Sinus Heart Rate Research Articles

Automatic Detection of Congestive Heart Failure Based on a Hybrid Deep Learning Algorithm in the Internet of Medical Things

Congestive heart failure (CHF) is a chronic heart condition with heart function decline caused by various heart diseases that requires long-term treatment and affects personal life safety. Presently, CHF diagnosis is being conducted by experts, which is a nonspecific mode that is time consuming and depends on experience. Therefore, it is of great clinical value to conduct CHF recognition through automatic detection. This article proposed an automatic CHF detection model based on a hybrid deep learning algorithm that is composed of a convolutional neural network (CNN) and a recursive neural network (RNN). We also classified normal sinus heart rate signals and CHF signals based on electrocardiography (ECG) and time-frequency spectra during the RR interval. The accuracy of this algorithm was 99.93%, the sensitivity was 99.85%, and the specificity was 100% when 5-min ECG signals were analyzed. It showed a certain improvement over previous studies. We also investigated the detection of CHF patients from healthy subjects by ultrashort-term ECG, and good performance was obtained. The hybrid deep learning algorithm can make objective, accurate classifications of CHF signals and serve as an effective auxiliary tool for the clinical detection of CHF patients.

Abstract 316: Influence of Aging and Na Channels on Sinus Rhythm and Heart Rate Variability

Heart rate variability (HRV) is an index of cardiovascular health and reflects the ability of the heart to adjust sinus rhythm in response to autonomic regulation, a process affected by age. Importantly, Na channels have emerged as key components of discharge and conduction of the sino-atrial node, but whether altered Na channels affect HRV remains to be established. Thus, we studied effects of aging and altered Na channels on heart rate and HRV using wild type (WT) mice and mice with phosphomimetic mutation of Na channel Nav1.5 at Ser571 (S571E mice). Electrocardiograms (ECG) were obtained in male conscious mice at ~4, ~12, ~18, and ~24 months of age (n=13-51). The mean RR interval of the ECG was similar in WT mice at ~4, ~12, and ~18 months (83±4, 81±2, 83±2 ms, respectively), but increased at ~24 months (85±5 ms). In contrast, mean RR interval in S571E mice was maximal at ~4 months (86±6 ms) and progressively decreased at ~12 (83±9 ms), ~18 (79±2 ms), and ~24 months (80±3 ms). Standard deviation of RR intervals (SDRR), an indicator of RR variability, was maximal in WT at ~4 months (3.8±1.6 ms) and was reduced at ~12, ~18, and ~24 months (2.1±0.9, 2.4±1, and 2.6±1.2 ms). Similarly, SDRR was maximal in S571 at ~4 (5.1±2.6 ms) and ~12 months (4.3±1.5 ms), and decreased at ~18 and ~24 months of age (2.6±1.0 and 3.1±1.1 ms). Standard deviation of instantaneous (SD1) and long-term (SD2) RR interval variability, indicative of parasympathetic and sympathetic influence, respectively, were derived from Poincaré plots of RR i and RR i+1 intervals. Overall, SD1 was preserved for the two groups of aging mice, whereas SD2 was maximal at ~4 months and decreased at ~18 and ~24 months. In the presence of complete autonomic block (propranolol and atropine), RR interval increased in young (~4 months, +10%) and old (~24 months, +16%) WT mice. Similarly, autonomic block increased RR interval in young (~4 months, +12%) and old (~24 months, +14%) S571E, but it abrogated RR interval differences between young and old. For the two genotypes, autonomic block reduced SDRR and SD2 exclusively in young animals, abolishing age-related differences in HRV. Overall, these data suggest that Na + channel function conditions heart rate and its age-related adaptations, but does not interfere with the decline of HRV occurring with age.

Assessment of left atrial mechanics and left ventricular functions using 3D speckle-tracking echocardiography in patients with inappropriate sinus tachycardia.

Inappropriate sinus tachycardia (IST) is defined as a sinus heart rate > 100 bpm at rest (with a mean 24-h heart rate > 90 bpm not due to primary causes) and is associated with distressing symptoms of palpitations. The effect of IST on left atrial (LA) and left ventricular (LV) myocardial dynamics is uncertain. Thus, the aim of this study was to identify early changes in LA mechanics and LV myocardial functions in patients with IST using 3D-STE. Sixty patients with IST and 65 age- and gender-matched controls were enrolled into the study. Conventional 2D echocardiography and 3D-STE were performed, and LAS-r, LAS-active, LAS-passive, LAEF, LAEF-active, LAEF-passive, LV-GLS, LV-GCS, LV-GAS, and LV-GRS were obtained for every patient. The LAS-r and LAS-active were significantly decreased in the IST group than in the control group (p < 0.001, p = 0.004, respectively). The multivariate logistic regression models revealed that LAS-r (p = 0.008, Odds ratio (OR) 5.98, 95% confidence interval (CI) 2.36-11.18), and LAS-active (p = 0.032, OR 2.16, 95% CI 1.97-4.69) were found to be independent factors for predicting IST. The present study is the first to evaluate the left atrial mechanics and left ventricular functions in the patients with IST using 3D-STE. We found that IST had a negative effect on left atrial mechanics. According to our findings, we can say that IST is not a completely innocent, benign clinical condition, but rather, it causes subclinical left atrial dysfunction.

