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Background: Detection of pulmonary perfusion defects is the recommended approach for diagnosing chronic thromboembolic pulmonary hypertension (CTEPH). This is currently achieved in a clinical setting using scintigraphy. Phase‐resolved functional lung (PREFUL) magnetic resonance imaging (MRI) is an alternative technique for evaluating regional ventilation and perfusion without the use of ionizing radiation or contrast media. Purpose: To assess the feasibility and image quality of PREFUL‐MRI in a multicenter setting in suspected CTEPH. Study Type: This is a prospective cohort sub‐study. Population: Forty‐five patients (64 ± 16 years old) with suspected CTEPH from nine study centers. Field Strength/Sequence: 1.5 T and 3 T/2D spoiled gradient echo/bSSFP/T2 HASTE/3D MR angiography (TWIST). Assessment: Lung signal‐to‐noise ratio (SNR) and contrast‐to‐noise ratio (CNR) were compared between study centers with different MRI machines. The contrast between normally and poorly perfused lung areas was examined on PREFUL images. The perfusion defect percentage calculated using PREFUL‐MRI (QDPPREFUL) was compared to QDP from the established dynamic contrast‐enhanced MRI technique (QDPDCE). Furthermore, QDPPREFUL was compared between a patient subgroup with confirmed CTEPH or chronic thromboembolic disease (CTED) to other clinical subgroups. Statistical Tests: t‐Test, one‐way analysis of variance (ANOVA), Pearson's correlation. Significance level was 5%. Results: Significant differences in lung SNR and CNR were present between study centers. However, PREFUL perfusion images showed a significant contrast between normally and poorly perfused lung areas (mean delta of normalized perfusion −4.2% SD 3.3) with no differences between study sites (ANOVA: P = 0.065). QDPPREFUL was significantly correlated with QDPDCE (r = 0.66), and was significantly higher in 18 patients with confirmed CTEPH or CTED (57.9 ± 12.2%) compared to subgroups with other causes of PH or with excluded PH (in total 27 patients with mean ± SD QDPPREFUL = 33.9 ± 17.2%). Data Conclusion: PREFUL‐MRI could be considered as a non‐invasive method for imaging regional lung perfusion in multicenter studies. Level of Evidence: 3 Technical Efficacy: Stage 1 [ABSTRACT FROM AUTHOR]

Aims: The purpose of this study was to evaluate the effect of transient local myocardial gene transfer of iNOS on cardiac function in a large mammal animal model of heart failure induced by chronic ischemia. Methods: Chronic myocardial ischemia was induced using a minimally invasive model in 16 landrace pigs. Upon demonstration of heart failure, eight animals were treated with liposome-mediated iNOS-gene-transfer by local intramyocardial injection; eight animals received a sham procedure to serve as control. Results: The transmurality of late enhancement (control: 46.4%, iNOS: 35.9%; p < 0.05) was significantly decreased in the ischemic area in the iNOS-treated group. Wall thickness at end-systole (6.8 mm vs. 5.9 mm, p < 0.001) and at end-diastole (5.4 mm vs. 4.2 mm, p < 0.001) were significantly higher in the therapy group. Additionally, the regional wall motion at the level of the ischemic region was 3.5 mm in the therapy group while it was significantly less (3.0 mm, p < 0.001) in the control group. Conclusions: Our findings demonstrate that transient iNOS overexpression potentially leads to a significant decrease of regional late enhancement with a positive effect on regional cardiac function in the ischemic area in a large animal model of postischemic heart failure. [ABSTRACT FROM AUTHOR]

