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Background: The role and optimal sequence of ventricular tachycardia (VT) induction, mapping, and ablation when combined with substrate modification is unclear.Objective: The purpose of this study was to test the benefits of starting the scar-related VT ablation procedure with substrate modification vs the standard protocol of VT induction, mapping, and ablation as the first step.Methods: Forty-eight consecutive patients with structural heart disease and clinical VTs were randomized to simplified substrate ablation procedure with scar dechanneling as the first step (group 1, n = 24) or standard procedure with VT induction, mapping, and ablation followed by scar dechanneling (group 2, n = 24). Procedure and fluoroscopy times, the need for external cardioversion, acute results, and VT recurrence during follow-up were compared between groups.Results: Thirty-seven patients had ischemic cardiomyopathy, 10 nonischemic cardiomyopathy, and 1 arrhythmogenic cardiomyopathy. Before substrate ablation, 32 VTs were induced and targeted for ablation in 23 patients of group 2. Procedure time (209 ± 70 minutes vs 262 ± 63 minutes; P = .009), fluoroscopy time (14 ± 6 minutes vs 21± 9 minutes; P = .005), and electrical cardioversion (25% vs 54%; P = .039) were lower in group 1. After substrate ablation, 16 patients (66%) of group 1 and 12 patients (50%) of group 2 were noninducible (P = .242). End-procedure success (after residual inducible VT ablation) was achieved in 87.5% and 70.8% of patients, respectively (P = .155). There were no differences in VT recurrence rate between groups during a mean follow-up of 22 ± 14 months (log rank, P = .557).Conclusion: VT induction and mapping before substrate ablation prolongs the procedure, radiation exposure, and the need for electrical cardioversion without improving acute results and long-term ablation outcomes. [ABSTRACT FROM AUTHOR]

The United States Food and Drug Administration has approved the wearable cardioverter defibrillator (WCD) for use in patients who are at high risk for sudden cardiac arrest (SCA) and who do not yet have an established indication for an implantation cardioverter defibrillator (ICD) or have contraindications for device implantation for various reasons. The WCD is typically used for primary prevention in (1) high-risk patients with reduced left ventricular ejection fraction (LVEF) ≤35 % after recent acute myocardial infarction (MI) during the 40-day ICD waiting period, (2) before and after coronary artery bypass graft or percutaneous coronary intervention during the 90-day ICD waiting period, (3) after recently diagnosed nonischemic dilated cardiomyopathy (NICM) during the 3- to 9-month medical therapy optimization period, or (4) for those with inherited proarrhythmic conditions such as long QT syndrome or hypertrophic cardiomyopathy. Unlike the automatic external defibrillator, the WCD does not require assistance from bystanders for therapy and conscious patients can delay or avert therapy with the use of response buttons. The WCD exhibits a small risk of inappropriate shock, mostly due to supraventricular tachycardia and/or electrical noise. Multiple non-randomized observational studies have shown high efficacy in detection and appropriate shock therapy for sustained ventricular tachyarrhythmias. This paper discusses the use of the WCD for prevention of SCA in patients with various cardiac substrates. [ABSTRACT FROM AUTHOR]