Predictors of cardiac neuromodulation achieved by cryoballoon ablation performed in patients with atrial fibrillation who were in sinus rhythm before the ablation

BackgroundThe impact of pulmonary vein isolation (PVI) performed with cryoballoon (CB) on the intrinsic cardiac autonomic nervous system (ICANS) remains unclear. ObjectiveThe purpose of this study was to evaluate the predictors and the clinical meaning of cardiac neuromodulation achieved by CB-ablation as assessed by sinus heart rate (HR) response after the procedure. MethodsPatients who underwent CB-ablation for drug-resistant atrial fibrillation (AF) from January 2014 to October 2018 were included. Twelve‑leads rest ECG was taken both before and after the procedure. After discharge, patients were scheduled for follow-up visits at 1, 3, 6, and 12 months and 24 h Holter recordings were obtained at each follow-up visit. All documented AF episodes of >30 s were considered as recurrence. ResultsFour-hundred seventy-two patients (62.3% male, age 56.7 ± 13.6 years, 97.2% paroxysmal AF) were included. Mean HR before the procedure was 60.17 ± 10.4 bpm, while the morning after the procedure mean HR was 75.48 ± 12.0 bpm. Age at enrollment (R = −0.26; p < 0.001), baseline HR before the CB-A (R = −0.32; p < 0.001), nadir temperature in each right pulmonary vein (R = −0.11, p = 0.022; R = −0.16; p = 0.001) were significantly associated with the ∆HR. At 2-year follow-up, freedom from recurrences was 83.1% for the patients with HR increase ≥15 bpm after CB-A and 66.3% in patients with HR increase ˂15 bpm (p = 0.021). ConclusionSinus HR increase is a frequent phenomenon after CB-A, that can be predicted by both clinical and procedural factors and that correlates with better outcome after cryo-PVI.

P1917Can cryoballoon ablation produce alterations in cardiac and extra-cardiac autonomic nervous system in patients with atrial fibrillation?

Abstract Background Cryoballoon ablation (CBA) during pulmonary vein isolation (PVI) for atrial fibrillation (AF) can cause direct thermal injury to structures adjacent to the left atrium, including the periatrial ganglionated plexi (GP). In contrast, it has not been clarified whether cardiac autonomic nervous system (CANS) modification by CBA could indirectly affect extra-CANS. Purpose This study was aimed to investigate the impact of CBA on extra-CANS as well as CANS in AF patients. Methods Ninety-three Consecutive patients who underwent initial CBA in our institute were enrolled. Among them, 64 subjects (age 67±9 years; male gender 52%; CHADS2 score 1.2±1.0; diabetes mellitus 16%; β-blocker therapy 23%) had paroxysmal AF (G-P) and 29 (age 66±7 years; male gender 90%; CHADS2 score 1.3±1.0; diabetes mellitus 24%; β-blocker therapy 34%) had sustained AF (G-S). In G-P, resting sinus heart rate (R-HR) and coefficient of variation of the R-R intervals (CVR-R) during sinus rhythm were measured in resting 12-lead electrocardiogram before and after CBA as an index of CANS. Decrease in CVR-R after PVI reflects the vagal nerve injury by the procedure. Pupil movement reflects the autonomic nervous function. In both groups, pupillary light reflex, as an indicator of extra-CANS activity, was measured by infrared videopupillography (Iriscorder® Dual C10641, Hamamatsu Photonics, Hamamatsu, Japan) before and after CBA. Velocity of dilatation (VD) is related to sympathetic function, and velocity of contraction (VC) is associated with the balance between sympathetic and vagal tone. All CBA were treated with second generation 28mm cryoballoons (CB). CB temperature was down to a minimum of −60°C and target application time was 180 seconds. Results Complete PVI was achieved in all patients, in which touch-up radiofrequency ablation for the PVI was required in 4 cases of G-S. In G-P, R-HR significantly increased (59.2±9.2bpm to 72.5±8.3bpm, p&lt;0.01) and CVR-R significantly decreased (2.32±1.1% to 1.61±0.61%, p&lt;0.01) after CBA, while VC and VD did not significantly change (3.83±1.03mm2/sec to 3.64±0.96mm2/sec and 1.83±0.62mm2/sec to 1.86±0.84mm2/sec, respectively). In G-S, there were not significant changes between before and after CBA in VC and VD (3.77±0.80mm2/sec to 3.71±0.99mm2/sec and 1.81±0.49mm2/sec to 1.80±0.59mm2/sec, respectively). There were no significant differences between two groups in VC and VD before the procedure. Conclusion These results suggest that CBA seems to result in local parasympathetic denervation due to damage of adjacent structures including ganglionated plexi while the alteration of CANS by CBA does not seem to efferently affect extra-CANS.

