Sei Iwai

Reversal of Cardiomyopathy in Patients With Repetitive Monomorphic Ventricular Ectopy Originating From the Right Ventricular Outflow Tract

Background—Tachycardia-induced cardiomyopathy caused by ventricular tachycardia is a well-defined clinical entity. Less well appreciated is whether simple ventricular ectopy can result in cardiomyopathy. We sought to examine a potential causal relationship between repetitive monomorphic ventricular ectopy originating from the right ventricular outflow tract and cardiomyopathy and the role of ablation in reversing this process. Methods and Results—The study consisted of 27 patients (11 men; age, 47±15 years) with repetitive monomorphic ventricular ectopy, including 8 patients (30%) with depressed ventricular function (ejection fraction ≤45%). All patients underwent assessment of cardiac structure and function. The burden of ectopy was quantified through 24-hour Holter monitoring. Patients then underwent ablation guided by 3D mapping. After ablation, patients underwent repeated Holter monitoring and reassessment of cardiac function. Patients with depressed ventricular function were more likely to be older than patients with normal function (58±14 versus 42±18 years; P=0.013). However, the burden of ventricular ectopy was similar in patients with (17 859±13 488 ectopic beats per 24 hours) and without (17 541±11 479 ectopic beats per 24 hours; P=0.800) preserved ventricular function. Successful ablation was performed in 23 patients (85%), including 7 of 8 patients with depressed ventricular function. In this latter group, ventricular function improved in all patients (from 39±6% to 62±6%; P=0.017). Conclusions—Repetitive monomorphic ventricular ectopy (in the absence of sustained ventricular tachycardia) originating from the right ventricular outflow tract is an underappreciated cause of unexplained cardiomyopathy. Successful ablation of the focal source of ventricular ectopy results in normalization of left ventricular function. Patients with ectopy-induced cardiomyopathy are significantly older than patients with preserved ventricular function, which suggests either that older patients are more susceptible to the development of a cardiomyopathy or that the cardiomyopathy has had a longer period of time in which to evolve.

Right and left ventricular outflow tract tachycardias : Evidence for a common electrophysiologic mechanism

Introduction:“Idiopathic” ventricular arrhythmias most often arise from the right ventricular outflow tract (RVOT), although arrhythmias from the left ventricular outflow tract (LVOT) are also observed. While previous work has elucidated the mechanism and electropharmacologic profile of RVOT arrhythmias, it is unclear whether those from the LVOT share these properties. The purpose of this study was to characterize the electropharmacologic properties of RVOT and LVOT arrhythmias.

Nonlinear-dynamical arrhythmia control in humans

Nonlinear-dynamical control techniques, also known as chaos control, have been used with great success to control a wide range of physical systems. Such techniques have been used to control the behavior of in vitro excitable biological tissue, suggesting their potential for clinical utility. However, the feasibility of using such techniques to control physiological processes has not been demonstrated in humans. Here we show that nonlinear-dynamical control can modulate human cardiac electrophysiological dynamics by rapidly stabilizing an unstable target rhythm. Specifically, in 52/54 control attempts in five patients, we successfully terminated pacing-induced period-2 atrioventricular-nodal conduction alternans by stabilizing the underlying unstable steady-state conduction. This proof-of-concept demonstration shows that nonlinear-dynamical control techniques are clinically feasible and provides a foundation for developing such techniques for more complex forms of clinical arrhythmia.

Multidetector row computed tomography for identification of left atrial appendage filling defects in patients undergoing pulmonary vein isolation for treatment of atrial fibrillation: Comparison with transesophageal echocardiography

