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

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

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

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

Echocardiographic (echo) markers in the different CRT modes.

(A) 3D LVEF (echo); (B) Systolic dyssynchrony index (SDI; echo). (3D - 3-dimensional, BiV–biventricular pacing, LV—left ventricle, LVEF–left ventricular ejection fraction, tLVp—triggered left ventricular pacing).</p

Patient characteristics (n = 17).

Patient characteristics (n = 17).</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

Intermediate CD14⁺⁺CD16⁺ monocytes decline after transcatheter aortic valve replacement and correlate with functional capacity and left ventricular systolic function

<div><p>Background</p><p>Transcatheter aortic valve replacement (TAVR) is the method of choice for patients with severe aortic valve stenosis, who are ineligible or at high risk for surgery. Though TAVR leads to a significant reduction in mortality, a notable amount of patients are re-hospitalized early after TAVR. Parameters or biomarkers predicting outcome are therefore needed to identify patients who benefit most. Specific monocyte subsets have been associated with cardiovascular diseases and were shown to possess prognostic value.</p><p>Methods</p><p>Peripheral blood was drawn before and after transfemoral TAVR with the self-expanding CoreValve, Boston Lotus or the balloon-expanding Edwards Sapien prosthesis. Classical (CD14⁺⁺CD16⁻), intermediate (CD14⁺⁺CD16⁺) and non-classical (CD14⁺CD16⁺⁺) monocyte subsets were determined by flow cytometry. Transthoracic echocardiography was performed before, early after as well as 3 months after the TAVR procedure.</p><p>Results</p><p>No significant differences in the absolute monocyte counts were found after TAVR. A significant decline in the intermediate monocyte population was though observed early after TAVR (pre 4.01±0.38%, post 2.803±0.34%, <i>p≤0</i>.<i>05</i>). Creatinine levels stayed stable after TAVR procedure and intermediate monocytes were associated with worse renal function. Monocyte decline was not related to changes in CRP-, noradrenaline, cortisol or aldosterone-levels. The amount of intermediate monocytes correlated with worse cardiac function and predicted the possibility to reach an improvement in NYHA functional class at 3 months after TAVR.</p><p>Conclusions</p><p>A significant decline of intermediate monocytes occurs shortly after TAVR. High levels of intermediate monocytes were associated with worse cardiac function and predicted poor functional capacity, hinting at a possible prognostic value.</p></div

General traits, comorbidities and functional parameters before TAVR.

<p>General traits, comorbidities and functional parameters before TAVR.</p