The MetaPost AP-VS-Visualizer.

<p>A short software script utilizes the patient´s heart rate (JET simulator rate) and the AV delay as adjusted by the tester to calculate and graphically to display the interval between atrial pacing and sensing of the subsequent QRS complex. AP: atrial pacing, VS: ventricular sensing, AV: atrioventricular, bpm: beats per minute, ms: milliseconds, mV: millivolt.</p

The simulation model.

<p>The model is composed of the JET-Simulator, an ECG monitor, a simulation doll, and an external AVT capable pacemaker. The doll is fitted with atrial and ventricular external pacing wires, simulating an infant after cardiac surgery.</p

Principles of AVT pacing.

<p>(A) External pacing wires are switched at the pacemaker´s inputs. The pacemaker senses ventricular depolarization via the atrial channel and stimulates the atria before the next QRS complex, modified from [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0150704#pone.0150704.ref006" target="_blank">6</a>]. (B) Original electrocardiogram during AVT pacing in a 3-month-old child with postoperative JET. A: atrial input, V: ventricular input, PM: external pacemaker, VS: ventricular sensing, AP: atrial pacing, AV: atrioventricular, PVARP: postventricular atrial refractory period.</p

Simulator testing.

<p>Ten pediatric cardiologists were asked to establish AVT pacing. Ten working steps were assessed: ON, switching on the pacemaker; VDD, choosing the VDD mode; V-SENSE, adjusting ventricular sensing for maximal insensitivity; MTR, selecting the maximal tracking rate at a value 10–20 bpm above the patient´s heart rate; AV-DLY, setting the AV delay to the maximum allowed value; PVARP, adjusting the post ventricular atrial refractory period to 100 ms; RATE, selecting a basic stimulation rate clearly below the patient´s heart rate; R-WAVE, measuring the ventricular input signal; A-SENSE, selecting an atrial sensitivity 50% of the ventricular input signal; WIRES, connecting the pacing wires of the pacemaker. Three points indicate perfect, 2 points suboptimal performance, and 1 point a mistake that impairs safe or effective AVT pacing.</p

The custom-made JET simulator.

<p>JET rates are selected via a rotary switch in the middle of one face. Signals for an ECG monitor are provided at the lateral output sites. Output plugs at the top supply the input signal for the pacemaker. An on/off switch is located at the right side of the device. R: right, L: left, F: foot, N: neutral.</p

Data_Sheet_1_Impact of liver fibrosis and nodules formation on hemodynamics in young adults after total cavopulmonary connection. A magnetic resonance study.pdf

BackgroundThe aim of this study was to analyze the relation between the hepatic fibrosis markers, liver morphology and hemodynamics assessed by magnetic resonance imaging (MRI) after total cavopulmonary connection (TCPC).Materials and methodsAdult patients after TCPC performed in childhood between 1993 and 2003 are the subjects of this observational study. The follow-up protocol consisted of clinical and echocardiographic examination, liver elastography, cardiopulmonary exercise test, MRI hemodynamics and liver morphology assessment and direct enhanced liver fibrosis (ELF) test.ResultsThe cohort consisted of 39 patients (46% female) with a median age at study 26 (IQR 23–28) years and interval from TCPC 21 (IQR 20–23) years. There was no correlation between ELF test and any MRI variables, but procollagen III amino-terminal peptide (PIIINP), a single component of ELF test, correlated significantly with ventricular end-diastolic volume (r = 0.33; p = 0.042) and inferior vena cava flow (r = 0.47; p = 0.003). Fifteen (38%) patients with liver nodules had compared to other 24 patients higher end-diastolic volume (ml/m2) 102.8 ± 20.0 vs. 88.2 ± 17.7; p = 0.023, respectively. PIIINP correlated significantly with inferior vena cava flow (r = 0.56; p = 0.030) and with end-diastolic volume (r = 0.53; p = 0.043), but only in patients with liver nodules.ConclusionGradual progression of liver fibrosis, particularly hepatic arterialization caused by liver nodules formation, increases inferior vena cava flow and subsequent ventricular volume overload may further compromise single ventricle functional reserve in adult patients after TCPC.</p