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      Evaluating functional capacity, and mortality effects in the presence of atrial electromechanical conduction delay in patients with systolic heart failure

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          Abstract

          Objective:

          Atrial functions are relatively suppressed in heart failure (HF). We aimed to investigate the associations of intra- and inter-atrial electromechanical conduction delay (EMCD) with functional class and mortality over a 12-month follow-up period.

          Methods:

          The prospective study included 65 patients with systolic HF and 65 healthy subjects with normal sinus rhythm. Left ventricular (LV) systolic functions and left atrial (LA) dimensions and volumes were evaluated by transthoracic echocardiography. Tissue Doppler imaging (TDI) signals at the lateral border of the mitral annulus (lateral PA’), septal mitral annulus (septal PA’), and tricuspid annulus (tricuspid PA’) were measured. Intra- and inter-atrial EMCD were calculated.

          Results:

          Mitral inflow velocities were studied using pulsed-wave Doppler after placing the sample volume at the leaflets’ tips. The peak early (E wave) and late (A wave) velocities were measured. The septal annular E/E’ ratio was relatively higher and lateral, septal, and right ventricular S, E’, and A’ waves were significantly lower in the HF group than in the control group (12.49±6.03 – 7.16±1.75, pE/E’ <0.0001). Intra-atrial EMCD was detected as 117.5 ms and inter-atrial EMCD as 127.5 ms in patients with prolonged atrial EMCD. A significant increase was found in prolonged intra- and inter-atrial EMCD according to functional capacity increase (p=0.012 and p=0.031, respectively). The incidence of mortality was significantly higher in patients with prolonged atrial EMCD (p=0.025), and 5 patients in the HF group died during the study over the 12-month follow-up period.

          Conclusions:

          In this study, we found a relationship between prolonged atrial conduction time and increased functional class and mortality in patients with systolic HF. (Anatol J Cardiol 2016; 16: 579-86)

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          Most cited references21

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          New Doppler echocardiographic applications for the study of diastolic function.

          Doppler echocardiography is one of the most useful clinical tools for the assessment of left ventricular (LV) diastolic function. Doppler indices of LV filling and pulmonary venous (PV) flow are used not only for diagnostic purposes but also for establishing prognosis and evaluating the effect of therapeutic interventions. The utility of these indices is limited, however, by the confounding effects of different physiologic variables such as LV relaxation, compliance and filling pressure. Since alterations in these variables result in changes in Doppler indices of opposite direction, it is often difficult to determine the status of a given variable when a specific Doppler filling pattern is observed. Recently, color M-mode and tissue Doppler have provided useful insights in the study of diastolic function. These new Doppler applications have been shown to provide an accurate estimate of LV relaxation and appear to be relatively insensitive to the effects of preload compensation. This review will focus on the complementary role of color M-mode and tissue Doppler echocardiography and traditional Doppler indices of LV filling and PV flow in the assessment of diastolic function.
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            Remodeling of sinus node function in patients with congestive heart failure: reduction in sinus node reserve.

            Experimental and clinical studies have demonstrated diffuse atrial remodeling in congestive heart failure (CHF). We hypothesized that patients with CHF would demonstrate derangement of sinus node function. Eighteen patients with symptomatic CHF (left ventricular ejection fraction, 26+/-5%) and 18 age-matched control subjects were studied. Under autonomic blockade, the following were evaluated: intrinsic sinus cycle length, corrected sinus node recovery time (CSNRT), sinoatrial conduction time, number and duration of fractionated electograms or double potentials along the crista terminalis, and location of the earliest sinus activity. Electroanatomic mapping was performed to evaluate the location and nature of the sinus node complex, to characterize sinoatrial propagation, and to evaluate conduction abnormalities and voltage amplitude along the crista terminalis. Patients with CHF demonstrated the following findings compared with age-matched control subjects: prolongation of the intrinsic sinus cycle length (P=0.005), prolongation of CSNRT (P<0.0001), caudal localization of sinus activity both during sinus rhythm (P=0.03) and after pacing (P=0.002), prolongation of sinoatrial conduction time (P=0.02), greater number (P<0.0001) and duration (P<0.0001) of fractionated electrograms or double potentials along the crista terminalis, loss of voltage amplitude along the crista terminalis (P=0.02), and abnormal and circuitous propagation of the sinus impulse. This study demonstrates that patients with CHF have significant sinus node remodeling characterized by anatomic and structural changes along the crista terminalis with a reduction in functional sinus node reserve. This finding may have implications for the development of clinical bradycardia in CHF and for the use of negatively chronotropic agents and pacing in this condition.
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              Differences in atrial versus ventricular remodeling in dogs with ventricular tachypacing-induced congestive heart failure.