BACKGROUND Advances in multidetector computed tomography (MDCT) technology now permit three-dimensional cardiac imaging with high spatial and temporal resolution. Historically, transesophageal echocardiography (TEE) has been the gold standard for assessment of the left atrial appendage (LAA) in patients with atrial fibrillation and other atrial arrhythmias. Findings on TEE, including demonstration of LAA thrombus and dense nonclearing spontaneous echocardiographic contrast (SEC), predict future fatal and nonfatal thromboembolic events. OBJECTIVE The purpose of this study was to compare the diagnostic performance of 64-detector row MDCT in detecting LAA thrombus and dense nonclearing SEC as identified by TEE in patients undergoing pulmonary vein isolation for treatment of atrial fibrillation. METHODS A total of 72 consecutive patients (69.4% male; mean age 56.1 +/- 10.3 years) underwent both MDCT and TEE for evaluation of the LAA (median intertest interval 0 days, interquartile range 0-5 days). MDCT assessment of the LAA was performed by two methods: (1) comparison of Hounsfield unit (HU) densities in the LAA apex to the ascending aorta (AscAo) in the same axial plane and (2) nonquantitative visual identification of a filling defect in the LAA. TEE evaluation of the LAA included identification of echodense intracavitary masses in the LAA as well as pulsed-wave Doppler interrogation of the LAA ostium. RESULTS Patients with LAA thrombus or dense nonclearing SEC by TEE exhibited significantly lower LAA/AscAo HU ratios than patients who did not (0.82 +/- 0.22 vs 0.39 +/- 0.19, P <.001). LAA/AscAo HU cutoff ratios < or = 0.75 correlated to LAA thrombus or dense nonclearing SEC by TEE, with 100% sensitivity, 72.2% specificity, 28.6% positive predictive value, and 100% negative predictive value. HU ratios < or = 0.75 were associated with pulsed-wave Doppler velocities <50 cm/s of the LAA ostium (P <.001). In multivariable analysis, LAA/AscAo HU ratio < or = 0.75 remained a robust predictor of LAA thrombus or dense nonclearing SEC by TEE (P <.001). In contrast, MDCT identification of TEE-identified LAA thrombus or dense nonclearing SEC by visual detection of LAA filling defects resulted in lower sensitivity (50%) and negative predictive value (95.1%). CONCLUSION Current-generation MDCT successfully identifies LAA thrombus and dense nonclearing SEC with high sensitivity and moderate specificity. Importantly, LAA/AscAo HU ratios >0.75 demonstrate 100% negative predictive value for exclusion of LAA thrombus or dense nonclearing SEC. These results suggest that in patients undergoing pulmonary vein isolation procedures, MDCT examinations that demonstrate LAA/AscAo HU ratios >0.75 may preclude the need for preprocedural TEE.

Lesional tachycardias related to mitral valve surgery.

OBJECTIVES The purpose of this study was to define the anatomic distribution of electrically abnormal atrial tissue and mechanisms of atrial tachycardia (AT) after mitral valve (MV) surgery. BACKGROUND Atrial tachycardia is a well-recognized long-term complication of MV surgery. Because atrial incisions from repair of congenital heart defects provide a substrate for re-entrant arrhythmias in the late postoperative setting, we hypothesized that atriotomies or cannulation sites during MV surgery also contributed to postoperative arrhythmias. METHODS In 10 patients with prior MV surgery, electroanatomic maps were constructed of 11 tachycardias (6 right atrium [RA], 4 left atrium [LA] and 1 biatrial). Activation and voltage maps were used to identify areas of low voltage, double potentials and conduction block. RESULTS Lesions were present in the lateral wall of the RA (six of seven maps) and in the LA along the septum adjacent to the right pulmonary veins (four of five maps). In 8 of 10 patients, these findings corresponded to atrial incisions or cannulation sites. Arrhythmia mechanisms were identified for 9 of 11 tachycardias. A macro-re-entrant circuit was mapped in six cases, three involving lesions in the lateral wall of the RA and three involving the LA septum and right pulmonary veins. In three of these cases figure-of-eight re-entry was demonstrated, and in the other three a single macro-re-entrant circuit was observed. In three other cases, a focal origin was identified adjacent to abnormal tissue in the RA (two cases) or within a pulmonary vein (one case). CONCLUSIONS Surgical incisions for MV surgery provide a substrate for atrial arrhythmias. Both macro-re-entrant and focal mechanisms contribute to AT after MV surgery.

