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Purpose:  The purpose of this study was to assess the diagnostic accuracy of computed tomography pulmonary angiogram (CTPA) including dual energy and reconstruction of iodine maps for diagnosing CTEPH. This method for detecting embolisms and perfusion failures was compared with V/Q-SPECT. An additional purpose was to compare the applied radiation dose of both techniques., Materials and Methods:  71 patients (49 women) with suspected CTEPH were included in this prospective study. The patients received a V/Q-SPECT and a dual-energy CTPA. Iodine maps were reconstructed from the data set. CTPA and the iodine maps were read by an experienced radiologist unaware of the clinical information as well as the results of the V/Q-SPECT. Results were compared to the V/Q-SPECT. DLP and the applied amount of radionuclides (MAA, Technegas) were obtained for comparison of radiation dose., Results:  For the diagnosis of CTEPH, the sensitivity of DECT was 1.000, specificity 0.966, PPV 0.867 and NPV 1.000, respectively. There was not a considerable difference in the x-ray exposure between the DECT examination and the V/Q-SPECT (1.892 mSv vs. 1.911 mSv; p = 0.6115). Both examination modalities were highly consistent regarding the classification of pathological segments (1177/1278 segments, 92,09 %, κ = 0,5938)., Conclusion:  This study presents the DECT, in combination with reconstructed iodine maps, as a potential alternative to the current imaging technique of first choice, V/Q-SPECT. For creating future prospective diagnostic algorithms, the implementation of DECT screening with iodine maps should be considered., Key Points: · DECT correctly identified all CTEPH patients.. · There is substantial agreement between DECT and V/Q-SPECT in the classification of pathological segments.. · There is no significant difference in radiation exposure during DECT examination and V/Q-SPECT examination.. · Reduced radiation dose does not negatively impact image quality.., Citation Format: · Schüßler A, Richter M, Tello K et al. Evaluation der diagnostischen Genauigkeit und der Strahlendosis der Dual-Energy-Computertomografie (DECT) bei chronisch thromboembolischer pulmonaler Hypertonie (CTEPH). Fortschr Röntgenstr 2021; 193: 1318 - 1326., Competing Interests: The authors declare that they have no conflict of interest., (Thieme. All rights reserved.)

