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      Heart rate variability improvement in children using transcatheter atrial septal defect closure

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          Abstract

          Objective:

          We evaluated autonomic behavior by examining heart rate variability (HRV) in the time domain and frequency domain in pediatric patients who underwent transcatheter closure of atrial septal defect (ASD).

          Methods:

          A prospective study design was used. Holter ECG was performed in a control group of 30 healthy subjects and a group of 47 patients who underwent transcatheter ASD closure. ECG was taken one day before, one day after, and six months after the procedure to evaluate changes in the time domain [SDNN, rMSSD, NN, pNN50(%), and SDANN] and frequency domain (VLF, LF, HF, VHF, and LF/HF) in the patient group. Student’s t-test was used to evaluate changes prior to and after the procedure.

          Results:

          There were 28 females (60%) in the patient group and 21 females (70%) in the control group. The mean age and weight of the participants in the patient group were 9.61±4.72 years and 32.40±19.60 kg, respectively; the mean age and weight of the control subjects were 10.43±5.31 years and 32.83±13.00 kg, respectively. In both the time domain and frequency domain analyses, the patient group values were found to be lower than those in the control group prior to the procedure; the values in the patient group were found to approach the values in the control group following the procedure. By the sixth month, the values in the patient group reached the control levels with no statistically significant difference (SDNN: 145±0.84, 137.50±42.50; r MSSD: 72.18±48.22, 58.14±28.49; SDANN: 125.13±13.50, 122.40±41.06; VLF: 112.85±29.07, 114.41±98.39; LF: 50.40±24.09, 45.69±15.13; HF: 39.28±19.86, 44.29±13.14; VHF: 10.29±4.24, 9.99±6.47; LF/HF: 1.90±1.44, 1.24±0.81; p>0.05).

          Conclusion:

          The transcatheter closure of secundum ASDs was found to have a positive effect on HRV. Consequently, it may contribute to reduced mortality and morbidity. We can conclude that in children, HRV recovers approximately six months after transcatheter ASD closure.

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          Most cited references26

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          Atrial arrhythmia after surgical closure of atrial septal defects in adults.

          Atrial flutter and atrial fibrillation are causes of morbidity in adults with an atrial septal defect. In this study, we attempted to identify risk factors for atrial flutter and fibrillation both before and after the surgical closure of an atrial septal defect. We searched for preoperative and postoperative atrial flutter or fibrillation in 213 adult patients (82 men and 131 women) who underwent surgical closure of atrial septal defects because of symptoms, a substantial left-to-right shunt (ratio of pulmonary to systemic blood flow, >1.5:1), or both at Toronto Hospital between 1986 and 1997. Forty patients (19 percent) had sustained atrial flutter or fibrillation before surgery. As compared with the patients who did not have atrial flutter or fibrillation before surgery, those who did were older (59+/-11 vs. 37+/-13 years, P 40 years) at the time of surgery (P=0.001), the presence of preoperative atrial flutter or fibrillation (P<0.001), and the presence of postoperative atrial flutter or fibrillation or junctional rhythm (P=0.02) were predictive of late postoperative atrial flutter or fibrillation. The risk of atrial flutter or atrial fibrillation in adults with atrial septal defects is related to the age at the time of surgical repair and the pulmonary arterial pressure. To reduce the morbidity associated with atrial flutter and fibrillation, the timely closure of atrial septal defects is warranted.
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            A comparison of surgical and medical therapy for atrial septal defect in adults.

