Long-term follow-up in patients with arrhythmogenic right ventricular cardiomyopathy

Long‐Term Prognosis in Patients with ARVC. Introduction: Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a major cause of sudden cardiac death due to tachyarrhythmias. The purpose of this study was to investigate the long‐term prognosis in patients with ARVC and the incidence of rapid ventricular arrhythmias during follow‐up. Methods: Thirty ARVC patients (19 male, 63.3%, mean age 48 ± 15 years) fulfilling modified Task Force criteria 2010 were included. Of them, 13 patients (43.3%) received implantable cardioverter‐defibrillator (ICD) implantation. Rapid ventricular arrhythmia was defined as electrical storm or the occurrence of ventricular tachycardia (VT) or ventricular fibrillation (VF) with a cycle length of 240 ms or less that necessitate shock delivery to 2 or more times within a 24‐hour period. Results: With a mean follow‐up of 68 ± 10 months, 6 patients (20%) with ICD implantation had recurrent rapid VT/VF. One (3.3%) of them died of multiple shocks and SCD, and 5 (16.7%) had multiple ICD therapies due to VT/VF and electrical storm. The interval between the diagnosis of ARVC and occurrence of rapid VT/VF was 13.4 ± 4.9 months. Most (5/6, 83.3%) events of recurrent rapid VT/VF occurred within 2 years. Ablated patients who did not receive an ICD implant were totally free of rapid VT/VF. Conclusions: For patients with ARVC, long‐term prognosis is favorable. During a long‐term follow‐up, patients meeting the criteria for ICD implantation have a higher rate of rapid and potentially life‐threatening arrhythmias. However, early and clustered recurrence of rapid VT/VF in patients with an ICD is common, whereas late occurrence of rapid VT/VF is very rare. (J Cardiovasc Electrophysiol, Vol. 23, pp. 750‐756, July 2012)     

Indications and outcome of implantable cardioverter-defibrillators for primary and secondary prophylaxis in patients with noncompaction cardiomyopathy

Prophylactic ICDs for Noncompaction Cardiomyopathy . Background: Noncompaction cardiomyopathy (NCCM) is a rare, primary cardiomyopathy, with initial presentation of heart failure, emboli, or arrhythmias, including sudden cardiac death. Implantable cardioverter‐defibrillators (ICDs) are frequently used for primary and secondary prevention in different cardiomyopathy patients, but data about ICD in NCCM are scarce. The aim of this study was, therefore, to investigate ICD indications and outcomes in NCCM patients. Methods and Results: We collected prospective data from our NCCM cohort (n = 77 pts, mean age: 40 ± 14 years). ICD was implanted in 44 (57%) patients with NCCM according to the current ICD guidelines for nonischemic cardiomyopathies: in 12 for secondary prevention (7 × ventricular fibrillation, 5 × sustained ventricular tachycardia [VT]) and in 32 patients for primary prevention (heart failure/severe LV dysfunction). During a mean follow‐up of 33 ± 24 months, 8 patients presented with appropriate ICD shocks due to sustained VT after median 6.1 [1–16] months. This included 4 of 32 (13%) patients in the primary prevention group and 4 of 12 (33%) in the secondary prevention group (P = 0.04). 9 patients presented with inappropriate ICD therapy: 6 (19%) in the primary and 3 (25%) in the secondary prevention group, at a median follow‐up of 4 (2–23) months. Conclusions: In our cohort of NCCM patients, an ICD was frequently implanted for primary or secondary prevention of sudden cardiac death. At follow‐up, frequent appropriate ICD therapy was observed in both groups, supporting the application of current ICD guidelines for primary and secondary prevention of sudden cardiac death in NCCM. (J Cardiovasc Electrophysiol, Vol. 22, pp. 898‐904, August 2011)     

Temporal associations between thoracic volume overload and malignant ventricular arrhythmias: a study of intrathoracic impedance

Volume Overload and Ventricular Arrhythmias . Background : Acute exacerbations of heart failure (HF) are believed to trigger malignant ventricular arrhythmias, but the temporal association between fluid accumulation and ventricular arrhythmias has not been evaluated in an objective manner. We hypothesized that increased intrathoracic fluid accumulation in patients with HF, as measured by an index of intrathoracic impedance, is associated with an increased risk of ventricular arrhythmias. Methods and Results : We analyzed interrogations in a cohort of 96 patients with left ventricular dysfunction (EF ≤ 35%) with devices that monitor intrathoracic impedance (OptiVol fluid index). Treated episodes of ventricular tachycardia or fibrillation (VT/VF) were adjudicated and stratified according to predetermined fluid index thresholds (OptiVol indices of 15, 30, 45, 60 Ω‐days). VT/VF episodes occurred in 16 patients (17%). VT/VF was more common on days when the fluid index was elevated using threshold values of 15, 30, and 45 Ω‐days (P = 0.006, 0.04, 0.02, respectively). There were no differences in the percent of time above any threshold between patients with and without VT/VF. Conclusions : In patients with HF who develop VT/VF, volume overload, as detected by an index incorporating changes in intrathoracic impedance, was temporally associated with malignant ventricular tachyarrhythmias. (J Cardiovasc Electrophysiol, Vol. 22, pp. 293‐299, March 2011)     

