Sudden death during follow-up after new-onset ventricular tachycardia in vascular surgery patients.

BACKGROUND: Vascular surgery patients are at increased risk for late sudden cardiac death. Identification of patients at risk during surgery offers the opportunity for focused therapy. METHODS: We monitored 483 vascular surgery patients who had no documented history of arrhythmias to identify perioperative new-onset ventricular tachyarrhythmia (VT) and myocardial ischemia using a continuous electrocardiographic (ECG) device for 72 hours. Cardiac risk factors, left ventricular ejection fraction (LVEF), medical therapy, inflammation status, and perioperative ischemia in relation to arrhythmia were noted in all patients. During follow-up, event-based outcomes analysis was used to describe survival. RESULTS: New-onset perioperative VT was detected in 33 patients (6.8%). A higher percentage of patients experiencing perioperative VT had reduced LVEF preoperatively than those without VT (24% vs 12%; P = .04). Additionally, fewer patients experiencing VT were receiving statins than those without (70% vs 85%; P = .02). Patients experiencing VT had a higher incidence of myocardial ischemia (30% vs 18%; P = .10). Perioperative VT was preceded by ischemia in only 60% of the cases. The overall cohort survival was 83% at 24-month follow-up (interquartile range [IQR], 1.1-1.3). Sudden cardiac death free survival among patients experiencing VT was less than in those without (79% vs 92%; P = .02). After adjusting for gender, cardiac risk factors, and type of surgery, new-onset perioperative VT was associated with sudden cardiac death (hazard ratio [HR], 2.6; 95% confidence interval [CI], 1.1-5.8). CONCLUSION: Perioperative VT is likely to be associated with late sudden cardiac death and decreased survival. Continuous perioperative ECG is an effective method to identify VT and may allow improved management of these patients.

Acute haemodynamic effects of increase in paced heart rate in heart failure patients recorded with an implantable haemodynamic monitor.

AIMS: The aim of this study was to investigate the acute effects of different biventricularly paced heart rates (pHRs) on right ventricular (RV) haemodynamics in heart failure (HF) patients with an implantable haemodynamic monitor (IHM). METHODS AND RESULTS: At rest, seven pHRs, range 60-120 bpm (steps of 10), were randomly programmed and maintained for 60 s in 10 patients (male, 65±12 years, New York Heart Association II-III). Right ventricular systolic (RVSP) and diastolic pressures, estimated pulmonary artery diastolic (ePAD) pressure, and RV+dP/dt were recorded beat-to-beat using the IHM. Cardiac output (CO) was estimated from the RV pressure waveforms and arterial blood pressure was measured (Portapres®). To compare the haemodynamic effects of increased pHR at rest to that of spontaneous, sinus-driven heart rate (HR) increase, patients also performed a symptom-limited bicycle exercise. At rest, RV+dP/dt increased significantly with elevated pHR (P, main effect, <0.001), whereas filling pressures (ePAD and RVSP) decreased significantly in the range 60-100 bpm (P<0.03 and P<0.003, respectively) but tended to increase or level out at pHRs>00 bpm. At a pHR of 100 bpm, ePAD was 1.4 mmHg lower compared with 60 bpm (P<0.01). Cardiac output increased gradually with elevated pHR at rest (P<0.001). Both total peripheral and estimated pulmonary arterial resistance significantly decreased with increased pHR. During exercise-induced maximum HR increase, RV+dP/dt, ePAD, and CO were all significantly higher compared with the corresponding pHR at rest. CONCLUSION: During cardiac resynchronization therapy in HF patients, the force frequency relationship is present in the RV, as increasing the pHR in the range 60-100 bpm results in decreased filling pressures and increased CO.

Cardiac resynchronization therapy and atrial overdrive pacing for the treatment of central sleep apnoea.

AIMS: The combined therapeutic impact of atrial overdrive pacing (AOP) and cardiac resynchronization therapy (CRT) on central sleep apnoea (CSA) in chronic heart failure (CHF) so far has not been investigated. We aimed to evaluate the effect of CRT alone and CRT + AOP on CSA in CHF patients and to compare the influence of CRT on CHF between CSA positive and CSA negative patients. METHODS AND RESULTS: Thirty patients with CRT indication underwent full night polysomnography, echocardiography, exercise testing, and neurohumoral evaluation before and 3 months after CRT implantation. In CSA positive patients (60%), two additional sleep studies were conducted after 3 months of CRT, with CRT alone or CRT + AOP, in random order. Cardiac resynchronization therapy resulted in significant improvements of NYHA class, left ventricular ejection fraction, N-terminal pro-brain natriuretic peptide, VO(2)max, and quality of life irrespective of the presence of CSA. Cardiac resynchronization therapy also reduced the central apnoea-hypopnoea index (AHI) (33.6 +/- 14.3 vs. 23.8 +/- 16.9 h(-1); P < 0.01) and central apnoea index (17.3 +/- 14.1 vs. 10.9 +/- 13.9 h(-1); P < 0.01) without altering sleep stages. Cardiac resynchronization therapy with atrial overdrive pacing resulted in a small but significant additional decrease of the central AHI (23.8 +/- 16.9 vs. 21.5 +/- 16.9 h(-1); P < 0.01). CONCLUSION: In this study, CRT significantly improved CSA without altering sleep stages. Cardiac resynchronization therapy with atrial overdrive pacing resulted in a significant but minor additional improvement of CSA. Positive effects of CRT were irrespective of the presence of CSA.

Reduction of atrial fibrillation burden by atrial overdrive pacing: experience with an improved algorithm to reduce early recurrences of atrial fibrillation.

