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      Intermittent Advanced Atrial Depolarization Abnormality?

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          Abnormal atrial depolarization, characterized by P waves ≧110 ms on the electrocardiogram, can manifest as partial or advanced interatrial block (IAB). Advanced IAB, denoted by biphasic P waves in leads II, II and aVF, is considered to confer increased severity in interatrial conduction delay, and is now perceived to be a result of continued deterioration in interatrial impulse propagation between the atria. While progression from partial to advanced IAB has been described, the converse, resolution of advanced IAB, which has often been touted as ‘complete block’ to its partial, ‘incomplete’ type, i.e. the occurrence of intermittent advanced IAB, has escaped observations so far. We present the first known report of such a scenario.

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          Most cited references 7

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          Electromechanical dysfunction of the left atrium associated with interatrial block.

          Our purpose was to determine the effect of interatrial block (IAB, P-wave duration >/=120 ms) on left atrial (LA) dynamics. IAB is associated with LA enlargement (LAE). LA dysfunction is associated with decreased left ventricular filling, a propensity for LA appendage thrombus formation, and reduced atrial natriuretic peptide levels. We evaluated LA function in patients with and without IAB matched for LA size. Echocardiograms with LA enlargement were analyzed. Twenty-four patients had IAB, and 16 patients without IAB formed the control group. LA volumes, A-wave acceleration times (At), LA stroke volume (LASV), ejection fraction (LAEF), and kinetic energy (LAKE) were calculated. The control group and patients with IAB had comparable maximal LA volume and diameter (P >.05). Patients with IAB had significantly longer At (115 +/- 39 ms vs 83 +/- 24 ms, P <.01) and smaller LASV (7 +/- 5 mL vs 17 +/- 6 mL, P <.01), LAEF (9% +/- 6% vs 25% +/- 8%, P <.01), and LAKE (20 +/- 14 vs 65 +/- 44 Kdyne/cm/s, P <.01). LAKE varied inversely with P-wave duration (r = -0.51, P <.01). P-wave duration and minimal LA volume were independent determinants of LAEF. Patients with IAB have a sluggish, poorly contractile LA, and the extent of dysfunction is related to the degree of electrical delay from IAB. IAB should be considered a marker of an electromechanically dysfunctional LA and hence a risk factor for atrial fibrillation and congestive heart failure.
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            Tumor necrosis factor alpha induces human atrial myofibroblast proliferation, invasion and MMP-9 secretion: inhibition by simvastatin.

            Tumor necrosis factor alpha (TNFalpha) is implicated in myocardial remodeling, a process in which activated cardiac fibroblasts (myofibroblasts) secrete matrix-degrading metalloproteinases (MMPs) and undergo increased proliferation and invasion. Statins are cholesterol-lowering drugs that also have direct cellular effects, which may underlie their ability to reduce myocardial remodeling. This study investigated the effect of TNFalpha on human cardiac myofibroblast proliferation, invasion and MMP-9 secretion, and determined whether these properties were modulated by simvastatin. Human cardiac myofibroblasts were cultured from right atrial appendage. TNF receptor expression was quantified by immunoblotting. Cell proliferation, invasion, MMP-9 secretion and MMP-9 mRNA expression were determined by cell counting, Matrigel-coated modified Boyden chamber assays, gelatin zymography and RT-PCR, respectively. Human atrial myofibroblasts expressed the TNF-RI and TNF-RII receptor subtypes. TNFalpha (1 ng/ml) induced a 23.1+/-3.9% increase in cell number after 4 days (P<0.001). Additionally, TNFalpha (1-10 ng/ml) significantly (P<0.01) increased myofibroblast invasion, with a concomitant increase in MMP-9 secretion, that was due to increased MMP-9 mRNA levels. Using TNF-R-specific neutralizing antibodies, we determined that these cellular effects of TNFalpha were predominantly TNF-RI-mediated. Simvastatin (0.1-10 mumol/l) concentration dependently inhibited TNFalpha-induced myofibroblast proliferation, invasion and MMP-9 secretion. TNFalpha, acting predominantly via the TNF-R1 receptor, increased human atrial myofibroblast proliferation, invasion and MMP-9 secretion, all of which were inhibited by simvastatin. Inhibition of cytokine-induced cardiac myofibroblast activation by statins provides a rationale for their use in patients with cardiac pathologies characterized by adverse myocardial remodeling.
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              Angiotensin-converting enzyme inhibitors as adjunctive therapy in patients with persistent atrial fibrillation.

              The purpose of the current study was to assess the effect of angiotensin-converting enzyme inhibitor (ACEI) therapy in facilitating cardioversion from persistent atrial fibrillation (AF) and maintaining sinus rhythm. Pharmacologic therapy and electrical cardioversion for AF are often unsuccessful in maintaining long-term sinus rhythm. The current study, a 1-year, prospective follow-up, comprised 47 patients with persistent AF undergoing electrical cardioversion. Patients receiving ACEI were compared with those receiving other medications. The study end point was the number of defibrillation attempts required for atrial defibrillation and the number of hospital admissions. A secondary end point was change in signal-averaged P-wave duration (SAPD) 1 year after successful electrical cardioversion. Of those admitted and requiring electrical defibrillation, the number of defibrillation attempts required for successful cardioversion was significantly less in the ACEI group (P <.001). The incidence rate ratio for admissions comparing recipients of ACEI with others was 0.14 (P =.03). Patients receiving ACEI therapy had significantly lower SAPD at 1 year when compared with the no-ACEI group (135 ms +/- 3 vs 150 ms +/- 2, P =.002). The use of long-term ACEI therapy facilitated electrical defibrillation in patients with persistent AF. ACEI therapy also reduced SAPD, suggesting amelioration of the arrhythmogenic substrate. Furthermore, we confirmed that SAPD is prolonged in patients with persistent AF.

                Author and article information

                S. Karger AG
                April 2008
                10 October 2007
                : 110
                : 1
                : 68-72
                aDivision of Cardiology, Department of Medicine, St. Boniface General Hospital, University of Manitoba, Winnipeg, Man., Canada; bDivision of Cardiology, Department of Medicine, Saint Vincent Hospital, University of Massachusetts, Worcester, Mass., USA
                109409 Cardiology 2008;110:68–72
                © 2007 S. Karger AG, Basel

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                Page count
                Figures: 2, References: 14, Pages: 5
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