Antiarrhythmic and proarrhythmic effects of subcutaneous nerve stimulation in ambulatory dogs

High output subcutaneous nerve stimulation (ScNS) remodels the stellate ganglia and suppresses cardiac arrhythmia. The purpose of this study was to test the hypothesis that long duration low output ScNS causes cardiac nerve sprouting and increases plasma norepinephrine concentration and the duration of paroxysmal atrial tachycardia (PAT) in ambulatory dogs. We prospectively randomized 22 dogs (11 males and 11 females) into 5 different output groups for 2 months of ScNS: 0 mA (sham) (n = 6), 0.25 mA (n = 4), 1.5 mA (n = 4), 2.5 mA (n = 4), and 3.5 mA (n = 4). As compared with baseline, the changes in the durations of PAT episodes per 48 hours were significantly different among different groups (sham, -5.0 ± 9.5 seconds; 0.25 mA, 95.5 ± 71.0 seconds; 1.5 mA, -99.3 ± 39.6 seconds; 2.5 mA, -155.3 ± 87.8 seconds; and 3.5 mA, -76.3 ± 44.8 seconds; P< .001). The 3.5 mA group had a greater reduction in sinus heart rate than did the sham group (-29.8 ± 15.0 beats/min vs -14.5 ± 3.0 beats/min; P = .038). Immunohistochemical studies showed that the 0.25 mA group had a significantly increased while 2.5 mA and 3.5 mA stimulation had significantly reduced growth-associated protein 43 nerve densities in both atria and ventricles. The plasma norepinephrine concentrations in the 0.25 mA group was 5063.0 ± 4366.0 pg/mL, which was significantly higher than that in the other groups of dogs (739.3 ± 946.3; P = .009). There were no significant differences in the effects of simulation between males and females. In ambulatory dogs, low output ScNS causes cardiac nerve sprouting and increases plasma norepinephrine concentration and the duration of PAT episodes while high output ScNS is antiarrhythmic.

Model of evaluation of the dynamics of left ventricular diastolic function in acute decompensated heart failure. Effect of ivabradin

Aim — to reveal the connection between the initial morphofunctional characteristics of patients and the dyna mics of changes in the diastolic function at the time, as well as during 6 months of observation after the episode of acute decompensated heart failure against the background of standard therapy and with the addition of the If-channel blocker ivabradine.&#x0D; Material and methods. We examined 127 patients hospitalized for the episode of the acute decompensated heart failure with a sinus rhythm and heart rate more than 85 beats per minute. Of these, 67 patients received ivabradine in addition to standard therapy, 60 patients were in control group. A 6-minute walk test, echocardiography assessment of systolic and diastolic function, electrocardiography (heart rate and rhythm) were performed on the day of admission (except for the 6-minute walk test), in 1 and 6 months later.&#x0D; Results. A scoring of the chance for positive dynamics of diastolic function was obtained in patients with acute decompensated heart failure, in the presence of certain initial characteristics of patients, such as: systolic pulmonary artery pressure &lt; 37 mmHg (p &lt; 0.005), heart rate &lt; 95 beats per minute (p &lt; 0.05), end diastolic size &lt; 50 mm (p &lt; 0.005), VE/Em* &lt; 18 (p &lt; 0.0005), end systolic size &lt; 40 mm (p &lt; 0.0005), and end systolic volume index &lt; 40 ml/m2 (p &lt; 0.0005), end diastolic volume index &lt; 73 ml/m2 (p &lt; 0.005), ejection fraction &gt; 50% (p &lt; 0.005), ivabradine intake (p &lt; 0.05), relative wall thickness &gt; 0,46 (p &lt; 0.005), female sex. A relationship between improvement in diastolic function and improvement in results of 6-minute walk test was found: with a positive dynamics of diastolic function, patients began to walk a distance in the 6-minute walk test more by 6,9 ± 2,9 meters (p &lt; 0.0005).&#x0D; Conclusion. The data obtained in our study confirm the advisability of addition ivabradine to the standard therapy of patients with acute decompensated heart failure with the found “useful” morphofunctional characteristics.

