Wideband arrhythmia-Insensitive-rapid (AIR) pulse sequence for cardiac T1 mapping without image artifacts induced by an implantable-cardioverter-defibrillator.

PURPOSE: To develop and evaluate a wideband arrhythmia-insensitive-rapid (AIR) pulse sequence for cardiac T1 mapping without image artifacts induced by implantable-cardioverter-defibrillator (ICD). METHODS: We developed a wideband AIR pulse sequence by incorporating a saturation pulse with wide frequency bandwidth (8.9 kHz) to achieve uniform T1 weighting in the heart with ICD. We tested the performance of original and "wideband" AIR cardiac T1 mapping pulse sequences in phantom and human experiments at 1.5 Tesla. RESULTS: In five phantoms representing native myocardium and blood and postcontrast blood/tissue T1 values, compared with the control T1 values measured with an inversion-recovery pulse sequence without ICD, T1 values measured with original AIR with ICD were considerably lower (absolute percent error > 29%), whereas T1 values measured with wideband AIR with ICD were similar (absolute percent error < 5%). Similarly, in 11 human subjects, compared with the control T1 values measured with original AIR without ICD, T1 measured with original AIR with ICD was significantly lower (absolute percent error > 10.1%), whereas T1 measured with wideband AIR with ICD was similar (absolute percent error < 2.0%). CONCLUSION: This study demonstrates the feasibility of a wideband pulse sequence for cardiac T1 mapping without significant image artifacts induced by ICD.

"Vasovagal" response during ventricular fibrillation: incidence and implications.

BACKGROUND: The purpose of this study was to assess the relationship between changes in sinus node cycle length (SNCL) during ventricular fibrillation (VF) and the peripheral changes in blood pressure (BP) and sympathetic nerve activity (SNA) in human subjects. We hypothesized that patients with no SNCL shortening during VF have a vasovagal-like response with a greater decrease in BP and SNA when compared to patients with SNCL shortening. METHODS: SNCL, BP, and SNA recordings were attempted in 24 patients undergoing the implantation of a dual-chamber implantable defibrillator. Changes were measured during the first 5 seconds of VF and compared with the 5 seconds prior to VF induction. RESULTS: SNCL shortened during VF in nine patients (mean%∆SNCL = -12 ± 8%) and remained unchanged or lengthened in seven patients (mean%∆SNCL = 7 ± 7%). Eight patients had ventriculoatrial (VA) conduction prohibiting assessment of SNCL changes. In patients with SNCL shortening, the %∆MBP (mean BP) was -47 ± 6% compared to -58 ± 8% in patients with no SNCL shortening (P < 0.01). In patients with VA conduction, the %∆MBP was -54 ± 3%. SNA recordings were successfully obtained in four patients. When compared to baseline, SNA increased by 34 ± 30% in two patients with SNCL shortening, decreased by 25% in one patient with SNCL lengthening, and by 90% in the fourth patient with VA conduction. CONCLUSIONS: We have shown that patients with no SNCL shortening have a significantly greater decrease in MBP during VF when compared to patients with SNCL shortening. The underlying mechanism appears to be reflex mediated with a vasovagal-like response in patients with no SNCL shortening.

Implantation of cardiac rhythm devices during concomitant anticoagulation or antiplatelet therapy.

Cardiac rhythm devices are increasingly being utilized as the population ages and the incidence of chronic heart failure, bradyarrhythmias and the indications for pacing and prevention of sudden cardiac arrest expand. The number of patients receiving oral anticoagulants and dual antiplatelet therapy is similarly increasing. Implantation of cardiac rhythm devices during concomitant use of oral anticoagulants or antiplatelet regimens poses an increased risk of perioperative bleeding complications. Traditionally, heparin-based bridging protocols have been recommended for such patients to mitigate the bleeding risk while reducing the risk of thrombotic complications. Although the literature is limited, an appraisal of the literature reveals that bridging may not be the best strategy. We review the literature and propose strategies to promote successful perioperative outcomes, while reducing the risk of bleeding or thrombosis during the time of implantation for patients on chronic anticoagulation and antiplatelet therapies.

Cardiac resynchronization therapy device implantation in patients with therapeutic international normalized ratios.

