Redo procedures after sinus node sparing hybrid ablation for inappropriate sinus tachycardia/postural orthostatic sinus tachycardia.

AIMS: A novel sinus node (SN) sparing hybrid ablation for inappropriate sinus node tachycardia (IST)/postural orthostatic tachycardia syndrome (POTS) has been demonstrated to be an effective and safe therapeutic option in patients with symptomatic drug-resistant IST/POTS. The aim of this study was to evaluate the long-term rate of redo procedures after hybrid IST ablation and procedural strategy, outcomes and safety of redo procedures. METHODS AND RESULTS: All consecutive patients from 2015 to 2023 were prospectively enrolled in the UZ Brussel monocentric IST/POTS registry. They were analysed if the following inclusion criteria were fulfilled: 1) diagnosis of IST or POTS, 2) symptomatic IST/POTS refractory or intolerant to drugs, and 3) hybrid SN sparing ablation performed. The primary endpoint was redo procedure. The primary safety endpoint was pacemaker (PM) implantation. A total of 220 patients undergone to hybrid IST ablation were included, 185 patients (84.1%) were treated for IST and 61 patients (27.7%) for POTS.After a follow-up of 73.3 ± 16.2 months, 34 patients (15.4%) underwent a redo. A total of 23 patients (67.6%) had a redo for IST recurrence and 11 patients (32.4%) for other arrhythmias. Pacemaker implantation was performed in 21 patients (9.5%). Nine patients (4.1%) had no redo procedure and experienced sick sinus syndrome requiring a PM. Twelve patients (5.4%) received a PM as a shared therapeutic choice combined with SN ablation procedure. CONCLUSION: In a large cohort of patients the long-term free survival from redo procedure after hybrid IST ablation was 84.6% with a low PM implantation rate.

Rebound hyperkalemia in a dog with albuterol toxicosis after cessation of potassium supplementation.

OBJECTIVE: To describe the presentation of rebound hyperkalemia as a delayed side effect of albuterol toxicity in a dog. CASE SUMMARY: A 3-year-old female neutered mixed-breed dog was presented for albuterol toxicosis that led to a severe hypokalemia, hyperlactatemia, and hyperglycemia. The dog also experienced sinus tachycardia and generalized weakness. Treatment was instituted with intravenous fluid therapy and potassium supplementation, and the dog was monitored with a continuous electrocardiogram. Resolution of hypokalemia was documented 12 hours after initial presentation, at which time fluid therapy and potassium supplementation were discontinued. There were no further periods of sinus tachycardia, but instead the dog developed ventricular ectopy with rapid couplets (instantaneous rates of 300/min). An echocardiogram revealed normal cardiac size and function. Twenty-four hours after presentation, the patient developed severe hyperkalemia, despite discontinuation of fluids and potassium supplementation for 12 hours. Serial venous and urinary electrolytes were performed for determination of the fractional excretion of electrolytes. These data confirmed rebound hyperkalemia (7.0 mmol/L), consistent with a markedly increased fractional excretion of potassium, and secondary to the release of potassium from inside the cells. Fluid therapy with dextrose supplementation was provided until 36 hours postpresentation. The hyperkalemia resolved, and the dog was discharged after 44 hours of hospitalization. NEW OR UNIQUE INFORMATION PROVIDED: This case documents rebound hyperkalemia following treatment of albuterol toxicosis in a dog. This case highlights the importance of understanding the distribution of total body potassium when treating serum hypokalemia. Transcellular shifts of potassium, as in the case of albuterol toxicosis, can lead to rebound hyperkalemia even after discontinuation of potassium supplementation. This case further explores the utility of fractional excretion of electrolytes in elucidating the etiology and management of electrolyte disturbances.

Ivabradine in the treatment of non-paroxysmal junctional tachycardia with interference atrioventricular dissociation: A case report.

