Yacoub M.,Imperial College London |
Yacoub M.,Aswan Heart Center |
Yacoub M.,Harefield Heart Science Center |
ElGuindy A.,Aswan Heart Center |
And 3 more authors.
Journal of Cardiovascular Translational Research | Year: 2014
Cardiovascular disease (CVD) is currently the leading cause of mortality in the world, and it is estimated that 80 % of the disease burden is encountered in low- and middle-income countries (LMICs). While numerous wake-up calls have been issued in the recent years to face this emerging epidemic, little has been achieved. One particularly deficient area is cardiac surgery. This article aims to address the challenges and barriers to establishing cardiac surgery programs in LMICs and some of the existing efforts to overcome them, focusing on a center in Aswan, Egypt, as an example. © 2014, Springer Science+Business Media New York.
Gogas B.D.,National and Kapodistrian University of Athens |
Gogas B.D.,Erasmus Medical Center |
Parissis J.T.,National and Kapodistrian University of Athens |
Iliodromitis E.K.,National and Kapodistrian University of Athens |
And 6 more authors.
Hellenic Journal of Cardiology | Year: 2010
Infection following the implantation of a left ventricular assist device (LVAD) is a life-threatening complication with mortality rates ranging from 15% to 44%. Staphylococcus aureus and Staphylococcus epidermidis are the most frequently identified pathogensand are responsible for 60% of LVAD-related infections, local as well as systemic. In this report we describe the successful therapeutic management of a patient who received a Heart Mate II as "bridging-to-recovery", which was complicated by device infection that was managed without device explantation.
Ibrahim M.,Harefield Heart Science Center |
Navaratnarajah M.,Harefield Heart Science Center |
Siedlecka U.,Harefield Heart Science Center |
Rao C.,Harefield Heart Science Center |
And 5 more authors.
European Journal of Heart Failure | Year: 2012
Aim sCa 2+-induced Ca 2+ release (CICR) is critical for contraction in cardiomyocytes. The transverse (t)-tubule system guarantees the proximity of the triggers for Ca 2+ release [L-type Ca 2+ channel, dihydropyridine receptors (DHPRs)] and the sarcoplasmic reticulum Ca 2+ release channels [ryanodine receptors (RyRs)]. Transverse tubule disruption occurs early in heart failure (HF). Clinical studies of left ventricular assist devices in HF indicate that mechanical unloading induces reverse remodelling. We hypothesize that unloading of failing hearts normalizes t-tubule structure and improves CICR.Methods and resultsHeart failure was induced in Lewis rats by left coronary artery ligation for 12 weeks; sham-operated animals were used as controls. Failing hearts were mechanically unloaded for 4 weeks by heterotopic abdominal heart transplantation (HF-UN). HF reduced the t-tubule density measured by di-8-ANEPPS staining in isolated left ventricular myocytes, and this was reversed by unloading. The deterioration in the regularity of the t-tubule system in HF was also reversed in HF-UN. Scanning ion conductance microscopy showed the reappearance of normal surface striations in HF-UN. Electron microscopy revealed recovery of normal t-tubule microarchitecture in HF-UN. L-type Ca 2+ current density, measured using whole-cell patch clamping, was reduced in HF but unaffected by unloading. The variance of the time-to-peak of the Ca 2+ transient, an index of CICR dyssynchrony, was increased in HF and normalized by unloading. The increased Ca 2+ spark frequency observed in HF was reduced in HF-UN. These results could be explained by the recoupling of orphaned RyRs in HF, as indicated by immunofluorescence.ConclusionsOur data show that mechanical unloading of the failing heart reverses the pathological remodelling of the t-tubule system and improves CICR. © 2012 The Author.