Abstract 17278: Concomitant Use of Ivabradine in the Setting of Cardiogenic Shock: A Case Series

Background: Ivabradine, a selective sinus node inhibitor, is indicated for patients with chronic heart failure with reduced ejection fraction (HFrEF). Use in cardiogenic shock is currently contraindicated. However, studies have suggested increasing heart rate may be deleterious for patients with HFrEF due to an inverted Bowditch-Treppe response. Limited case series have suggested use of Ivabradine in decompensated HFrEF may be beneficial. We present a case series of patients who presented with severely decompensated HFrEF and received inotropic support and concomitant ivabradine. Methods: We selected four patients with HFrEF presenting with elevated sinus heart rate and cardiogenic shock (cardiac index &lt;2.0L/min*m2with pulmonary artery wedge pressure &gt; 20 mmHg by invasive hemodynamic monitoring) while on inotropic therapy and were intolerant of beta blockade due to hypotension. Ivabradine 2.5 mg 12 h was initiated and subsequently titrated with continued monitoring with baseline, 24 h and latest obtained parameters recorded. Other treatments occurred at the discretion of the attending physician. Results: Four male patients (mean age 44 years) with non-ischemic cardiomyopathy (mean EF 17%, mean NT-pro-BNP 5104 pg/ml) were included. Ivabradine was tolerated in all cases, with a mean dose of 6 mg q12h. Mean heart rate and pulmonary wedge pressure fell 20% and 32% respectively from baseline to last measurement, while stroke volume increased with an overall improvement in cardiac index. (Table 1) There were no changes noted in mean arterial blood pressure. All patients underwent successful wean of inotropic support within 48 hours and were discharged alive on beta blocker and ACE inhibitor therapy. No adverse events attributed to use of Ivabradine were observed. Conclusion: In our small series of patients with cardiogenic shock, beta blocker intolerance and elevated sinus heart rate, Ivabradine was added without any deleterious hemodynamic effect and associated with early clinical improvement. Further studies are needed to better assess its potential use in this population.

Acute echocardiographic effects of sotalol on ventricular systolic function in dogs with ventricular arrhythmias.

BackgroundSotalol is a commonly used antiarrhythmic drug that may alter ventricular function.ObjectiveTo determine the effect of sotalol on echocardiographic indices of ventricular systolic function in dogs with ventricular arrhythmias.AnimalsThirty‐five client‐owned dogs with ventricular arrhythmias.MethodsDogs with ventricular arrhythmias (n = 27) had an echocardiogram and 5‐minute ECG performed at baseline and 2‐4 hours post‐sotalol (2‐2.5 mg/kg PO once). Eight additional dogs underwent the same protocol but did not receive sotalol (within‐day variability controls). Left ventricular (LV) internal dimension at end‐systole normalized to bodyweight (LVIDs_N), LV ejection fraction (LV EF), LV shortening area, LV fractional shortening, tricuspid annular plane systolic excursion (TAPSE), and right ventricular systolic myocardial velocity were evaluated as indices of systolic function.ResultsAll indices except TAPSE had mild decreases in systolic function post‐sotalol (all P ≤ .0007) compared with baseline but only the percent change in LVIDs_N and LV EF were significantly (P ≤ .0079) different from the percent change of the same indices in control dogs. Sinus heart rate, ventricular premature complexes/5‐minutes, and arrhythmia grade also were decreased post‐sotalol (all P ≤ .01) compared with baseline when assessed by a 5‐minutes ECG. No dog experienced an adverse event post‐sotalol, including dogs with systolic dysfunction or atrial enlargement.Conclusions and Clinical ImportanceA single dose of sotalol may cause a mild decrease in LV systolic function in dogs with ventricular arrhythmias. Sotalol appears to be well tolerated, even in dogs with atrial enlargement or systolic dysfunction.

Challenges in Treatment of Inappropriate Sinus Tachycardia.