Ivabradine reduces the heart rate by selectively inhibiting the If current of the sinoatrial node, mainly for the treatment of chronic heart failure with decreased left ventricular systolic function and inappropriate sinus tachycardia, but the inhibitory effect on the atrioventricular node is rarely reported. The patient was admitted to hospital mainly because of intermittent chest pain for 7 years, which worsened for 10 days. Admission electrocardiogram (ECG) considered sinus tachycardia, with QS wave and T wave inversion in II, III, aVF, V3 R-V5 R, V4 -V9 leads, and non-paroxysmal junctional tachycardia (NPJT) with interference atrioventricular dissociation. After treatment with ivabradine the ECG returned to normal conduction sequence. NPJT with interference atrioventricular dissociation is a fairly rare electrocardiographic phenomenon. This case reports for the first time that ivabradine is used in the treatment of NPJT with interference atrioventricular dissociation. It is speculated that ivabradine has a potential inhibitory effect on the atrioventricular node.

Ivabradine for Uncontrolled Sinus Tachycardia in Thyrotoxic Cardiomyopathy - Case Report.

BACKGROUND: Beta-blockers, mainly propranalol, are usually administered to control heart rate in patients with thyrotoxicosis, especially when congestive heart failure presents. However, when thyrotoxicosis is not controlled, heart rate may be difficult to control even with maximal doses of propranolol. This presentation alerts physicians to the possibility of using ivabradine, a selective inhibitor of the sinoatrial pacemaker, for the control of heart rate. CASE PRESENTATION: We present a 37-year-old woman with thyrotoxicosis and congestive heart failure whose heart rate was not controlled with a maximal dose of beta blockers during a thyroid storm. The addition of ivabradine, a selective inhibitor of the sinoatrial pacemaker, controlled her heart rate within 48 hours. CONCLUSION: Ivabradine should be considered in patients with thyrotoxicosis, including those with heart failure, in whom beta blockers are insufficient to control heart rate.

Heart rate control with landiolol hydrochloride in infants with ventricular dysfunction and pulmonary hypertension.

AIMS: Sinus tachycardia potentially leads to a deterioration of cardiac function in critically ill infants. The ultrashort-acting beta-blocker landiolol hydrochloride is a new pharmacological option for a selective heart rate (HR) control in patients with sinus tachycardia and heart failure. METHODS AND RESULTS: This study was a monocentric retrospective medical chart review study at the University Children's Hospital Bonn (Germany) from 01 January 2018 until 30 June 2020. This study included a cohort of 62 term and preterm infants with a diagnosis of ventricular dysfunction and/or pulmonary hypertension (PH), in combination with preexisting tachycardia and treatment with landiolol hydrochloride. Infants were allocated to subgroups according to weeks of gestational age (GA): born at <35 weeks of GA (Group A) and born at >35 weeks of GA (Group B). Tachycardia was defined depending on GA (<35 weeks of GA: >170 b.p.m.; ≥ 35 weeks of GA: >150 b.p.m.). The primary endpoint was defined as percentage of patients achieving HR normalization during the first 24 h of landiolol treatment. Twenty-nine infants were allocated to Group A and 33 infants to Group B. The overall median GA of the infants was 35.3 (23.3/41.3), with 53% female infants. The primary endpoint was achieved in 57 patients (91.9%). The median time to reach target HR was 1.8 (0.3-24) h. The median starting dose of landiolol was 8.8 (3.9-25.3) µk/kg/min, with a median dosing during the first 24 h of landiolol treatment of 9.9 (2.8-35.4) µk/kg/min. The median landiolol dose while achieving the target HR was 10 (2.4-44.4) µk/kg/min. The right ventricular dysfunction improved significantly in both groups 24 h after onset of landiolol infusion (P = 0.001 in Group A and P = 0.045 in Group B). The left ventricular and biventricular dysfunction improved significantly 24 h after onset of landiolol infusion in infants of Group B (P = 0.004 and P = 0.006, respectively). The severity of PH improved significantly after 24 h in infants of Group A (P < 0.001). During landiolol treatment, no severe drug-related adverse event was noted. CONCLUSIONS: The use of landiolol hydrochloride for HR control of non-arrhythmic tachycardia in critically ill infants is well tolerated. Reduction of HR can be guided quickly and landiolol treatment is associated with an improvement of ventricular dysfunction and PH.

Successful use of ivabradine in a 10-year-old patient with graft failure after heart transplantation.