Dofetilide reduces the frequency of ventricular arrhythmias and implantable cardioverter defibrillator therapies

Dofetilide Reduces VT/VF and ICD Therapies . Background: Patients with an implanted cardioverter defibrillator (ICD) and ventricular arrhythmias leading to ICD therapies have poor clinical outcomes and quality of life. Antiarrhythmic agents and catheter ablation are needed to control these arrhythmias. Dofetilide has only been approved for the treatment of atrial fibrillation. The role of dofetilide in the control of ventricular arrhythmias in patients with an ICD has not been established. Objective: Evaluate the safety and efficacy of dofetilide in a consecutive group of patients with an ICD and recurrent ventricular tachycardia (VT) and/ or ventricular fibrillation (VF) after other antiarrhythmic drugs have failed to suppress these arrhythmias. Methods: We studied 30 patients (age 59 ± 11; 5 women) with symptomatic VT or VF and ICDs for secondary prevention of sudden cardiac death. These patients had an average of 1.8 ± 4.5 episodes of VT/VF per month despite antiarrhymic therapy. Twenty‐one patients (70%) had recurrent appropriate ICD therapies prior to initiation of dofetilide, and 9 (30%) VTs below the programmed detection rate of the ICD. Twenty‐three patients (77%) had coronary artery disease. Mean ejection fraction was 30 ± 14% and 26/30 (87%) had congestive heart failure. All patients had previously failed 2 ± 1 antiarrhythmic drugs including amiodarone (n = 19) and sotalol (n = 10). Results: During the first month of treatment, 25 patients (83%) had complete suppression of VT/VF and of the 21 patients with ICD therapies 16 (76%) had no therapies during the first month of treatment. During a follow‐up period of 32 ± 32 months, dofetilide reduced the monthly episodes of VT/VF from 1.8 ± 4.5 to 1.0 ± 3.5 (P = 0.006). Monthly ICD therapies decreased from 0.9 ± 1.4 to 0.4 ± 1.7 (P = 0.037). In 9 patients that presented with slow VTs under the ICD detection zone, dofetilide reduced monthly VT/VF episodes from 0.7 ± 0.6 to 0.1 ± 0.1 (P = 0.01) and 6 (67%) had no further ICD therapies. Dofetilide was discontinued in 13 patients (43%) after 24 ± 30 months due to failure to control VT/VF (n = 7), placement of a left ventricular assist device (n = 3), catheter ablation (n = 1), heart transplantation (n = 1), and left ventricular restoration surgery (n = 1). There were 7 documented deaths (2 patients died suddenly; 3 patients of progressive heart failure; and 2 of non‐cardiac causes). Conclusions: In patients with an ICD and ventricular arrhythmias, dofetilide decreases the frequency of VT/VF and ICD therapies even when other antiarrhythmic agents, including amiodarone, have previously been ineffective. Recurrences still occur in some patients requiring catheter ablation, mechanical support, or heart transplantation. (J Cardiovasc Electrophysiol, Vol. 23 p. 296‐301, March 2012.)     

Sudden cardiac death after acute heart failure hospital admission: insights from ASCEND‐HF

Aims

The incidence of and factors associated with sudden cardiac death (SCD) early after an acute heart failure (HF) hospital admission have not been well defined.

Methods and results

We assessed SCD and ventricular arrhythmias in the Acute Study of Clinical Effectiveness of Nesiritide in Decompensated Heart Failure (ASCEND‐HF) trial, which included patients with acute HF with reduced or preserved ejection fraction. SCD, resuscitated SCD (RSCD), and sustained ventricular tachycardia/ventricular fibrillation (VT/VF) were adjudicated from randomization through 30 days and were combined into a composite endpoint. Baseline characteristics associated with this composite were determined by logistic regression. RSCD and VT/VF were included as time‐dependent variables in a Cox model evaluating the association of these variables with 180‐day all‐cause mortality. Among 7011 patients, the 30‐day all‐cause mortality rate was 3.8%; SCD accounted for 17% of these deaths. The 30‐day composite event rate was 1.8% (n = 121). Ten patients had more than one event with 30‐day Kaplan–Meier event rates of 0.6% for SCD [95% confidence interval (CI) 0.5%–0.9%, n = 43], 0.4% for RSCD (95% CI 0.2%–0.5%, n = 24), and 0.9% for VT/VF (95% CI 0.7%–1.2%, n = 64). In the multivariable model, chronic obstructive pulmonary disease, history of VT, male sex, and longer QRS duration were associated with SCD, RSCD, or VT/VF. A RSCD or VT/VF event was associated with higher 180‐day mortality (adjusted hazard ratio 6.6, 95% CI 4.8–9.1, P < 0.0001).

