8 research outputs found

    Mean P-wave duration measured in a single lead over all sectors (95% CI).

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    <p>The two sectors which comprise the manoeuvres are shaded grey. We observed significant differences for ITH and MM vs BL during the manoeuvre (both p<0.001). The P-wave duration did not change during the course of the BL (p = 0.99) and AP (p = 0.94) manoeuvre. All analyses were adjusted for PAF status, heart rate, age, BMI, and sex. BL = baseline (normal breathing). ITH = inspiration through a threshold load (simulating an obstructive hypopnea). MM = Mueller manoeuvre (simulating an obstructive apnea). AP = end-expiratory breath holding (simulating central apnea).</p

    Simulated Obstructive Sleep Apnea Increases P-Wave Duration and P-Wave Dispersion

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    <div><p>Background</p><p>A high P-wave duration and dispersion (Pd) have been reported to be a prognostic factor for the occurrence of paroxysmal atrial fibrillation (PAF), a condition linked to obstructive sleep apnea (OSA). We tested the hypothesis of whether a short-term increase of P-wave duration and Pd can be induced by respiratory manoeuvres simulating OSA in healthy subjects and in patients with PAF.</p><p>Methods</p><p>12-lead-electrocardiography (ECG) was recorded continuously in 24 healthy subjects and 33 patients with PAF, while simulating obstructive apnea (Mueller manoeuvre, MM), obstructive hypopnea (inspiration through a threshold load, ITH), central apnea (AP), and during normal breathing (BL) in randomized order. The P-wave duration and Pd was calculated by using dedicated software for ECG-analysis.</p><p>Results</p><p>P-wave duration and Pd significantly increased during MM and ITH compared to BL in all subjects (+13.1ms and +13.8ms during MM; +11.7ms and +12.9ms during ITH; p<0.001 for all comparisons). In MM, the increase was larger in healthy subjects when compared to patients with PAF (p<0.05).</p><p>Conclusion</p><p>Intrathoracic pressure swings through simulated obstructive sleep apnea increase P-wave duration and Pd in healthy subjects and in patients with PAF. Our findings imply that intrathoracic pressure swings prolong the intra-atrial and inter-atrial conduction time and therefore may represent an independent trigger factor for the development for PAF.</p></div

    Patient characteristics.

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    <p>AU = Agatston units; CACS = coronary artery calcium score; COPD = chronic obstructive lung disease; CRP = C-reactive protein; FEV<sub>1</sub> = forced expiration in one second; FVC = forced vital capacity; GOLD = Global Initiative for Obstructive Lung Disease; MACE = major adverse cardiovascular event; PY = pack years of smoking; SPECT = single-photon emission computerized tomography</p><p><sup>a</sup> Data available from 71 (87.7%) COPD subjects and 67 (82.7%) control subjects</p><p><sup>b</sup> Data available from 79 (97.5%) COPD subjects and 49 (60.5%) control subjects</p><p>Patient characteristics.</p

    Predictors of MACE in multivariable analysis adjusted for age, male sex, and number of cardiovascular risk factors.

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    <p>AU = Agatston units; BMI = body mass index; CACS = coronary artery calcium score; GOLD = Global Initiative for Chronic Obstructive Lung Disease; MACE = major adverse cardiovascular event; SPECT = single-photon emission computerized tomography</p><p>Predictors of MACE in multivariable analysis adjusted for age, male sex, and number of cardiovascular risk factors.</p
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