The ESC/ERS guidelines (published at the end of 2015) and other international recommendations defined pulmonary hypertension (PH) by an invasively measured mean pulmonary arterial pressure (mPAP) ≥ 25 mmHg at rest. At the 6 th World Symposium on Pulmonary Hypertension in Nice a modification of this hemodynamic definition in the sense of lowering the threshold to > 20 mmHg was proposed. A pulmonary vascular resistance (PVR) ≥ 3 Wood units (WU) is additionally required for the diagnosis of pre-capillary PH. This modification must be critically reviewed with regard to the underlying rationale and possible consequences. Therefore, a detailed explanation is required. In particular, it must be made clear that this change currently has no influence on the evidence-based and approval-compliant prescription of drugs for the targeted therapy of pulmonary arterial hypertension (PAH)., Competing Interests: S. Rosenkranz: Honorare für Vorträge und/oder Beratertätigkeiten von Abbott, Actelion, Arena, Bayer, Ferrer, GSK, MSD, Novartis, Pfizer und United Therapeutics. Forschungsunterstützung an Institutionen von Actelion, Bayer, Novartis, Pfizer und United Therapeutics. G.P. Diller: Forschungsunterstützung und/oder Konferenz-Teilnahme und/oder Honorare für Vorträge und/oder Beratertätigkeit von Actelion, Pfizer, Daiichi-Sankyo, AOP Orphan Therapeuticals. D. Dumitrescu: Honorare für Vorträge und/oder Beratertätigkeiten von Actelion, Bayer, GSK, MSD, Novartis, Pfizer, Servier. Forschungsunterstützung an Institution von Actelion. R. Ewert: Honorare für Vorträge und/oder Beratertätigkeiten von Actelion, Bayer, GSK, Merck, OMT, Pfizer, United Therapeutics. H.A. Ghofrani: Honorare für Vorträge und/oder Konsultationen von Actelion, Bayer, Gilead, GSK, MSD, Novartis, Pfizer und United Therapeutics. E. Grünig: Honorare für Beratertätigkeiten und/oder Vorträge von Actelion, Bayer, GSK, Novartis, Pfizer und United Therapeutics. M. Halank: Honorare für Vorträge und/oder Beratertätigkeiten von Actelion, AOP orphan/OMT, Bayer, Gilead, GSK, MSD, Novartis und Pfizer. M. Held: Honorare für Vorträge und/oder Beratertätigkeiten von Actelion, Bayer, Berlin Chemie, Boehringer, GSK, MSD, Novartis, Pfizer, United Therapeutics. H. Kaemmerer: Forschungsunterstützung und/oder Konferenz-Teilnahme und/oder Honorare für Vorträge und/oder Beratertätigkeit von Actelion, Bayer, Pfizer. H. Klose: Honorare für Vorträge und/oder Beratertätigkeiten und Kongressteilnahmeunterstützung von Actelion, Bayer, MSD, GSK, UT, Novartis, OMT und Pfizer; Forschungsunterstützung von GSK, Actelion und Bayer. G. Kovacs: Honorare für Vorträge und/oder Beratertätigkeiten von Actelion, Bayer, GSK, MSD, Novartis, Pfizer, Chiesi, Boehringer-Ingelheim. S. Konstantinides: Honorare für Vorträge und/oder Beratertätigkeiten von Actelion, Bayer, Boehringer. I.M. Lang: Honorare für Beratertätigkeiten und/oder Vorträge von Actelion, AOP Orphan, Astra-Zeneca, Bayer-Schering, Cordis, Daiichi-Sankyo, Edwards, GSK, Medtronic, Novartis, Pfizer, Servier, United Therapeutics. T.J. Lange: Honorare für Vorträge und/oder Beratertätigkeiten und/oder Forschungsunterstützung an Institutionen von Actelion, AOP orphan/OMT, Bayer, GSK, Pfizer and United Therapeutics. H. Leuchte: Honorare für Vorträge und/oder Beratertätigkeiten von Actelion, Bayer, GSK, Merck, und Pfizer. E. Mayer: Honorare für Vorträge und/oder Beratertätigkeiten von Actelion, Bayer, MSD und Pfizer. A. Olschewski: Honorare für Vorträge und/oder Beratertätigkeiten und/oder Forschungsunterstützung an Institutionen von Bayer, GSK, Pfizer. H. Olschewski: Honorare für Vorträge und/oder Beratertätigkeiten und/oder Forschungsunterstützung an Institutionen von Actelion, Bayer, Belerophon, Boehringer, GSK, Menarini, MSD, Novartis, Pfizer, Roche. K.M. Olsson: Honorare für Vorträge und/oder Beratertätigkeiten von Actelion, Bayer, GSK, Pfizer und United Therapeutics. C. Opitz: Keine persönlichen Einkünfte als mögliche Interessenkonflikte. R.T. Schermuly: Honorare für Vorträge und/oder Beratertätigkeiten und/oder Forschungsunterstützung an Institutionen von Bayer, Gilead, MSD, Novartis, United Therapeutics. W. Seeger: Honorare für Vorträge und/oder Beratertätigkeiten und/oder Forschungsunterstützung an Institutionen von Actelion, Bayer, Pfizer, Novartis. H. Wilkens: Honorare für Beratertätigkeiten und/oder Vorträge von Actelion, Bayer, Boehringer-Ingelheim, GSK, MSD, Novartis, Pfizer und Roche. M.M. Hoeper: Honorare für Beratertätigkeiten und/oder Vorträge von Actelion, Bayer, Gilead, GSK, Merck und Pfizer., (© Georg Thieme Verlag KG Stuttgart · New York.)

Metabolism and nutrition of the critical ill are dynamic parameters of the severe disease influencing the blood glucose concentration. After the finding of increased survival in an initial study in tight glucose control, further large multicenter trials could not show such a benefit and even an increased mortality has been found. Hyperglycemia may be a feature of the stress metabolism and is possibly an adaptive process. Next to the endogenous response, therapy with catecholamines and glucosteroids impacts the response to insulin and the glucose metabolism. Hypo- and hypercaloric nutrition also interact with the insulin therapy. Nutritional therapy should be adapted to the actual state of the patient avoiding hypercaloric feeding and an energy deficit. Using this framework, therapy with insulin may be used to achieve a targeted range of glucose avoiding an increased risk of hypoglycaemia., (© Georg Thieme Verlag Stuttgart · New York.)