Background Previous studies reported that left ventricular noncompaction (LVNC) is a cardiomyopathy, familial or sporadic, arising from arrest of the normal process of trabecular remodeling during embryonic development. The diagnosis is usually made by echocardiography, but to date, there has been little research on the occurrence and clinicopathological features of LVNC in the explanted hearts of orthotopic heart transplant (OHT) recipients. Design The clinical, echocardiographic, and pathologic findings were reviewed for evidence of LVNC, diagnosed by echocardiographic criteria, in 105 patients with end-stage heart failure (HF) undergoing OHT. Analyses of multiple sections of the explanted hearts were carried out. The hearts were evaluated for grades (0, negative; 1, mild/occasional foci; 2, moderate/multiple foci; 3, severe/extensive, diffuse) of fibrosis, reactive and replacement, hypertrophy, myocytolysis in left ventricle, right ventricle, interventricular septum, and atria. Absolute measurements of noncompacted and compacted portions of the left ventricle wall and noncompacted/compacted ratios were calculated. Results Isolated LVNC was observed in 0 of 54 ischemic cardiomyopathy and in 4 of 51 (7.8%) nonischemic cardiomyopathy patients — 2 men and 2 women, with a mean age ± SEM of 34.2 ± 6.9 years. The echocardiogram disclosed marked left ventricular dilatation, prominent trabeculations, and left ventricle ejection fraction < 20%. Mural thrombi were seen in 3 of 4 (75%) patients. The heart weight mean ± SEM was 468 ± 55.3 g (range, 340–600 g); noncompacted myocardium was 22 ± 5.8 mm, compacted myocardium was 13.2 ± 3.5 mm, and noncompacted/compacted ratio was 1.7/1 ± 0.2. The total scores of hypetrophy, myocytolysis, and fibrosis were as follows: left ventricle, 7.7 ± 0.2; right ventricle, 6.2 ± 0.5; interventricular septum, 6.7 ± 0.2; and atria, 7.5 ± 0.3. Conclusions LVNC is an unusual form of nonischemic cardiomyopathy in patients suffering from end-stage HF undergoing OHT. The variability in the noncompacted/compacted ratio and discordance between the echocardiographic and pathological findings points to the need for further clarification of diagnostic imaging and diagnostic criteria for LVNC. Further studies in larger series, correlating the anatomoclinical and genetic variables, also would improve our understanding of LVNC as a cause of advanced HF leading to OHT. [ABSTRACT FROM AUTHOR]

Background Left ventricular ejection fraction (LVEF) recovers during follow-up in a significant proportion of patients implanted with a cardioverter defibrillator (ICD) for primary prevention. Little is known about the midterm arrhythmic risk in this population, particularly in relation to the presence or absence of ischemic cardiomyopathy. Methods and Results We retrospectively analyzed 286 patients with an ICD implanted for primary prevention between 2002 and 2010. Patients were divided into two groups based on their last LVEF assessment: (1) Recovery, defined as an LVEF > 35%; and (2) No-Recovery, defined as an LVEF ≤ 35%. Kaplan-Meir curves and multivariate Cox regression analysis were performed separately for patients with ischemic (211 patients) and nonischemic (75 patients) cardiomyopathy. Forty-nine patients (17.1%) had LVEF recovery to >35% at last follow-up. Overall, 72 patients (25.2%) experienced ventricular arrhythmias requiring ICD therapy during a median follow-up of 4.4 years. With multivariate Cox regression, LVEF recovery was associated with a lower arrhythmic risk in the whole cohort (hazard ratio [HR]: 0.38 [0.13-0.85]; P = 0.02) and in the nonischemic cardiomyopathy cohort (HR: 0.10 [0.005-0.55]; P = 0.005), but not in the ischemic cardiomyopathy cohort (HR: 0.84 [0.25-2.10]; P = 0.74). Conclusion In conclusion, patients with nonischemic cardiomyopathy who improved their LVEF to >35% after primary prevention ICD implantation were at very low absolute arrhythmic risk. Our study raises the possibility that the LVEF cutoff to safely withhold ICD replacement might be higher in patients with ischemic compared to nonischemic cardiomyopathy. This will need to be confirmed in prospective studies. [ABSTRACT FROM AUTHOR]

Background: Left ventricular ejection fraction (LVEF) response to guideline-directed medical therapy (GDMT) and to early cardiac resynchronization therapy (CRT) in new-onset idiopathic nonischemic cardiomyopathy (NICM) and left bundle branch block (LBBB) is not well described. CRT is recommended if LVEF remains ≤35% after at least 3 months of GDMT. Objective: The purpose of this study was to describe LVEF response to GDMT at 3 months and to early CRT in new-onset LBBB-associated idiopathic NICM. Methods: A retrospective cohort study was performed in subjects with new-onset idiopathic NICM, LVEF ≤35%, and LBBB or narrow (<120 ms) QRS complex morphology. LVEF response between groups was evaluated with log-binomial and linear regression. LVEF response within groups was evaluated using the paired Student t test. Results: In 102 subjects (70 with narrow QRS complex and 32 with LBBB), post-GDMT LVEF was >35% in 39 narrow QRS complex subjects (56%) and 2 LBBB subjects (6%) (P < .0001). The absolute difference between post-GDMT LVEF and initial LVEF was greater in the narrow QRS complex group (16.1% ± 14.6% vs. 3.3% ± 10.7%; P < .0001). Narrow QRS complex, referenced to LBBB, was significantly associated with post-GDMT LVEF >35% (relative risk 10.30; 95% confidence interval 2.63-40.27; P = .0008) and absolute difference between post-GDMT LVEF and initial LVEF (β = 16.296; standard error = 2.977; P < .0001) in final multivariable analyses. CRT super-response, defined as post-CRT LVEF ≥50%, was observed in 8 of LBBB subjects (35%) who received CRT. Conclusion: GDMT did not significantly improve LVEF in new-onset LBBB-associated idiopathic NICM at 3 months. Most remained candidates for CRT, and a high percentage were super-responders. Optimal timing for CRT implantation requires further investigation. [ABSTRACT FROM AUTHOR]