Conclusions

Approximately 2% of patients admitted for acute HF experienced SCD, RSCD, or VT/VF within 30 days of admission, and SCD accounted for 17% of all deaths within 30 days.     

Long-term incidence of malignant ventricular arrhythmia and shock therapy in patients with primary defibrillator implantation does not differ from event rates in patients treated for survived cardiac arrest

INTRODUCTION: Recent trials have demonstrated benefit of prophylactic defibrillator (ICD) implantation compared to conventional treatment in high-risk patients. However, many patients have rare or no sustained arrhythmias following implantation. Our study addresses the question, whether patients with prophylactic defibrillator implantation have a lower risk for life-threatening ventricular tachycardia (VT) or ventricular fibrillation (VF) compared to sudden cardiac death (SCD) survivors. METHODS AND RESULTS: Over 7 years we enrolled 245 patients. Occurrence of spontaneous sustained VT/VF resulting in adequate ICD treatment was the endpoint. Incidence, type, and treatment of sustained arrhythmia in 43 previously asymptomatic ICD recipients (group B) were compared to data of 202 survivors of imminent SCD (group A). All patients had severely impaired left ventricular ejection fraction (<45%). Group B patients had long runs (>6 cycles, <30 s) of VT during Holter monitoring and inducible sustained arrhythmia. Incidence of rapid VT and VF (cycle length <240 ms/heart rate >250 bpm) after 4 years (35% in both groups, P = ns) and adequate defibrillator therapies (57% vs 55%, P = ns) were similar in both groups after univariate and multivariate analysis. Cumulative mortality tended to be lower in group B compared to group A, but the difference was not statistically significant. CONCLUSION: During long-term follow-up, incidence of sustained rapid ventricular arrhythmia in prophylactically treated patients is as high as that of SCD survivors. Benefit from defibrillator implantation for primary prevention (group B) appears to be comparable to that for survived cardiac arrest (group A).     

Inducibility of life-threatening ventricular arrhythmias is related to maximum left ventricular thickness and clinical markers of sudden cardiac death in patients with hypertrophic cardiomyopathy attributable to the Asp175Asn mutation in the alpha-tropomyosin gene

We investigated inducibility of life-threatening arrhythmias with programmed ventricular stimulation (PVS) in relation to clinical markers of sudden cardiac death (SCD) in subjects with hypertrophic cardiomyopathy (HCM) attributable to the Asp175Asn mutation in the α-tropomyosin gene (TPM1-Asp175Asn). PVS was performed with up to three extrastimuli and distribution of markers of SCD was evaluated in 21 adult subjects with the TPM1-Asp175Asn. Sustained polymorphic ventricular tachycardia (VT) or ventricular fibrillation (VF) was induced in seven of 21 subjects (33%). Inducible subjects had more severe left ventricular hypertrophy (LVH) and an increased number of markers of SCD (family history of SCD, syncope or presyncope, fall in systolic blood pressure (BP) during exercise, documented non-sustained VT (NSVT), and marked LVH) compared to non-inducible subjects (IVS 2.4 ± 0.3 cm vs. 1.6 ± 0.5 cm, P < 0.001; and two to three vs. one to two markers of SCD, P = 0.007, respectively). In conclusion, in HCM attributable to the Asp175Asn mutation in the α-tropomyosin gene, life-threatening arrhythmias were induced in one third of the patients. Inducibility was associated with the maximum left ventricular (LV) thickness and the number of markers of SCD, suggesting that in HCM patients with an identical causative mutation, susceptibility to ventricular arrhythmias is related to the cardiomyopathic phenotype.     

