Effects of long-term beta-blocker therapy on P-wave duration and dispersion in patients with rheumatic mitral stenosis

Erbay, Ali Rıza; Turhan, Hasan; Yaşar, Ayşe Saatçı; Biçer, Asuman; Şenen, Kubilay; Şaşmaz, Hatice; Sabah, İrfan; Yetkın, Ertan

doi:10.1016/j.ijcard.2004.03.079

Cited by 32 publications

(39 citation statements)

References 20 publications

(35 reference statements)

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“…Thus, elevated plasma Hcy level may be partly responsible for the impairment of coronary blood flow in patients with CSF. Erbay et al [3] and Barutcu et al [4] found the Hcy level was higher in patients with CSF compared to patients with normal coronary flow, similar to our results. So they reported that elevated Hcy levels may be associated with endothelial dysfunction, which may lead to CSF, and Hcy lowering therapies may have a role in improvement of endothelial function and coronary blood flow in patients with CSF.…”

Section: Discussionsupporting

confidence: 92%

“…This angiographic finding showing slow contrast progression was first described in six patients with typical angina pectoris by Tambe et al [1] and there are just a few studies reported about the etiology of this phenomenon since this date. Although the knowledge concerning the etiopathogenesis of CSF was very scarce, it was thought to be due to the coronary microvascular endothelial dysfunction and elevated level of plasma homocysteine (Hcy) [1,2,3,4]. The elevated Hcy level has been reported to be associated with endothelial dysfunction and contributes to increased risk of cardiovascular disease regardless of conventional risk factors [5].…”

Section: Introductionmentioning

confidence: 99%

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Effect of Homocysteine-Induced Oxidative Stress on Endothelial Function in Coronary Slow-Flow

Tanrıverdi¹,

Evrengül²,

Enli³

et al. 2007

Cardiology

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Background and Objective: Coronary slow-flow (CSF) phenomenon is characterized by delayed opacification of vessels in a normal coronary angiogram, but its etiopathogenesis remains unclear. Plasma homocysteine (Hcy) level can severely disturb vascular endothelial function and may play a role in the pathogenesis of CSF. In our study, endothelial function in patients with CSF and their relationship with Hcy and oxidative stress parameters are investigated. Method: Forty-four patients with angiographically proven CSF and 44 cases with normal coronary flow pattern with similar risk profile were enrolled in the study. Coronary flow patterns of the cases are determined by Thrombolysis in Myocardial Infarction (TIMI) frame count method. Endothelium dependent flow mediated dilatation (FMD) and independent vasodilatation characteristics are evaluated by high frequency ultrasound over the brachial artery. Superoxide dismutase (SOD) and reduced glutathione (GSH) and reduction of oxidative material in the body and the end product of lipid peroxidation, malondialdehyde (MDA) are measured as oxidative stress markers in blood samples. Results: Plasma Hcy level (µmol/l) of patients with CSF was found to be significantly higher than in controls (12.2 ± 4.9 vs. 8.5 ± 2.8, p = 0.0001). FMD was 7.87 ± 2.0% in controls and 4.98 ± 1.1% in patients with CSF (p = 0.0001). GSH was reduced in patients with CSF. SOD and MDA activity were found higher in patients with CSF than control subjects. Plasma Hcy level was significantly positively correlated with mean TIMI frame count and negatively correlated with FMD in correlation analysis (r = 0.58, p = 0.0001; r = –0.41, p = 0.022; respectively). Conclusion: The present findings allow us to conclude that patients with CSF have increased levels of Hcy and oxidative stress markers and impaired endothelial cell function.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Effect of Homocysteine-Induced Oxidative Stress on Endothelial Function in Coronary Slow-Flow

Tanrıverdi¹,

Evrengül²,

Enli³

et al. 2007

Cardiology

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“…Heath et al [44] reported that propofol may alter the ion channel in the myocardium which could have an effect on the QTc interval, due to block the delayed rectifier potassium current. Several studies showed that Pd has a predictive value for atrial fibrillation in patients without apparent heart disease [8,9]. To our knowledge, this study is the first one in investigation Pd during FFB.…”

Section: Discussionmentioning

confidence: 73%

“…It has been observed that the laryngoscopy and tracheal intubation associated with significant stimulation of sympathetic activity may cause a prolonged QTc interval during anesthetic induction in healthy patients [7]. Furthermore, it has been reported that the increased P wave dispersion (Pd) are connected with increased risk of atrial fibrillation [8,9].…”

Section: Introductionmentioning

confidence: 99%

Changes on QT, Qtc and P Dispersion during Flexible Bronchoscopy under Propofol and 12121 Remifentanil Sedation. A Double-Blind Randomized Trial

