LVOT and LVOT calcium load, baseline right bundle branch block, and implantation depth were identified as independent predictors of the need for PPMI post-TAVR. Patient groups with different PPMI risk could be stratified using these 4 predictors. A slightly higher valve implantation site may prevent excessive PPMI rates.

The incidence of blunt chest trauma (BCT) is greater than 15% of all trauma admissions to the emergency departments worldwide and is the second leading cause of death after head injury in motor vehicle accidents. The mortality due to BCT is inhomogeneously described ranging from 9% to 60%. BCT is commonly caused by a sudden high-speed deceleration trauma to the anterior chest, leading to a compression of the thorax. All thoracic structures might be injured as a result of the trauma. Complex cardiac arrhythmia, heart murmurs, hypotension, angina-like chest pain, respiratory insufficiency or distention of the jugular veins may indicate potential cardiac injury. However, on admission to emergency departments symptoms might be missing or may not be clearly associated with the injury. Accurate diagnostics and early management in order to prevent serious complications and death are essential for patients suffering a BCT. Optimal initial diagnostics includes echocardiography or CT, Holter-monitor recordings, serial 12-lead electrocardiography and measurements of cardiac enzymes. Immediate diagnostics leading to the appropriate therapy is essential for saving a patient's life. The key aspect of the entire management, including diagnostics and treatment of patients with BCT, remains an interdisciplinary team involving cardiologists, cardiothoracic surgeons, imaging radiologists and trauma specialists working in tandem.

Innate immune responses and rapid recruitment of leukocytes, which regulate inflammation and subsequent healing, play a key role in acute myocardial infarction (MI). Peptidylarginine deiminase 4 (PAD4) is critically involved in chromatin decondensation during the release of Neutrophil Extracellular Traps (NETs) by activated neutrophils. Alternatively, activated macrophages (M2) and accurate collagen deposition determine the repair of the infarcted heart. In this study, we investigated the impact of NETs on macrophage polarization and their role for acute cardiac inflammation and subsequent cardiac healing in a mouse model of acute MI. NETs were found to promote in vitro macrophage polarization toward a reparative phenotype. NETs suppressed pro-inflammatory macrophages (M1) under hypoxia and diminished IL-6 and TNF-α expression. Further on, NETs strongly supported M2b polarization and IL-10 expression. In cardiac fibroblasts, NETs increased TGF-ß expression under hypoxic culture conditions. PAD4−/− mice subjected to permanent ligation of the left anterior descending artery suffered from overwhelming inflammation in the acute phase of MI. Noteworthy, PAD4−/− neutrophils were unable to release NETs upon ex vivo stimulation with ionomycin or PMA, but produced significantly higher amounts of reactive oxygen species (ROS). Increased levels of circulating cell-free DNA, mitochondrial DNA and cardiac troponin were found in PAD4−/− mice in the acute phase of MI when compared to WT mice. Reduced cardiac expression of IL-6, IL-10, and M2 marker genes, as well as increased TNF-α expression, suggested a pro-inflammatory state. PAD4−/− mice displayed significantly increased cardiac MMP-2 expression under baseline conditions. At day 1, post-MI, PAD4−/− mice showed increased end-diastolic volume and increased thinning of the left ventricular wall. Interestingly, improved cardiac function, as demonstrated by significantly increased ejection fraction, was found at day 21. Altogether, our results indicate that NETs support macrophage polarization toward an M2 phenotype, thus displaying anti-inflammatory properties. PAD4 deficiency aggravates acute inflammation and increases tissue damage post-MI, partially due to the lack of NETs.