BACKGROUND: Many patients who need cardiac resynchronization therapy (CRT) require chronic anticoagulation. Current guidelines recommend discontinuation of warfarin and the initiation of anticoagulant "bridging" therapy during these procedures. We evaluated the safety of CRT-device (CRT-D) implantation without interruption of warfarin therapy. METHODS: A total of 123 consecutive patients requiring CRT-D therapy were enrolled, 49 identified as high risk for thromboembolic events who received either intravenous heparin, low molecular weight heparin, or warfarin therapy. The control group comprised 74 patients with low risk of thromboembolic events who required only cessation of warfarin perioperatively. Patients were evaluated at discharge and 15 and 30 days postoperatively for pocket hematomas, thromboembolic events, and bleeding. Patients' length of stay was also catalogued. RESULTS: Patients in the bridging arm had a significant increase in the rate of pocket hematomas (4.1%[control] vs 5.0%[warfarin] vs 20.7%[bridging], P = 0.03) and subsequent longer length of stay (1.6 +/- 1.6 [control] vs 2.9 +/- 2.7 [warfarin] vs 3.7 +/- 3.2 [bridging], P < 0.001). Hematoma formation postoperatively was not different among patients undergoing an upgrade procedure versus those without preexisting cardiac rhythm devices (12% vs 6.2%, P = NS). Patients with a prosthetic mechanical mitral valve had a higher incidence of pocket hematoma formation (1.8% vs 20%, P = 0.03). CONCLUSIONS: Our findings suggest that implantation of CRT-Ds without interruption of warfarin therapy in patients at high risk of thromboembolic events is a safe alternative to routine bridging therapy. This strategy is associated with reduced risk of pocket hematomas and shorter length of hospital stay. (PACE 2010; 400-406).

Scatter in repolarization timing predicts clinical events in post-myocardial infarction patients.

BACKGROUND: Increased spatial and temporal dispersion of repolarization contributes to ventricular arrhythmogenesis. Beat-to-beat fluctuations in T-wave timing are thought to represent such dispersion and may predict clinical events. OBJECTIVE: The purpose of this study was to assess whether a novel noninvasive measure of beat-to-beat instability in T-wave timing would provide additive prognostic information in post-myocardial infarction patients. METHODS: We studied 678 patients from 12 hospitals with 32-lead 5-minute electrocardiogram recordings 6-8 weeks after myocardial infarction. Custom software identified R wave-to-T wave intervals (RTIs) and diastolic intervals (DIs). Repolarization scatter (RTI:DI(StdErr)) was then calculated as the standard error about the RTI:DI regression line. In addition, left ventricular ejection fraction (LVEF), short-term heart rate variability (HRV) parameters, and QT variability index were measured. Patients were followed for the composite endpoint of death or life-threatening ventricular arrhythmia. RESULTS: After a mean follow-up of 63 months, 134 patients met the composite endpoint. An RTI:DI(StdErr) >5.50 ms was associated with a 210% increase in arrhythmias or deaths (P <.001). After adjusting for LVEF, RTI:DI(StdErr) remained an independent predictor (P <.001). RTI:DI(StdErr) was also independent of short-term HRV parameters and the QT variability index. CONCLUSIONS: Increased repolarization scatter, a measure of high-frequency, cycle-length-dependent repolarization instability, predicts poor outcomes in patients after myocardial infarction.

Heart rate turbulence parameters correlate with post-premature ventricular contraction changes in muscle sympathetic activity.

BACKGROUND: Heart rate turbulence (HRT) has been shown to be vagally mediated with a strong correlation to baroreflex indices. However, the relationship between HRT and peripheral sympathetic nerve activity (SNA) after a premature ventricular contraction (PVC) remains unclear. OBJECTIVE: We sought to evaluate the relationship between HRT and the changes in peripheral SNA after PVCs. METHODS: We recorded postganglionic muscle SNA during electrocardiogram monitoring in eight patients with spontaneous PVCs. Fifty-two PVCs were observed and analyzed for turbulence onset (TO) and slope (TS). SNA was quantified during (1) the dominant burst after the PVC (dominant burst area) and (2) the 10 seconds after the dominant burst (postburst SNA). RESULTS: The mean TO was 0.1% +/- 4.6%, and the mean TS was 6.1 +/- 6.6. The dominant burst area negatively correlated with TO (r = -0.50, P = .0002). The postburst SNA showed a significant positive correlation with TO (r = 0.44, P = .001) and a negative correlation with TS (r = -0.42, P = .002). These correlations remained significant after controlling for either the PVC coupling interval or the left ventricular ejection fraction. CONCLUSIONS: Our findings highlight the relationship between perturbations in HRT and pathology in the sympathetic limb of the autonomic nervous system. Future studies are needed to evaluate the prognostic role of baroreflex control of sympathetic activity in patients with structural heart disease.

The effects of rate and irregularity on sympathetic nerve activity in human subjects.