Background: Progressive activation delay after premature stimulation has been associated with ventricular fibrillation in nonischemic cardiomyopathy (NICM).Objectives: The objectives of this study were (1) to investigate prolongation of the paced QRS duration (QRSd) after premature stimulation as a marker of activation delay in NICM, (2) to assess its relation to induced ventricular arrhythmias, and (3) to analyze its underlying substrate by late gadolinium enhancement cardiac magnetic resonance imaging (LGE-CMR) and endomyocardial biopsy.Methods: Patients with NICM were prospectively enrolled in the Leiden Nonischemic Cardiomyopathy Study and underwent a comprehensive evaluation including LGE-CMR, electrophysiology study, and endomyocardial biopsy. Patients without structural heart disease served as controls for electrophysiology study.Results: Forty patients with NICM were included (mean age 57 ± 14 years; 33 men [83%]; left ventricular ejection fraction 30% ± 13%). After the 400-ms drive train and progressively premature stimulation, the maximum increase in QRSd was larger in patients with NICM than in controls (35 ± 18 ms vs. 23 ± 12 ms; P = .005) and the coupling interval window with QRSd prolongation was wider (47 ± 23 ms vs. 31 ± 14 ms; P = .005). The maximum paced QRSd exceeded the ventricular effective refractory period, allowing for pacing before the offset of the QRS complex in 20 of 39 patients with NICM vs. 1 of 20 controls (P < .001). In patients with NICM, QRSd prolongation was associated with the inducibility of polymorphic ventricular tachycardia (16 of 39 patients) and was related to long, thick strands of fibrosis in biopsies, but not to focal enhancement on LGE-CMR.Conclusion: QRSd is a simple parameter used to quantify activation delay after premature stimulation, and its prolongation is associated with the inducibility of polymorphic ventricular tachycardia and with the pattern of myocardial fibrosis in biopsies. [ABSTRACT FROM AUTHOR]

VT and MRI Background Ventricular tachycardia (VT) in patients with cardiomyopathy originates in scar tissue. Intramural or epicardial scar may result in ineffective ablation if mapping and ablation are limited to the endocardium. The purpose of this study was to investigate whether preprocedural magnetic resonance imaging (MRI) is beneficial in patients with failed endocardial VT ablations in determining an appropriate ablation strategy. Methods and Results A cardiac MRI was performed in 20 patients with a failed ablation procedure and cardiomyopathy (nonischemic n = 12, ischemic n = 8). A subsequent ablation strategy was determined by a delayed enhanced MRI (DE-MRI) and an epicardial subxyphoid access was planned only in patients with epicardial or intramural free-wall scar. MRIs were performed in all patients with or without an implanted cardioverter defibrillator (ICD). The location of scar tissue in the MRI predicted the origin of VT in all patients. In 9/20 patients an epicardial procedure was performed based on the result of the MRI. An endocardial procedure was performed in the remaining 11 patients who had either endocardial or septal scarring and one patient in whom the MRI only showed artifact. Five patients remained inducible postablation and four patients had VT recurrence within a follow-up period of 17 ± 22 months. All of the latter patients had an intramural scar pattern. Conclusions Imaging with DE-MRI prior to VT ablation in patients with previously failed endocardial ablation procedures is beneficial in identifying an ablation strategy, helps to focus on an area of interest intraprocedurally, and provides valuable outcomes information. [ABSTRACT FROM AUTHOR]