Response to Adenosine Differentiates Focal From Macroreentrant Atrial Tachycardia Validation Using Three-Dimensional Electroanatomic Mapping

Background—We previously proposed that adenosine has mechanism-specific effects on atrial tachycardia (AT), such that adenosine terminates AT attributable to triggered activity, transiently suppresses automatic rhythms, and has no effect on macroreentrant AT. This, however, remains controversial, because other studies have reported that adenosine terminates reentrant AT. To clarify this issue, we used 3D electroanatomic mapping to delineate the tachycardia circuit and thereby determine whether the response to adenosine differentiates focal from macroreentrant AT. Methods and Results—We examined the effect of adenosine on 43 ATs in 42 consecutive patients (59±15 years of age; 26 female) who received adenosine during tachycardia and whose mechanism of AT was characterized by pharmacological perturbation, entrainment, 3D electroanatomic mapping, and results of radiofrequency ablation. Eight tachycardias were macroreentrant (noncavotricuspid isthmus-dependent), and 35 ATs were focal (either triggered or automatic). Adenosine administered during AT (at doses sufficient to result in AV block) terminated or transiently suppressed focal AT in 33 of 35 cases, whereas 8 of 8 macroreentrant ATs were adenosine insensitive (P <0.001). Twenty-eight of 35 focal ATs were located along the crista terminalis or tricuspid annulus. Conclusions—The response of AT to adenosine can immediately differentiate atrial tachycardia arising from a focal source from that attributable to macroreentry. This finding can be exploited to facilitate developing a focused, strategic ablative approach at the onset of a procedure.

Chapter 72 – Ventricular Tachycardia in Patients with Structurally Normal Hearts

Idiopathic ventricular tachycardia is a generic term that refers to ventricular arrhythmias that originate in hearts without structural disease. Several discrete forms of idiopathic ventricular tachycardia have been identified, and electropharmacologic data suggest that multiple arrhythmogenic mechanisms may account for these arrhythmias. 1 2 Idiopathic ventricular tachycardia has been classified with respect to the ventricle of origin, the response to pharmacologic agents, evidence for catecholamine dependence, and the morphologic features of the arrhythmia (QRS configuration and axis and whether repetitive, nonsustained, or sustained). A mechanistically oriented classification has also been developed and is summarized in Table 72-1 . In general, the response of the arrhythmia to programmed stimulation and to adenosine, verapamil, and propranolol differentiates nearly all forms of idiopathic ventricular tachycardia.

Long-term outcome of patients with unexplained syncope treated with an electrophysiologic-guided approach in the implantable cardioverter-defibrillator era.

OBJECTIVES We evaluated the long-term outcome of patients with coronary artery disease and unexplained syncope who were treated with an electrophysiologic (EP)-guided approach. BACKGROUND Electrophysiologic studies are frequently performed to evaluate unexplained syncope in patients with coronary artery disease. Patients with this profile who have inducible ventricular tachycardia are considered at high risk for sudden death and increased overall mortality, and therefore are often treated with an implantable cardioverter-defibrillator (ICD). The impact of this EP-guided strategy is unknown because there are no data comparing the long-term outcome of ICD recipients with that of noninducible patients. METHODS We evaluated 67 consecutive patients with coronary artery disease and unexplained syncope. All patients were treated with an EP-guided approach that included ICD implantation in patients with inducible ventricular tachycardia. RESULTS Electrophysiologic testing suggested a plausible diagnosis in 32 (48%) of these patients. Inducible monomorphic ventricular tachycardia was the most common abnormality. Despite frequent appropriate therapy with ICDs, the total mortality for patients with inducible monomorphic ventricular tachycardia was significantly higher than for noninducible patients. The respective one- and two-year survival rates were 94% and 84% in noninducible patients and 77% and 45% in inducible patients (p = 0.02). CONCLUSIONS Electrophysiologic testing suggests an etiology for unexplained syncope in approximately 50% of patients and risk stratifies these patients with regard to long-term outcome. Patients who receive an ICD for the management of inducible ventricular tachycardia have a high incidence of spontaneous ventricular arrhythmias requiring ICD therapy. However, despite ICD implantation and frequent appropriate delivery of ICD therapies, patients with inducible ventricular tachycardia have a significantly worse prognosis than do those who are noninducible.