The number of adults with congenital heart defects (CHD) is steadily rising and amounts to approximately 360,000 in Germany. CHD is often associated with pulmonary hypertension (PH), which may develop early in untreated CHD. Despite timely treatment of CHD, PH not infrequently persists or recurs in older age and is associated with significant morbidity and mortality.The revised European Society of Cardiology/European Respiratory Society 2022 guidelines for the diagnosis and treatment of PH represent a significant contribution to the optimized care of those affected. However, the topic of "adults with congenital heart disease" is addressed only relatively superficial in these guidelines. Therefore, in the present article, this topic is commented in detail from the perspective of congenital cardiology., Competing Interests: Harald Kaemmerer: Unabhängig von diesem Manuskript Sponsorship and honoraria Janssen/Johnson & Johnson; Bristol Myers Squibb. Steering Board COMPERA International.Gerhard Paul Diller: Advisory consultancy work for Janssen/Johnson & Johnson.Ingo Dähnert: Proctortätigkeit für Occlutech und Medtronic, Studien für Janssen und Novartis, Advisory Board für Actelion/Janssen.Christina A. Eichstaedt: C. A. E. ist Miterfinderin des europäischen Patents (EP3507380) “Gene panel specific for pulmonary hypertension and its uses”. CAE hat von msd Vortragshonorare erhalten, unabhängig von dieser Arbeit.Andreas Eicken: Keine Interessenkonflikte.Annika Freiberger: Keine Interessenkonflikte.Sebastian Freilinger: Keine Interessenkonflikte.Ralf Geiger: Keine Interessenkonflikte.Matthias Gorenflo: Advisory Board für Janssen.Ekkehard Grünig: E. G. hat Honorare für Vorträge/Konsultationen von Bayer/MSD, Ferrer, GEBRO, GSK, Janssen und OMT erhalten. Forschungsförderung für klinische Studien wurde von Acceleron, Actelion, BayerHealthCare, MSD, Bellerophon, GossamerBio, Janssen, Novartis, OMT, Pfizer, REATE und United Therapeutics erhalten.Alfred Hager: Unabhängig von diesem Manuskript erhielt A. H. Reisekostenerstattungen von Actelion, Pfizer, GlaxoSmithKline, Lilly und OMT; Rednergelder von Encysive, Pfizer, Actelion, Medtronic, Schiller, GlaxoSmithKline, OMT, AOP Orphan und Janssen; Autorenvergütungen von Actelion; Beraterhonorare von Actelion, Bayer, Ethypharm und GlaxoSmithKline; er hält Aktien von Merck Inc., Merck KGaA, Johnson & Johnson, Pfizer und Abbott.Michael Huntgeburth: Honorare Advisory-Board Janssen-Cilag, Johnson & Johnson.Ann-Sophie Kaemmerer-Suleiman: Keine Interessenkonflikte.Rainer Kozlik-Feldmann: Teaching-Kurse für Occlutech, Proktortätigkeit für Abbott (Amplatzer).Astrid E. Lammers: CEC chair and advisory consultancy work for Janssen/Johnson & Johnson.Nicole Nagdyman: Keine Interessenkonflikte.Sebastian Michel: Keine Interessenkonflikte.Kai Helge Schmidt: Vortragshonorare von Janssen, MSD und Abbott.Anselm Uebing: Keine Interessenkonflikte.Fabian von Scheidt: Keine Interessenkonflikte.Christian Apitz: Honorare für Vortragstätigkeit und Advisory Board für Janssen., (Thieme. All rights reserved.)

The number of adults with congenital heart disease (CHD) is steadily rising and amounts to approximately 360,000 in Germany. CHD is often associated with pulmonary arterial hypertension (PAH), which may develop early in untreated CHD. Despite timely treatment of CHD, PAH often persists or recurs in older age and is associated with significant morbidity and mortality.The revised European Society of Cardiology/European Respiratory Society 2022 guidelines for the diagnosis and treatment of PH represent a significant contribution to the optimized care of those affected. However, the topic of "adults with congenital heart defects" is addressed only relatively superficially in these guidelines. Therefore, this article addresses the perspective of congenital cardiology in greater depth., Competing Interests: Harald Kaemmerer: Unabhängig von diesem Manuskript Sponsorship and honoraria Janssen/Johnson & Johnson; Bristol Myers Squibb. Steering Board COMPERA International.Gerhard Paul Diller: Advisory consultancy work for Janssen/Johnson & Johnson.Ingo Dähnert: Proctortätigkeit für Occlutech und Medtronic, Studien für Janssen und Novartis, Advisory Board für Actelion/Janssen.Christina A. Eichstaedt: