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Aims: The combined therapeutic impact of atrial overdrive pacing (AOP) and cardiac resynchronization therapy (CRT) on central sleep apnoea (CSA) in chronic heart failure (CHF) so far has not been investigated. We aimed to evaluate the effect of CRT alone and CRT + AOP on CSA in CHF patients and to compare the influence of CRT on CHF between CSA positive and CSA negative patients., Methods and Results: Thirty patients with CRT indication underwent full night polysomnography, echocardiography, exercise testing, and neurohumoral evaluation before and 3 months after CRT implantation. In CSA positive patients (60%), two additional sleep studies were conducted after 3 months of CRT, with CRT alone or CRT + AOP, in random order. Cardiac resynchronization therapy resulted in significant improvements of NYHA class, left ventricular ejection fraction, N-terminal pro-brain natriuretic peptide, VO(2)max, and quality of life irrespective of the presence of CSA. Cardiac resynchronization therapy also reduced the central apnoea-hypopnoea index (AHI) (33.6 +/- 14.3 vs. 23.8 +/- 16.9 h(-1); P < 0.01) and central apnoea index (17.3 +/- 14.1 vs. 10.9 +/- 13.9 h(-1); P < 0.01) without altering sleep stages. Cardiac resynchronization therapy with atrial overdrive pacing resulted in a small but significant additional decrease of the central AHI (23.8 +/- 16.9 vs. 21.5 +/- 16.9 h(-1); P < 0.01)., Conclusion: In this study, CRT significantly improved CSA without altering sleep stages. Cardiac resynchronization therapy with atrial overdrive pacing resulted in a significant but minor additional improvement of CSA. Positive effects of CRT were irrespective of the presence of CSA.

Background: In patients with chronic heart failure (CHF) and conduction delay, biventricular (BiV) and left ventricular (LV) pacing similarly improve systolic function at resting heart rates. We hypothesized that BiV and univentricular pacing differentially affect contractile function at increasing heart rates., Methods and Results: Twenty-two patients (aged 66+/-2 years, QRS 179+/-8 ms, LV ejection fraction 23+/-1%) underwent cardiac catheterization before device implantation to measure LV hemodynamics at baseline (rate 68+/-2 bpm; sinus rhythm n=18; atrial fibrillation n=4) and during BiV, LV, and right ventricular (RV) stimulation at 80, 100, 120, and 140 bpm. BiV and LV pacing at 80 bpm equally augmented dP/dtmax as compared with baseline and RV pacing (P<0.001). Stimulation rate significantly interacted with the effect of BiV, LV, and RV pacing on LV end-diastolic pressure (LVEDP), systolic pressure (LVSP), and dP/dtmax. Increasing the rate from 80 to 140 bpm enhanced dP/dtmax from 913+/-28 to 1119+/-50 mm Hg/s during BiV stimulation (P<0.001) but had no significant effect on contractility during single-site LV (951+/-47 versus 1002+/-54 mm Hg/s) or RV (800+/-46 versus 881+/-49 mm Hg/s) pacing. At 140 bpm, LVEDP was lower and LVSP higher during BiV pacing than during RV and LV pacing (LVEDP 12+/-1 versus 17+/-1 and 16+/-1 mm Hg, P<0.001; LVSP 112+/-5 versus 106+/-5 and 108+/-6 mm Hg, P<0.01 and P=0.09; BiV versus RV and LV pacing, respectively)., Conclusions: Different modes of ventricular stimulation alter the in vivo force-frequency relation of CHF patients. In contrast to single-site LV and RV pacing, contractile function improves with increasing heart rates during BiV stimulation. This effect may contribute to the enhanced exercise capacity during BiV pacing and could provide a functional benefit over LV-only pacing in patients for whom resynchronization therapy is indicated.

