Cara N. Pellegrini

Dual-chamber implantable cardioverter-defibrillator selection is associated with increased complication rates and mortality among patients enrolled in the NCDR implantable cardioverter-defibrillator registry.

OBJECTIVES The aim of this study was to compare single- versus dual-chamber implantable cardioverter-defibrillator (ICD) implantation and complication rates in a large, real-world population. BACKGROUND The majority of patients enrolled in ICD efficacy trials received single-chamber devices. Although dual-chamber ICDs offer theoretical advantages over single-chamber defibrillators, the clinical superiority of dual-chamber models has not been conclusively proven, and they may increase complications. METHODS The National Cardiovascular Data Registry ICD Registry was used to examine the association between baseline characteristics and device selection in 104,049 patients receiving single- and dual-chamber ICDs between January 1, 2006, and December 31, 2007. A longitudinal cohort design was then used to determine in-hospital complication rates. RESULTS Dual-chamber devices were implanted in 64,489 patients (62%). Adverse events were more frequent with dual-chamber than with single-chamber device implantation (3.17% vs. 2.11%, p < 0.001), as was the rate of in-hospital mortality (0.40% vs. 0.23%, p < 0.001). After adjusting for demographics, medical comorbidities, diagnostic test data, and ICD indication, the odds of any complication (odds ratio: 1.40; 95% confidence interval: 1.28 to 1.52; p < 0.001) and in-hospital mortality (odds ratio: 1.45; 95% confidence interval: 1.20 to 1.74; p < 0.001) were increased with dual-chamber versus single-chamber ICD implantation. CONCLUSIONS In this large, multicenter cohort of patients, dual-chamber ICD use was common. Dual-chamber device implantation was associated with increases in periprocedural complications and in-hospital mortality compared with single-chamber defibrillator selection.

Impact of advanced age on survival in patients with implantable cardioverter defibrillators

AIMS Given the selectivity of clinical trial patients and meager representation of elderly in the major implantable cardioverter defibrillator (ICD) randomized trials (<25%), whether such data apply to elderly patients overall is unclear. The purpose of our study is to understand the influence of age on mortality after ICD implantation. METHODS AND RESULTS We performed a retrospective cohort study of 502 consecutive patients receiving ICDs from 1993 to 2003 at a single university hospital. The primary predictor was patient age, categorized as <65, 65-75, and >75 years at ICD implantation. The primary outcome was time to death. Mean follow-up was 4 years. Median survival after ICD implantation was 5.3 years among subjects >75 years, less than half that of the youngest group. After adjusting for potential confounders, compared with subjects <65 years of age, patients >75 years [hazard ratio (HR), 4.7; 95% confidence interval (CI), 2.8-7.9; P < 0.001] and those 65-75 years (HR, 2.8; 95% CI, 1.7-4.8; P < 0.001) were at greater risk of death. Increased age was associated with higher total, cardiac, and non-cardiac mortality (all P <or= 0.001). CONCLUSION Age at ICD implantation is strongly and independently associated with mortality. Age should be considered among potential co-morbidities in anticipating survival of the elderly patient prior to ICD implantation.

Statin Use is Associated with Lower Risk of Atrial Fibrillation in Women with Coronary Disease: The HERS Trial

Objective: To determine the efficacy of statin treatment in atrial fibrillation (AF) prevention in women. Design: Cohort study using data obtained in the Heart and Estrogen/Progestin Replacement Study (HERS). Setting: Secondary analysis of a multicentre, randomised controlled clinical trial. Patients: 2673 Postmenopausal women with coronary disease. Main outcome measures: AF prevalence at baseline and incident AF over a mean follow-up of 4.1 years. Results: 88 Women with AF were identified: 29 at baseline and 59 during follow-up. Women with AF were significantly less likely to be taking a statin at study enrolment than those without AF (22% vs 37%, p = 0.003). Baseline statin use was associated with a 65% lower odds of having AF at baseline after controlling for age, race, history of myocardial infarction or revascularisation and history of heart failure (odds ratio 0.35, 95% confidence interval (CI) 0.13 to 0.93, p = 0.04). The risk of developing AF during the study among those free from AF at baseline, adjusted for the same covariates, was 55% less for those receiving statin treatment (hazard ratio 0.45, 95% CI 0.26 to 0.78, p = 0.004). Conclusions: Statin treatment is associated with a lower prevalence and incidence of AF after adjustment for potential confounders in postmenopausal women with coronary disease.

Clinical management of ventricular tachycardia.