Background: Inappropriate Sinus Tachycardia (IST) is a clinical syndrome characterized by a sinus heart rate inexplicably higher than one hundred beats per minute at rest that is associated with symptoms like palpitations, dyspnea or dizziness in the absence of primary causes of tachycar-dia.The diagnosis requires exclusion of other causes of tachycardia including medications/substances (such as anti-cholinergic, beta-blocker withdrawal, caffeine, and alcohol) or medical conditions (such as panic attacks, pulmonary embolism, fever, hyperthyroidism, hypovolemia, anemia, and pain).Methods: Work up should include an EKG to differentiate other causes of tachycardia, 24 hour-Holter monitor if indicated, serum thyroid levels, hemoglobin levels and toxicology screen. Electro-physiological studies are not routinely recommended, but should be considered in certain patients in whom concurrent supraventricular tachycardia is suspected.Conclusion: The underlying pathology in IST is yet to be completely understood. However, it is thought that the causes of IST can be broadly classified into two groups; either as an intrinsic increase in sinus node automaticity or an extrinsic cause. Among extrinsic causes, there is evolving evidence that IgG anti-β receptor antibodies are found in IST causing tachycardia.Managing patients with IST includes lifestyle modification, non-pharmacological and pharmacologi-cal interventions. Ivabradine has recently emerged as an effective treatment of IST and was shown to be superior to beta-blockers.

Сдвиги в структуре иерархической системы гомеокинеза больных ИБС на фоне стрессорного воздействия

The article presents the data on the possibility of obtaining additional diagnostic information about the reactions of the systemic regulation of the body under stressful conditions implemented as a part of the stress-test in patients with coronary artery disease: stable exertional angina. The implementation of an alternative approach to the assessment of adaptation processes arising against the background of measured physical activity is based on the assessment of the shifts in the topology of the entropic attractor model of the sinus heart rate reflecting the phenomenon of systemic homeokinesis. Against the background of the transition process in systemic regulation during stress-test, at the attractor structure has been revealed the development of the heart rate entropy, being a complex object, with the effects of activation and consolidation of its levels, which are significantly more pronounced during the formation of myocardial ischemia. The proposed digital indicators reflecting the identified topological changes can be used for an objective quantitative diagnosis of the phenomenon of destabilization of the systemic body resistance during the exacerbation of acute somatic pathology.

Influence of increased heart rate and aortic pressure on resting indices of functional coronary stenosis severity

Baseline assessment of functional stenosis severity has been proposed as a practical alternative to hyperemic indices. However, intact autoregulation mechanisms may affect intracoronary hemodynamics. The aim of this study was to investigate the effect of changes in aortic pressure (Pa) and heart rate (HR) on baseline coronary hemodynamics and functional stenosis assessment. In 15 patients (55 ± 3% diameter stenosis) Pa, intracoronary pressure (Pd) and flow velocity were obtained at control, and during atrial pacing at 120 bpm, increased Pa (+30 mmHg) with intravenous phenylephrine (PE), and elevated Pa while pacing at sinus heart rate (PE + sHR). We derived rate pressure product (RPP = systolic Pa × HR), baseline microvascular resistance (BMR = Pd/velocity), and stenosis resistance [BSR = (Pa − Pd)/velocity] as well as whole-cycle Pd/Pa. Tachycardia (120 ± 1 bpm) raised RPP by 74% vs. control. Accordingly, BMR decreased by 27% (p < 0.01) and velocity increased by 36% (p < 0.05), while Pd/Pa decreased by 0.05 ± 0.02 (p < 0.05) and BSR remained similar to control. Raising Pa to 121 ± 3 mmHg (PE) with concomitant reflex bradycardia increased BMR by 26% (p < 0.001) at essentially unchanged RPP and velocity. Consequently, BSR and Pd/Pa were only marginally affected. During PE + sHR, velocity increased by 21% (p < 0.01) attributable to a 46% higher RPP (p < 0.001). However, BMR, BSR, and Pd/Pa remained statistically unaffected. Nonetheless, the interventions tended to increase functional stenosis severity, causing Pd/Pa and BSR of borderline lesions to cross the diagnostic threshold. In conclusion, coronary microvascular adaptation to physiological conditions affecting metabolic demand at rest influences intracoronary hemodynamics, which may lead to altered basal stenosis indices used for clinical decision-making.

Impact of Ivabradine on Health-Related Quality of Life of Patients with Ischaemic Chronic Heart Failure.

