Datasheet1_Incidence and prognostic significance of malignant arrhythmias during (repetitive) Holter electrocardiograms in patients with pulmonary hypertension.docx

BackgroundIn patients with pulmonary hypertension (PH), increased pulmonary vascular resistance (PVR) may lead to increased right ventricular afterload and cardiac remodelling, potentially providing the substrate for ventricular arrhythmias. Studies dealing with long term monitoring of patients with PH are rare. The present study evaluated the incidence and the types of arrhythmias retrospectively recorded by Holter ECG in patients with newly detected PH during a long-term Holter ECG follow-up. Moreover, their impact on patient survival was evaluated.Patients and methodsMedical records were screened for demographic data, aetiology of PH, incidence of coronary heart disease, level of brain natriuretic peptide (BNP), results from Holter ECG monitoring, 6-minute walk test distance, echocardiographic data and hemodynamic data derived from right heart catheterization. Two subgroups were analyzed: 1. patients (n = 65) with PH (group 1 + 4) and derivation of at least 1 Holter ECG within 12 months from initial detection of PH and 2. patients (all PH etiologies, n = 59) with 3 follow-up Holter ECGs. The frequency and complexity of premature ventricular contractions (PVC) was classified into “lower” and “higher” (=non sustained ventricular tachycardia, nsVT) burden.ResultsHolter ECG revealed sinus rhythm (SR) in most of the patients (n = 60). Incidence of atrial fibrillation (AFib) was low (n = 4). Patients with premature atrial contractions (PAC) tend to have a shorter period of survival (p = 0.098), PVC were not correlated with significant survival differences. During follow-up PAC and PVC were common in all PH groups. Holter ECG revealed non sustained ventricular tachycardia in 19/59 patients [(32.2%); n = 6 during first Holter-ECG, n = 13 during second/third Holter-ECG]. In all patients suffering from nsVT during follow-up previous Holter ECG revealed multiform/repetitive PVC. PVC burden was not linked to differences in systolic pulmonary arterial pressure, right atrial pressure, brain natriuretic peptide and results of six-minute walk test.ConclusionPatients with PAC tend to have a shortened survival. None of the evaluated parameters (BNP, TAPSE, sPAP) was correlated with the development of arrhythmias. Patients with multiform/repetitive PVC seem to be at risk for ventricular arrhythmias.</p

Writing Kingship and Power:Studies in Honour of Simon Keynes

<p>Scatter plots and results of linear regression analyses are shown for 6MWD (A), mean pulmonary arterial pressure (B), pulmonary vascular resistance (C), cardiac index (D), and pulmonary arterial wedge pressure (E). 6MWD, 6-minute walk distance; iPAH, idiopathic pulmonary arterial hypertension.</p

Angiopoetin-1 levels and baseline parameters as predictors of clinical worsening according to patient population.

<p>Angiopoetin-1 levels and baseline parameters as predictors of clinical worsening according to patient population.</p

Angiopoietin-1 levels and other baseline parameters as predictors of overall mortality/transplant in patients with different PH subtypes.

<p>Angiopoietin-1 levels and other baseline parameters as predictors of overall mortality/transplant in patients with different PH subtypes.</p

Baseline characteristics.

<p>Baseline characteristics.</p

Associations of angiopoietin-1 with 6MWD and pulmonary hemodynamics in PH-LHD.

<p>Scatter plots and results of linear regression analyses are shown for 6MWD (A), mean pulmonary arterial pressure (B), pulmonary vascular resistance (C), cardiac index (D), and pulmonary arterial wedge pressure (E). 6MWD, 6-minute walk distance; PH-LHD, pulmonary hypertension due to left heart disease.</p

Kaplan—Meier survival and time to clinical worsening curves stratified by angiopoietin-1 quartile.

<p>Analyses were conducted separately in patients with idiopathic pulmonary arterial hypertension (A–B), connective tissue disease-associated pulmonary arterial hypertension (C–D), pulmonary hypertension due to left heart disease (E–F), and chronic thromboembolic pulmonary hypertension (G–H).</p

Additional file 1: Figure S1. of Survival with sildenafil and inhaled iloprost in a cohort with pulmonary hypertension: an observational study

Kaplan–Meier plots of cumulative transplant-free survival in patients with pulmonary arterial hypertension associated with collagen-vascular disease, idiopathic pulmonary arterial hypertension, and pulmonary arterial hypertension associated with systemic-to-pulmonary shunt. Data are shown for patients who were treated with iloprost followed by addition of sildenafil (iloprost/sildenafil) or sildenafil followed by addition of iloprost (sildenafil/iloprost). (PDF 853 kb

Data_Sheet_1_Hepatorenal dysfunction in patients with chronic thromboembolic pulmonary hypertension.docx

BackgroundCardiac interactions with organs such as the liver or kidneys have been described in different cardiovascular diseases. However, the clinical relevance of hepatorenal dysfunction in chronic thromboembolic pulmonary hypertension (CTEPH) remains unclear. We determined the association of hepatorenal dysfunction (measured using the Model for End-stage Liver Disease Sodium [MELDNa] score) with right heart function and survival in patients with CTEPH.MethodsWe analyzed all patients with CTEPH in the Giessen Pulmonary Hypertension Registry who had available MELDNa scores and were not taking vitamin K antagonists. The MELDNa score was calculated as MELD score − serum Na − (0.025 * MELD score * (140 − serum Na)) + 140; the MELD score was calculated as 10*(0.957*ln(creatinine)+0.378*ln(bilirubin)+1.12*ln(International Normalized Ratio))+6.43.ResultsSeventy-two patients were included (74% female; median [Q1, Q3] MELDNa: 9 [6, 11]). MELDNa correlated well with right atrial and ventricular function and pulmonary hemodynamics. Forward regression analysis revealed that hepatorenal dysfunction mainly depends on right atrial strain and tricuspid regurgitation, but not right ventricular systolic dysfunction. Hepatorenal dysfunction predicted mortality at baseline and follow-up (adjusted hazard ratios [95% confidence intervals] per unit increase of MELDNa: 1.6 [1.1, 2.4] and 1.8 [1.1, 2.9], respectively). Changes in hepatorenal function also predicted mortality.ConclusionHepatorenal dysfunction in CTEPH is primarily associated with venous congestion rather than cardiac forward failure. As a surrogate parameter for hepatorenal dysfunction, MELDNa is a simple method to identify at-risk patients at baseline and follow-up.</p

Flow chart of patient selection.

<p>RHC: right heart catheterization; PEA: pulmonary endarterectomy; PH: pulmonary hypertension.</p