Heart Failure: Will There be Any light at the End of the Tunnel with Stem Cell Therapy?

Cardiac regeneration using stem cells emerges as a noveltreatment option for heart failure. Clinical applications havereported encouraging but modest favorable results, concerningcardiac functional recovery. However, many issues need clarification.The most appropriate cell type, the optimal number ofinjected cells and time for cell delivery, as well as the mode ofcell function remain to be elucidated. Furthermore, ways to improve cell survival and long term engraftment are being sought, in an effort to enhance the regenerative capability of the cells. A substantial amount of basic, translational and clinical research is still needed, in order to take advantage of the full therapeuticpotential of stem cell treatments for heart failure

Persistent Left Superior Vena Cava With Absent Right Superior Vena Cava

We report the case of a 52-year-old patient who referred to our hospital with the indication for a pacemaker implantation. The attempt to implant the pacemaker lead through the right subclavian vein revealed an unusual course of the lead. The phlebography through the right subclavian vein revealed the presence of a persistent left superior vena cava and the absence of right superior vena cava

Perfusion defect size predicts engraftment but not early retention of intra-myocardially injected cardiosphere-derived cells after acute myocardial infarction

Therapeutic cell retention and engraftment are critical for myocardial regeneration. Underlying mechanisms, including the role of tissue perfusion, are not well understood. In Wistar Kyoto rats, syngeneic cardiosphere-derived cells (CDCs) were injected intramyocardially, after experimental myocardial infarction. CDCs were labeled with [18F]-FDG (n = 7), for quantification of 1-h retention, or with sodium-iodide-symporter gene (NIS; n = 8), for detection of 24-h engraftment by reporter imaging. Perfusion was imaged simultaneously. Infarct size was 37 ± 9 and 38 ± 9% of LV in FDG and NIS groups. Cell signal was located in the infarct border zone in all animals. No significant relationship was observed between infarct size and 1-h CDC retention (r = −0.65; P = 0.11). However, infarct size correlated significantly with 24-h engraftment (r = 0.75; P = 0.03). Residual perfusion at the injection site was not related to cell retention/engraftment. Larger infarcts are associated with improved CDC engraftment. This observation encourages further investigation of microenvironmental conditions after ischemic damage and their role in therapeutic cell survival

Inotropic therapy in patients with advanced heart failure. A clinical consensus statement from the Heart Failure Association of the European Society of Cardiology

This clinical consensus statement reviews the use of inotropic support in patients with advanced heart failure. The current guidelines only support use of inotropes in the setting of acute decompensated heart failure with evidence of organ malperfusion or shock. However, inotropic support may be reasonable in other patients with advanced heart failure without acute severe decompensation. The clinical evidence supporting use of inotropes in these situations is reviewed. Particularly, patients with persistent congestion, systemic hypoperfusion, or advanced heart failure with need for palliation, and specific situations relevant to implantation of left ventricular assist devices or heart transplantation are discussed. Traditional and novel drugs with inotropic effects are discussed and use of guideline-directed therapy during inotropic support is reviewed. Finally, home inotropic therapy is described, and palliative care and end-of-life aspects are reviewed in relation to management of ongoing inotropic support (including guidance for maintenance and weaning of chronic inotropic therapy support)

Myocardial Substrate Determines Acute Cardiac Retention and Lung Biodistribution of Intramyocardially Injected Cardiac-Derived Stem Cells—A PET/CT Experimental Study

Abstract 1080 Michael Bonios, Johns Hopkins University, Baltimore, MD; John Terrovitis, Cedars Sinai Medical Ctr, Los Angeles, CA; Brian O’Rourke, James Fox, Jianhua Yu, James M Engles, Takahiro Higuchi, Riikka Lautamäki, Martin Pomper, Richard L Wahl, Benjamin M Tsui, Frank M Bengel, Johns Hopkins University, Baltimore, MD; Eduardo Marbαn, Cedars Sinai Medical Ctr, Los Angeles, CA; M. Roselle Abraham, Johns Hopkins University, Baltimore, MD Michael Bonios, 2008 Finalist and Presenting Author </jats:p

The effect of intra-aortic baloon counterpulsation of coronary blood flow in the intact myocardium and during reperfusion following a long period of ischemia: experimental study

