Background: Incessant focal atrial tachycardia (FAT), if untreated, can lead to ventricular dysfunction and heart failure (tachycardia-induced cardiomyopathy). Drug therapy of FAT is often difficult and ineffective. The efficacy of ivabradine has not been systematically evaluated in the treatment of FAT. Methods: The study group consisted of patients with incessant FAT (lasting >24 hours) and structurally normal hearts. Patients with ventricular dysfunction as a consequence of FAT were not excluded. All antiarrhythmic drugs were discontinued at least 5 half-lives before the initiation of ivabradine. Oral ivabradine (adults, 10 mg twice 12 hours apart; pediatric patients: 0.28 mg/kg in 2 divided doses) was initiated in the intensive care unit under continuous electrocardiographic monitoring. A positive response was defined as the termination of tachycardia with the restoration of sinus rhythm or suppression of the tachycardia to <100 beats per minute without termination within 12 hours of initiating ivabradine. Results: Twenty-eight patients (mean age, 34.6±21.5 years; women, 60.7%) were included in the study. The most common symptom was palpitation (85.7%) followed by shortness of breath (25%). The mean atrial rate during tachycardia was 170±21 beats per minute, and the mean left ventricular ejection fraction was 54.7±14.3%. Overall, 18 (64.3%) patients responded within 6 hours of the first dose of ivabradine. Thirteen of 18 ivabradine responders subsequently underwent successful catheter ablation. FAT originating in the atrial appendages was a predictor of ivabradine response compared with those arising from other atrial sites ( P =0.046). Conclusions: Ivabradine-sensitive atrial tachycardia constitutes 64% of incessant FAT in patients without structural heart disease. Incessant FAT originating in the atrial appendages is more likely to respond to ivabradine than that arising from other atrial sites. Our findings implicate the funny current in the pathogenesis of FAT.
There is increasing evidence that the ABO blood group phenotypes modulates Plasmodium falciparum rosetting and may influence the clinical manifestation of severe malaria. Whether blood group phenotypes are associated with risk of severe falciparum malaria in Odisha, we analyzed 343 adult malaria patients. The results showed high prevalence of blood group B in both mild (n=110) and severe malaria (cerebral malaria [CM]; n=130 and non-cerebral severe malaria [NCSM]; n=103) categories among the non-O group and while type O is significantly associated with protection against CM, patients with type A and B group had increased risk for developing CM. Further, the strength of association for B group (p=< 0.0001) was high and has double the risk of (OR=5.0) of developing CM compared to blood group A (OR=2.5). Such findings may probably be due to strain specific blood group preferences of P. falciparum and high prevalence of B group. However, the ABO blood group distribution of mild malaria was comparable with that of the NCSM group of patients. The lack of association of ABO phenotypes with NCSM is evidence for the hypothesis that the underlying pathogenesis cascades are different in CM and NCSM clinical presentations.
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Background Reflex syncope (RS), the most common cause of syncope is usually recurrent, associated with decreased quality of life, and frustrates both the clinicians and the patients with a paucity of effective treatment options. Purpose To assess the effectiveness of yoga therapy on the recurrence of reflex syncope. Methods Subjects with recurrent RS (>3 episodes) and positive head-up tilt test were enrolled prospectively, and randomized to conventional therapy with physical maneuvres (Group 1) and yoga therapy (Group 2). Group 1 patients were taught physical counter-pressure maneuvers as per guidelines. Group 2 patients were taught yoga for 7 sessions by a certified Yoga instructor/therapist, and then advised to perform yoga for 60 minutes at least five days/week for six months. The Yoga module consisted of Pranayama (breathing techniques), Asanas (Postures) and Dhyana (Meditation) for 60 minutes/session. Both groups were followed up monthly for 6 months in the syncope clinic noting down the recurrences and the quality of life using the syncope functional status questionnaire score. Result The study group consisted of 97 patients (group 1: 46 patients and group 2: 51 patients) enrolled prospectively between June 2015 to February 2017. The mean age was 33.1±16.6 years, with male: female ratio 1.1:1, and a mean of 6.4±6.06 syncope episodes (group 1: 6.8±8.0 vs. group 2: 6.0±4.0; p=0.551). The mean duration of symptoms was 17.1±20.71 months (group 1: 16.1±22.8 months vs. group 2: 17.8±19.1 months; p=0.694). There was a significant decrease in the recurrences of syncope in the yoga group compared to the conventional group at three months (group 1: 1.8±1.4 vs group 2: 0.8±0.9, P<0.001) as well as six months follow-up (group 1: 3.38±3.0 vs group 2: 0.98±1.23, P<0.001). The quality of life score at 6 months improved in 20 patients in group 1 and in 45 patients in group 2 (<0.001). Conclusion Guided yoga therapy is superior to conventional measures in reducing the number of syncopal episodes and improves the quality of life in patients with reflex syncope. Yoga therapy should be considered as treatment strategy for patients with reflex syncope.
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