We encountered a paediatric case of graft failure due to antibody-mediated rejection after heart transplantation in which ivabradine was effective. Inappropriate sinus tachycardia in denervated transplanted hearts is a good indication for ivabradine administration as beta-blockers have a limited efficacy. To our knowledge, this is the first report on the effectiveness of ivabradine in a paediatric heart transplant rejection case.

Five-year results of heart rate control with ivabradine or metoprolol succinate in patients after heart transplantation.

BACKGROUND: Cardiac graft denervation causes inadequate sinus tachycardia in patients after heart transplantation (HTX) which is associated with reduced survival. This study investigated the 5-year results of heart rate control with ivabradine or metoprolol succinate in patients after HTX. METHODS: This registry study analyzed 104 patients receiving either ivabradine (n = 50) or metoprolol succinate (n = 54) within 5 years after HTX. Analysis included patient characteristics, medication, echocardiographic features, cardiac catheterization data, cardiac biomarkers, heart rates, and post-transplant survival including causes of death. RESULTS: Demographics and post-transplant medication revealed no significant differences except for ivabradine and metoprolol succinate use. At 5-year follow-up, patients with ivabradine had a significantly lower heart rate (73.3 bpm) compared to baseline (88.6 bpm; P < 0.01) and to metoprolol succinate (80.4 bpm; P < 0.01), a reduced left ventricular mass (154.8 g) compared to baseline (179.5 g; P < 0.01) and to metoprolol succinate (177.3 g; P < 0.01), a lower left ventricular end-diastolic pressure (LVEDP; 12.0 mmHg) compared to baseline (15.5 mmHg; P < 0.01) and to metoprolol succinate (17.1 mmHg; P < 0.01), and a reduced NT-proBNP level (525.4 pg/ml) compared to baseline (3826.3 pg/ml; P < 0.01) and to metoprolol succinate (1038.9 pg/ml; P < 0.01). Five-year post-transplant survival was significantly better in patients with ivabradine (90.0%) versus metoprolol succinate (68.5%; P < 0.01). CONCLUSION: Patients receiving ivabradine showed a superior heart rate reduction and a better left ventricular diastolic function along with an improved 5-year survival after HTX.

Ivabradine versus bisoprolol in the treatment of inappropriate sinus tachycardia: a long-term follow-up study.

AIM: The aim of our study was to compare ivabradine versus bisoprolol in the short-term and long-term treatment of inappropriate sinus tachycardia. METHODS: From this prospective, parallel-group, open-label study, consecutive patients affected by inappropriate sinus tachycardia received ivabradine or bisoprolol and were evaluated with Holter ECG, ECG stress test, European Heart Rhythm Association score and Minnesota Living With Heart Failure Questionnaire at baseline, after 3 and 24 months. RESULTS: Overall, 40 patients were enrolled. Baseline parameters were comparable in the ivabradine and bisoprolol subgroups. Two patients had transient phosphenes with ivabradine and two others interrupted the drug after 3 months as they planned to become pregnant. Eight individuals treated with bisoprolol experienced hypotension and weakness, which caused drug discontinuation in five of them. Ivabradine was superior to bisoprolol in reducing Holter ECG mean heart rate (HR) and mean HR during daytime at short- and long-term follow-up. Moreover, ivabradine but not bisoprolol significantly reduced Holter ECG mean HR during night-time as well as maximal and minimal HR and significantly increased the time duration and maximal load reached at ECG stress test. The quality of life questionnaires significantly improved in both subgroups. CONCLUSION: This study suggests that ivabradine is better tolerated than bisoprolol and seems to be superior in controlling the heart rate and improving exercise capacity in a small population of individuals affected by inappropriate sinus tachycardia during a short-term and long-term follow-up.

Comparative effectiveness of metoprolol, ivabradine, and its combination in the management of inappropriate sinus tachycardia in coronary artery bypass graft patients.