AIMS: Two independent studies have revealed a potential limitation of post-mode switch overdrive pacing (PMOP), which is its delayed start. METHODS AND RESULTS: We conducted a prospective, randomized, single blind, crossover design study (the post-long pause overdrive pacing study) to test the efficacy of an improved version of PMOP (PMOP(enhanced)). A total of 45 patients were enrolled, of whom 41 were analysed. The median number of atrial tachycardia/atrial fibrillation (AT/AF) episodes per day (1.38 vs. 1.19), the median number of early recurrences of atrial fibrillation (ERAF) per day (0.56 vs. 0.51), and the median AT/AF burden (time per day spent in AT/AF) (2.47 vs. 2.51 h) were not significantly different during the control and active study periods. Based on the median number of episodes per week recorded 90 days prior to enrollment, the patients were stratified by the median and then split into two groups, Group A (lower 2-Quartiles) and Group B (upper 2-Quartiles). The median AT/AF burden was significantly lower in Group B during the active study period (3.71 vs. 1.71 h, P = 0.02).The median number of AT/AF episodes per day and the median number of ERAF per day in Group B showed a trend towards reduction when the algorithm was turned on (3.79 vs. 2.44 and 2.77 vs. 1.86, respectively). In contrast, in Group A we did not demonstrate any difference in AT/AF frequency, ERAF frequency, or burden. CONCLUSION: The main finding of this study is that temporary overdrive pacing at 90 bpm for 10 min starting just prior to device-classified AT/AF termination does not show a positive effect on the overall study population. However, when enabled in patients who suffer from a high percentage of ERAF, a significant reduction in the AT/AF burden could be demonstrated. Based on these findings, further prospective studies on a more targeted patient population are needed to confirm our results.

Stimulation of the intra-cardiac vagal nerves innervating the AV-node to control ventricular rate during AF: specificity, parameter optimization and chronic use up to 3 months.

BACKGROUND: Stimulation of the intra-cardiac vagal nerves innervating the AV-node (AVNS) is a promising approach to slow down ventricular rate (VR) during atrial fibrillation (AF). Our purpose was to demonstrate that effects on R-R-interval during stable AF can be maintained for several months once optimized and that AVNS affects specifically the nerves innervating the AV-node. METHODS: Our study included both an acute and chronic phase. Fifteen goats were implanted with a pacemaker connected to an atrial and ventricular lead and a neurostimulator connected to an atrial lead placed at a certain septal site, to induce an AV prolongation. In the chronic experiments (n = 9), after assessment of optimal AVNS parameters, the effect of continuous AVNS on VR was studied during stable AF for up to 3 months. The mechanism of AVNS was studied using atropine and esmolol. Next, the effects of AVNS during the atrial refractory period on electrophysiological and hemodynamic parameters were investigated acutely (n = 7). RESULTS: The maximal effect was found at a stimulation frequency of 40 Hz, and increased with increasing pulse width (at lower voltages) and increasing voltage. After 0, 1, and 3 months of AVNS during stable AF, AVNS decreased average VR, respectively, 55% (n = 9), 48% (n = 8), and 28% (n = 6). The AVNS effect appeared to be dominantly parasympathetic. AVNS did not influence (1) the sinus node, (2) the refractory period of the atrial, ventricular tissue, and His and (3) hemodynamic parameters. CONCLUSION: AVNS is efficient in reducing ventricular rate for at least 3 months using optimized parameters and specifically affects the parasympathetic nerves innervating the AV-node.

Continuous monitoring of intrathoracic impedance and right ventricular pressures in patients with heart failure.

BACKGROUND: Hemodynamic monitoring using implantable devices may provide early warning of volume overload in patients with heart failure (HF). This study was designed to prospectively compare information from intrathoracic impedance monitoring and continuous right ventricular pressure measurements in patients with HF. METHODS AND RESULTS: Sixteen patients with HF (age, 63.5+/-13.8 years; left ventricular ejection fraction, 23.2+/-11.3%; New York Heart Association, II and III) and a previous HF decompensation received both a cardiac resynchronization therapy defibrillator providing a daily average of intrathoracic impedance and an implantable hemodynamic monitor providing an estimate of the pulmonary artery diastolic pressure. At the end of a 6-month investigator-blinded period, baseline reference hemodynamic values were determined over 4 weeks during which the patient was clinically stable. A major HF event was defined as HF decompensation requiring hospitalization, IV diuretic treatment, or leading to death. Sixteen major HF events occurred in 10 patients. Within 30 days and 14 days before a major HF event, impedance decreased by 0.12+/-0.21 Omega/d and 0.20+/-0.20 Omega/d, respectively, whereas estimated pulmonary arterial diastolic pressure increased by 0.10+/-0.20 mm Hg/d and 0.16+/-0.15 mm Hg/d, respectively. During these periods, impedance decreased by 3.8+/-5.4 Omega (P<0.02) and 4.9+/-6.1 Omega (P<0.007), respectively, whereas estimated pulmonary arterial diastolic pressure increased by 5.8+/-5.7 mm Hg (P<0.002) and 6.8+/-6.1 mm Hg (P<0.001), respectively, compared with baseline. In all patients, impedance and estimated pulmonary arterial diastolic pressure were inversely correlated (r = -0.48+/-0.25). Within 30 days preceding a major HF event, this correlation improved to r =-0.58+/-0.24. CONCLUSIONS: Decompensated HF develops based on hemodynamic derangements and is preceded by significant changes in intrathoracic impedance and right ventricular pressures during the month prior to a major clinical event. Impedance and pressure changes are moderately correlated. Future research may establish the complementary contribution of both parameters to guide diagnosis and management of patients with HF by implantable devices.