Mode of Onset of Malignant Ventricular Arrhythmias in Idiopathic Ventricular Fibrillation

Mode of Onset of Idiopathic VF. Introduction : The mode of onset of malignant ventricular arrhythmias (ventricular tachycardia [VT] or ventricular fibrillation [VF] has been well described in patients with organic heart disease and in patients with the long QT syndromes. Less is known about the mode of onset of VF in patients with out-of-hospital VF who have no evidence of organic heart disease or identifiable etiology.
Methods and Results : We reviewed the ECGs of all our patients with Idiopathic VF. Documentation of the onset of spontaneous arrhythmias was available for 22 VK episodes in 9 patients (6 men and 3 women; age 41 ± 16 years). In all instances, spontaneous VF followed a rapid polymorphic VT, which was initiated by premature ventricular complexes (PVCs) with very short coupling intervals. The PVC initiating VF had a coupling interval of 302 ± 52 msec and a prematurity index of 0.4 ± 0.07. These PVCs occurred within 40 msec of the peak of the preceding T wave. Pause-dependent arrhythmias were never observed.
Concltision : Cardiac arrest among patients with idiopathic VF has a very distinctive mode of onset. Documentation of a polymorphic VT that is not pause dependent is of diagnostic value.     

Prolonged repolarization after ventricular assist device support is associated with arrhythmias in humans with congestive heart failure

BACKGROUND: Recent observations indicate that the QTc interval often increases in the early postoperative period (<1 week) after mechanical unloading of severely failing hearts with a left ventricular assist device (LVAD). The present study examined whether early changes in ventricular repolarization after LVAD placement are associated with ventricular arrhythmias. METHODS AND RESULTS: An electrocardiogram was obtained within 4 days before LVAD placement, <12 hours after LVAD placement, and weekly thereafter. Patient records were reviewed for documented ventricular tachycardia (VT) or ventricular fibrillation (VF) for 1 week preoperatively and the first 2 weeks postoperatively. Differences in QTc interval between patients with and without VT were evaluated. Ten of 17 patients enrolled (59%) had VT or VF after LVAD placement. Of these, 4 required therapeutic intervention because of clinical instability or symptoms. The change in the QTc (DeltaQTc) between the preoperative and immediate postoperative period was significantly different among patients with VT/VF compared with patients without VT/VF (+23 ms vs. -68 ms, P < .001). CONCLUSION: The early period after initiation of LVAD support of the failing human heart is associated with a relatively high incidence of significant ventricular arrhythmias after LVAD placement. Beyond the impact of myocardial inflammation and wound healing occurring after all LVAD implants, early postoperative increases in the QTc interval after cardiac unloading appear to predispose to ventricular arrhythmias.     

Postextrasystolic Repolarization Abnormalities in ST‐U Segment in Patients with Ventricular Arrhythmias

Background: Changes in U‐wave amplitude after premature ventricular contractions (PVC) are known as prognostic markers in the long QT syndrome dependent on bradycardia. The purpose of the study was to find correlation between postextrasystolic ST‐U segment changes and a history of sustained ventricular tachycardia or ventricular fibrillation (VT/VF). Methods: The ST‐U segment configurations were taken from the 24‐hour ambulatory ECG. The comparison of the morphology of these segments was performed between sinus beats preceding PVC's and first postextrasystolic beats. Population: Two groups of patients were evaluated: 1) 32 patients with VT/VF history (VT/VF group), and 2) 36 patients with potentially malignant arrhythmia (structural heart disease with frequent PVCs and/or nonsustained VT‐nsVT) tnon‐VT/VF group). Results: We found T‐wave changes in 8 patients (25%) from the VT/VF group and in 12 patients (33.3%) from the nonVT/VF group (P = NS) and U‐wave changes in 13 patients (40.6%) and 3 patients (8.3%), respectively (P < 0.05). Other ECG indexes related to PVC's were also considered: RR interval, coupling interval (Cl), prematurity index (Pl), and postextrasystolic pause (PP). The analysis of these ECG indices revealed, when compared with patients without T‐U‐wave changes, that the occurrence of U‐wave changes was significantly related to longer RR interval of the sinus rhythm preceding PVC: 1025 ± 211 vs 918 ± 200 ms (P < 0.05). The prematurity index was lowest in patients with U‐wave changes: 0.54 ± 0.12 vs 0.65 ± 0.16 (P < 0.01) while postextrasystolic pauses leading to the postextrasystolic U‐wave changes were significantly longer: 1383 ± 223 vs 1130 ± 247 ms (P < 0.001). Cl did not differentiate patients: 556 ± 108 vs 584 ± 117 ms (P = NS). Conclusions: Postextrasystolic changes in ST‐U segment configuration are dependent on bradycardia, low prematurity index of the PVC, and the lengthening of the postextrasystolic pause. U‐wave changes more frequently appeared in patients with malignant arrhythmias. Follow‐up study is needed to assess if they might be predictive for the occurrence or reoccurrence of arrhythmic episodes. A.N.E. 2002;7(1):17–21     

Obesity as a risk factor for sustained ventricular tachyarrhythmias in MADIT II patients

