Resection of hypertrophic papillary muscles and mitral valve replacement in a patient with midventricular hypertrophic obstructive cardiomyopathy - a new approach.

Midventricular hypertrophic obstructive cardiomyopathy (HOCM) is characterized by hypertrophy of the interventricular septum (IVS) and - in rare cases - of the papillary muscles (PM), which subsequently can cause dynamic left ventricular outflow tract obstruction (LVOTO) and severe heart failure symptoms. We report on a rare case of a 44-year-old patient suffering from midventricular HOCM with hypertrophic anterolateral PM and an additional chorda between the PM and the IVS.We describe a new surgical approach via right anterolateral thoracotomy in 3-dimensional (3D) video-assisted minimal-invasive technique with resection of hypertrophic PMs as well as the entire mitral valve-apparatus and valve replacement avoiding septal myectomy and potentially associated complications. After an uneventful procedure clinical symptoms improved from NYHA III-IV at baseline to NYHA 0-I postoperatively and remained stable over a follow-up period of 24 months. Therefore, the presented technique may be considered as a new and alternative approach in patients with hypertrophic PMs and hypertrophic IVS as subtype of midventricular HOCM.

Machine-Learning-Based Diagnostics of Cardiac Sarcoidosis Using Multi-Chamber Wall Motion Analyses.

BACKGROUND: Hindered by its unspecific clinical and phenotypical presentation, cardiac sarcoidosis (CS) remains a challenging diagnosis. OBJECTIVE: Utilizing cardiac magnetic resonance imaging (CMR), we acquired multi-chamber volumetrics and strain feature tracking for a support vector machine learning (SVM)-based diagnostic approach to CS. METHOD: Forty-five CMR-negative (CMR(-), 56.5(53.0;63.0)years), eighteen CMR-positive (CMR(+), 64.0(57.8;67.0)years) sarcoidosis patients and forty-four controls (CTRL, 56.5(53.0;63.0)years)) underwent CMR examination. Cardiac parameters were processed using the classifiers of logistic regression, KNN(K-nearest-neighbor), DT (decision tree), RF (random forest), SVM, GBoost, XGBoost, Voting and feature selection. RESULTS: In a three-cluster analysis of CTRL versus vs. CMR(+) vs. CMR(-), RF and Voting classifier yielded the highest prediction rates (81.82%). The two-cluster analysis of CTRL vs. all sarcoidosis (All Sarc.) yielded high prediction rates with the classifiers logistic regression, RF and SVM (96.97%), and low prediction rates for the analysis of CMR(+) vs. CMR(-), which were augmented using feature selection with logistic regression (89.47%). CONCLUSION: Multi-chamber cardiac function and strain-based supervised machine learning provides a non-contrast approach to accurately differentiate between healthy individuals and sarcoidosis patients. Feature selection overcomes the algorithmically challenging discrimination between CMR(+) and CMR(-) patients, yielding high accuracy predictions. The study findings imply higher prevalence of cardiac involvement than previously anticipated, which may impact clinical disease management.

Maslinic acid alleviates ischemia/reperfusion-induced inflammation by downregulation of NFκB-mediated adhesion molecule expression.

Ischemia/reperfusion (I/R)-induced inflammation is associated with enhanced leukocyte rolling, adhesion and transmigration within the microcirculation. These steps are mediated by hypoxia-triggered signaling pathways, which upregulate adhesion molecule expression on endothelial cells and pericytes. We analyzed whether these cellular events are affected by maslinic acid (MA). Mitochondrial activity and viability of MA-exposed endothelial cells and pericytes were assessed by water-soluble tetrazolium (WST)-1 and lactate dehydrogenase (LDH) assays as well as Annexin V/propidium iodide (PI) stainings. Effects of MA on hypoxia and reoxygenation-induced expression of E-selectin, intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1 were determined by flow cytometry. The subcellular localization of the NFκB subunit p65 was analyzed by immunofluorescence and Western blot. I/R-induced leukocytic inflammation was studied in MA- and vehicle-treated mouse dorsal skinfold chambers by intravital fluorescence microscopy and immunohistochemistry. MA did not affect viability, but suppressed the mitochondrial activity of endothelial cells. Furthermore, MA reduced adhesion molecule expression on endothelial cells and pericytes due to an inhibitory action on NFκB signaling. Numbers of adherent and transmigrated leukocytes were lower in post-ischemic tissue of MA-treated mice when compared to vehicle-treated controls. In addition, MA affected reactive oxygen species (ROS) formation, resulting in a diminished oxidative DNA damage. Hence, MA represents an attractive compound for the establishment of novel therapeutic approaches against I/R-induced inflammation.