NICM VT Ablation Aim To determine whether ventricular tachycardia (VT) recurrences in arrhythmogenic RV cardiomyopathy (ARVC) and nonischemic cardiomyopathy (NICM) are related to incomplete ablation or disease progression. Methods ARVC and NICM patients with two substrate maps of the same diseased ventricle with an interprocedural delay of ≥12 months were included. Disease progression was defined as ≥1 factor: scar area progression (PROG, +5%), ventricular remodeling (dilatation [+25 mL] or decreased ejection fraction [-5%EF]). Incomplete ablation was defined as index VT recurrence or ablation in previously unablated regions inside index scar without PROG. Results Twenty patients from nine centers were included (80% male 55 ± 16 years, 7 ARVC and 13 NICM, LVEF 43 ± 14%). Mean delay was 28 ± 18 months. Disease progression occurred in 75% with ventricular remodeling in 70%: ventricular dilation in 45% (ARVC [71%]; NICM [38%]), decreased EF in 60% [RVEF in ARVC (71%); LVEF in NICM (54%)], and scar progression in 50% (in ARVC [57%] and NICM [46%]). Index VT recurrence was observed in 40%. Redo ablation sites were located in previously unablated regions inside the index scar in 70% of patients. VT recurrence following the second procedure was seen in 25%. Fifteen percent died during a follow-up of 17 ± 17 months. Conclusion Disease progression is the rule in ARVC and NICM while scar progression occurs in half. However, even if disease progression is frequently observed, incomplete index ablation is the most common finding, strongly suggesting the need for more extensive ablation. [ABSTRACT FROM AUTHOR]

Objectives The study sought to examine prognostic relevance of T1 mapping parameters (based on a T1 mapping method) in nonischemic dilated cardiomyopathy (NIDCM) and compare them with conventional markers of adverse outcome. Background NIDCM is a recognized cause of poor clinical outcome. NIDCM is characterized by intrinsic myocardial remodeling due to complex pathophysiological processes affecting myocardium diffusely. Lack of accurate and noninvasive characterization of diffuse myocardial disease limits recognition of early cardiomyopathy and effective clinical management in NIDCM. Cardiac magnetic resonance (CMR) supports detection of diffuse myocardial disease by T1 mapping. Methods This is a prospective observational multicenter longitudinal study in 637 consecutive patients with dilated NIDCM (mean age 50 years [interquartile range: 37 to 76 years]; 395 males [62%]) undergoing CMR with T1 mapping and late gadolinium enhancement (LGE) at 1.5-T and 3.0-T. The primary endpoint was all-cause mortality. A composite of heart failure (HF) mortality and hospitalization was a secondary endpoint. Results During a median follow-up period of 22 months (interquartile range: 19 to 25 months), we observed a total of 28 deaths (22 cardiac) and 68 composite HF events. T1 mapping indices (native T1 and extracellular volume fraction), as well as the presence and extent of LGE, were predictive of all-cause mortality and HF endpoint (p < 0.001 for all). In multivariable analyses, native T1 was the sole independent predictor of all-cause and HF composite endpoints (hazard ratio: 1.1; 95% confidence interval: 1.06 to 1.15; hazard ratio: 1.1; 95% confidence interval: 1.05 to 1.1; p < 0.001 for both), followed by the models including the extent of LGE and right ventricular ejection fraction, respectively. Conclusions Noninvasive measures of diffuse myocardial disease by T1 mapping are significantly predictive of all-cause mortality and HF events in NIDCM. We provide a basis for a novel algorithm of risk stratification in NIDCM using a complementary assessment of diffuse and regional disease by T1 mapping and LGE, respectively. [ABSTRACT FROM AUTHOR]

Abstract: A 58‐year‐old man with dilated cardiomyopathy was admitted with heart failure. He had a history of two catheter ablation procedures for ventricular tachycardia (VT) originating from the intraventricular septum (IVS). Before dual valve replacement (DVR), he suffered a VT storm. An electrophysiological study revealed an extended low‐voltage area at the IVS with the exit of the induced VT at the anterior side. Radiofrequency application was performed at the VT exit as a landmark for surgical cryoablation (SA). During the DVR, SA was performed at the IVS using this landmark. After SA, the patient had no ventricular tachyarrhythmia. [ABSTRACT FROM AUTHOR]

Sudden cardiac death (SCD) is an important cause of mortality worldwide. Although SCD is most often associated with coronary heart disease, the risk of SCD in patients without ischemic heart disease is well-established. Nonischemic cardiomyopathies, including idiopathic dilated cardiomyopathy, hypertrophic cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy represent three unique disease entities that have been shown to be highly associated with SCD and ventricular arrhythmias. A variety of risk stratification tools have been investigated, although the optimal strategy remains unknown. Identification of the arrhythmogenic substrate and treatment of ventricular arrhythmias in these subgroups can be challenging. Herein, we aim to discuss the current understanding of the anatomic and electrophysiologic substrate underlying ventricular arrhythmias and highlight features that may be associated with a higher risk of SCD in these 3 conditions.