Background: Obesity, as defined by body mass index ≥30 kg/m², has been shown to be a risk factor for cardiovascular disease. However, data on the relationship between body mass index (BMI) and the risk of ventricular arrhythmias and sudden cardiac death are limited. The aim of this study was to evaluate the risk of ventricular tachyarrhythmias and sudden death by BMI in patients after myocardial infarction with severe left ventricular dysfunction.
Methods : The risk of appropriate defibrillator therapy for ventricular tachycardia or ventricular fibrillation (VT/VF) by BMI status was analyzed in 476 nondiabetic patients with left ventricular dysfunction who received an implantable cardioverter defibrillator (ICD) in the Multicenter Automatic Defibrillator Implantation Trial-II (MADIT II).
Results : Mean BMI was 27 ± 5 kg/m². Obese patients comprised 25% of the study population. After 2 years of follow-up, the cumulative rates of appropriate ICD therapy for VT/VF were 39% in obese and 24% in nonobese patients, respectively (P = 0.014). In multivariate analysis, there was a significant 64% increase in the risk for appropriate ICD therapy among obese patients as compared with nonobese patients, which was attributed mainly to an 86% increase in the risk of appropriate ICD shocks (P = 0.006). Consistent with these results, the risk of the combined endpoint of appropriate VT/VF therapy or sudden cardiac death (SCD) was also significantly increased among obese patients (Hazard Ratio 1.59; P = 0.01).
Conclusions : Our findings suggest that in nondiabetic patients with ischemic left ventricular dysfunction, a BMI ≥30 kg/m² is an independent risk factor for ventricular tachyarrhythmias.     

Prognostic significance of the Holter-derived T-wave variability in patients with ventricular tachyarrhythmias complicating acute coronary syndrome—TWIST study

Background

We aimed to investigate the association between ventricular repolarization instability and sustained ventricular tachycardia and ventricular fibrillation (VT/VF) occurring within 48 h (acute-phase VT/VF) after the onset of acute coronary syndrome (ACS) and the prognostic role of repolarization instability and heart rate variability (HRV) after discharge from the hospital.

Methods

We studied 572 ACS patients with a left ventricular ejection fraction >35%. The ventricular repolarization instability was assessed by the beat-to-beat T-wave amplitude variability (TAV) using high-resolution 24-h Holter ECGs recorded at a median of 11 days from the date of admission. We calculated the HRV parameters including the deceleration capacity (DC) and non-Gaussian index calculated on a 25 s timescale (λ25s). The DC and λ25s were dichotomized based on previous studies' thresholds.

Results

Acute-phase VT/VF developed in 43 (7.5%) patients. In-hospital mortality was significantly higher among VT/VF patients (4.7% vs. 0.9%, p = .03). An adjusted logistic model showed that the maximum TAV (odds ratio 1.02, 95% confidence interval [CI] 1.00–1.29, p = .04) was associated with acute-phase VT/VF. During a median follow-up period of 2.1 years, 19 (3.3%) patients had cardiac deaths or resuscitated cardiac arrest. Acute-phase VT/VF (p = .12) and TAV (p = .72) were not significant predictors of survival. An age and sex-adjusted Cox model showed that the DC (p < .01), λ25s (p < .01), and emergency coronary intervention (p < .01) were independent predictors.

Conclusion

T-wave amplitude variability was associated with acute-phase VT/VF, but the TAV was not predictive of survival post-discharge. The DC, λ25s, and emergency coronary intervention were independent predictors of survival.     

Dispersion of repolarization and beta-thalassemia major: the prognostic role of QT and JT dispersion for identifying the high-risk patients for sudden death

Background: Patients with beta‐thalassemia major (β‐TM) are at increased risk for sudden cardiac death (SCD). Heterogeneity of ventricular repolarization is considered to provide an electrophysiological substrate for malignant arrhythmias. QT dispersion (QTc‐D) and JT dispersion (JTc‐D) are electrocardiographic parameters indicative of heterogeneity of ventricular repolarization. The aim of our study was to evaluate the heterogeneity of ventricular repolarization in patients with beta‐thalassemia and to test the hypothesis that an abnormal QTc and JTc dispersion may predict SCD in this population. Materials and Methods: The study involved 51 patients with β‐TM (age 33.9 ± 8.4; 33 M) and 51 healthy subjects used as controls, matched for age, gender, and body mass index (BMI). Among the β‐TM group, 14 patients with β‐TM (age 27 ± 6.64; 11 M) died from SCD during follow‐up. For each patient, QTD and JTD intervals were calculated. Results: Compared to the healthy control group, β‐TM group presented increased values of the QTc‐D (65.36 ± 33.95 vs. 37, 62 ± 17.65; P < 0.003) and JTc‐D (74.64 ± 33.27 vs. 40.32 ± 12.45; P < 0.001). In the β‐TM sudden death group, QTc‐D and JTc‐D were significantly greater than in survived β‐TM group (92.70 ± 44.24 vs. 56.14 ± 23.80, P = 0.0001; 101.54 ± 47.93 vs. 64.47 ± 17.90, P = 0.0001). A cutoff value of 70 ms for QTc‐D had a sensitivity and specificity of 77% in identifying patients at risk for SCD. A cutoff value of 100 ms for JTc‐D had a sensitivity of 65% and a specificity of 94% in identifying this category of patients. Conclusion: β‐TM is associated with significant changes in heterogeneity of ventricular repolarization. QTc and JTc dispersion are useful markers of risk of SCD in patients with β‐TM.     