              Congestive heart failure (CHF) causes arrhythmogenic remodeling in both atria and ventricles, but differences between atrial and ventricular remodeling in CHF have not been well characterized. We examined atrial and ventricular tissues from dogs with CHF induced by ventricular tachypacing (220-240/min) for 0 (control) or 24 h, or 1, 2 or 5 weeks. Histopathology was used to assess apoptosis, fibrosis, white blood cell infiltration and cell death, ELISA to measure angiotensin-II concentration and Western blot to evaluate protein expression. Ventricular tachypacing-induced CHF was associated with substantially more fibrosis in left atrium (maximum 10 +/- 1% at 5 weeks) than in left ventricle (0.4 +/- 0.1% at 5 weeks, P < 0.01 versus left atrium). Tissue angiotensin-II concentration increased to steady state in atrial tissue at 24 h but increased more slowly in left ventricle, with a maximum that was significantly higher in atrium than ventricle. Ventricular tachypacing caused tissue apoptosis, inflammatory cell infiltration and cell death, with maximum changes in left atrium being faster, transient and larger than in left ventricle. Mitogen activated protein kinase activation was rapid (within 24 h) in left atrium, but smaller and slower (p38, c-Jun N-terminal kinase) or non-significant (extracellular signal-related kinase) in left ventricle. The 25-kDa activated form of transforming growth factor-beta1, a particularly important profibrotic mediator in atrium, increased significantly in left atrium, from 2.6 +/- 0.6 (control) to 9.2 +/- 1.7 (24 h) and 8.1 +/- 1.8 optical density units (1 week), but was not significantly changed in ventricle. There are qualitative and quantitative differences in atrial versus ventricular remodeling in experimental ventricular tachypacing-induced CHF, with potentially important consequences for understanding underlying mechanisms and developing new therapeutic approaches. Copyright 2004 European Society of Cardiology
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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
                August 2016
                21 October 2015
                : 16
                : 8
                : 579-586
                Affiliations
                [1]Department of Cardiology, Ankara Dışkapı Training and Research Hospital; Ankara- Turkey
                [1 ]Department of Cardiology, Faculty of Medicine, Pamukkale University; Denizli- Turkey
                [2 ]Department of Cardiology, İzmir Karşıyaka State Hospital; İzmir- Turkey
                [3 ]Department of Cardiology, Faculty of Medicine, İzmir Şifa University; İzmir- Turkey
                [4 ]Department of Cardiology, Faculty of Medicine, Ege University; İzmir- Turkey
                [5 ]Department of Cardiology, İzmir Tepecik Training and Research Hospital; İzmir- Turkey
                Author notes
                Address for correspondence: Dr. Murat Bilgin, Pamukkale Üniversitesi Tıp Fakültesi Kardiyoloji Anabilim Dalı, P: 20100, Denizli- Türkiye Phone: +90 535 519 74 72 Fax: +90 312 323 06 32 E-mail: drbilginmurat@ 123456hotmail.com
                Article
                AJC-16-579
                10.5152/AnatolJCardiol.2015.6445
                5368513
                27004707
                95435f65-8603-4f56-bb33-1f1a90e8b133
                Copyright © 2016 Turkish Society of Cardiology

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

                History
                : 04 August 2015
                Categories
                Original Investigation

                heart failure,atrial electromechanical delay,functional class,mortality

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