Ventricular Fibrosis in Patients With NICM Background Current guidelines recommend the implantation of an implantable cardioverter-defibrillator (ICD) for primary prevention of sudden cardiac death (SCD) in a subgroup of patients with nonischemic cardiomyopathy (NICM) who have a left ventricular ejection fraction (LVEF) ≤ 30-35%, and are NYHA functional class II or III. However, the majority of patients with an ICD implantation for primary prevention did not receive appropriate ICD therapy. The purpose of this study was to evaluate the association between myocardial fibrosis detected by cardiovascular magnetic resonance (CMR) imaging and life-threatening ventricular arrhythmic events in NICM patients. Methods One hundred and seventy-five NICM patients with an LVEF ≦ 35 % and NYHA functional class II or III, (60 ± 15 years, LVEF 29 ± 5.4%) were studied. Myocardial fibrosis was identified with a late gadolinium enhancement (LGE) on CMR. Clinical events were defined as SCD or life-threatening ventricular arrhythmic events and were followed up for 5.1 ± 3.3 years. Results The presence of an LGE was detected in 122 patients (70%). No life-threatening ventricular arrhythmia events occurred in patients with the absence of an LGE. A total of 18 ventricular tachycardia and 8 ventricular fibrillation events were found in patients with the presence of an LGE (P < 0.01). Sensitivity, specificity, and positive and negative predictive value of LGE in predicting life-threatening ventricular arrhythmia events were 100%, 34%, and 15% and 100%, respectively. Multivariate analysis showed that the presence of both septal and lateral mid-wall LGE was associated with life-threatening ventricular arrhythmic events (hazard ratio 23.1 CI; 2.88-184.9, P = 0.003). Conclusions The absence of an LGE predicts a low potential risk of SCD and life-threatening ventricular arrhythmia events in the near future. CMR may be a useful tool for selecting suitable patients for primary ICD implantations in NICM patients. [ABSTRACT FROM AUTHOR]

Background Many nonischemic cardiomyopathy (NICMP) patients referred for catheter ablation of ventricular tachycardia (VT) undergo an initial epicardial approach under general anesthesia (GA). However, GA may suppress inducibility and decrease tolerance of induced VT, leaving substrate modification as the sole ablation method. Objectives Determine the utility of a strategy of initial programmed electrical stimulation (PES) under light sedation in patients referred for epicardial ablation of VT. Methods Of 68 NICMP patients referred for VT ablation, 25 were referred specifically for epicardial ablation. All patients underwent PES under conscious sedation, with conversion to GA and epicardial access only if VT morphology and/or endocardial mapping suggested an epicardial substrate. Results VT was induced with PES in 24 of 25 patients (mean age 52 years; 76% male; ejection fraction 38 ± 18%). VT was hemodynamically tolerated in 63% and unstable in 38% of patients. The noninducible/unstable VT patients underwent substrate modification based on voltage and pace mapping. Of the patients with stable VT, 73% were mapped and ablated endocardially (six right ventricle, three left ventricle, one left coronary cusp, one middle cardiac vein), and 33% were successfully ablated in areas of normal endocardial voltage. After ablation, the clinical VT was noninducible in all patients. After mean follow-up of 10 months, 80% were free of implantable cardioverter defibrillator shocks or sustained VT. Conclusions An initial approach of PES and entrainment mapping under conscious sedation is critically important for patients with NICMP referred for epicardial ablation. Empiric ablation of endocardial/epicardial scar would have missed the clinical VT in 20% of patients. [ABSTRACT FROM AUTHOR]

