Introduction. For pulmonary vein isolation in patients with atrial fibrillation (AF), some centers use the double transseptal puncture technique for catheter access in order to facilitate catheter manipulation within the left atrium. However, no safety data has so far been published using this approach. Method. 269 ablation procedures were performed in 243 patients (mean age 56.6 ± 9.3 years, 75% men) using the double transseptal puncture for catheter access in all cases. Patients were considered for ablation of paroxysmal (80%), persistent (19%), and permanent (1%) AF. 230 procedures were performed on an outpatient basis (85.5%), and 26 were repeat procedures (9.7%). Results. The double transseptal puncture catheter access was successfully achieved in all patients. The procedural success with the endpoint of pulmonary vein isolation was reached in 255 procedures (95%). A total of 1048 out of 1062 pulmonary veins (99%) were successfully isolated. Major complications occurred in eight patients (3.0%). Of these, seven patients (2.6%) had pericardial effusion requiring percutaneous drainage, and one patient (0.4%) suffered a minor reversible stroke. One patient (0.4%) had a minor air embolism with transient symptoms. Conclusion. The double transseptal puncture catheterization technique allows easy catheter manipulation within the left atrium to reach the goal of acute procedural success in AF ablation. Procedure-related complications are rare, and the technique can be used safely for AF ablation in the outpatient setting.
Oral anticoagulant use is common among patients undergoing pacemaker or defibrillator surgery. BRUISE CONTROL (Bridge or Continue Coumadin for Device Surgery Randomized Controlled Trial; NCT00800137) demonstrated that perioperative warfarin continuation reduced clinically significant hematomas (CSH) by 80% compared with heparin bridging (3.5% versus 16%). BRUISE-CONTROL-2 (NCT01675076) observed a similarly low risk of CSH when comparing continued versus interrupted direct oral anticoagulant (2.1% in both groups). Using patient level data from both trials, the current study aims to: (1) evaluate the effect of concomitant antiplatelet therapy on CSH, and (2) understand the relative risk of CSH in patients treated with direct oral anticoagulant versus continued warfarin.We analyzed 1343 patients included in BRUISE-CONTROL-1 and BRUISE-CONTROL-2. The primary outcome for both trials was CSH. There were 408 patients identified as having continued either a single or dual antiplatelet agent at the time of device surgery.Antiplatelet use (versus nonuse) was associated with CSH in 9.8% versus 4.3% of patients (P<0.001), and remained a strong independent predictor after multivariable adjustment (odds ratio, 1.965; 95% CI, 1.202-3.213; P=0.0071). In multivariable analysis, adjusting for antiplatelet use, there was no significant difference in CSH observed between direct oral anticoagulant use compared with continued warfarin (odds ratio, 0.858; 95% CI, 0.375-1.963; P=0.717).Concomitant antiplatelet therapy doubled the risk of CSH during device surgery. No difference in CSH was found between direct oral anticoagulant versus continued warfarin. In anticoagulated patients undergoing elective or semi-urgent device surgery, the patient specific benefit/risk of holding an antiplatelet should be carefully considered.URL: https://www.clinicaltrials.gov. Unique identifiers: NCT00800137, NCT01675076.
Hospitalization due to heart failure (HF) exacerbation represents a major burden in health care and portends a poor long-term prognosis for patients. As a result, there is considerable interest to develop novel tools and strategies to better detect onset of volume overload, as HF hospitalizations may be reduced if appropriate interventions can be promptly delivered. One such innovation is the use of device-based diagnostic parameters in HF patients with implantable cardioverter defibrillators (ICD) and/or cardiac resynchronization therapy (CRT) devices. These diagnostic algorithms can effectively monitor and detect changes in patients' HF status, as well as predict one's risk of HF hospitalization. This paper will review the role of these device diagnostics parameters in the assessment and management of HF patients in ambulatory settings. In addition, the integration of these novel algorithms in existing HF disease management models will be discussed.