BACKGROUND: Inappropriate sinus tachycardia (IST) is an arrhythmic complication observed after coronary artery bypass graft (CABG) surgery which left untreated, commonly increases chances of postoperative stroke. The primary study objective was comparing effectiveness of beta blocker-metoprolol; a specific If blocker-ivabradine and its combination in patients who develop IST as a complication following CABG. MATERIALS AND METHODS: An open-labeled, investigator initiated, clinical study was conducted on 150 patients who developed IST (heart rate [HR] >100 beats/min) following elective CABG surgery. The patients were randomized into three treatment groups. Group I - received ivabradine (5 mg), Group II - metoprolol (25 mg), and Group III - ivabradine (5 mg) and metoprolol (25 mg). Treatment was given orally, twice a day for 7 days in all the three groups postoperatively. Primary endpoints were comparative effectiveness in HR and blood pressure reduction following treatment. RESULTS: IST was diagnosed by an electrocardiogram (12-lead) considering morphological features of P-wave and with 32% increase from baseline HR in all the three groups. Compared to IST arrthymic rate, HR was reduced in all groups following respective treatment (P = 0.05). Reduction in HR was significant (P < 0.05) in combination group followed by ivabradine which was significantly greater than metoprolol treated group. None of the treatments clinically changed the systolic, diastolic and mean blood pressure till discharge. No surgery/treatment-related complications were observed in any groups. CONCLUSION: Ivabradine stands as a pharmacological option for controlling HR and rhythm without associated side effects in postoperative CABG patients with IST.

COVID-19-induced postural orthostatic tachycardia syndrome treated with ivabradine.

A 22-year-old woman was referred with exertional dyspnoea and chest tightness 3 weeks following a diagnosis of COVID-19. Evaluation revealed a resting sinus tachycardia and criteria for postural orthostatic tachycardia syndrome were met. After non-pharmacological interventions failed to yield symptomatic improvement, ivabradine was commenced. This intervention was followed by a substantial improvement in the patient's exercise tolerance and energy levels and an objective reduction in supine and standing heart rate.

Efficacy of medical and ablation therapy for inappropriate sinus tachycardia: A single-center experience.

BACKGROUND: Effective therapy for inappropriate sinus tachycardia (IST) remains challenging with high rates of treatment failure and symptom recurrence. It is uncertain how effective pharmacotherapy and procedural therapy are long-term, with poor response to medical therapy in general. METHODS: We retrospectively reviewed all patients with the diagnosis of IST at a tertiary academic medical center from 1998 to 2018. We extracted data related to prescribing patterns and symptom response to medical therapy and sinus node modification (SNM), assessing efficacy and periprocedural complication rates. RESULTS: A total of 305 patients with a formal diagnosis of IST were identified, with 259 (84.9%) receiving at least one prescription medication related to the condition. Beta-blockers were the most commonly used medication (n = 245), with a majority of patients reporting no change or worsening of symptoms, and poor response was seen to other medication classes. Improvement was seen significantly more often with ivabradine than beta blockers, though the sample size was limited (p = .003). Fifty-five patients (18.0% of all IST patients), mean age 32.0 ± 9.1 years, underwent a SNM procedure, with an average of 1.8 ± 0.9 procedures per patient. Acute symptomatic improvement (<6 months) was seen in 58.2% of patients. Long-term complete resolution of symptoms was seen in 5.5% of patients, modest improvement in 29.1%, and no long-term benefit was seen in 65.5% of patients. CONCLUSIONS: Among all medical therapies, there were high rates of treatment failure or symptom worsening in over three-quarters of patients in our study. Ivabradine was most beneficial, though the sample size was small. While most patients receiving SNM ablation for IST perceive an acute symptomatic improvement, almost two-thirds of patients have no long-term improvement, and resolution of symptoms is quite rare. AV node ablation with pacemaker implantation following lack of response to SNM offered increased success, though the sample size was limited.

Ivabradine in Cardiovascular Disease Management Revisited: a Review.

Ivabradine is a unique agent that is distinct from beta-blockers and calcium channel blockers as it reduces heart rate without affecting myocardial contractility or vascular tone. Ivabradine is a use-dependent inhibitor targeting the sinoatrial node. It is approved for use in the United States as an adjunct therapy for heart rate reduction in patients with heart failure with reduced ejection fraction. In this scenario, ivabradine has demonstrated improved clinical outcomes due to reduction in heart failure readmissions. However, there has been conflicting evidence from prospective studies and randomized controlled trials for its use in stable ischemic heart disease regarding efficacy in symptom reduction and mortality benefit. Ivabradine may also play a role in the treatment of patients with inappropriate sinus tachycardia, who often cannot tolerate beta-blockers and/or calcium channel blockers. In this review, we highlight the evidence for the nuances of using ivabradine in heart failure, stable ischemic heart disease, and inappropriate sinus tachycardia to raise awareness for its vital role in the treatment of select populations.