            The surgical closure of an atrial septal defect is frequently recommended for patients over 40 years of age. However, the prognosis for such patients with unrepaired defects is largely unknown, and the outcome for patients operated on after the fourth decade of life has not yet been compared with that for medically treated patients in a controlled follow-up study. In a retrospective study, we examined the clinical course of 179 consecutive patients with isolated atrial septal defects diagnosed after the age of 40. The 84 patients (47 percent) who underwent surgical repair were compared with the 95 patients (53 percent) who were treated medically. The mean (+/-SD) follow-up period was 8.9 +/- 5.2 years (range, 1 to 26). Multivariate analysis revealed that surgical closure of the defect significantly reduced mortality from all causes (relative risk, 0.31; 95 percent confidence interval, 0.11 to 0.85). The adjusted 10-year survival rate of surgically treated patients was 95 percent, as compared with 84 percent for the medically treated patients. In addition, surgical treatment prevented functional deterioration, as measured by the New York Heart Association class (relative risk, 0.21; 95 percent confidence interval, 0.08 to 0.55). However, the incidence of new atrial arrhythmias or of cerebrovascular insults in the two groups was not significantly different. The surgical repair of an atrial septal defect in patients over 40 years of age, as compared with medical therapy, increases long-term survival and limits the deterioration of function due to heart failure. However, surgically treated patients should be followed closely for the onset of atrial arrhythmias so as to reduce the risk of thromboembolic complications.
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              Atrial stretch, not pressure, is the principal determinant controlling the acute release of atrial natriuretic factor.

              The current studies were designed to investigate the mechanisms in the intact anesthetized dog that control the release of atrial natriuretic factor (ANF). In vitro, mechanical stretch of atrial tissue produces an increased release of ANF. In vivo, changes in atrial pressure correlate positively with circulating ANF levels. The present investigations used 6 open-chest anesthetized dogs to evaluate the role of atrial pressure versus atrial stretch, the latter determined by atrial transmural pressure, in the release of ANF. In a paired design, animals underwent cardiac tamponade followed by constriction of the aorta and pulmonary artery. Tamponade produces a balanced increase in intra-atrial and pericardial pressures. Thus, despite an elevated atrial pressure, there is no increase in transmural pressure producing atrial stretch. Great artery constriction increases intra-atrial but not pericardial pressure, resulting in an increase in atrial transmural pressure and atrial stretch. Cardiac tamponade increased right atrial pressure (0.8 +/- 0.3 to G.6 +/- 0.6 mm Hg, p less than 0.001) and pulmonary capillary wedge pressure (3.7 +/- 0.6 to 8.8 +/- 0.6 mm Hg, P less than 0.001). Constriction of the aorta and pulmonary artery also increased right atrial pressure (1.5 +/- 0.8 to 6.3 +/- 0.8 mm Hg, p less than 0.05) and pulmonary capillary wedge pressure (4.6 +/- 0.3 to 7.8 +/- 1.0 mm Hg, p less than 0.05). Atrial transmural pressure increased only during great artery constriction.(ABSTRACT TRUNCATED AT 250 WORDS)
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                Author and article information

                Journal
                Anatol J Cardiol
                Anatol J Cardiol
                Anatolian Journal of Cardiology
                Kare Publishing (Turkey )
                2149-2263
                2149-2271
                April 2016
                04 March 2015
                : 16
                : 4
                : 290-295
                Affiliations
                [1]Department of Pediatric Cardiology, Mehmet Akif Ersoy Thoracic and Cardiovascular Surgery Center and Research Hospital; İstanbul- Turkey
                [* ]Department of Cardiology, Mehmet Akif Ersoy Thoracic and Cardiovascular Surgery Center and Research Hospital; İstanbul- Turkey
                [** ]Department of Pediatric Cardiovascular Surgery, Mehmet Akif Ersoy Thoracic and Cardiovascular Surgery Center and Research Hospital; İstanbul- Turkey
                Author notes
                Address for Correspondence: Dr. İsa Özyılmaz, Mehmet Akif Ersoy Kalp ve Damar Eğitim ve Araştırma Hastanesi Pediyatrik Kardiyoloji Bölümü, Halkalı, Küçükçekmece, İstanbul- Türkiye Phone: +90 212 692 20 00-1134 Fax: +90 212 471 94 94 E-mail: isaozy@ 123456hotmail.com
                Article
                AJC-16-290
                10.5152/akd.2015.5922
                5368440
                26642471
                0b465f6a-126b-4fa6-a11a-9a9594680d07
                Copyright © 2016 Turkish Society of Cardiology

                This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License

                History
                : 06 February 2015
                Categories
                Original Investigation

                heart rate variability,atrial septal defect,closure,transcatheter,children

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