We conclude that LOX-1 is regulated by Ang II in vitro and in vivo, that induction of LOX-1 is mediated by the AT(1) receptor, and that repression of LOX-1 by long-term ACE inhibitor treatment may contribute to the antiatherosclerotic potential of this therapy.
Background-This study aimed to assess if clampless off-pump coronary artery bypass grafting (CABG) decreases risk-adjusted mortality, stroke rate, and morbidity in unselected patients in comparison to conventional CABG. Methods and Results-Between July 2009 and November 2010, data of 1282 consecutive patients undergoing isolated CABG were prospectively recorded. In 30.8% (nϭ395), clampless off-pump revascularization was used, either with the PAS-Port automated central venous anastomosis system (nϭ310) or as total arterial revascularization without central anastomoses (nϭ85). Propensity score (PS) matching was performed based on 15 preoperative risk variables to correct for selection bias. In-hospital mortality and stroke rate as primary end point, as well as major complications and follow-up outcome of clampless off-pump (lessOPCAB) and conventional CABG (cCABG) were compared in 394 matched patient pairs (total: 788 patients). The clampless off-pump technique decreased the in-hospital rate of death (odds ratio, 0.25; 95% confidence interval, 0.05-1.18, Pϭ0.080) and stroke (odds ratio, 0.36; 95% confidence interval, 0.13-0.99, Pϭ0.048) significantly. Complications such as low cardiac output syndrome, prolonged ventilation and rethoracotomy were also reduced by lessOPCAB. Over a 2-year follow-up period overall survival, cerebrovascular and major adverse event rate were significantly lower in the lessOPCAB group, while the repeat revascularization rate was comparable. Conclusions-In a retrospective PS-matched analysis, clampless off-pump CABG lowers mortality, stroke rate and other morbidity in an unselected group of patients with coronary artery disease. (Circulation. 2012;126[suppl 1]:S176 -S182.)
In end-stage heart failure, cardiac beta-adrenoceptors are decreased and cardiac Gi protein is increased. We assessed beta-adrenoceptors, G proteins, and effects of several beta-adrenoceptor agonists, histamine, and 5-HT on adenylyl cyclase activity in right and left atria and left ventricles and on left ventricular contractility in six potential heart transplant donors (nonfailing hearts; NFHs) and in nine patients with end-stage dilated cardiomyopathy (DCM) and 11 patients with end-stage ischemic cardiomyopathy (ICM) to establish whether the functional responsiveness of all cardiac Gs-coupled receptors is reduced. Beta-adrenoceptors were reduced in all three tissues; in DCM, beta1-adrenoceptors were more markedly downregulated; in ICM, both beta1- and beta2-adrenoceptors were diminished. In all three tissues, isoprenaline-, terbutaline-, histamine- and 5-HT-induced adenylyl cyclase activation was reduced similarly in DCM and ICM. Moreover, in DCM and ICM, guanosine triphosphate (GTP)- (involving Gs and Gi) activated adenylyl cyclase was significantly diminished, whereas NaF-activated (involving only Gs) and Mn2+-activated (acting at the catalytic unit of the enzyme) adenylyl cyclase was unaltered. Left ventricular positive inotropic responses to beta1- (noradrenaline, dopamine, and dobutamine), beta2- (terbutaline), and beta1- and beta2-adrenoceptors (isoprenaline, adrenaline, and epinine), as well as H2-receptor (histamine) stimulation were significantly reduced. The extent of reduction was not different for each agonist in ICM and DCM. We conclude that in DCM and ICM, functional responsiveness of all cardiac Gs-coupled receptors is similarly reduced.
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