Activation of circulating platelets in CHF.

<p>Platelet-bound fibrinogen is significantly increased in CHF-placebo (mean fluorescence intensity (MFI): Sham 88±4, CHF-placebo 104±6, p<0.05) and reduced following treatment with PETN (89±7, p<0.05 vs. CHF-placebo), n = 8–12.</p

Hemodynamics and descriptive parameters from placebo- and PETN-treated CHF rats compared with sham-operated placebo-treated rats.

<p>CHF was defined by elevated left ventricular end-diastolic pressure (LVEDP, >15 mmHg) and impaired left ventricular function, values are means ± standard error (* = p<0.01 vs. Sham;^# = p<0.05 vs. CHF Placebo). MI = myocardial infarction; LV = left ventricle; RV = right ventricle; BW = body weight; LVSP = left-ventricular systolic pressure; LVEDP = left-ventricular end-diastolic pressure; MPV = mean platelet volume</p><p>Hemodynamics and descriptive parameters from placebo- and PETN-treated CHF rats compared with sham-operated placebo-treated rats.</p

Maximal aggregation of platelets from CHF rats ex vivo.

<p>Maximal ADP-induced aggregation was significantly enhanced in CHF-placebo vs. sham-operated animals at different ADP concentrations and normalized and partly even decreased following chronic PETN treatment, n = 10–12; <b>I-V</b> = different ADP concentrations in detail (1/2/5/10/20μM ADP).</p

Final aggregation of platelets from CHF rats ex vivo.

<p>Final ADP-induced aggregation was significantly enhanced in CHF-placebo vs. sham-operated animals at different ADP concentrations and normalized and partly even decreased following chronic PETN treatment, n = 10–12; <b>I-V</b> = different ADP concentrations in detail (1/2/5/10/20μM ADP).</p

Fig 5 -

(A) QRS width; (B) Max. LV delay depending on the amount of QRS shortening by tLVp with regard to intrinsic QRS complex (BiV–biventricular pacing, LV—left ventricle, tLVp—triggered left ventricular pacing); n = 9 for ≤20ms, n = 8 for >20ms.</p

LV delay, measured by 2D strain (echo) in the different CRT modes.

Max. (BiV–biventricular pacing, LV—left ventricle, LVEF–left ventricular ejection fraction, tLVp—triggered left ventricular pacing).</p

Fig 1 -

Electrogram (EGM) and electrocardiogram (ECG) of the three different settings: 1. optimized bi-ventricular-stimulation (BiV); 2. Physiological AV nodal conduction without triggered left ventricular pacing (tLVp-off); 3. TLVp algorithm turned on (tLVp-on) with physiological AV nodal conduction (a), and after premature ventricular contraction (PVC; b). (ECG–electrocardiogram, IEGM–internal electrogram, PVC—premature ventricular contraction, tLVp—triggered left ventricular pacing).</p

Correlations of intermediate monocytes with cortisol, aldosterone and noradrenaline.

<p>Correlations (Spearman) between intermediate monocyte measured by flow cytometry and cortisol (cor), aldosterone (aldo) as well as noradrenaline (nor). (a) Intermediate monocyte pre TAVR vs. cor, aldo, nor pre TAVR. (b) Intermediate monocyte post TAVR vs. cor, aldo, nor post TAVR. Correlations among cor, aldo and nor are also shown. On the top of each graph: pairwise correlation value and relative significance (negative value indicates inverse correlation); on bottom: bivariate scatterplot. ** p<0.01.</p

QRS width (ecg) in the different CRT modes.

(BiV–biventricular pacing, LV—left ventricle, tLVp—triggered left ventricular pacing).</p

Electrocardiographic and echocardiographic markers depending on the amount of QRS shortening by tLVp with regard to intrinsic QRS complex.

Electrocardiographic and echocardiographic markers depending on the amount of QRS shortening by tLVp with regard to intrinsic QRS complex.</p