events after myocardial infarction.

2 : MADIT II (second Multicenter Automated Defibrillator Implantation Trial) debate: risk stratification, costs, and public policy.

3 : 2015 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: The Task Force for the Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death of the European Society of Cardiology (ESC). Endorsed by: Association for European Paediatric and Congenital Cardiology (AEPC).

4 : 2014 AHA/ACC Guideline for the Management of Patients with Non-ST-Elevation Acute Coronary Syndromes: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines.

5 : 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines.

6 : 2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society.

7 : Modes and timing of death in 66 252 patients with non-ST-segment elevation acute coronary syndromes enrolled in 14 TIMI trials.

8 : Trends in acute coronary heart disease mortality, morbidity, and medical care from 1985 through 1997: the Minnesota heart survey.

9 : Contribution of modern cardiovascular treatment and risk factor changes to the decline in coronary heart disease mortality in Scotland between 1975 and 1994.

10 : Sudden death after myocardial infarction.

11 : Sudden death in patients with myocardial infarction and left ventricular dysfunction, heart failure, or both.

12 : Temporal trends on the risk of arrhythmic vs. non-arrhythmic deaths in high-risk patients after myocardial infarction: a combined analysis from multicentre trials.

13 : Early recovery of left ventricular function after thrombolytic therapy for acute myocardial infarction: an important determinant of survival.

14 : Recovery of ventricular function after myocardial infarction in the reperfusion era: the healing and early afterload reducing therapy study.

15 : Prophylactic use of an implantable cardioverter-defibrillator after acute myocardial infarction.

16 : Defibrillator implantation early after myocardial infarction.

17 : Electrophysiology-guided defibrillator implantation early after ST-elevation myocardial infarction.

18 : Risk stratification and survival after myocardial infarction.

19 : Risk factors for sudden death after acute myocardial infarction: two-year follow-up.

20 : Value of radionuclide rest and exercise left ventricular ejection fraction in assessing survival of patients after thrombolytic therapy for acute myocardial infarction: results of Thrombolysis in Myocardial Infarction (TIMI) phase II study. The TIMI Study Group.

21 : The relationships of left ventricular ejection fraction, end-systolic volume index and infarct size to six-month mortality after hospital discharge following myocardial infarction treated by thrombolysis.

22 : A randomized study of the prevention of sudden death in patients with coronary artery disease. Multicenter Unsustained Tachycardia Trial Investigators.

23 : Improved survival with an implanted defibrillator in patients with coronary disease at high risk for ventricular arrhythmia. Multicenter Automatic Defibrillator Implantation Trial Investigators.

24 : Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction.

25 : Early protection against sudden death by n-3 polyunsaturated fatty acids after myocardial infarction: time-course analysis of the results of the Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto Miocardico (GISSI)-Prevenzione.

26 : Effect of ACE inhibitor trandolapril on life expectancy of patients with reduced left-ventricular function after acute myocardial infarction. TRACE Study Group. Trandolapril Cardiac Evaluation.

27 : Nonsustained ventricular tachycardia and other high-risk predictors following myocardial infarction: implications for prophylactic automatic implantable cardioverter-defibrillator use.

28 : Prediction of sustained ventricular tachycardia inducible by programmed stimulation in patients with coronary artery disease. Utility of clinical variables.

29 : Electrophysiologic testing to identify patients with coronary artery disease who are at risk for sudden death. Multicenter Unsustained Tachycardia Trial Investigators.

30 : Nonsustained, asymptomatic ventricular tachycardia in patients with coronary artery disease: prognosis and incidence of sudden death of patients who are noninducible by electrophysiological testing.

31 : Prognostic significance of ventricular tachycardia and fibrillation induced at programmed stimulation and delayed potentials detected on the signal-averaged electrocardiograms of survivors of acute myocardial infarction.

32 : Identifying patients at risk of sudden death after myocardial infarction: value of the response to programmed stimulation, degree of ventricular ectopic activity and severity of left ventricular dysfunction.

33 : Programmed ventricular stimulation in survivors of an acute myocardial infarction.

34 : Frequency and significance of induced sustained ventricular tachycardia or fibrillation two weeks after acute myocardial infarction.

35 : Value of electrophysiologic testing in patients with previous myocardial infarction and nonsustained ventricular tachycardia. Philadelphia Arrhythmia Group.

36 : Risk stratification following myocardial infarction in the thrombolytic era: a two-step strategy using noninvasive and invasive methods.

37 : Risk stratification following myocardial infarction in the thrombolytic era: a two-step strategy using noninvasive and invasive methods.

38 : Clinical significance of ventricular tachycardia (3 beats or longer) detected during ambulatory monitoring after myocardial infarction.

39 : Prevalence, characteristics and significance of ventricular tachycardia detected by 24-hour continuous electrocardiographic recordings in the late hospital phase of acute myocardial infarction.

40 : Prevalence and prognostic significance of ventricular arrhythmias after acute myocardial infarction in the fibrinolytic era. GISSI-2 results.

41 : Prevalence, characteristics and prognostic value during long-term follow-up of nonsustained ventricular tachycardia after myocardial infarction in the thrombolytic era.

42 : Variability of Holter electrocardiographic findings in patients fulfilling the noninvasive MADIT criteria. Multicenter Automatic Defibrillator Implantation Trial.

43 : Changing late prognosis of acute myocardial infarction: impact on management of ventricular arrhythmias in the era of reperfusion and the implantable cardioverter-defibrillator.

44 : Depressed heart rate variability identifies postinfarction patients who might benefit from prophylactic treatment with amiodarone: a substudy of EMIAT (The European Myocardial Infarct Amiodarone Trial).

45 : Prophylactic implantable cardioverter-defibrillators after myocardial infarction--not for everyone.

46 : Pathophysiological basis and clinical application of T-wave alternans.

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