Prevalence, predictors, and mortality significance of the causative arrhythmia in patients with electrical storm

INTRODUCTION: Electrical storm (ES) is characterized by either refractory ventricular tachycardia (VT) or ventricular fibrillation (VF). However, little is known about the prevalence, predictors, and mortality implications of the causative arrhythmia in ES. We sought to assess the prevalence, predictors, and survival significance of VT and VF as the causative arrhythmia of ES in implantable cardioverter defibrillator (ICD) patients. METHODS AND RESULTS: Consecutive patients from January 2000 to December 2002 who presented to the ICD clinic with > or = 2 separate ventricular arrhythmic episodes requiring shock within 24 hours were included in the study. ICD interrogation confirmed the number of shocks and provided electrograms for interpretation of the causative arrhythmia. Patients were grouped as VF or VT according to the causative arrhythmia. Their prevalence, predictors, and mortality rates were compared. Of 2,028 patients assessed in the ICD clinic, 208 (10%) presented with ES. VF was the cause of ES in 99 of 208 patients, for an overall prevalence of 48%. Original ICD indication, coronary artery disease, and amiodarone therapy were predictive for the causative arrhythmia. There was no mortality difference between the VT and VF groups; however, both groups had significantly increased mortality compared to a control ICD population without ES. CONCLUSION: VF is the causative arrhythmia for a sizable proportion of patients with ES. The initial ICD indication, coronary artery disease, and amiodarone therapy are predictors of the causative arrhythmias in ES. There does not appear to be any mortality difference between ES patients with VT and VF, but mortality is increased in patients with ES versus control ICD patients without ES.     

J-wave syndromes. from cell to bedside

The J wave, a deflection that follows the QRS complex of the surface electrocardiogram, is usually partially buried in the R wave in humans, appearing as a J-point elevation. An early repolarization (ER) pattern characterized by J-point elevation, slurring of the terminal part of the QRS, and ST-segment elevation has long been recognized and considered to be totally benign. Recent studies have presented evidence demonstrating that an ER pattern in inferior leads or inferolateral leads is associated with increased risk for life-threatening arrhythmias, named early repolarization syndrome. Early repolarization syndrome and Brugada syndrome share similar electrocardiographic characteristics, clinical outcomes, risk factors, as well as a common arrhythmic platform related to amplification of I_to-mediated J waves. Although Brugada syndrome and early repolarization syndrome differ with respect to the magnitude and lead location of abnormal J wave manifestation, they can be considered to represent a continuous spectrum of phenotypic expression, termed J-wave syndromes. Early repolarization syndrome has been proposed to be divided into 3 subtypes: type 1, displaying an ER pattern predominantly in the lateral precordial leads, is prevalent among healthy male athletes and rarely seen in ventricular fibrillation survivors; type 2, displaying an ER pattern predominantly in the inferior or inferolateral leads, is associated with a higher level of risk; whereas type 3, displaying an ER pattern globally in the inferior, lateral, and right precordial leads, is associated with the highest level of risk for development of malignant arrhythmias and is often associated with ventricular fibrillation storms.     

Dynamicity of Early and Late Phases of Repolarization in Patients with Remote Anterior Myocardial Infarction: The Interlead Differences