Background: The relation between myocardial scar and different types of ventricular arrhythmias in patients with nonischemic dilated cardiomyopathy (NIDCM) is unknown.Objectives: The purpose of this study was to analyze the effect of myocardial scar, assessed by late gadolinium enhancement cardiac magnetic resonance imaging (LGE-CMR), on the occurrence and type of ventricular arrhythmia in patients with NIDCM.Methods: Consecutive patients with NIDCM who underwent LGE-CMR and implantable cardioverter-defibrillator (ICD) implantation at either of 2 centers were included. LGE was defined by signal intensity ≥35% of maximal signal intensity, subdivided into core and border zones (≥50% and 35%-50% of maximal signal intensity, respectively), and categorized according to location (basal or nonbasal) and transmurality. ICD recordings and electrocardiograms were reviewed to determine the occurrence and type of ventricular arrhythmia during follow-up.Results: Of 87 patients (age 56 ± 13 y, 62% male, left ventricular ejection fraction 29% ± 12%), 55 (63%) had LGE (median 6.3 g, interquartile range 0.0-13.8 g). During a median follow-up of 45 months, monomorphic ventricular tachycardia (VT) occurred in 18 patients (21%) and polymorphic VT/ventricular fibrillation (VF) in 10 (11%). LGE predicted monomorphic VT (log-rank, P < .001), but not polymorphic VT/VF (log-rank, P = .40). The optimal cutoff value for the extent of LGE to predict monomorphic VT was 7.2 g (area under curve 0.84). Features associated with monomorphic VT were core extent, basal location, and area with 51%-75% LGE transmurality.Conclusions: Myocardial scar assessed by LGE-CMR predicts monomorphic VT, but not polymorphic VT/VF, in NIDCM. The risk for monomorphic VT is particularly high when LGE shows a basal transmural distribution and a mass ≥7.2 g. Importantly, patients without LGE on CMR remain at risk for potentially fatal polymorphic VT/VF. [ABSTRACT FROM AUTHOR]

Background To date, there has been little research, if any, on the pathological correlates of end-stage heart failure in the explanted hearts of orthotopic heart transplant (OHT) recipients in correlation with the patients’ hemodynamics. We sought to compare the gross and histopathological parameters in hearts explanted—native or previously transplanted—from patients with end-stage heart failure with the clinical hemodynamics parameters at the time of OHT. Methods Forty patients undergoing OHT were enrolled in this study and divided into two groups according to whether they suffered from ischemic (ICMP) or nonischemic cardiomyopathy (NICMP). All study patients were treated with OHT for end-stage heart failure at The University of Texas Health Science Center at Houston. The pathological investigations of the hearts were focused on the study of the underlying cause of heart failure leading the patient to OHT; on the quantification of the extent and severity of fibrosis, hypertrophy, and myocytolysis; and on validating a semiquantitative grading scale. Analyses of multiple sections of the explanted hearts were carried out. The heart weights were recorded and compared with the grades of fibrosis, hypertrophy of cardiomyocytes, and myocytolysis. The grades of fibrosis, hypertrophy, and myocytolysis were evaluated in right and left ventricles and atria (with areas of confluent infarction excluded). The pathological parameters were correlated with the patients’ clinical parameters. Results Twenty-two patients (20 men, 2 women, mean age±S.E.M., 62.3±2.2 years) suffered from ICMP and 18 patients (9 men, 9 women, mean age±S.E.M., 56.3±2.8 years) from NICMP. All the clinical and pathological measured variables were comparable between the two groups, except for pulmonary vascular resistance, which was higher in the NICMP group of patients, and the grade of myocytolysis, which was significantly higher in the ICMP vs. NICMP group. Most of the clinical and pathological variables were overall linearly correlated. Conclusions Both ICMP and NICMP groups of end-stage heart failure requiring OHT presented high grades of fibrosis, hypertrophy, and myocytolysis. Heart failure is the final common pathway of a variety of primary cardiovascular diseases regardless of the ischemic or nonischemic nature of the cardiomyopathy. [ABSTRACT FROM AUTHOR]