The clinical spectrum of obstructive sleep apnea-(OSA-)related cardiovascular disease (CVD) comprises systemic arterial hypertension (prevalence: 40-60%), pulmonary hypertension (20-30%), coronary artery disease (20-30%), congestive heart failure (5-10%), and stroke (5-10%). During sleep, heart rhythm disorders such as atrioventricular blocks, sinus arrests and atrial fibrillation can be induced by OSA. OSA-related CVD mainly affects those patients with an apnea-hypopnea index > 30/h and, if left untreated, is linked to increased mortality. Epidemiologic data have clearly shown that cardiovascular risk is increased in OSA independent of confounding factors such as obesity and concomitant metabolic disease. In recent years, the pathophysiology of OSA-related CVD has been further elucidated showing that apart from the well-known sympathetic activation, increased oxidative stress and pro-inflammatory changes seem to play major roles. Furthermore, studies using high resolution ultrasonography have demonstrated endothelial dysfunction and enhanced atherosclerosis in these patients. Finally, animal models of OSA have delineated that daytime arterial hypertension is the consequence of the OSA-associated chronic intermittent hypoxia. Therapy of OSA by continuous positive airway pressure (CPAP) ventilation exerts cardioprotective effects. It has been shown to rectify the vascular micromilieu, restore endothelium-dependent vasodilation, lower 24-h blood pressure, eliminate nocturnal heart rhythm disorders, and improve left ventricular function. Furthermore, long-term CPAP therapy leads to a reduction in important clinical endpoints such as the rates of myocardial infarction and stroke.

The idiopathic interstitial pneumonias, especially the idiopathic pulmonary fibrosis (IPF), are life-threatening lung disorders, for which no effective treatment option exists. In view of IPF, the American Thoracic Society (ATS)/European Respiratory Society (ERS) consensus statement recommends a combined therapy with corticosteroids and azathioprine or cyclophosphamide, although data from conclusive clinical trials are yet missing and the recurrent clinical experience is that these drugs do not really help in IPF. Up to now, lung transplantation represents the last and only therapeutic option for IPF subjects. Based on new pathophysiological concepts of IPF, there are meanwhile a couple of different agents under preclinical and clinical assessment, and the increasing number of clinical trials ongoing in IPF raise the hope that an effective treatment comes into reach. The agents investigated and their targets are: acetylcysteine (reactive oxygen species [ROS] scavenging), interferon-gamma 1b (modulation of Th1/Th2 balance, direct antifibrotic effects), pirfenidone and GC 1008 (blockade of transforming growth factor-beta), FG 3019 (blockade of connective tissue growth factor), imatinib mesylate (blockade of platelet-derived growth factor), bosentan (blockade of endothelin), zileutin (blockade of leukotrienes), etanercept (blockade of tumor necrosis factor-alpha), heparin (alveolar anticoagulation). Hopefully, these new therapeutic strategies may help to improve prognosis of IPF in the future.

Besides all progress in the therapy of pulmonary arterial hypertension over the past years, there is still no cure for this devastating disease. By introducing effective and nonparenteral medications (e. g., oral endothelin receptor antagonists [ERAs], inhaled prostanoids), quality of life, exercise tolerance and prognosis of patients have substantially improved. However, applicability of these therapies can be hampered by serious side effects and/or the necessity for elaborate application techniques. Whether selective ERAs--due to their specificity for the A-type receptor--have potential benefits over the nonselective ERA bosentan remains to be answered by the analysis of pivotal trials recently carried out with ambrisentan and sitaxsentan. Inhaled treprostinil can potentially have benefits over the already approved inhaled iloprost, related to its higher pulmonary selectivity as well as to the longer biological half-life. However, this has yet to be proven in long-term randomized controlled trials. In comparison to the previously mentioned substances, the selective phosphodiesterase-5 (PDE5) inhibitor sildenafil approached approval closest as new therapy for pulmonary arterial hypertension. Oral sildenafil has proven its efficacy as a selective pulmonary vasodilator in various forms of pulmonary hypertension. The results of the pivotal phase III trial have confirmed the strong efficacy and excellent tolerability of this substance. Combination therapies, despite all progress seen for single agents, can be regarded as the most promising therapeutic approach for the future. However, controlled randomized trials that are currently under consideration have to confirm this notion.