Best of heart failure

49 ivabradine was discontinued for no change in symptoms (after 30 days). Sixteen patients were followed up for more than 3 months: in one ivabradine was discontinued for no improvement in symptoms (after 14.5 months) (Table 3 ). In 15 patients (68%), the symptoms improved according to the treating clinician: reduced syncopal episodes and resolution of symptoms (Table 4 ). 3.2 Side Effects One patient (4.5%) experienced mild phosphenes (flashing lights). The ivabradine dosage was slightly reduced, from 10 to 7.5 mg/day, with improvement of the symptoms. No patient experienced symptomatic bradycardia. 3.3 Electrocardiograms EKGs were retrospectively available for analysis in 19 of the 22 patients (86%) after starting ivabradine. Changes to heart rate and QTc are shown in Table 5 . Table 2 Medications taken prior to starting ivabradine. Some were discontinued when it was started Number of medications prior to ivabradine Medication Number of patients 1 Fludrocortisone Beta-blocker Midodrine Sodium supplement 7 2 4 0 2 Fludrocortisone Beta-blocker Midodrine Sodium supplement 1 0 0 1 Table 3 Follow-up (total patients, n = 22) Number of patients Ivabradine discontinued Follow-up \ 3 month 6 4 Follow-up [ 3 months 16 1 Table 4 Evaluation of symptoms after starting ivabradine Improvement Unchanged Deterioration 22 patients 15 (68%) 6 (27%) 1 (4.5%) Ivabradine in POTS: Preliminary Experience in Children management of t making. The patie compassionate bas benefits and side e their parents. 2 Methods We evaluated pa institution for who February 2008 to pharmacy databas starting the medi POTS was specifi heart rate increase 120 bpm within t with symptoms significant orthost age at commence up-titration, reaso treatment, medica medications with worsening of sym and at follow-up cardiogram (EKG dine and at follo 2.1 Statistical An Normally distribut and standard devi were described w pendent t test was nificant level was Table 1 Demographi clinician’s stated indi starting ivabradine 60 ivabradine was discontinued for no change in symptoms (after 30 days). Sixteen patients were followed up for more than 3 months: in one ivabradine was discontinued for no improvement in symptoms (after 14.5 months) (Table 3 ). In 15 patients (68%), the symptoms improved according to the treating clinician: reduced syncopal episodes and resolution of symptoms (Table 4 ). 3.2 Side Effects One patient (4.5%) experienced mild phosphenes (flashing lights). The ivabradine dosage was slightly reduced, from 10 to 7.5 mg/day, with improvement of the symptoms. No patient experienced symptomatic bradycardia. 3.3 Electrocardiograms EKGs were retrospectively available for analysis in 19 of the 22 patients (86%) after starting ivabradine. Changes to heart rate and QTc are shown in Table 5 . None of the patients had an abnormal QTc interval when on ivabradine. There was a reduction in heart rate on resting EKG, from a mean (SD) of 82.5 (13.6) bpm to a mean of 71.3 (16.5) bpm ( p = 0.007). None of the patients developed symptomatic bradycardia. 4 Discussion This is the first observational study to describe the use of ivabradine in patients under 18 years of age with POTS. The study was retrospective and purely descriptive, with no attempt made to influence the patients’ management. The data should therefore be regarded as preliminary, but as it is the first documentation of a group of pediatric patients with POTS receiving ivabradine, it is important to report initial outcome and side effects. In this group, just over two-thirds reported improvement of symptoms. The dosage was 0.1 mg/kg wice a day. Side effects were rare, with less than 5% developing temporary and mild phosphenes that did not warrant suspension of the drug; the symptom resolved on reducing the dose. There were concerning side effects. Ivabradine is a promising and relatively new drug. It is a selective inhibitor of the I(f) current that contributes to sinus node automaticity. The echanism of action has been studied in detail in isolated rabbit sinoatrial node cells [ 7 ]. Ivabradine was approved by the European Medicines Agency in 2005, and it is the first clinically approved drug that targets the hyperpolarization-activated cyclic nucleo- tide-gated (HCN) channels. The therapeutic indications in the adult population are the symptomatic treatment of chronic stable angina in patients intolerant to, or inade- quately controlled by, beta-blockers and hose heart rate exceeds 60 bpm in sinus rhythm and heart failure [ 1 , 8 – 13 ]. The Euro ean Societ of Cardiology guidelines on heart failure suggest considering ivabradine to reduce the risk of hospitalization due to heart failure in patients in sinus rhythm with an ejection fraction of B 35%, heart rate remaining at C 70 bpm, and persisting symptoms [New York Heart Association (NYHA) class II–IV] despite treatment with an evidence-based dose of beta-blocker (or maximum tolerated dose below that), angiotensin Table 2 Medications taken prior to starting ivabradine. Some were discontinued when it was started Number of medications prior to ivabradine Medication Number of patients 1 Fludrocortisone Beta-blocker Midodrine Sodium supplement 7 2 4 0 2 Fludrocortisone Beta-blocker Midodrine Sodium supplement 1 0 0 1 Table 3 Follow-up (total patients, n = 22) Number of patients Ivabradine discontinued Follow-up \ 3 month 6 4 Follow-up [ 3 months 16 1 Table 4 Evaluation of symptoms after starting ivabradine Improvement Unchanged Deterioration 22 patients 15 (68%) 6 (27%) 1 (4.5%) Table 5 Changes to heart rate and QTc on starting ivabradine Baseline, mean (SD) Foll w-up, mean (SD) p Heart rate (bpm) 82.5 (13.6) 71.3 (16.5) \ 0.05 QTc (ms) 397.6 (20.2) 398.7 (29.1) 0.44 SD standard deviation Ivabradine in POTS: Preliminary Experience in Children 61