ICD Programming in Ischemic and Nonischemic Cardiomyopathy Introduction The MADIT-RIT trial demonstrated reduction of inappropriate and appropriate ICD therapies and mortality by high-rate cut-off and 60-second-delayed VT therapy ICD programming in patients with a primary prophylactic ICD indication. The aim of this analysis was to study effects of MADIT-RIT ICD programming in patients with ischemic and nonischemic cardiomyopathy. Methods and Results First and total occurrences of both inappropriate and appropriate ICD therapies were analyzed by multivariate Cox models in 791 (53%) patients with ischemic and 707 (47%) patients with nonischemic cardiomyopathy. Patients with ischemic and nonischemic cardiomyopathy had similar incidence of first inappropriate (9% and 11%, P = 0.21) and first appropriate ICD therapy (11.6% and 14.1%, P = 0.15). Patients with ischemic cardiomyopathy had higher mortality rate (6.1% vs. 3.3%, P = 0.01). MADIT-RIT high-rate cut-off (arm B) and delayed VT therapy ICD programming (arm C) compared with conventional (arm A) ICD programming were associated with a significant risk reduction of first inappropriate and appropriate ICD therapy in patients with ischemic and nonischemic cardiomyopathy (HR range 0.11-0.34, P < 0.001 for all comparisons). Occurrence of total inappropriate and appropriate ICD therapies was significantly reduced by high-rate cut-off ICD programming and delayed VT therapy ICD programming in both ischemic and nonischemic cardiomyopathy patients. Conclusion High-rate cut-off and delayed VT therapy ICD programming are associated with significant reduction in first and total inappropriate and appropriate ICD therapy in patients with ischemic and nonischemic cardiomyopathy. [ABSTRACT FROM AUTHOR]

Nonischemic cardiomyopathy can complicate antineoplastic therapy and lead to irreversible heart failure. We evaluated structural changes at the time of left ventricular assist device implantation in heart failure patients who had been exposed to anthracycline, and we correlated those changes with clinical presentation. We retrospectively studied left ventricular core samples taken at implantation of the HeartMate II left ventricular assist device in 12 heart failure patients (mean age, 46 ± 16 yr) who had histories of anthracycline exposure. We evaluated those samples for hypertrophy, myocytolysis, and fibrosis. Histopathologic findings showed moderate-to-severe myocyte hypertrophy, moderate myocytolysis, and perivascular and interstitial fibrosis with areas of replacement fibrosis. Ultrastructural studies revealed marked decreases in myofibrils, diffuse mitochondrial swelling, and disorganization of the sarcoplasmic reticulum. The interval between anthracycline therapy and heart failure was a mean of 6.8 ± 5.7 years; duration of heart failure symptoms, 38 ± 47 months; and duration of device support, 414 ± 266 days. Four patients are continuing on device support, 3 have undergone transplantation, 3 have undergone device explantation, and 2 have died. The time of heart failure onset and the duration of symptoms did not correlate with the severity and extent of the histopathologic changes. The histopathologic findings and the clinical course varied in heart failure patients with anthracycline exposure. No correlation was observed between anthracycline therapy and the development or duration of heart failure symptoms, severity of histopathologic changes, or outcomes. [ABSTRACT FROM AUTHOR]

Background Frequent idiopathic premature ventricular complexes (PVCs) can result in PVC-induced cardiomyopathy. Frequent PVCs can also aggravate ischemic cardiomyopathy. Objective The purpose of this study was to investigate the impact of frequent PVCs on nonischemic cardiomyopathy. Methods This was a consecutive series of 30 patients (mean age 59.1 ± 12.1; 18 men; mean ejection fraction [EF] 38% ± 15%) with structurally abnormal hearts based on the presence of scar on cardiac magnetic resonance imaging and/or a history of cardiomyopathy before the presence of frequent PVCs who were referred for ablation of frequent PVCs. Results Ablation was successful in 18 of 30 patients (60%), resulting in an increase of mean EF from 33.9% ± 14.5% to 45.7% ± 17% ( P < .0001) during mean follow-up of 30 ± 28 months. The PVC burden in these patients was reduced from 23.1% ± 8.8% to 1.0% ± 0.9% ( P < .0001). Mean EF did not change in patients with a failed ablation procedure (44.4 ± 16 vs 43.5 ± 21, P = .85). The PVC site of origin was in scar tissue in 14 of 18 patients with a successful ablation procedure. Mean New York Heart Association functional class improved from 2.3 ± 0.6 to 1.1 ± 0.2 ( P < .0001) in patients with a successful outcome and remained unchanged in patients with an unsuccessful outcome (1.9 ± 0.9 vs 1.9 ± 0.7, P = 1). Conclusion In patients with frequent PVCs and nonischemic cardiomyopathy, EF and functional class can be improved but not always normalized by successful PVC ablation. In most patients with an effective ablation, the arrhythmogenic substrate was located in scar tissue. [ABSTRACT FROM AUTHOR]