Background: Repolarization dynamicity (QT/RR) is supposed to be a prognostic marker in post‐MI patients. However, data on the relationships between early and late phases of QT and RR intervals (QT peak/RR and T peak–T end/RR) are insufficient, and which ECG lead should be used for the analysis is unclear. We analyzed repolarization dynamicity in patients after anterior MI with and without VT/VF history using two leads of Holter recordings‐ modified V₅ and V₃. The daytime and nighttime periods were also analyzed. Methods: Cohort of 88 patients after anterior MI (>6 months) consisted of 43 patients without VT/VF (33 males; 59 ± 12 years; LVEF: 41 ± 7%; NoVT/VF), and 45 patients with VT/VF history‐ ICD implanted as secondary prevention (40 males; 64 ± 10 years; LVEF: 32 ± 8%; VT/VF). QT/RR, QT peak/RR and T peak–T end/RR were calculated from 24‐hour ECG for the entire recording, daytime and nighttime periods, from V₅ and V₃ leads, respectively. Results: VT/VF patients had lower LVEF (P = 0.001). There were no differences in age and gender. VT/VF group had steeper QT/RR, QT peak/RR, and T peak–T end/RR in V₅: 0.233 ± 0.04 versus 0.150 ± 0.05, P = 0.0001, 0.181 ± 0.04 versus 0.120 ± 0.04, P = 0.0001, 0.052 ± 0.02 versus 0.030 ± 0.02, P = 0.0001, and in V₃: 0.201 ± 0.04 versus 0.149 ± 0.05, P = 0.0001, 0.159 ± 0.03 versus 0.118 ± 0.04, P = 0.0001, and 0.042 ± 0.02 versus 0.031 ± 0.02, P = 0.004; respectively. VT/VF patients had higher indices in V₅ than in V₃ lead (P = 0.001). QT/RR and QT peak/RR were steeper at daytime period in both leads. It was not found for T peak–T end/RR. Conclusions : Patients with VT/VF history are characterized by steeper relationships between repolarization duration and RR intervals. These findings are more evident in modified V₅ lead.     

The Relation of QT Dispersion to Spontaneous Ventricular Arrhythmias During the Acute Phase of Myocardial Infarction

Background: QT dispersion is associated with ventricular arrhythmias and sudden death among patients with a previous myocardial infarction (Ml). The relationship between QT dispersion and ventricular arrhythmias during the acute phase of Ml is uncertain. Methods: Patients enrolled in the Multicenter Study of Silent Myocardial Ischemia who had first Q wave myocardial infarctions (n = 363) were screened for the presence of ventricular arrhythmias during the initial hospitalization. Twelve patients had ventricular fibrillation, and 18 patients had an episode of monomorphic ventricular tachycardia. Each patient who had ventricular arrhythmias was matched with four controls on the basis of age, peak creatine kinase, thrombolysis, and the presence of congestive heart failure. The final study population consisted of 150 patients: 12 patients with ventricular fibrillation (VF+) who were compared to 48 controls (VF—), and 18 patients with ventricular tachycardia (VT+) who were compared to 72 controls (VT–). The RR, QRS, and QT intervals were measured manually using standard 12-lead ECGs (25 mm/s) obtained after hospital admission. The maximal QT dispersion (maximum — minimum value) was calculated. Multivariate logistic regression analysis was performed to determine if QT dispersion was independently associated with ventricular arrhythmias during the acute phase of Ml. Results: QT dispersion was significantly greater in VF+ patients compared to VF— patients (89 ± 18 ms vs 66 ± 22 ms, P > 0.01). QT dispersion was similar in VT+ and VT— patients (68 ± 25 ms vs 68 ± 26 ms, P = NS). QT dispersion was the only variable that was independently associated with ventricular fibrillation (OR 1.7 for each 10-ms increment in QT dispersion; 95% Cl 1.2–2.6; P = 0.008). QT dispersion was not associated with monomorphic ventricular tachycardia (OR 1.0; 95% Cl 0.8–1.2; P = NS). Conclusion: QT dispersion is independently associated with ventricular fibrillation, but not monomorphic ventricular tachycardia, during the acute phase of Ml.     

心电图对急性心肌梗死高危猝死患者的预警作用研究

目的：探讨心电图联合临床危险因素在急性心肌梗死猝死高危患者中的预警作用。方法选择急性心肌梗死伴有恶性心律失常（室性心动过速、心室颤动）患者为恶性心律失常组（n=148）,急性心肌梗死不伴恶性心律失常患者为对照组（n=52）,测量患者的各心电指标,包括QRS时间、Q- T间期和Tp- e间期、J波、碎裂QRS波群,计算Q- Td及Tp- eC,记录左心室射血分数（LVEF）,并随访调查6个月内心脏性猝死的发生情况,比较两组上述指标。根据LVEF值将所有患者分为LVEF≤30%,30%＜LVEF≤40%,40%＜LVEF≤50%,LVEF＞50%,比较不同LVEF者室性心动过速/心室颤动、心脏性猝死发生情况。纳入常见的临床危险因素后,采用Logistic回归分析筛选恶性心律失常的预测因子。结果恶性心律失常组合并糖尿病者、QRS时间、Q- Td、Tp- e间期、Tp- eC、J波、碎裂QRS波群、BNP值和心脏性猝死的发生率均高于对照组（P＜0.05或0.01）,而LVEF值低于对照组（P＜0.01）。随着LVEF的降低,室性心动过速/心室颤动的发生率明显增高,其中30%＜LVEF≤40%所占比例最高（85.5%）。Logistic回归分析结果显示Tp- e间期、LVEF、J波是患者发生恶性心律失常的独立预测因子（r=0.72、0.62、0.49,OR=4.68、3.63、2.46）,Tp- e间期的相关性最强（r=0.72）,相对危险度最高（OR=4.68）。结论Tp- e间期、LVEF、J波是急性心肌梗死患者恶性心律失常发生的危险因素,Tp- e间期的预测价值最高,优于LVEF、J波。LVEF的降低与急性心肌梗死恶性心律失常的发生密切相关。     