Catheter ablation of postinfarction ventricular tachycardia: Ten-year trends in utilization, in-hospital complications, and in-hospital mortality in the United States

BACKGROUND There is a paucity of data regarding the complications and in-hospital mortality after catheter ablation for ventricular tachycardia (VT) in patients with ischemic heart disease. OBJECTIVE The purpose of this study was to determine the temporal trends in utilization, in-hospital mortality, and complications of catheter ablation of postinfarction VT in the United States. METHODS We used the 2002-2011 Nationwide Inpatient Sample (NIS) database to identify all patients ≥18 years of age with a primary diagnosis of VT (International Classification of Diseases, Ninth Edition, Clinical Modification [ICD-9-CM] code 427.1) and who also had a secondary diagnosis of prior history of myocardial infarction (ICD-9-CM 412). Patients with supraventricular arrhythmias were excluded. Patients who underwent catheter ablation were identified using ICD-9-CM procedure code 37.34. Temporal trends in catheter ablation, in-hospital complications, and in-hospital mortality were analyzed. RESULTS Of 81,539 patients with postinfarct VT, 4653 (5.7%) underwent catheter ablation. Utilization of catheter ablation increased significantly from 2.8% in 2002 to 10.8% in 2011 (Ptrend < .001). The overall rate of any in-hospital complication was 11.2% (523/4653), with vascular complications in 6.9%, cardiac in 4.3%, and neurologic in 0.5%. In-hospital mortality was 1.6% (75/4653). From 2002 to 2011, there was no significant change in the overall complication rates (8.4% to 10.2%, Ptrend = .101; adjusted odds ratio [per year] 1.02, 95% confidence interval 0.98-1.06) or in-hospital mortality (1.3% to 1.8%, Ptrend = .266; adjusted odds ratio [per year] 1.03, 95% confidence interval 0.92-1.15). CONCLUSION The utilization rate of catheter ablation as therapy for postinfarct VT has steadily increased over the past decade. However, procedural complication rates and in-hospital mortality have not changed significantly during this period.

Regional Variation in the Incidence and Outcomes of In-Hospital Cardiac Arrest in the United States

Background— Regional variation in the incidence and outcomes of in-hospital cardiac arrest (IHCA) is not well studied and may have important health and policy implications. Methods and Results— We used the 2003 to 2011 Nationwide Inpatient Sample databases to identify patients ≥18 years of age who underwent cardiopulmonary resuscitation (International Classification of Diseases, Ninth Edition, Clinical Modification procedure codes 99.60 and 99.63) for IHCA. Regional differences in IHCA incidence, survival to hospital discharge, and resource use (total hospital cost and discharge disposition among survivors) were analyzed. Of 838 465 patients with IHCA, 162 270 (19.4%) were in the Northeast, 159 581 (19.0%) were in the Midwest, 316 201 (37.7%) were in the South, and 200 413 (23.9%) were in the West. Overall IHCA incidence in the United States was 2.85 per 1000 hospital admissions. IHCA incidence was lowest in the Midwest and highest in the West (2.33 and 3.73 per 1000 hospital admissions, respectively). Compared with the Northeast, risk-adjusted survival to discharge was significantly higher in the Midwest (odds ratio, 1.33; 95% confidence interval, 1.31–1.36), South (odds ratio, 1.21; 95% confidence interval, 1.19–1.23), and West (odds ratio, 1.25; 95% confidence interval, 1.23–1.27). IHCA survival increased significantly from 2003 to 2011 in the United States and in all regions (all Ptrend<0.001). Total hospital cost was highest in the West, whereas discharge to skilled nursing facility and use of home health care among survivors was highest in the Northeast. Conclusions— We observed significant regional variation in IHCA incidence, survival, and resource use in the United States. This variation was explained only partially by differences in patient and hospital characteristics. Further studies are needed to identify other potential factors responsible for these regional differences to improve outcomes after IHCA.