Association of GT-repeat length polymorphism with HO-1 expression in atrial tissues.

<p>Representative confocal images show the expression of HO-1 in the atria of 8 AF patients and 4 controls (sinus rhythm subjects [SR], left). The number represents the size of GT-repeats in each subject. Relative intensity of HO-1 measured in the α-actin-expressing areas was quantified (right). S/S denotes 4 of 6 patients with shorter GT-repeat (<27 GT) homozygous genotype and L/L denotes 4 of 6 patients with longer (≧27 GT) homozygous genotype. At least 5 random fields were chosen to observe >30 myocytes with scanning and averaging. Data are expressed as mean ± SE. P<0.05; *, #: the different symbols represent the significant difference among groups.</p

GT-repeats modulate the transcriptional activity of HO-1 gene and its responsiveness to rapid pacing.

<p>(<b>A</b>) HL-1 cells were transfected with plasmids containing various lengths of GT-repeats in the HO-1 promoter for 24 hours. The luciferase activity was assayed as described in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0108773#s2" target="_blank">Methods</a>. (<b>B</b>) HL-1 cells were transfected with plasmids containing various lengths of GT-repeats in the HO-1 promoter for 24 hours and/or subsequently received tachypacing (4 Hz) for 2 hours. Each value (mean ± SE, [n = 4]) is expressed as a fold change of luciferase activity relative to the control condition. P<0.05; *, #: the different symbols represent the significant difference among groups.</p

Association of the GT-repeat length polymorphism with fibrosis in AF tissues.

<p>Representative confocal images show fibrosis in the atria of 8 AF patients and 4 controls (sinus rhythm subjects [SR], left). Relative intensity of collagen I was quantified (right). Data are expressed as mean ± SE. P<0.05; *, #: the different symbol represents the significant difference among groups.</p

Demographic and Clinical Characteristics of the Study Population.

<p>ACE = angiotensin converting enzyme; ARB = angiotensin receptor blocker;</p><p>BMI = body mass index; CAD = coronary artery disease; LA = left atrium.</p><p>Demographic and Clinical Characteristics of the Study Population.</p

Association of the GT-repeat length polymorphism with oxidative stress in AF tissues.

<p>An identical paradigm was followed as described in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0108773#pone-0108773-g001" target="_blank">Figure 1</a>. Atrial tissues were stained with DHE to detect ROS generation as described in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0108773#s2" target="_blank">Methods</a>. Representative confocal images show ROS production in the atria of 8 AF patients and 4 controls (sinus rhythm subjects [SR], left). Relative fluorescence density in the α-actin-expressing area was quantified (right). Data are expressed as mean ± SE. P<0.05; *, #: the different symbols represent the significant difference among groups.</p

Association of the GT-repeat length polymorphism with myofibril degradation in AF tissues.

<p>Representative confocal images show myosin degradation in the atria of 8 AF patients and 4 controls (sinus rhythm subjects [SR], left). Relative intensity of MHC in the α-actin-expressing area was quantified (right). Data are expressed as mean ± SE. P<0.05; *: the different symbol represents the significant difference among groups.</p

Cerebral desaturation in heart failure: Potential prognostic value and physiologic basis

<div><p>Cerebral tissue oxygen saturation (SctO₂) reflects cerebral perfusion and tissue oxygen consumption, which decline in some patients with heart failure with reduced ejection fraction (HFrEF) or stroke, especially during exercise. Its physiologic basis and clinical significance remain unclear. We aimed to investigate the association of SctO₂ with oxygen transport physiology and known prognostic factors during both rest and exercise in patients with HFrEF or stroke. Thirty-four HFrEF patients, 26 stroke patients, and 17 healthy controls performed an incremental cardiopulmonary exercise test using a bicycle ergometer. Integrated near-infrared spectroscopy and automatic gas analysis were used to measure cerebral tissue oxygenation and cardiac and ventilatory parameters. We found that SctO₂ (rest; peak) were significantly lower in the HFrEF (66.3±13.3%; 63.4±13.8%,) than in the stroke (72.1±4.2%; 72.7±4.5%) and control (73.1±2.8%; 72±3.2%) groups. In the HFrEF group, SctO₂ at rest (SctO_2rest) and peak SctO₂ (SctO_2peak) were linearly correlated with brain natriuretic peptide (BNP), peak oxygen consumption (), and oxygen uptake efficiency slope (<i>r</i> between -0.561 and 0.677, <i>p</i> < 0.001). Stepwise linear regression showed that SctO_2rest was determined by partial pressure of end-tidal carbon dioxide at rest (P_ETCO_2rest), hemoglobin, and mean arterial pressure at rest (MAP_rest) (adjusted R = 0.681, <i>p</i> < 0.05), while SctO_2peak was mainly affected by peak carbon dioxide production () (adjusted R = 0.653, <i>p</i> < 0.05) in patients with HFrEF. In conclusion, the study delineates the relationship of cerebral saturation and parameters associated with oxygen delivery. Moreover, SctO_2peak and SctO_2rest are correlated with some well-recognized prognostic factors in HFrEF, suggesting its potential prognostic value.</p></div

Area under curve of hemodynamic variables during 1^st PLRT and VO_2VAT at 1st CPET.

<p>VAT: ventilatory anaerobic threshold; CD: change difference from HU to LR; CR: change ratio from HU to LR = CD/HU; HU: head-up; LR: leg raise; LR5: leg raise at the 5th minute; SR: supine rest; CO: cardiac output; CI: cardiac index; SV: stroke volume; SVCom: stroke volume compliance; SVIcom: stroke volume index compliance; TFC: thoracic fluid content; TPR: total peripheral resistance; TPRI: total peripheral resistance index</p><p>Area under curve of hemodynamic variables during 1^st PLRT and VO_2VAT at 1st CPET.</p

Risk of Ischemic Thromboembolism in AF Patients with One Additional Risk Factor of CHA₂DS₂-VASc Score^*.

<p>Risk of Ischemic Thromboembolism in AF Patients with One Additional Risk Factor of CHA₂DS₂-VASc Score^{<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0151485#t004fn001" target="_blank">*</a>}.</p

AnnuaI Risk of Ischemic thromboembolism by CHA₂DS₂-VASc Score among AF patients without anticoagulants.

<p>AnnuaI Risk of Ischemic thromboembolism by CHA₂DS₂-VASc Score among AF patients without anticoagulants.</p