CategoriesClick here to see recent updates
Prof. Dr. med. Carsten Tschöpe, Charité, CVK Ventricular Unloading and Inflammation - The Role of Impella in Myocarditis
Dr. Tschöpe speaking on how he used Impella support to bridge a patient through myocarditis.VIEW
This first of its kind iPad app is an interactive simulation-based textbook of cardiovascular physiology and hemodynamics. The textbook is divided into 4 parts and will cover a full range of topics relevant to the understanding of hemodynamics in health and disease. This app includes Part 1: Basic Physiological Concepts, and covers topics including the cardiac cycle, pressure-volume relations, preload, afterload, contractility, lusitropy and ventricular-vascular coupling. Parts II, III and IV will cover advanced physiological concepts, pathophysiology, disease states and therapeutics and mechanical circulatory support. The full simulation is available from any place in the app, simply by rotating iPad into a landscape orientation. The simulation, linked with end-of-chapter questions and problem sets allow for a flexible “learn-by-doing” environment for experimentation and discovery.VIEW
Left Ventricular Unloading Using an Impella CP Improves Coronary Flow and Infarct Zone Perfusion in Ischemic Heart Failure
Background-—Delivering therapeutic materials, like stem cells or gene vectors, to the myocardium is difficult in the setting of
ischemic heart failure because of decreased coronary flow and impaired microvascular perfusion (MP). The aim of this study was to
determine if mechanical left ventricular (LV) unloading with the Impella increases coronary flow and MP in a subacute myocardial
Methods and Results-—Anterior transmural myocardial infarction (infarct size, 26.03.4%) was induced in Yorkshire pigs. At 2
weeks after myocardial infarction, 6 animals underwent mechanical LV unloading by Impella, whereas 4 animals underwent
pharmacological LV unloading using sodium nitroprusside for 2 hours. LV unloading with Impella significantly reduced end-diastolic
volume (1611mL, P=0.02) and end-diastolic pressure (EDP; 3223 mm Hg, P=0.03), resulting in a significant decrease in LV
end-diastolic wall stress (EDWS) (infarct: 71.614.7 to 43.310.8 kdynes/cm2 [P=0.02]; remote: 66.620.9 to 40.613.3 kdynes/
cm2 [P=0.02]). Coronary flow increased immediately and remained elevated after 2 hours in Impella-treated pigs. Compared
with the baseline, MP measured by fluorescent microspheres significantly increased within the infarct zone (10981%, P=0.003),
but not in the remote zone. Although sodium nitroprusside effectively reduced LV-EDWS, 2 (50%) of sodium nitroprusside–treated
pigs developed profound systemic hypotension. A significant correlation was observed between the infarct MP and EDWS (r2=0.43,
P=0.03), suggesting an important role of EDWS in regulating MP during LV unloading in the infarcted myocardium.
Conclusions-—LV unloading using an Impella decreased EDWS and increased infarct MP without hemodynamic decompensation.
Mechanical LV unloading is a novel and efficient approach to increase infarct MP in patients with subacute myocardial infarction.