The rationale for repurposing funny current inhibition for management of ventricular arrhythmia.

Management of ventricular arrhythmia in structural heart disease is complicated by the toxicity of the limited antiarrhythmic options available. In others, proarrhythmia and deleterious hemodynamic and noncardiac effects prevent practical use. This necessitates new thinking in therapeutic agents for ventricular arrhythmia in structural heart disease. Ivabradine, a funny current (If) inhibitor, has proven safety in heart failure, angina, and inappropriate sinus tachycardia. Although it is commonly known that funny channels are primarily expressed in the sinoatrial node, atrioventricular node, and conducting system of the ventricle, ivabradine is known to exert effects on metabolism, ion homeostasis, and membrane electrophysiology of remodeled ventricular myocardium. This review considers novel concepts and evidence from clinical and experimental studies regarding this paradigm, with a potential role of ivabradine in ventricular arrhythmia.

Long-term outcomes of sinus node modification in patients with severely symptomatic drug-refractory inappropriate sinus tachycardia: a single-center experience.

BACKGROUND: The purpose of the study was to evaluate the long-term outcomes of sinus node modification (SNM) in treating patients with severely symptomatic drug-refractory inappropriate sinus tachycardia (IST). METHODS: The study included 39 patients with symptomatic drug-refractory IST who have undergone SNM at Saint Louis University Hospital. Data was reviewed retrospectively. Recurrence of symptoms was assessed at 3-6-month follow-up intervals. RESULTS: The mean age of our cohort was 31.5 ± 11. The mean HR at diagnosis was 135 ± 25.4 beats per minute (BPM). Thirty-seven of 39 (94.8%) patients had complete resolution of symptoms. Of these 37 patients, 16 required 1 SNM, 17 patients required 2 SNM, and 4 patients required 3 SNM in order to achieve complete symptom resolution. Mean HR post-procedure was 78.6 ± 12.3 BPM. Thirteen of 39 patients required rate control medication post-procedure, all of whom were prescribed beta-blockers. Patients were followed every 3 to 6 months with a mean follow-up duration of 62.3 ± 42.9 months from the patient's last SNM procedure. Thirteen of those 37 patients (35.1%) developed intermittent symptomatic bradycardia requiring permanent pacemaker implantation. Two of the 39 patients had phrenic nerve injury, and 6 patients had post-procedure pericarditis. CONCLUSIONS: This study provides additional information to the limited dataset available in the literature and shows that SNM might provide patients with long-term symptomatic relief bearing in mind the potential increased risk for the need for permanent pacing.

Inadequate, inappropriate sinus-node tachycardia: an old cardiac arrhythmia in a new perspective (II.): Our experiences with the pharmacological treatment / Inadekvát, aránytalan sinuscsomó-tachycardia: egy régi szívritmuszavar új megvilágításban (II.).