BACKGROUND: We have recently shown that atrial fibrillation is associated with an increase in sympathetic nerve activity (SNA) compared with sinus rhythm. It remains unclear, however, whether these findings are true at various rates and whether the magnitude of sympathoexcitation is related to the degree of irregularity. OBJECTIVE: To determine the role of irregularity in mediating the SNA changes at various pacing rates. Univariate analysis showed that as the irregularity increased, SBP increased (r = 0.44, P < .001) but that MAP and DBP did not change significantly. METHODS: Using custom-made software, atrioventricular sequential pacing with predetermined rates (100, 120, and 140 bpm) and irregularities (standard deviation = 0%, 5%, 15%, and 25% of mean cycle length) was performed in 23 patients referred for electrophysiologic evaluation. Pacing at each rate/irregularity was performed for 2 minutes, with 2 minutes of recovery in between. Systolic, diastolic, and mean arterial blood pressure (SBP, DBP, and MAP), central venous pressure (CVP), and SNA were measured at baseline and during pacing. RESULTS: Univariate analysis showed that as the irregularity increased, SBP increased (r = 0.44, P < .001 but that MAP and DBP did not change significantly. A significant correlation was found between the pacing irregularity and SNA, with greater sympathoexcitation noted at greater degrees of irregularity (r = 0.2, P = .04). A five-variable linear model using DBP, MAP, CVP, and degree of pacing irregularity to predict SNA was highly statistically significant (r = 0.46, P < .001). After controlling for hemodynamic changes, for every 1% increase in irregularity, there was a 6.1% increase in SNA. CONCLUSION: We have shown that greater degrees of irregularity cause greater sympathoexcitation and that the effects of irregular pacing on SNA are independent of the hemodynamic changes.

The magnitude of sinus cycle length change during ventricular tachycardia is predictive of successful antitachycardia pacing.

BACKGROUND: Despite the wide use of antitachycardia pacing (ATP) in patients with implantable cardioverter defibrillators (ICDs), predictors of ATP success remain poorly understood. We hypothesize that the degree of sympathoexcitation, as measured by the sinus cycle length (SCL) shortening during ventricular tachycardia (VT), is a predictor of ATP success. METHODS AND RESULTS: The charts of 462 patients with dual-chamber ICDs were reviewed. A total of 88 events in 26 patients met the inclusion criteria and were analyzed. The mean SCL during the 4 seconds preceding the VT onset (SCL-baseline), and during the 4 seconds prior to ATP delivery (SCL-VT) was measured. The percent shortening in SCL was calculated as ((SCL-baseline) - (SCL-VT))/(SCL-baseline) x 100. Patients were classified into the ATP-success and ATP-failure groups depending on the VT(s) response to ATP. Using a t-test analogue for clustered data, patients in the ATP-success group exhibited a greater shortening in SCL when compared with the ATP-Failure group (5.8% compared to 4.7%, P = 0.007). The successful ATP events displayed an average SCL shortening of 6.0% compared to 1.8% in the unsuccessful ATP events (P = 0.029). When the events were analyzed, the sensitivity and specificity of a shortening in SCL of >10% in predicting ATP success were 0.29 and 1. CONCLUSION: We have shown that the SCL change during VT, a marker of the autonomic changes that accompany a tachycardia, is useful in predicting ATP success. Our findings suggest that analysis of the SCL during VT might play a role in future programming of ATP in patients with ICDs.

Klebsiella pneumoniae: a rare cause of device-associated endocarditis.

Intravascular infections involving implanted pacemakers and defibrillators are being seen with increasing frequency. This report describes a case of intravascular infection of an implanted defibrillator with Klebsiella pneumoniae, an unusual pathogen for pacemaker or defibrillator infection.

Ventricular tachycardia in structurally normal hearts.

This review focuses on four distinct syndromes of ventricular tachycardia that occur in the structurally normal heart. Recent advances in the fields of molecular biology and genetics, along with intracardiac mapping techniques, have led to a greater understanding of the underlying mechanisms of and therapeutic options for these syndromes. The cyclic AMP-mediated triggered activity tachycardias, including exercise-induced right ventricular outflow track tachycardia and repetitive monomorphic ventricular tachycardia, are the most common of these syndromes. Idiopathic left ventricular tachycardia, for which there is significant evidence for re-entry within the Purkinje network, is largely curable with catheter ablation. The long QT syndrome comprises a heterogeneous group of ion channel defects leading to prolongation of myocyte repolarization and Torsade de Pointes ventricular tachycardia. Brugada syndrome, a familial disorder of transmembrane ion transport, is felt to be the result of a group of sodium channel defects leading to characteristic electrocardiographic abnormalities, and syncope and sudden death. Primary focus is given to recent advances in our understanding of the underlying mechanism and current therapeutic approaches.