Novel vendor-independent 3DE software enables an accurate, reproducible and faster quantitation of RV volumes and ejection fraction. Rather than optional, systematic verification of border tracking quality and manual editing are mandatory to ensure accurate 3DE measurements. These findings are relevant for echocardiography laboratories aiming to implement 3DE for RV analysis for both research and clinical purposes.

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It was shown recently that angiotensin-converting enzyme activity is limited by endogenous inhibition in vivo, highlighting the importance of angiotensin II (ACE2) elimination. The potential contribution of the ACE2 to cardiovascular disease progression was addressed. Serum ACE2 activities were measured in different clinical states (healthy, n=45; hypertensive, n=239; heart failure (HF) with reduced ejection fraction (HFrEF) n=141 and HF with preserved ejection fraction (HFpEF) n=47). ACE2 activity was significantly higher in hypertensive patients (24.8±0.8 U/ml) than that in healthy volunteers (16.2±0.8 U/ml, p=0.01). ACE2 activity further increased in HFrEF patients (43.9±2.1 U/ml, p=0.001) but not in HFpEF patients (24.6±1.9 U/ml) when compared with hypertensive patients. Serum ACE2 activity negatively correlated with left ventricular systolic function in HFrEF, but not in hypertensive, HFpEF or healthy populations. Serum ACE2 activity had a fair diagnostic value to differentiate HFpEF from HFrEF patients in this study. Serum ACE2 activity correlates with cardiovascular disease development: it increases when hypertension develops and further increases when the cardiovascular disease further progresses to systolic dysfunction, suggesting that ACE2 metabolism plays a role in these processes. In contrast, serum ACE2 activity does not change when hypertension progresses to HFpEF, suggesting a different pathomechanism for HFpEF, and proposing a biomarker-based identification of these HF forms.

Mild-to-moderate subclinical glomerular and tubular damage can be identified in many childhood cancer survivors. However, most patients experience some spontaneous recovery from acute nephrotoxicity.

The effect of hydrostatic pressure on physiological intracoronary measurements is usually ignored in the daily clinical practice. Our aim was to investigate this effect on Pd/Pa (distal/aortic pressure) and FFR (fractional flow reserve). 41 FFR measurements between 0.7 and 0.9 were selected. The difference in the height of the orifice and that of the sensor was defined in mm on the basis of 3D coronary reconstruction. Resting Pd/Pa and FFR were adjusted by subtracting the hydrostatic pressure gradient from the distal pressure. Height measurements were also performed from 2D lateral projections for each coronary segment (n = 305). In case of the LAD, each segment was located higher (proximal: