beta 1AR and beta 2AR coexist and function on human ventricular myocytes. At low (-)-epinephrine concentrations, contractile responses are predominantly mediated by beta 2AR rather than beta 1AR in myocytes from failing hearts.

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Background-Postinfarction ventricular septal defect carries a grim prognosis. Surgical repair offers reasonable outcomes in patients who survive a healing phase. Percutaneous device implantation represents a potentially attractive early alternative. Methods and Results-Postinfarction ventricular septal defect closure was attempted in 53 patients from 11 centers (1997)(1998)(1999)(2000)(2001)(2002)(2003)(2004)(2005)(2006)(2007)(2008)(2009)(2010)(2011)(2012); aged 72±11 years; 42% female). Nineteen percent had previous surgical closure. Myocardial infarction was anterior (66%) or inferior (34%). Time from myocardial infarction to closure procedure was 13 (first and third quartiles, 5-54) days. Devices were successfully implanted in 89% of patients. Major immediate complications included procedural death (3.8%) and emergency cardiac surgery (7.5%). Immediate shunt reduction was graded as complete (23%), partial (62%), or none (15%). Median length of stay after the procedure was 5.0 (2.0-9.0) days. Fifty-eight percent survived to discharge and were followed up for 395 (63-1522) days, during which time 4 additional patients died (7.5%).

Clenbuterol induces significant hypertrophy of the LDM associated with specific changes in cardiac gene expression.

LAAO can be performed safely in a real world setting with good implant success rates and procedural outcomes. The long-term benefits of the procedure are reassuring in terms of both ischemic events and avoidance of severe bleeding associated with anticoagulation in this patient group. © 2016 Wiley Periodicals, Inc.

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1 The decreased response to P-adrenoceptor stimulation seen in heart failure may be related to a defect in cyclic AMP production. The inotropic effects of the selective phosphodiesterase (PDE) III inhibitors, SK&F 94120 and SK&F 94836, and the non-selective PDE inhibitor, 3-isobutyl-1-methylxanthine (IBMX), alone and when combined synergistically with isoprenaline, were studied in control and P-adrenoceptor-desensitized ventricular myocytes.2 Myocytes isolated from noradrenaline-treated guinea-pigs had a reduced maximum response to isoprenaline compared with control animals (60.0 ± 2.5%, n = 42 vs 79.5 ± 1.7% maximum calcium: n = 46, P <0.001). Together with an approximately 20 fold increase in the isoprenaline EC", this is indicative of ,-adrenoceptor desensitization as a result with chronic infusion with noradrenaline. 3 The maximum inotropic response of IBMX was depressed following noradrenaline treatment, from 74.9 ± 4.6% (n = 7) in control, to 61.7 ± 2.70% (n = 6), as a percentage of maximum calcium in noradrenaline-treated guinea-pig ventricular myocytes (P<0.02). The pD2 value for IBMX was also reduced (P <0.02). No significant differences in the inotropic effects of SK&F 94120 and SK&F 94836 were seen between control and P-adrenoceptor desensitized myocytes.4 Threshold inotropic concentrations of SK&F 94120 and SK&F 94836 caused a five fold decrease in the EC50 of control myocytes for isoprenaline, and an 11 fold decrease in the noradrenaline-treated guinea-pig ventricular myocytes. 5 The maximum response to isoprenaline in myocytes isolated from normal guinea-pigs was unaffected by PDE inhibition; either at threshold or maximum inotropic concentrations, or by CPT cyclic AMP, an analogue of cyclic AMP. 6 A significant potentiation of the maximum isoprenaline response by threshold inotropic concentrations was observed with SK&F 94120 (P<0.05), but not with IBMX or SK&F 94836, in myocytes isolated from noradrenaline-treated guinea-pig hearts. This potentiation, however, did not completely restore the response to levels seen in control myocytes. 7 The extent of potentiation of the maximum isoprenaline response by maximum inotropic concentrations of either IBMX or CPT cyclic AMP, was no greater than that by threshold concentrations of IBMX, in myocytes isolated from noradrenaline-treated guinea-pig hearts. 8 In cardiac myocytes isolated from the explanted hearts of 16 patients with heart failure, threshold concentrations of IBMX and SK&F 94120 decreased the isoprenaline EC50 by a factor of four and six, respectively, but potentiation of the maximum isoprenaline response occurred only with SK&F 94120. The attenuated isoprenaline response was increased from 60.3 ± 4.5% to 74.3 ± 4.2% as a % maximum calcium (P<0.05, n = 6), but remained substantially lower than the 116 ± 7% (P<0.001, n = 6) seen in myocytes isolated from non-failing hearts. 9 We conclude that the reduced maximum contraction amplitude with isoprenaline in cardiac myocytes from either patients in end-stage failure, or noradrenaline-treated guin...