Chronic heart failure (CHF) remains a major health problem, with high levels of morbidity and mortality and a low health-related quality of life (HRQoL). We assessed the impact on HRQoL of adding the If channel blocker, ivabradine, to a standard treatment regimen of patients with ischaemic CHF (I-CHF) and heart rate (HR) ≥70 beats/min (bpm). A randomized prospective study of 100 consecutive patients presenting with stable I-CHF, left ventricular ejection fraction (LVEF) <40% and a sinus HR ≥70 bpm. New York Heart Association (NYHA) class, overall summary score (OSS) and clinical summary score (CSS) of the Kansas City Cardiomyopathy Questionnaire (KCCQ) were used to assess HRQoL. The patients were randomized into 2 groups: carvedilol only (group I (n=50)) and carvedilol + ivabradine (group II (n=50)). The patients were followed up for 12 weeks and their HRQoL scores were monitored and compared. The overall mean age of the cohort was 63±10 years with 70% (n=70) males. HRQoL scores had significantly improved in group II after 12 weeks of follow-up. The net proportion of patients with a 5-point improvement in CSS was 30% higher in group II (p=0.002), whereas that for the OSS, it was 24% (p=0.001), when compared with group I. These improvements were accompanied by a significant HR reduction (69 vs 78 bpm; p=0.002). Adding ivabradine to the standard drug regimen, currently advocated by guidelines for CHF with a heart rate ≥70 bpm, resulted in a significant improvement in HRQoL.

The effect of ivabradine on functional capacity in patients with chronic obstructive pulmonary disease

Increased sympathetic tone and use of bronchodilators increase heart rate and this may worsen functional capacity in patients with chronic obstructive pulmonary disease (COPD). The aim of this study was to look at the short-term effect of the heart rate lowering drug ivabradine on clinical status in COPD patients.We randomised 80 COPD patients with sinus heart rate ≥90 bpm into either taking ivabradine 7.5 mg twice per day or placebo for two weeks. We assessed all patients using the modified Borg scale and 6-minute walk test at baseline and then again 2 weeks after randomisation.There were no significant differences in age, sex, severity of airway obstruction (measured using forceful exhalation), severity of diastolic dysfunction or pulmonary artery systolic pressure between the two groups. The ivabradine group showed significant improvement in 6-minute walk distance (from 192.6±108.8 m at baseline to 285.1±88.9 m at the end of the study) compared with the control group (230.6±68.4 at baseline and 250.4±65.8 m at the end of study) (p<0.001). This improvement in the drug group was associated with significant improvement of dyspnea on modified Borg scale (p=0.007).Lowering heart rate with ivabradine can improve exercise capacity and functional class in COPD patients with resting heart rate >90 bpm.

Prognosis of high sinus heart rate after catheter ablation for atrial fibrillation.

Although atrial fibrillation (AF) catheter ablation increases sinus heart rate (HR), its mechanism and prognosis have not yet been clearly elucidated. We hypothesize that post-AF ablation high sinus HR (PA-HSR) is associated with a better clinical outcome of AF ablation without adverse cardiac effects. We studied 991 AF patients (75% male, 58 ± 11 years old, 70% paroxysmal AF) with HR variability (HRV) at 3 months and 1 year after catheter ablation, and pre- and post-1-year echocardiograms. Post-AF ablation high sinus HR was defined as an average HR greater than 2 SD (≥92 bpm) as measured by 24 h Holter. (1) Average HR increased significantly (P< 0.001), and PA-HSR was observed in 28 patients (2.8%) 3 months after AF ablation. At 1 year after catheter ablation, 21% were taking β-blockers and 36% maintained an average HR of ≥92 bpm. (2) Post-AF ablation high sinus HR was independently associated with pre-procedural high average HR (OR 1.097; 95% CI 1.029-1.169, P= 0.005), high left atrium (LA) electrogram voltage (OR 3.545; 95% CI 1.183-10.618, P= 0.024), and reduced root mean square of differences between successive NN intervals (rMSSD) at 3 months HRV (OR 0.959; 95% CI 0.919-0.999, P= 0.047). (3) At 1 year echocardiography, size reduction of LA (P= 0.055) or LV (P= 0.372) and the improvement in ejection fraction (P= 0.529) were not significantly different between patients with PA-HSR and those without. (4) Throughout 27 ± 17 months of follow-up, patients with PA-HSR showed significantly lower clinical recurrence than those without (log rank, P= 0.020). Post-AF ablation high sinus HR was observed in patients with smaller LA size and higher LA electrogram voltage and significant vagal modulation without adverse cardiac effects. Post-AF ablation high sinus HR was associated with a significantly lower clinical recurrence of AF after catheter ablation.

