Polymorphic PVCs refractory to medication therapy may be modifiable by RSD in patients without structural heart disease. Although encouraging, our data are preliminary and need to be validated in a large population and in long term.
Cocaine abuse continues to be a serious problem worldwide [1], and the global number of annual cocaine users in 2010 ranged from 13.3 million to 19.7 million [2]. In the US alone, there were 1.4 million cocaine users in 2011 with as much as 19% of the US population admitting usage [2].Unfortunately, in addition to numerous complications in target organs, such as heart, liver, kidney, and central nervous system [3], cocaine is the most frequent cause of drugrelated deaths and emergency room visits in the U.S [4][5][6]. Since the re-emergence of recreational cocaine use in the late 1980s and the recent appearance of inexpensive freebase Introduction: Ventricular arrhythmias related to cocaine may not respond to antiarrhythmic drugs and may need treatment with radiofrequency ablation.
Case presentation:In this case we describe a 33-year-old man that presented to the emergency room complaining of chest discomfort and slight palpitations predominantly in the precordium, starting for 1 hour ago. The patient reports rare episodes of non tachycardic palpitations in the past, short-lived. He denied syncope or pre-syncope and did not show low output objective signs. After exams, he was diagnosed with sustained ventricular tachycardia confirmed by all used electrocardiographic criteria; the emergency medical team chose to use intravenous amiodarone, which reverted the arrhythmia. The patient was hospitalized, and continued intravenous amiodarone, sedation with benzodiazepines and 24-hour continuous monitoring electrocardiographic (Holter) were conducted. Amiodarone was suspended and was initiated oral diltiazem 80 mg in 8/8 hours. We requested a cardiac nuclear magnetic resonance image that showed normal perfusion and contractility, the absence of delayed enhancement, mild hypertrophy of the basal septum and lack of arrhythmogenic substrate. Electrophysiological study (EPS) was performed.
Conclusion:During the EPS, the ECG at baseline was normal. The programmed electrical stimulation induced atrioventricular nodal reentrant tachycardia (AVNRT) with aberrant conduction. The ablation of the slow pathway was successful, and the patient did not present new tachycardia episodes.
Purpose: This study examined patients who had a DDDR pacemaker and were exposed to different degrees of atrial and ventricular pacing. We aimed to determine the relationships between baseline features and percentages of atrial pacing (%AP), and ventricular pacing (%VP) in the first month post implant and subsequent onset of atrial fibrillation (AF) (primary outcomes). We also aimed to determine the relationships between time-dependent changes in %AP and %VP and AF recurrence (secondary outcomes).Methods: Three hundred six patients were evaluated every 6 months up to 3 years of follow-up. The %AP and %VP were assessed at each follow-up visit.
Results:The mean time to the first episode of AF (n=227) was 15.3 ± 10.7 months. At the end of 3 years of follow-up, 74.2% patients developed AF events. At baseline, the mean %AP was significantly higher inpatients who subsequently developed AF than in those who did not (68.5% ± 19.7% versus 33.3% ± 23.2%, P<0.0001). Similarly, mean %VP was significantly higher in patients who developed AF than in those without AF events (25.8% ± 14.5% versus 14.4% ± 11.9%, P<0.0001). Kaplan-Meier survival analysis demonstrated a significant increased risk of AF events in patients who subsequently developed AF compared with those who did not (log-rank test, P<0.0001).
Conclusions:Our study shows an association between %AP and %VP at baseline and time to appearance of the first AF episode after pacemaker implantation. During 3 years of follow-up, we also observed a significantly increased risk of AF events in the high %AP and high %VP groups at baseline.
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