C.A.E. ist Miterfinderin des europäischen Patents (EP3507380) “Gene panel specific for pulmonary hypertension and its uses”. CAE hat von msd Vortragshonorare erhalten, unabhängig von dieser Arbeit.Andreas Eicken: keine Interessenkonflikte.Annika Freiberger: keine Interessenkonflikte.Sebastian Freilinger: keine Interessenkonflikte.Ralf Geiger: keine Interessenkonflikte.Matthias Gorenflo: Advisory Board für Janssen.Ekkehard Grünig: E.G. hat Honorare für Vorträge/Konsultationen von Bayer/MSD, Ferrer, GEBRO, GSK, Janssen und OMT erhalten. Forschungsförderung für klinische Studien wurde von Acceleron, Actelion, BayerHealthCare, MSD, Bellerophon, GossamerBio, Janssen, Novartis, OMT, Pfizer, REATE und United Therapeutics erhalten.Alfred Hager: Unabhängig von diesem Manuskript erhielt A.H. Reisekostenerstattungen von Actelion, Pfizer, GlaxoSmithKline, Lilly und OMT; Rednergelder von Encysive, Pfizer, Actelion, Medtronic, Schiller, GlaxoSmithKline, OMT, AOP Orphan und Janssen; Autorenvergütungen von Actelion; Beraterhonorare von Actelion, Bayer, Ethypharm und GlaxoSmithKline; er hält Aktien von Gilead, Merck Inc., Merck KGaA, Johnson &Johnson, Pfizer, Abbvie und Takeda.Ulrike Herberg: keine Interessenkonflikte.Michael Huntgeburth: Honorare Advisory-Board Janssen-Cilag, Johnson & Johnson.Ann-Sophie Kaemmerer: keine Interessenkonflikte.Rainer Kozlik-Feldmann: Teaching Kurse für Occlutech, Proktortätigkeit für Abbott (Amplatzer).Astrid E. Lammers: CEC chair and advisory consultancy work for Janssen/Johnson & Johnson.Nicole Nagdyman: keine Interessenkonflikte.Sebastian Michel: keine Interessenkonflikte.Kai Helge Schmidt: Vortragshonorare von Janssen, MSD und Abbott.Anselm Uebing: keine Interessenkonflikte.Fabian von Scheidt: keine Interessenkonflikte.Christian Apitz: Honorare Janssen., (Thieme. All rights reserved.)

Pulmonary hypertension associated with left heart disease (PH-LHD) corresponds to group two of pulmonary hypertension according to clinical classification. Haemodynamically, this group includes isolated post-capillary pulmonary hypertension (IpcPH) and combined post- and pre-capillary pulmonary hypertension (CpcPH). PH-LHD is defined by an mPAP > 20 mmHg and a PAWP > 15 mmHg, pulmonary vascular resistance (PVR) with a cut-off value of 2 Wood Units (WU) is used to differentiate between IpcPH and CpcPH. A PVR greater than 5 WU indicates a dominant precapillary component. PH-LHD is the most common form of pulmonary hypertension, the leading cause being left heart failure with preserved (HFpEF) or reduced ejection fraction (HFmrEF, HFrEF), valvular heart disease and, less commonly, congenital heart disease. The presence of pulmonary hypertension is associated with increased symptom burden and poorer outcome across the spectrum of left heart disease. Differentiating between group 1 pulmonary hypertension with cardiac comorbidities and PH-LHD, especially due to HFpEF, is a particular challenge. Therapeutically, no general recommendation for the use of PDE5 inhibitors in HFpEF-associated CpcPH can be made at this time. There is currently no reliable rationale for the use of PAH drugs in IpcPH, nor is therapy with endothelin receptor antagonists or prostacyclin analogues recommended for all forms of PH-LHD., Competing Interests: A.S.: Vortragshonorare im Zusammenhang hiermit: Actelion, Abbott, Edwards, MSD, Forschungsgrands: Abbott.S.S.: Vortragshonorare und Reiseunterstützung von MSD und Johnson & Johnson.A.Y.: Reports personal fees from MSD outside the submitted work.A.J.R.: Vortragshonorare von AstraZeneca und Bayer sowie Reisekostenunterstützung von Johnson & Johnson und Servier, alles ohne Zusammengang mit dem vorliegenden Manuskript.E.P.-J.: Reisekostenunterstützung OMT, Actelion, Boehringer-Ingelheim sowie Honorar von Actelion.K.H.S.: Vortragshonorare von Janssen, MSD und Abbott.Die weiteren Autoren haben keine Interessenkonflikte angegeben., (Thieme. All rights reserved.)