Összefoglaló. Bevezetés: Az inadekvát, aránytalan sinuscsomó-tachycardia a szív nomotop ingerképzési zavarával járó, nem ritka klinikai szindróma. A szívritmuszavar-entitást a nem paroxysmalis, magas nyugalmi sinusfrekvencia, a fizikai/pszichés stresszre adott aránytalan sinustachycardia, valamint foként palpitációs panaszok jellemzik. Célkituzés: Az aránytalan sinuscsomó-tachycardiás betegeink gyógyszeres kezelésével szerzett tapasztalataink ismertetése. Módszerek: 2008 és 2018 között 104 beteget (92 no, 12 férfi; átlagéletkor 31 ± 10 év) kezeltünk ezzel a szívritmuszavarral. A betegek kivizsgálásuk után 12 elvezetéses EKG-, terheléses EKG-, valamint 24 órás Holter-monitoros EKG-megfigyeléseken vettek részt a gyógyszeres kezelés elott és után (bizoprolol: 2 × 5 mg/nap; ivabradin: 2 × 5 mg/nap). Az életminoség változását a European Heart Rhythm Association (EHRA) tüneti skálája szerint állapítottuk meg. Eredmények: Mindkét gyógyszer jelentosen csökkentette a nyugalmi sinusfrekvenciát (kontroll: 102 ± 10/min; bizoprolol: 78 ± 6/min; ivabradin: 74 ± 8/min, mindketto: p<0,0001). A gyógyszeres kezelés nélküli, 24 órás Holter-monitoros EKG-felvételek során mért szívfrekvenciák (minimum-maximum [átlag] sinusfrekvencia/min) a kontrollértékekrol (58 ± 8-159 ± 14 [94 ± 6]/min) mindkét gyógyszerre egyaránt szignifikánsan csökkentek (bizoprolol: 53 ± 7-132 ± 13 [77 ± 9]/min [mindhárom: p<0,0001]; ivabradin 51 ± 6-134 ± 18 [77 ± 8]/min [mindhárom: p<0,0001]). A terheléses EKG-vizsgálatok elott (kontroll: 99 ± 13/min; bizoprolol 81 ± 11/min [p<0,0001]; ivabradin: 84 ± 10/min [p<0,0001]) és a terhelés csúcspontján mért sinusfrekvenciák (kontroll: 164 ± 15/min; bizoprolol: 140 ± 16/min [p<0,0001]; ivabradin: 142 ± 14/min [p<0,0001]) is jelentosen mérséklodtek. Az azonos dózisban adott két gyógyszer szívfrekvencia-csökkento hatásai között számottevo különbséget nem tapasztaltunk. Az életminoséget tükrözo EHRA tüneti skálán (kontroll: 2,3 ± 0,7) mind a bizoprolol (1,4 ± 1,4; p<0,0001), mind az ivabradin (1,1 ± 0,2; p<0,0001) egyformán csökkentette a betegek tüneteit, panaszait. Számottevo cardiovascularis mellékhatás egyik betegcsoportban sem jelentkezett. Következtetések: Vizsgálati eredményeink alapján megállapítható, hogy az aránytalan sinuscsomó-tachycardiás betegek gyógyszeres kezelésére: (1) a kardiospecifikus adrenerg béta-blokkoló bizoprolol és az If-csatorna-gátló ivabradin egyaránt hatékonynak és biztonságosnak bizonyult; (2) az azonos adagban adott két gyógyszer hatékonysága között számottevo különbség nem volt; (3) a gyógyszeres kezelés nemcsak a sinusfrekvenciát csökkentette, hanem a betegek panaszait, tüneteit is mérsékelte. Orv Hetil. 2020; 161(46): 1953-1958. INTRODUCTION: The inadequate, inappropriate sinus-node tachycardia is not a rare clinical syndrome, defined as a disturbance of the nomotopic impulse formation of the heart. This cardiac arrhythmic entity is characterized by a non-paroxismal, increased sinus rate at rest, and/or inadequate response to physical and/or emotional stress and palpitations. OBJECTIVE: The aim of this study was to describe our experiences with pharmacological therapy of patients with inappropriate sinus tachycardia syndrome. METHODS: Between 2008 and 2018, 104 patients (92 women, 12 men, mean age: 31 ± 10 years) were treated with this cardiac arrhythmia entity. All patients underwent 12-lead ECG, 24-hour Holter-ECG monitoring and standard bicycle dynamic exercise tests before and after drug treatment (bisoprolol: 5 mg bid; ivabradine: 5 mg bid). Changes in the quality of life were estimated by using the European Heart Rhythm Association (EHRA) score. RESULTS: Both drugs decreased significantly the resting heart rate (control: 102 ± 10/min; bisoprolol 78 ± 6/min (p<0.0001), ivabradine: 74 ± 8/min (p<0.0001). The results of the parameters of the 24-hour Holter ECG recordings (expressed as minimal-maximal [average] heart rate/min) with drug therapy showed a significant decrease from control values in all three parameters: control 58 ± 8-159 ± 14 (94 ± 6)/min; bisoprolol 53 ± 7-132 ±13 (77 ± 9)/min (all three: p<0.0001); ivabradine: 51 ± 6-134 ± 18 (77 ± 8)/min (all three: p<0.0001). The sinus rate reduced significantly both before the bicycle dynamic exercise tests (control: 99 ± 13/min; bisoprolol: 81 ± 11/min [p<0.0001]; ivabradine: 84 ± 10/min [p<0.0001]) and at the peaks of the exercise test (control: 164 ± 15/min; bisoprolol: 140 ± 16/min [p<0.0001]; ivabradine 142 ± 14/min [p<0.0001]). The heart rate reducing effects of the two drugs did not differ significantly. The EHRA quality of life score was equally improved by the two drugs (control: 2.3 ± 0.7; bisoprolol: 1.4 ± 1.4 [p<0.0001]; ivabradine: 1.1 ± 0.2 [p<0.0001]). No cardiovascular side effects were observed while taking bisoprolol or ivabradine. CONCLUSIONS: Based on our clinical results, it can be pointed out that in the drug therapy of patients with inappropriate sinus node tachycardia: (1) bisoprolol (5 mg bid) and ivabradine (5 mg bid) proved to be equally effective and safe; (2) the heart rate reducing effect of the two drugs - given in the same dosage - did not differ considerably; (3) the pharmacological therapy significantly decreased not only the sinus frequency, but also reduced the symptoms of the patients. Orv Hetil. 2020; 161(46): 1953-1958.