Aims: Intravenous iron therapy (IVIT) is known to improve functional status in chronic heart failure (CHF) patients. The exact mechanism is not completely understood. We correlated magnetic resonance imaging (MRI) patterns of T2* iron signal in various organs to systemic iron and exercise capacity (EC) in CHF before and after IVIT. Methods and results: We prospectively analysed 24 patients with systolic CHF for T2* MRI pattern of the left ventricle (LV), small and large intestines, spleen, liver, skeletal muscle, and brain for iron. In 12 patients with iron deficiency (ID), we restored iron deficit by IVIT using ferric carboxymaltose. The effects after 3 months were analysed by spiroergometry and MRI. Patients with vs. without ID showed lower blood ferritin, haemoglobin (76 ± 63 vs. 196 ± 82 μg/L and 12.3 ± 1.1 vs. 14.2 ± 1.1 g/dL, all P < 0.002), and in trend a lower transferrin saturation (TSAT) (19.1 [13.1; 28.2] vs. 25.1 [21.3; 29.1] %, P = 0.05). Spleen and liver iron was lower as expressed by higher T2* value (71.8 [66.4; 93.1] vs. 36.9 [32.9; 51.7] ms, P < 0.002 and 33.5 ± 5.9 vs. 28.8 ± 3.9 ms, and P < 0.03). There was a strong trend for a lower cardiac septal iron content in ID (40.6 [33.0; 57.3] vs. 33.7 [31.3; 40.2] ms, P = 0.07). After IVIT, ferritin, TSAT, and haemoglobin increased (54 [30; 104] vs. 235 [185; 339] μg/L, 19.1 [13.1; 28.2] vs. 25.0 [21.0; 33.7] %, 12.3 ± 1.1 vs. 13.3 ± 1.3 g/L, all P < 0.04). Peak VO2 improved (18.2 ± 4.2 vs. 20.9 ± 3.8 mL/min/kg−1, P = 0.05). Higher peak VO2 at anaerobic threshold was associated with higher blood ferritin, reflecting higher metabolic exercise capacity after therapy (r = 0.9, P = 0.0009). Increase in EC was associated with haemoglobin increase (r = 0.7, P = 0.034). LV iron increased by 25.4% (48.5 [36.2; 64.8] vs. 36.2 [32.9; 41.9] ms, P < 0.04). Spleen and liver iron increased by 46.4 and 18.2%, respectively (71.8 [66.4; 93.1] vs. 38.5 [22.4; 76.9] ms, P < 0.04 and 33.5 ± 5.9 vs. 27.4 ± 8.6 ms, P < 0.007). Iron in skeletal muscle, brain, intestine, and bone marrow remained unchanged (29.6 [28.6; 31.2] vs. 30.4 [29.7; 30.7] ms, P = 0.7, 81.0 ± 6.3 vs. 82.9 ± 9.9 ms, P = 0.6, 34.3 ± 21.4 vs. 25.3 ± 14.1 ms, P = 0.2, 9.4 [7.5; 21.8] vs. 10.3 [6.7; 15.7] ms, P = 0.5 and 9.8 ± 1.5 vs. 13.7 ± 8.9 ms, P = 0.1). Conclusions: CHF patients with ID showed lower spleen, liver, and in trend lower cardiac septal iron. After IVIT, iron signal of the left ventricle as well as spleen and liver increased. Improvement in EC was associated with increase in haemoglobin after IVIT. In ID, liver, spleen, and brain but not heart iron were associated with markers of systemic ID. [ABSTRACT FROM AUTHOR]

Aims Ebstein's anomaly (EA) involves a displaced and dysplastic tricuspid valve resulting in an atrialized portion of the right ventricle and an en largement of the functional right ventricle and right atrium. Biomarkers targeting heart failure such as brain natriuretic peptide (BNP) or haematological parameters [haemoglobin (Hb) and haematocrit (Hct)] are upregulated in states of pulmonary hypoperfusion. We hypothesized that decreased pulmonary perfusion dependent on the stage of right heart failure is a possible mechanism in EA, and that it can be correlated with cardiac magnetic resonance (CMR) parameters. The aim of this study was to investigate the relationship between BNP and haematological parameters with functional parameters from CMR and exercise testing in patients with EA. Methods and results Twenty-five patients with non-corrected EA were studied prospectively (mean age 26 ± 14 years). BNP level was increased (74 ± 127 ng/L), and in 16% markedly above the heart failure cut-off level of 100 ng/L Hb and Hct were increased above normal levels in 20 and 24% of patients, respectively. BNP and Hct/Hb correlated with CMR [total right/left (R/L)-Volume-Index, right atrium-end-diastolic volume index (EDVi), functional right ventricle (fRV)-EDVi, fRV-ejection fraction (EF), tricuspid regurgitation, pulmonary artery flow, and left ventricular EF] and exercise testing [workload/kg, oxygen uptake (VO2), ventilatory response to carbon dioxide production (VE/VCO2), oxygen (O2) pulse, and heart rate reserve]. The higher BNP and haematological parameters, the higher was the disease severity and the more limited was the physical exercise capacity. Conclusion In this EA cohort, BNP levels and haematological parameters correlated well with functional data from CM Rand exercise testing. The total R/L-Volume-Index and BNP, and to some extent hematological parameters, may be useful as prognostic markers in patients with EA. [ABSTRACT FROM AUTHOR]