Aims: To systematically assess late outcomes of acute pulmonary embolism (PE) and to investigate the clinical implications of post-PE impairment (PPEI) fulfilling prospectively defined criteria., Methods and Results: A prospective multicentre observational cohort study was conducted in 17 large-volume centres across Germany. Adult consecutive patients with confirmed acute symptomatic PE were followed with a standardized assessment plan and pre-defined visits at 3, 12, and 24 months. The co-primary outcomes were (i) diagnosis of chronic thromboembolic pulmonary hypertension (CTEPH), and (ii) PPEI, a combination of persistent or worsening clinical, functional, biochemical, and imaging parameters during follow-up. A total of 1017 patients (45% women, median age 64 years) were included in the primary analysis. They were followed for a median duration of 732 days after PE diagnosis. The CTEPH was diagnosed in 16 (1.6%) patients, after a median of 129 days; the estimated 2-year cumulative incidence was 2.3% (1.2-4.4%). Overall, 880 patients were evaluable for PPEI; the 2-year cumulative incidence was 16.0% (95% confidence interval 12.8-20.8%). The PPEI helped to identify 15 of the 16 patients diagnosed with CTEPH during follow-up (hazard ratio for CTEPH vs. no CTEPH 393; 95% confidence interval 73-2119). Patients with PPEI had a higher risk of re-hospitalization and death as well as worse quality of life compared with those without PPEI., Conclusion: In this prospective study, the cumulative 2-year incidence of CTEPH was 2.3%, but PPEI diagnosed by standardized criteria was frequent. Our findings support systematic follow-up of patients after acute PE and may help to optimize guideline recommendations and algorithms for post-PE care., Competing Interests: Conflict of interest: A.C.M. was supported by a research grant from the German Academic Exchange Service (DAAD; 57440918). S.B. reports grants or contracts from Bayer, INARI, Boston Scientific, Medtronic, Bard, SANOFI, and Concept Medical; consulting fees from INARI; payment or honoraria from INARI, Boston Scientific, and Concept Medical; and support for attending meetings and/or travel from Bayer and Daiichi Sankyo. R.E. reports consulting fees from Actelion Germany, Boehringer Ingelheim, Janssen, AstraZeneca, OMT, and LungPacer; payment or honoraria from Janssen, Boehringer Ingelheim, AstraZeneca, OMT, Berlin Chemie, and Novartis; support for attending meetings and/or travel from Janssen, Boehringer Ingelheim, AstraZeneca, OMT, Berlin Chemie, and Novartis; and participation on a Data Safety Monitoring Board or Advisory Board for Janssen, Boehringer Ingelheim, AstraZeneca, and Berlin Chemie. M.F. reports payment or honoraria and support for attending meetings and/or travel from Janssen. F.G. reports grants or contracts from Janssen, Bayer; consulting fees from Bayer & Janssen and AstraZeneca; payment or honoraria from Bayer, Janssen, AstraZeneca, and MSD; payment for expert testimony from Janssen; and receipt of equipment, materials, drugs, medical writing, gifts, or other services from Janssen. H.-A.G. reports grants or contracts from Actelion/Janssen and Bayer; consulting fees from Actelion/Janssen, Bayer, MSD, Accelleron, MorphogenIX, and Gossamer Bio; payment or honoraria from Actelion/Janssen, Bayer, MSD, and Gossamer Bio; and support for attending meetings and/or travel from Actelion/Janssen, Bayer, and MSD. A.G. reports payment or honoraria from Bayer Vital, Roche, MSD, and Boehringer-Ingelheim; and support for attending meetings and/or travel from Bayer Vital. E.G. reports consulting fees from Actelion, Bayer/MSD, GSK, United Therapeutics, Novartis, REATA, OMT, and Pfizer; payment or honoraria from Actelion, Bayer/MSD, and GSK; participation on a Data Safety Monitoring Board or Advisory Board for