No abstract

Sex- and flow-related aortic valve calcification (AVC) studies are still limited in number, and data on the exact calcium quantity and distribution are scarce. Therefore, we aimed to (1) re-define the best threshold of AVC load to distinguish severe from moderate aortic stenosis (AS) in common AS entities and to (2) evaluate differences in the aortic annulus and left ventricular outflow tract (LVOT) calcium load. Nine hundred and thirty-eight patients with contrast-enhanced cardiac MSCT and moderate-to-severe aortic stenosis (AS) were retrospectively enrolled. Patients with severe AS ≤ 1.0 cm2 (n = 841) were further separated into three AS entities: high gradient (HGAS, n = 370, 44.0%), paradoxical low gradient (pLGAS, n = 333, 39.6%), and classical low gradient (LGAS, n = 138, 16.4%). AVC, leaflet, and LVOT calcification were quantified. Aortic valve calcification scores were highest in severe HGAS, and lower in severe pLGAS and classical LGAS. In all severity and AS entities, the non-coronary cusp (NCC) was the most calcified one. LVOT calcification was consistently comparable between gender and AS entities. Accuracy of logistic regression was the highest in HGAS (male vs. female: AVC > 2156 Agatston units (AU), c-index 0.76; vs. AVC > 1292 AU, c-index 0.85; or AVC density > 406 AU/cm2, c-index 0.82; vs. > 259 AU/cm2, c-index 0.86; each p < 0.0001*) to diagnose severe AS. AVC could only be used in men to differentiate between severe LGAS and moderate AS. Data from this retrospective analysis indicate that the NCC is subject to pre-dominant degeneration throughout gender, AS severity, and several AS entities. AVC was consistently comparable in severe pLGAS and classical LGAS, but only AVC in severe LGAS could sufficiently distinguish from moderate AS in men. LVOT calcification failed to be a reliable indicator of accelerating AS.

No abstract

Target temperature management is recommended in post-resuscitation care. Additionally, hypothermia is a promising option in adjunctive therapy of acute myocardial infarction (MI). However, first in men data are contradicting. There are still many open questions to identify the optimal regimen and target temperature. In this study, we aimed to investigate the effect of very mild hypothermia on infarct size (IS) in mice. Mice underwent cardiac ischemia by temporary occlusion of the left anterior descending (LAD) artery under conditions of very mild hypothermia (34-36 ℃). Hypothermia was reached within the first 5 minutes of ischemia (temperature: 34.6±0.5 vs. 36.8±1.1 ℃, P=0.035). Very mild hypothermia reduced IS in mice undergoing 30 minutes ischemia [IS/area at risk (AAR): 45±12% vs. 22±4%, P=0.018] as well as mice undergoing 60 minutes ischemia [IS/AAR: 67±7% vs. 28±2%, P=0.0003]. Very mild hypothermia reduces IS. This new approach in adjunctive therapy of patients with acute MI should be investigated in clinical trials.