Background: Studies of the IABP have reported conflicting results regarding the effects on coronary blood flow (CBF). The purpose of the present study was to measure the changes in coronary blood flow induced by intra-aortic balloon pump (IABP) counterpulsation in normal and reperfused porcine myocardium. Methods: A 30-ml IABP was placed in the descending aorta of 14 open-chest pigs. Each pig underwent occlusion of the mid left anterior descending (LAD) coronary artery for 1 h, followed by reperfusion for 2 h. The effects of IABP support on systolic aortic pressure (SAP) and aortic end-diastolic pressure were recorded. The mean CBF, distal to the LAD occlusion site was measured at baseline and during reperfusion, with and without IABP counterpulsation. Results: The IABP decreased SAP and aortic end-diastolic pressure in normal and reperfused myocardium, and maintained a peak aortic diastolic augmentation at the level of SAP. In normal myocardium, the IABP decreased mean CBF by 7.7±4.4% (p < 0.001). At 2, 15, 30, 60, 90 and 120 min of reperfusion, the IABP increased mean CBF by 11.5±6.8%, 8.0±7.0%, 11.2±6.9%, 12.4±12.9%, 23.5±9.9% and 8.9±6.9%, of the corresponding value without the assistance of the IABP (all p < 0.05). Conclusions: In the normal heart, IABP counterpulsation decreased CBF, probably because of a decrease in myocardial oxygen demand from a decreased afterload. During reperfusion the IABP increased CBF, suggesting that it might effectively mitigate the no-reflow phenomenon.Εισαγωγή: Μελέτες πάνω στη επίδραση της Ενδοαορτικής Αντλίας Αντιώθησης(ΕΑΑ) στη στεφανιαία ροή έχουν δώσει αντικρουόμενα αποτελέσματα. Σκοπός της παρούσας μελέτης ήταν η μέτρηση των μεταβολών της στεφανιαίας ροής υπό την επίδραση της ΕΑΑ τόσο σε φυσιολογικό μυοκάρδιο όσο και στη φάση της επαναιμάτωσης, μετά από παρατεταμένη ισχαιμία. Μέθοδος: Σε 14 πειραματόζωα (χοίροι) τοποθετήθηκε ασκός ΕΑΑ (30 cc) στην κατιούσα θωρακική αορτή. Ακολουθούσε διάνοιξη της θωρακικής κοιλότητας και απολίνωση του μέσου τμήματος της προσθίας κατιούσας στεφανιαίας αρτηρίας (ΠΚΣΑ) για 1 ώρα, ενώ ακολουθούσε επαναιμάτωση διάρκειας 2 ωρών. Η επίδραση της ΕΑΑ στη συστολική αορτική πίεση (ΣΑΠ) στην τελοδιαστολική αορτική πίεση (ΤΔΑΠ) και στη μέση τιμή της στεφανιαίας ροής μετρήθηκε στο φυσιολογικό μυοκάρδιο (πρό της πρόκλησης ισχαιμίας) και στη διάρκεια της επαναιμάτωσης, με την ΕΑΑ τόσο ενεργοποιημένη όσο και εκτός λειτουργίας Αποτελέσματα: Η ΕΑΑ επέφερε ελάττωση της ΣΑΠ και της ΤΔΑΠ τόσο στο φυσιολογικό όσο και στο επαναιματούμενο μυοκάρδιο. Στο φυσιολογικό μυοκάρδιο η ΕΑΑ επέφερε ελάτωση της μέσης τιμής της στεφανιαίας ροής κατά 7.7±4.4% (p<0.001). Στο 2ο, 15ο, 30ο, 60ο, 90ο και 120ο λεπτό της επαναιμάτωσης, η ενεργοποίηση της ΕΑΑ επέφερε αύξηση της μέσης τιμής της στεφανιαίας ροής κατά 11.5±6.8%, 8.0±7.0%, 11.2±6.9%, 12.4±12.9%, 23.5±9.9% και 8.9±6.9% αντίστοιχα (p<0.05). Συμπέρασμα: Στο φυσιολογικό μυοκάρδιο η ΕΑΑ προκάλεσε ελάττωση της στεφανιαίας ροής πιθανόν λόγω της ελάττωσης της μυοκαρδιακής κατανάλωσης οξυγόνου, ως αποτέλεσμα της ελάττωσης του μεταφορτίου της αριστερής κοιλίας. Αντίθετα, στη φάση της επαναιμάτωσης η ΕΑΑ προκάλεσε αύξηση της στεφανιαίας ροής και το αποτέλεσμα αυτό πιθανόν να έχει ευεργετική δράση στις περιοχές του μυοκαρδίου που χαρακτηρίζοται από το φαινόμενο μη επαναρροής