MSD, Janssen and Bayer; and leadership or fiduciary role for Actelion/Janssen. M.Ha. reports consulting fees from MSD; payment or honoraria from Actelion, AstraZeneca, Bayer, Berlin Chemie, Janssen-Cilag, and MSD; support for attending meetings and/or travel from Actelion; and participation on a Data Safety Monitoring Board or Advisory Board for Acceleron, Actelion, GSK, Janssen-Cilag, and MSD. M.He. reports consulting fees from Actelion, Bayer, Berlin Chemie, BMS, Boehringer Ingelheim, Janssen, MSD, and Pfizer; payment or honoraria from Actelion, AstraZeneca, Bayer, BMS, Berlin Chemie, Boehringer Ingelheim, Daiichi Sankyo, Janssen, MSD, and Pfuter Santis; and support for attending meetings and/or travel from Boehringer Ingelheim and Janssen. L.H. reports payment or honoraria from Actelion and MSD. M.M.H. reports consulting fees from Acceleron, Actelion, Bayer, GSK, Janssen, MSD, and Pfizer; and payment or honoraria from Actelion, Bayer, GSK, Janssen, MSD, and Pfizer. F.A.K. reports grants or contracts from Bayer, BMS, Boehringer Ingelheim, MSD, Daiichi Sankyo, Actelion. M.L. reports grants or contracts from Thermo Fisher Scientific, payment or honoraria from Actelion/Johnson & Johnson, Bayer, Daiichi Sankyo, MSD, Pfizer, and Georg Thieme Verlag Stuttgart Germany; support for attending meetings and/or travel from Actelion/Johnson & Johnson and Bayer; participation on a Data Safety Monitoring Board or Advisory Board for Thermo Fisher Scientific. H.H.L. reports travel fees for the study by Bayer, Germany, consulting fees, payment or honoraria, and payment for expert testimony from MSD, Germany; and participation on a Data Safety Monitoring Board or Advisory Board for MSD, Germany. E.M. reports payment or honoraria from Actelion/Janssen, MSD, and Bayer; support for attending meetings and/or travel from Actelion/Janssen, MSD, and Bayer; and participation on a Data Safety Monitoring Board or Advisory Board for Actelion/Janssen. H.-J.S. reports payment or honoraria from Janssen/Actelion, Bayer, GSK, and MSD; and participation on a Data Safety Monitoring Board or Advisory Board for Janssen. R.W. reports grants or contracts from Boehringer Ingelheim and Medtronic; and payment or honoraria from Abbott, AstraZeneca, Bayer, BMS, CVRx, Daichii Sankyo, Novartis, Pfizer, Pharmacosmos, Sanofi, Servier, and SOBI. H.W. reports payment or honoraria from Actelion/Janssen, Bayer, Biotest, Boehringer Ingelheim, MSD, Pfizer, and Roche; support for attending meetings and/or travel from Actelion and Boehringer Ingelheim; and participation on a Data Safety Monitoring Board or Advisory Board for Actelion/Janssen, Boehringer Ingelheim, and MSD. P.S.W. reports study grants from Bayer AG, grants or contracts from Boehringer Ingelheim, DiaSorin, Sanofi-Aventis, AstraZeneca, Bayer Health Care, Bayer Vital, Daiichy Sankyo Europe, and Novartis Pharma; payment or honoraria from Bayer Health Care, Pfizer Pharma, and Bristol Myers Squibb; and other non-financial support from Philips Medical Systems, DiaSorin, and IEM. S.V.K. reports grants or contracts from Bayer AG; consulting fees from Bayer AG, Daiichi Sankyo, and Boston Scientific; and payment or honoraria from Bayer AG, INARI Medical, MSD, Pfizer, and Bristol-Myers Squibb. S.R. reports grants or contracts from Actelion, AstraZeneca, Bayer, Janssen, and Novartis; consulting fees from Abbott, Acceleron, Actelion, Bayer, Janssen, MSD, Novartis, Pfizer, United Therapeutics, and Vifor; payment or honoraria from Actelion, Bayer, BMS, Ferrer, GSK, Janssen, MSD, Novartis, Pfizer, United Therapeutics, and Vifor. The remaining authors (A.C.M., C.A., D.B., L.B., D.F., N.M., F.J.M., C.N., C.O., and K.-H.S.) declare no conflict of interest., (© The Author(s) 2022. Published by Oxford University Press on behalf of European Society of Cardiology.)