Ventricular tachycardia (VT) may be monomorphic or polymorphic. Although commonly related to organic heart disease, a significant percentage of VTs are idiopathic (occurring in patients with otherwise normal hearts). Correctly identifying the substrate and mechanism of the tachycardia is essential for proper management. Although therapy for monomorphic VT associated with structural heart disease focuses on tachycardia suppression and reduction of sudden cardiac death (SCD) risk, idiopathic monomorphic VT generally does not entail an increased risk of SCD and treatment is aimed primarily at symptom reduction. Polymorphic VT associated with ischemia or an acquired precipitant that prolongs the QT interval should prompt reversal of underlying cause, in contrast to the congenital arrhythmia syndromes, which demand genetic testing to define the underlying problem. This review describes the diagnosis, mechanisms, etiology, and management of monomorphic and polymorphic VT, with attention to recent advances in biological understanding and the most current therapeutic recommendations.

Prevalence of Guideline-Directed Medical Therapy Among Patients Receiving Cardiac Resynchronization Therapy Defibrillator Implantation in the National Cardiovascular Data Registry During the Years 2006 to 2008

Cardiac resynchronization therapy (CRT) reduces morbidity and mortality among selected patients with left ventricular systolic dysfunction and severe heart failure symptoms despite guideline-directed medical therapy (GDMT). Contemporaneous guidelines provided clear recommendations regarding selection of patients for CRT, including that all patients should first receive GDMT with β blockers and renin-angiotensin axis antagonists. Prevalence of GDMT among real-world patients receiving CRT defibrillators (CRT-D) has not been well studied. We identified 45,392 patients in the National Cardiovascular Data Registry Implantable Cardioverter-Defibrillator Registry who underwent first CRT-D implantation for primary prevention of sudden death from January 2006 to June 2008. We calculated the proportion of patients with contemporaneous class I guideline indications for CRT-D, the proportion receiving GDMT for heart failure, and the proportion receiving GDMT who had class I guideline indications for CRT-D. Among patients without contraindications, 87% were prescribed β blockers, 78% an angiotensin-converting enzyme inhibitor or an angiotensin II receptor inhibitor, and 70% both a β blocker and an angiotensin-converting enzyme or angiotensin II receptor inhibitor at discharge. Finally, 50% of patients met class I guideline indications and were prescribed GDMT at discharge; 9% neither met class I indications nor were prescribed GDMT at discharge. The major limitation of this study is the lack of dosage information in the Implantable Cardioverter-Defibrillator Registry and lack of prescribing information at times other than discharge. In conclusion, many patients receiving CRT-D are not receiving GDMT at discharge. Ensuring that all patients receiving CRT-D are also receiving GDMT appears to be a quality improvement target.

His overdrive pacing during supraventricular tachycardia: a novel maneuver for distinguishing atrioventricular nodal reentrant tachycardia from atrioventricular reciprocating tachycardia.

BACKGROUND Because the His bundle is intrinsic to the circuit in orthodromic reciprocating tachycardia and remote from that of atrioventricular nodal reentrant tachycardia (AVNRT), pacing the His bundle during supraventricular tachycardia (SVT) may be useful to distinguish these arrhythmias. OBJECTIVE The purpose of this study was to test the hypothesis that His overdrive pacing (HOP) would affect SVT immediately for orthodromic reciprocating tachycardia and in a delayed manner for AVNRT. METHODS Once SVT was induced, HOP was performed by pacing the His bundle 10-30 ms faster than the SVT cycle length. The maneuver was determined to have entered the tachycardia circuit when a nonfused His-capture beat advanced or delayed the subsequent atrial electrogram by ≥10 ms or when the tachycardia was terminated. The number of beats required to enter each tachycardia with HOP was recorded. RESULTS HOP was performed during 66 SVTs (26 atrioventricular reciprocating tachycardia [AVRT] and 40 AVNRT). Entry into the tachycardia within 1 beat had sensitivity of 92%, specificity of 92%, positive predictive value (PPV) of 89% and negative predictive value (NPV) of 95% to confirm the diagnosis of AVRT. A cutoff ≥3 beats to enter the circuit had sensitivity of 90%, specificity of 92%, PPV of 95% and NPV of 86% to confirm the diagnosis of AVNRT. HOP had sensitivity, specificity, PPV, and NPV of 100% for distinguishing septal AVRT from atypical AVNRT. CONCLUSION HOP during SVT is a novel technique for distinguishing orthodromic reciprocating tachycardia from AVNRT. It can reliably distinguish between these arrhythmias with high sensitivity and specificity.

Idiopathic epicardial ventricular tachycardia with origin remote from vascular structures

We report a case of a patient with idiopathic left ventricular tachycardia (VT) successfully ablated from the epicardial aspect of the left ventricle, after a previous failed endocardial ablation. The VT appeared to be catecholamine sensitive. An excellent epicardial pacemap was found in the midlateral region of the left ventricle, remote from vascular structures. Following ablation, the patient discontinued antiarrhythmic drug use and has not experienced any recurrence of VT for more than 2 1/2 years.