Background— Unexplained cardiac arrest (UCA) may be explained by inherited arrhythmia syndromes. The Cardiac Arrest Survivors With Preserved Ejection Fraction Registry prospectively assessed first-degree relatives of UCA or sudden unexplained death victims to screen for cardiac abnormalities. Methods and Results— Around 398 first-degree family members (186 UCA, 212 sudden unexplained death victims’ relatives; mean age, 44±17 years) underwent extensive cardiac workup, including ECG, signal averaged ECG, exercise testing, cardiac imaging, Holter-monitoring, and selective provocative drug testing with epinephrine or procainamide. Genetic testing was performed when a mutation was identified in the UCA survivor or when the diagnostic workup revealed a phenotype suggestive of a specific inherited arrhythmia syndrome. The diagnostic strength was classified as definite, probable, or possible based on previously published definitions. Cardiac abnormalities were detected in 120 of 398 patients (30.2%) with 67 of 398 having a definite or probable diagnosis (17%), including Long-QT syndrome (13%), catecholaminergic polymorphic ventricular tachycardia (4%), arrhythmogenic right ventricular cardiomyopathy (4%), and Brugada syndrome (3%). The detection yield was similar for family members of UCA and sudden unexplained death victims (31% versus 27%; P =0.59). Genetic testing was performed more often in family members of UCA patients (29% versus 20%; P =0.03). Disease-causing mutations were identified in 20 of 398 relatives (5%). The most common pathogenic mutations were RyR2 (2%), SCN5A (1%), and KNCQ1 (0.8%). Conclusions— Cardiac screening revealed abnormalities in 30% of first-degree relatives of UCA or sudden unexplained death victims, with a clear working diagnosis in 17%. Long-QT, arrhythmogenic right ventricular cardiomyopathy, and catecholaminergic polymorphic ventricular tachycardia were the most common diagnoses. Systematic cascade screening and genetic testing in asymptomatic individuals will lead to preventive lifestyle and medical interventions with potential to prevent sudden cardiac death. Clinical Trial Registration— URL: http://www.clinicaltrials.gov . Unique identifier: NCT00292032.
Syncope in patients with supraventricular tachycardia has been suggested to be an ominous finding, predictive of rapid rates during tachycardia.To explore the mechanism of syncope during supraventricular tachycardia, tachycardia was induced in the supine position and after passive head-up tilting to 60 degrees in 13 patients with atrioventricular (AV) node reentry, eight patients with AV reentry, and one patient with atrial tachycardia. Tilt testing was also performed in sinus rhythm for 30 minutes (the last 15 minutes with isoproterenol infusion). Mean +/- SEM age was 38 +/- 3 years, and 11 patients had a history of syncope (median number of syncopal episodes, three; range, one to 30). The cycle length of tachycardia when upright was shorter than when supine (297 +/- 9 compared with 357 +/- 10 msec, p less than 0.001), and mean blood pressure fell to a greater extent after the onset of tachycardia (fall in mean blood pressure, 53 +/- 6 compared with 24 +/- 3 mm Hg, p less than 0.001). Mean blood pressure correlated significantly with tachycardia cycle length when supine (r = 0.58, p = 0.005) but not when tilted upright (r = 0.18, p = 0.45). Syncope occurred in seven patients during upright tachycardia. These seven patients had a greater fall in mean blood pressure with upright tachycardia than the 15 patients without syncope (fall in mean blood pressure, 70 +/- 4 compared with 45 +/- 5 mm Hg, p = 0.01), but there was no difference in the tachycardia cycle length (311 +/- 10 compared with 290 +/- 11 msec, p = 0.29). Six of the seven patients with tachycardia-induced syncope also had syncope with tilt testing in sinus rhythm compared with four of the 15 patients without tachycardia-induced syncope (p = 0.02).These data support the view that syncope during supraventricular tachycardia is related to vasomotor factors and does not predict a more rapid tachycardia rate.
The Canadian trial of physiologic pacing (CTOPP), published in 2000, demonstrated a reduction in atrial fibrillation (AF), stroke and death with preservation of atrioventricular synchrony, though only the lower rate of AF was statistically significant. The purpose of this study was to determine the effect of CTOPP on pacing mode selection in our region. The British Columbia Cardiac Registry contains prospectively entered data covering a population of 4 millions (M) and 17 implanting centers. It was examined for mode selection trends from 1997 to 2002. At examination, there were data on 22,446 pulse generators (PG) and 29,898 leads. New implant rates per M population were 1997:473; 1998:456; 1999:505; 2000:513; 2001:486; 2002:510. PG replacements also increased, resulting in a total implant rate of 667 PG per M in 2002. Over the 6‐year period, DDD use decreased from 321 to 306, but DDDR use, more than doubled from 317 to 750 PG/year. VVI use steadily decreased from 741 to 410 PG/year, while VVIR use increased more modestly from 1997 to 1999, then remained stable. During the 6‐year period bracketing CTOPP, use of modes maintaining AV synchrony increased by over 32%, to 53% of PG implanted in 2002. Our PG implant rate was much higher than expected from prior retrospective surveys, and similar to rates in Belgium, France, and Germany. CTOPP did not decrease our use of physiologic pacing but, instead, was associated with a brief pause, then progressively increased in both academic and community centers. Patients' need and widely accepted standards of care proved more important in clinical decision making than the results of a flawed randomized trial.