The use of ivabradine in a patient with inappropriate sinus tachycardia and cardiomyopathy due to limb girdle muscular dystrophy type 2I.

Muscular dystrophies are a heterogeneous group of disorders that commonly involve cardiac and skeletal muscle. Comprehensive guidelines for the management of cardiac failure and arrhythmias are available. However, the studies from which their recommendations are derived did not include any patients with muscular dystrophy. Some medications (eg, betablockers) may have significant side effects in this cohort. In some situations the use of agents with unique mechanisms of action such as ivabradine (a 'funny' channel inhibitor) may be more appropriate. Use of ivabradine has not previously been reported in limb girdle muscular dystrophy (LGMD). We describe the course of a patient with LGMD type 2I, cardiomyopathy and inappropriate sinus tachycardia treated with ivabradine. As advances in respiratory support have improved the outcomes of patients with muscular dystrophy; the prognostic significance of cardiac disease has increased. Ivabradine is tolerated and may reduce symptoms, morbidity and mortality in this cohort.

Baseline intrinsic heart rate and response to ivabradine treatment in patients with inappropriate sinus tachycardia.

BACKGROUND: Treatment with ivabradine became a new therapeutic alternative for patients with inappropriate sinus tachycardia (IST). The aim was to determine a relation between intrinsic heart rate (IHR) and response to ivabradine treatment. METHODS: Twenty-seven patients (mean age 37 ± 11; 23 women) with symptomatic IST despite medical treatment were recruited into the study. Resting ECG, 24-hr ECG monitoring (24hECG), exercise treadmill test, and symptoms evaluation were performed initially and after 60 days on ivabradine. IHR was acquired at baseline after pharmacological autonomic blockade. RESULTS: Nineteen patients (70%) were classified as abnormal IHR group (AIHR) while eight showed normal IHR (NIHR). No significant differences in ECG parameters were found between NIHR and AIHR subgroups, while baseline exercise capacity was higher in AIHR patients (10.9 vs. 9.5 METs, p < .05). Ivabradine treatment resulted in significant reduction in resting heart rate, average 24hECG heart rate, improvement in exercise capacity and reduction of symptoms in both subgroups. Nevertheless, favorable influence of ivabradine was significantly more exaggerated in AIHR subgroup (HR 116 vs. 90 bpm, av. HR 98 vs. 79 bpm, 10.9 vs. 13.6 METS, EHRA score 3.1 vs. 1.1, p < .001 for all) than in NIHR patients (HR 112 vs. 98 bpm, av. HR 97 vs. 88 bpm, 9.5 vs. 11.1 METs, EHRA score 3.1 vs. 1.9; p < .05 for all). CONCLUSIONS: Intrinsic heart rate may be useful in predicting response to ivabradine in patients with IST. More intense response to ivabradine in patients with AIHR may be attributed to different pathophysiological mechanisms underlying IST in AIHR and NIHR groups.