Background: Left-to-right (L-R) shunts are characterized by a pathological connection between high- and low-pressure systems, leading to a mixing of oxygen-rich blood with low oxygenated blood. They are typically diagnosed by phase-contrast cardiac magnetic resonance imaging (MRI) which requires extensive planning. T2 is sensitive to blood oxygenation and may be able to detect oxygenation differences between the left (LV) and right ventricles (RV) caused by L-R shunts., Purpose: To test the feasibility of routine T2 mapping to detect L-R shunts., Study Type: Retrospective., Population: Patients with known L-R shunts (N = 27), patients with RV disease without L-R shunts (N = 21), and healthy volunteers (HV; N = 52)., Field Strength/sequence: 1.5 and 3 T/balanced steady-state free-precession (bSSFP) sequence (cine imaging), T2-prepared bSSFP sequence (T2 mapping), and velocity sensitized gradient echo sequence (phase-contrast MRI)., Assessment: Aortic (Qs) and pulmonary (Qp) flow was measured by phase-contrast imaging, and the Qp/Qs ratio was calculated as a measure of shunt severity. T2 maps were used to measure T2 in the RV and LV and the RV/LV T2 ratio was calculated. Cine imaging was used to calculate RV end-diastolic volume index (RV-EDVi)., Statistical Tests: Wilcoxon test, paired t-tests, Spearmen correlation coefficient, receiver operating curve (ROC) analysis. Significance level P < 0.05., Results: The Qp/Qs and T2 ratios in L-R shunt patients (1.84 ± 0.84 and 0.89 ± 0.07) were significantly higher compared to those in patients with RV disease (1.01 ± 0.03 and 0.72 ± 0.10) and in HV (1.04 ± 0.04 and 0.71 ± 0.09). A T2 ratio of >0.78 showed a sensitivity, specificity, and negative predictive value of 100%, 73.9%, and 100%, respectively, for the detection of L-R shunts. The T2 ratio was strongly correlated with the severity of the shunt (r = 0.83)., Data Conclusion: RV/LV T2 ratio is an imaging biomarker that may be able to detect or rule-out L-R shunts. Such a diagnostic tool may prevent unnecessary phase-contrast acquisitions in cases with RV dilatation of unknown etiology., Level of Evidence: 3 TECHNICAL EFFICACY: Stage 2., (© 2021 The Authors. Journal of Magnetic Resonance Imaging published by Wiley Periodicals LLC on behalf of International Society for Magnetic Resonance in Medicine.)

Aims: The purpose of the study was to investigate, using cardiac magnetic resonance (CMR), the presence and time course of microvascular obstruction (MO) in patients with acute myocardial infarction (AMI), and to test its relationship with cardiac remodeling and clinical outcomes., Methods and Results: 53 patients with AMI and successful percutaneous reperfusion underwent CMR examination at four separate timepoints: within the first 48 hours, at 10 days, at six and twelve months after infarction. MO was quantified immediately (early imaging) and 10 minutes (late imaging) after contrast administration in each session. The extent of MO decreased from early to late imaging at both the first and the second CMR exam (p≤0.001). Early MO was absent in 18(36%) patients both at 48 hours and 10 days after AMI. At 1 year follow-up, LVEF in these patients improved to normal (median = 62% (53-70)). Early MO was present in the first but not in the second CMR in 13 (26%) patients; LVEF at one year in these patients reached a median = 52% (47-61). Finally, Early MO was present in both exams in 19 (38%) patients, who at 1 year after infarction had a LVEF of median = 49% (42-54, P≤0.001 across groups). The time course of MO was a predictor of prognosis upon Kaplan-Meier analysis (P = 0.035). The presence of MO at 10 days after AMI was associated with a higher risk of MACE during a 5-years follow-up., Conclusions: The presence of MO within 48 hours after AMI, and its time course in the following ten days, provides complementary information on both functional myocardial recovery and long-term outcome.