Abstract 17846: Prognosis of High Sinus Heart Rate After Catheter Ablation for Atrial Fibrillation

Introduction: Although radiofrequency catheter ablation (RFCA) for atrial fibrillation (AF) increases a sinus heart rate (HR) after rhythm control, its mechanism and prognosis have not yet been clearly elucidated. Hypothesis: We hypothesized that post-procedural high sinus HR is associated with better clinical outcome of AF ablation without hemodynamic adverse effects. Methods: We included 991 AF patients (75% male, 58 ± 11 years old, 70% paroxysmal AF [PAF]) who had analyzable HR variability (HRV) at 3-months and 1-year after RFCA, and pre- and post-1-year echocardiogram. Average HR measured by 24-hour Holter greater than 2SD (≥92bpm) was defined as post-ablation high sinus HR. Results: 1. Average heart rate was increased significantly (68.8±13.1 to 71.4±10.7bpm, p&lt;0.001), and high sinus HR (≥92bpm) was observed in 28 patients (2.8%) at 3-months after AF ablation. All of them tolerated well, 21% (6/28) were taking low dose β-blocker, and 36% (10/28) kept average HR≥92bpm at 1-year after RFCA. 2. High sinus HR was independently associated with pre-procedural high average HR (OR 1.097; 95% CI 1.029 to 1.169, p=0.005), high left atrial (LA) voltage (OR 3.545; 95% CI 1.183 to 10.618, p=0.024), and reduced rMSSD at 3-months HRV (OR 0.959; 95% CI 0.919 to 0.999, p=0.047). 3. At 1-year follow-up echocardiogram, LA reverse remodeling (ΔLA; -1.1±3.7 vs. -3.0±4.6mm, p=0.055) and the improvement of ejection fraction (ΔEF; 0.7±8.4 vs. 1.7±7.7%, p=0.529) were not significantly different between the patients with high sinus HR and those without. 4. During 27±17 months of follow-up, the patients with high sinus HR at 3-months after RFCA showed significantly lower clinical recurrence than those without (log rank, p=0.020). Conclusions: High sinus HR 3-months after AF ablation is observed in patients with less remodeled LA with significant post-procedure vagal modulation. High sinus HR after AF ablation did not show hemodynamic adverse effect and was associated with lower clinical recurrence rate of AF after RFCA.

I(f) current inhibitor ivabradine in patients with idiopathic dilated cardiomyopathy: Impact on the exercise tolerance and quality of life.

Evidence supported a beneficial effect of ivabradine on clinical outcome of patients with systolic heart failure, and a sinus heart rate (HR) ≥ 70 bpm. We explored the effect of ivabradine, vs. placebo, added to evidence-based treatment on exercise tolerance and quality of life in patients with idiopathic dilated cardiomyopathy. We enrolled 43 consecutive patients with dilated cardiomyopathy of no apparent cause, a left ventricular ejection fraction (LVEF) < 40%, New York Heart Association class ≥ II, sinus HR ≥ 70 bpm, and background evidence-based anti-failure medications. Ischemic heart disease was ruled out. Patients were randomized (1:1) to receive ivabradine or placebo. Ivabradine was titrated up gradually till 7.5 mg twice daily, or a HR < 60 bpm, and continued for 3 months. Symptom-limited exercise tolerance test was performed, and quality of life was assessed by the Minnesota Living With Heart Failure Questionnaire at 0, and 3 months. Forty-three patients were randomized to ivabradine (n = 20), or placebo (n = 23). Mean age was 50.8 ± 14.5 years (53.5% males). Mean HR was 85 ± 12 bpm, and mean LVEF was 32 ± 6%. Mean dose of carvedilol was 31.2% of the target dose. Baseline HR, blood pressure, exercise tolerance, Minnesota questionnaire score, and left ventricular systolic function were comparable between the two groups (p > 0.05 for all). At 3 months, mean dose of ivabradine was 6.8 mg bid. Ivabradine-treated patients had a lower HR, and improved left ventricular dimensions and systolic function, versus placebo-treated ones (p < 0.05 for all). HR dropped by a mean of 14 bpm in the ivabradine group, corrected for placebo. Both exercise tolerance, and Minnesota questionnaire score were better in the ivabradine group (p < 0.05 both). Ivabradine was well-tolerated. In symptomatic patients with idiopathic dilated cardiomyopathy, the addition of ivabradine, vs. placebo, to evidence-based treatment, reduced HR, and improved functional capacity, at short-term follow-up.

58. Cardiovascular responses in patients with symptoms of orthostatic intolerance

The inability to stand without orthostatic hypotension is the typical disabling clinical symptom of both Postural Tachicardia Syndrome (POTS) and Orthostatic Intolerance (OI). The increase of sinus heart rate of 30 beats/min or greater occurring within 10 min of head-up tilt test or standing, or a heart rate while upright of >120 beats/min. discriminates between the two conditions. To verify if others criteria, beside the difference in heart rate increase, can distinguish the two groups, we analyzed the cardiovascular responses during active standing and head – up tilt test. We analyzed 10 patients with POTS and 10 with OI. Power spectral analysis of blood pressure and heart rate variability, in resting condition and during a period of 30 min of head – up tilt test to 60°, was performed. Both clinical conditions were compared with each other and with a control group using the Student t test. During the head – up tilt both groups of patients showed a marked and comparable increase of LF-RRI and LF/HF ratio in the power spectrum of R–R interval compared to the baseline. This could suggest the hypothesis of OI as a condition preceding POTS.