Cardiac Output Is Not Affected During Intraoperative Testing of the Automatic Implantable Cardioverter Defibrillator

Cardiac Output and ICD Implantation. Introduction: Perioperative mortality of patients undergoing implantation of automatic implantable cardioverter defibrillators (ICDs) has been reduced dramatically following the availibility of trans venous-subcutaneous defibrillation leads. However, patients with severely reduced left ventricular function show a substantial rate of nonsudden cardiac mortality within the first year. Whether repeated intraoperative inductions of ventricular tachycardia/fibrillation (VT/VF) during implantation lead to hemodynamic deterioration and thus might contribute to development of end-stage heart failure in these patients is unknown. The purpose of the present study was to determine cardiac output and hemodynamic performance during transvenous-subcutaneous ICD implantation in patients with severe left ventricular dysfunction. Methods and Results: In 11 patients with a left ventricular ejection fraction (EF) ≤ 0.35, cardiac output was measured automatically with a combined continuous cardiac output/mixed venous oxygen saturation pulmonary artery catheter system. ICD implantation was performed during standardized general anesthesia. In the 11 patients (EF = 27 ± 2% [mean ± SEM]) a total of 95 episodes of VT/VF followed by defibrillation were induced (epsiodes per patient = 9 ± 1; range 6 to 11). Cardiac index was 2.2 ± 0.2 L·min^-1·min^-2 after induction of anesthesia (before start of surgery), and 1.9 ± 0.1 L·min^-1·m^-2 immediately before first induction of VT/VF. After the last episode of VT/VF, cardiac index was 2.1 ± 0.2 L·min^-1·m^-2. Cardiac index measured 1, 2, and 3 minutes after induction of VT/VF was not significantly different when compared to the preinduction value during any episode of VT/VF induction. Similarly, stroke volume index was 39 ± 5 mL·m^-2 immediately before first induction of VT/VF and 36 ± 3 mL·m^-2 after the last episode of VT/VF (NS). At the end of surgery, hemodynamic parameters did not exhibit any significant difference when compared to the data obtained before start of ICD implantation and testing. Conclusion: Extensive defibrillation tests during transvenous-subcutaneous ICD implantation in patients with severe left ventricular dysfunction are not associated with acute deterioration of cardiac performance.     

Cardiac arrest recorded on ambulatory electrocardiograms

To characterize the events that precede and precipitate sudden cardiac death (SCD), the long-term electrocardiograms of 27 patients who had SCD while being monitored were analyzed. In 20 patients, SCD was associated with ventricular tachyarrhythmias (ventricular tachyardia [VT]/ventricular fibrillation [VF]) and in 7 it was associated with bradyarrhythmias. Seventeen of the patients were men and 10 were women. Twenty-one patients had coronary artery disease, 2 had idiopathic dilated cardiomyopathy, 2 had mitral stenosis and 1 patient had mitral valve prolapse. Four patients with VT/VF had a previous nonfatal cardiac arrest. In the 20 patients with tachyarrhythmia-related SCD, 3 or more VT beats always preceded degeneration to VF. In 5 patients, the frequency or complexity of ventricular arrhythmias increased in the hour before SCD. In 11 of 20, there was a 20% or greater increase in underlying heart rate in the hour before SCD. The R-on-T phenomenon was observed in 4 patients. The long-short phenomenon initiated VT/VF in 2 patients. Only 2 patients with VT/VF were resuscitated. No patient with bradyarrhythmia-related SCD had manifest atrioventricular block or bundle branch block. Two of 7 patients had an episode of nonsustained bradycardia in the hour before arrest. No patient was resuscitated. In conclusion, VT that degenerates into VF is the most common arrhythmia associated with SCD. VT/VF is frequently preceded by an increase in heart rate and complex ectopy. VT is most often initiated by late ventricular premature complexes. Twenty-five percent of patients who have SCD have associated bradyarrhythmias that may occur without premonitory events.