Longer Ambulatory ECG Monitoring Increases Identification of Clinically Significant Ectopy

Frequent premature ventricular contractions (PVCs) can cause a reversible reduction in systolic function. Most studies use 24‐hour ambulatory electrocardiograms (AECGs) to assess PVC burden; however, PVC counts vary across 24‐hour periods. We hypothesized that extended AECG monitoring would better identify clinically significant ectopy.

Bradycardia: sinus and AV node dysfunction

The surface electrocardiogram (ECG) holds many clues with regard to the etiology of bradycardia and site of atrioventricular (AV) block. Bedside maneuvers may prove helpful in cases of 2:1 AV block or situations where the data is not all concordant. Wenckebach conduction may occur in any region of the heart, and there are nonpathologic mimickers of Mobitz II AV block as well. The surface ECG may aid in the inference of etiology for better than expected or slowed rather than blocked AV conduction. Sinus node dysfunction may present in several forms and often accompanies other conduction system disease. On occasion invasive studies may be required to help elucidate the mechanism of bradycardia. Das Oberflächen-EKG enthält viele Hinweise auf die Ursache einer Bradykardie und die Lokalisation eines AV-Blocks. Manöver am Patientenbett können hilfreich beim AV-Block II mit 2:1-Überleitung sein oder in Situationen, wo die Lokalisation und prognostische Bedeutung eines AV-Blocks nicht klar sind. Wenckebach-Leitung kann in jeder Region des Herzens auftreten ebenso wie es nicht-pathologische Arrhythmien gibt, die einen AV-Block II Typ Mobitz II nachahmen. Das Oberflächen-EKG kann dabei helfen, die Ursache einer Überleitung zu finden, die besser als erwartet ist oder bei der die AV-Überleitung eher verlangsamt als blockiert ist. Eine Sinusknoten-Dysfunktion kann sich in verschiedenen Formen zeigen und begleitet oft Reizleitungsstörungen. In Einzelfällen kann eine invasive elektrophysiologische Untersuchung notwendig sein, um den Mechanismus einer Bradykardie zu erhellen.The surface electrocardiogram (ECG) holds many clues with regard to the etiology of bradycardia and site of atrioventricular (AV) block. Bedside maneuvers may prove helpful in cases of 2:1 AV block or situations where the data is not all concordant. Wenckebach conduction may occur in any region of the heart, and there are nonpathologic mimickers of Mobitz II AV block as well. The surface ECG may aid in the inference of etiology for better than expected or slowed rather than blocked AV conduction. Sinus node dysfunction may present in several forms and often accompanies other conduction system disease. On occasion invasive studies may be required to help elucidate the mechanism of bradycardia.ZusammenfassungDas Oberflächen-EKG enthält viele Hinweise auf die Ursache einer Bradykardie und die Lokalisation eines AV-Blocks. Manöver am Patientenbett können hilfreich beim AV-Block II mit 2:1-Überleitung sein oder in Situationen, wo die Lokalisation und prognostische Bedeutung eines AV-Blocks nicht klar sind. Wenckebach-Leitung kann in jeder Region des Herzens auftreten ebenso wie es nicht-pathologische Arrhythmien gibt, die einen AV-Block II Typ Mobitz II nachahmen. Das Oberflächen-EKG kann dabei helfen, die Ursache einer Überleitung zu finden, die besser als erwartet ist oder bei der die AV-Überleitung eher verlangsamt als blockiert ist. Eine Sinusknoten-Dysfunktion kann sich in verschiedenen Formen zeigen und begleitet oft Reizleitungsstörungen. In Einzelfällen kann eine invasive elektrophysiologische Untersuchung notwendig sein, um den Mechanismus einer Bradykardie zu erhellen.

Episodic ventricular pacing with intact atrioventricular nodal function in a DDDR device: what is the rhythm and how can it be prevented?

m A b a t t c v i u. ase summary 67-year-old woman with a history of sick sinus syndrome nderwent placement of a dual-chamber pacemaker in 1993 nd generator change in 2001 (Integrity AFx DR 5342, St. ude Medical, Inc., St. Paul, MN, USA). Pacing was prorammed to DDDR mode with a lower rate limit of 70 ppm, pper rate limit of 120 ppm, and AV delay of 300 ms. While ospitalized for other reasons, she complained of palpitaions that correlated to periods of ventricular pacing. The nset is shown in Figure 1, and the termination is shown in igure 2. What is the explanation for the ventricular pacing? s the pacemaker malfunctioning? What reprogramming can e performed to prevent this rhythm, which is causing the alpitations?