Inducible cardiac arrhythmias caused by enhanced β1-adrenergic autoantibody expression in the rabbit

Previous studies demonstrated burst pacing and intravenous infusion of ACh induced sustained atrial tachycardia when rabbits were immunized to produce β2-adrenergic receptor (β2AR)-activating autoantibodies. The objective of this study was to examine the arrhythmogenic effect of β1-adrenergic receptor (β1AR)-activating autoantibodies in the rabbit. Eight New Zealand white rabbits were immunized with a β1AR second extracellular loop peptide to raise β1AR antibody titers. A catheter-based electrophysiological study was performed on anesthetized rabbits before and after immunization. Arrhythmia occurrence was determined in response to burst pacing before and after ACh infusion in incremental concentrations of 10 μM, 100 μM, and 1 mM. The baseline sinus heart rate before and after immunization averaged 149 ± 17 per min and 169 ± 16 per min, respectively (P < 0.05). In the preimmune studies, there were five sustained (≥10 s) arrhythmias in 32 induction attempts, which occurred in only four of eight rabbits. In the postimmune studies, there were 22 sustained arrhythmias in 32 induction attempts, which occurred in all eight rabbits (P < 0.0001 for the independent effect of immunization). Of the 22 sustained arrhythmias postimmunization, 15 were sinus tachycardia compared with only two before immunization (P < 0.01 for the independent effect of immunization). Postimmune (but not preimmune) rabbit sera demonstrated specific binding to β1AR and induced significant β1AR activation in transfected cells in vitro. No cross-reactivity with β2AR was observed. In conclusion, in contrast with rabbits with β2AR-activating autoantibodies that demonstrate predominantly atrial tachycardias, enhanced autoantibody activation of β1AR in the rabbit leads to tachyarrhythmias mainly in the form of sustained sinus tachycardia.

Slow Sinus Heart Rate as a Potential Predictive Factor of Paroxysmal Atrial Fibrillation in Stroke Patients

Background: Paroxysmal atrial fibrillation (PAF) is a strong independent risk factor for ischemic stroke and is also associated with stroke severity and mortality. However, the detection rate of PAF in patients with ischemic stroke is limited because they are often asymptomatic or present with sinus rhythm on electrocardiograms (ECGs). In the present study, we aimed to identify predictors of PAF in stroke patients by continuous ECG monitoring of the heart rate in sinus rhythm. Methods: We enrolled 741 consecutive patients with acute symptomatic ischemic stroke who were admitted to our hospital. Exclusion criteria were the following: (1) patients with persistent AF, (2) cardiac pacemaker users and (3) incomplete clinical investigations. Each patient was subject to 24-hour Holter ECG, cardiac monitoring by inpatient telemetry and routine transthoracic echocardiography. The minimum and mean sinus heart rates (SHRs) on 24-hour Holter ECGs were recorded. The presence of PAF was judged on the basis of previous history and cardiac studies during hospitalization. Clinical characteristics of the patients with and without PAF were compared, and multiple logistic regression analysis was performed to identify the predictors of PAF. Results: Of all enrolled patients, 606 (mean age 68.2 years, 63.4% male) were eligible for analysis, and the presence of PAF was confirmed in 116 subjects (19.1%). In the univariate analysis, the patients with and without PAF showed significant differences in age (74.3 vs. 66.7 years, p < 0.001), dyslipidemia (32.8 vs. 50.4%, p = 0.001), chronic heart failure (16.4 vs. 4.7%, p < 0.001), admission National Institute of Health Stroke Scale score (8.5 vs. 6, p < 0.001) and absence of vascular etiology (80.2 vs. 54.1%, p < 0.001). Furthermore, the minimum and mean SHRs were slower in the patients with than in those without PAF (46.5 vs. 54.0 bpm, p < 0.001 and 70.7 vs. 73.8 bpm, p = 0.009, respectively). In 501 (82.7%) out of 606 patients, minimum SHRs were detected at night (from 9:00 p.m. to 7:00 a.m.). A minimum SHR was an independent predictive factor of PAF in the multivariate analysis (odds ratio 1.08, 95% confidence interval 1.05 - 1.12, p < 0.001). Conclusions: A slow SHR on monitoring ECG is a potential predictive factor of PAF in patients with ischemic stroke.