Doğan¹

2012

J Anesthe Clinic Res

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Background: Serious hemodynamic alterations have been shown during flexible fiberoptic bronchoscopy (FFB). QT and P wave dispersion (QTd, Pd) may give us an significant information about cardiac status during FFB. This study aimed to compare the effect of propofol and remifentanil sedation on QTd, corrected QT dispersion (QTcd) and Pd during FFB.Method: Forty-nine ASA class I or II patients who were not pre-medicated were selected and allocated to receive either propofol 1 mg/kg (n=20) or remifentanil 1 µg/kg (n=20) and titrated to achieve Ramsey sedation score level of 5. QTd, QTcd and Pd were measured on electrocardiography baseline (T0), at the end of the infusion of drugs (T1), shortly after laryngoscopy (T2), at the end of bronchoscopy (T3) and the time of Modified Aldrete score to be achived 10 (T4) Heart rate, mean arterial pressure, respiratory rate and partial CO2 pressure in blood gas were recorded at these time points. Furthermore, recovery times (RT) were recordedResults: QTd at all measurement times, corrected QTd at T1 and T2, P dispersion at T1, T2 and T3 increased significantly in the propofol group compared to remifentanil group (p<0.05). Mean arterial pressure increased significantly in the propofol group compared to the remifentanil group at T2 (p<0.05). There was a significant decrease in respiratory rate at T1 and T3 in the remifentanil group (p<0.05). There were no significant differences in heart rate and partial CO2 pressure between groups. RT was shorter in the remifentanil group (p<0.05). Conclusion:Remifentanil shortened and propofol prolonged QTd, QTcd and Pd at sedative doses during FFB. Also we obtained the short RT with remifentanil. So remifentanil may be more suitable sedative agent during FFB.

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“…Accordingly, many investigators have searched the PD in many cardiac diseases to determine whether it is useful or not to predict the risk of AF. Based on the available data obtained from these investigations, PD may be considered as a noninvasive electrocardiographic marker to predict the risk of AF, especially in some cardiovascular disorders as cardiomyopathy, rheumatic mitral stenosis, ischemic heart disease, hypertension, and paroxysmal AF which characterized with a high prevalence of AF (7,8,(25)(26)(27)(28)(29)(30)(31).…”

Section: Discussionmentioning

confidence: 99%

The effect of nebivolol on P wave duration and dispersion in patients with Behçet’s disease; a prospective single-arm controlled study

Akkaya¹,

Karakaş²,

Şahin³

et al. 2013

Anadolu Kardiyol Derg

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Objective: Behçet's disease (BD) is a chronic multi-system disease presenting with recurrent oral and genital ulceration, and relapsing uveitis. Left ventricular diastolic dysfunction, ventricular arrhythmia and sudden cardiac death have been documented in BD. P wave dispersion (PD) has been reported to be associated with inhomogeneous and discontinuous propagation of sinus impulses. PD has been reported to be longer in patients with BD. Nebivolol, besides its selective beta1-blocking activity, causes an endothelium dependent vasodilatation through nitric oxide release. In this study, we searched for the effects of nebivolol on P wave duration and dispersion in patients with BD. Methods: This study was designed as prospective single-arm controlled study. We prospectively studied 35 Behçet's patients who were diagnosed according to the International Study Group criteria. Patients received 5 mg nebivolol per day for 3 months. The patients were evaluated with 12-leads electrocardiography at baseline and after for 3-month therapy. The difference between maximum and minimum P wave durations was defined as PD. The paired samples t test, Wilcoxon test were used for statistical analysis. Results: A significant decrease was observed in PD after therapy period (62.85±21.62 vs. 44.28±18.03 msec, p=0.001). No adverse effects were observed in treatment period. Conclusion: BD is associated with prolonged P wave duration and dispersion. We have shown for the first time that nebivolol causes a significant decrease in maximum P wave duration and PD in patients with BD. However, further comprehensive studies are needed to determine the long-term effects of nebivolol. (Anadolu Kardiyol Derg 2013; 13: 682-7) Key words: Behçet's disease, nebivolol, P wave dispersion Original Investigation Özgün Araşt›rma 682ÖZET Amaç: Behçet hastalığı (BH), tekrarlayıcı oral ve genital ülserasyon ve üveit atakları ile karakterize, kronik multisistemik bir hastalıktır. BH'da sol ventrikül diyastolik disfonksiyonu, ventriküler aritmi ve ani kardiyak ölüm vakaları bildirilmiştir. P dalga dispersiyonu (PD)'nun, sinüs uyarılarının homojen olmayan ve kesintili yayılımı ile ilişkili olduğu gösterilmiştir. PD'nin BH'da daha uzun olduğu gösterilmiştir. Selektif beta 1 bloker olan nebivolol, nitrik oksit salınımı sayesinde endotel bağımlı vazodilatasyon yapar. Bu çalışmada, BH'da nebivololün P dalga süresi ve PD üzerinde-ki etkisini araştırdık. Yöntemler: Bu araştırma prospektif, tek grup kontrollü çalışma olarak tasarlandı. Çalışmaya Uluslararası Çalışma Grubu kriterlerine uyan 35 BH alındı. Hastalara 3 ay süreyle 5 mg/gün nebivolol verildi. Hastalar başlangıçta ve 3 aylık tedavi sonrasında 12 kanallı elektrokardiyografi ile değerlendirildi. Maksimum ve minimum P dalga süresi arasındaki fark PD olarak belirlendi. Paired samples t-test, Wilcoxon testi istatistiksel değerlendirme için kullanıldı. Bulgular: Tedavi sonrasında PD'da belirgin azalma izlendi (62.85±21.62'e karşı 44.28±18.03 msn, p=0.001). Tedavi süresinde herhangi bir yan etki izlenmedi. So...

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Effects of long-term beta-blocker therapy on P-wave duration and dispersion in patients with rheumatic mitral stenosis

Cited by 32 publications

References 20 publications

Effect of Homocysteine-Induced Oxidative Stress on Endothelial Function in Coronary Slow-Flow

Effect of Homocysteine-Induced Oxidative Stress on Endothelial Function in Coronary Slow-Flow

Changes on QT, Qtc and P Dispersion during Flexible Bronchoscopy under Propofol and 12121 Remifentanil Sedation. A Double-Blind Randomized Trial

The effect of nebivolol on P wave duration and dispersion in patients with Behçet’s disease; a prospective single-arm controlled study

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