Permanent pacemaker implantation after isolated aortic valve replacement: incidence, risk factors and surgical technical aspects.

Abstract OBJECTIVES: Conducting system defects are common in patients with aortic valve disease. Aortic valve replacement may result in further conduction abnormalities requiring permanent pacemaker implantation. The aim of our study was to identify the incidence and predictors for postoperative 30-day permanent pacemaker implantation in patients undergoing isolated aortic valve replacement, and the effect of an accurate surgical technique in order to prevent permanent pacemaker implantation. METHODS: Data from 261 consecutive patients (mean age 69 +/- 12 years, 136 men) undergoing isolated aortic valve replacement from January 2004 to January 2008 were analyzed retrospectively. Indications for aortic valve replacement were aortic valve stenosis (n = 156), stenoinsufficiency (n = 63), regurgitation (n = 42). Aortic bicuspid valve was present in 25% of cases (n = 64), redo operation was the indication in 7% (n = 18). Preoperative conducting system disease, defined as first-degree atrioventricular block, left or right bundle-branch block or left anterior hemiblock, was present in 25.6% (n = 67) of patients. An accurate surgical technique for debridement of calcific material was performed. RESULTS: In-hospital mortality was 0.8% (2 out of 261 patients). Postoperatively, 8 out of 261 patients (3%) required permanent pacemaker implantation, for second-degree (n = 1) or complete atrioventricular block (n = 7). Incidence of permanent pacemaker implantation was similar for patients either with or without preoperative conducting system disease (25 vs. 25.7%, P = NS). Independent predictors of permanent pacemaker implantation were greater preoperative end-systolic diameter (P = 0.026) and left ventricular septum hypertrophy (P = 0.041). CONCLUSIONS: Need of permanent pacemaker implantation after aortic valve replacement seems to be related more to preoperative advanced aortic valve disease rather than pre-existing conducting system abnormalities. An accurate surgical technique for aortic valve replacement probably helps to prevent further impairment of conducting system function requiring early postoperative permanent pacemaker implantation

Mechanisms and predictors of transient left ventricular dysfunction early after successful percutaneous balloon mitral valvuloplasty.

BACKGROUND: The immediate effects of balloon mitral valvuloplasty (BMV) on left ventricular (LV) function in patients with mitral stenosis are still controversial. The aim of this study was to investigate the mechanisms and potential clinical, echocardiographic and hemodynamic predictors of transient LV dysfunction occurring in patients with mitral stenosis early after successful percutaneous BMV. METHODS: Sixty patients without residual mitral regurgitation were divided into two groups according to the changes in the left atrial (LA) pressure 15 min after successful BMV: 18 patients (group A) did not present with any reduction in LA pressure, and underwent nitroglycerin administration (0.4 mg, sublingually). The remaining 42 patients (group B) presented with a decrease in LA pressure. RESULTS: At baseline, both the mitral valve gradient and area assessed at echocardiography and during cardiac catheterization were similar in groups A and B. Group A patients presented with, however, higher LV early- and end-diastolic pressures and peak V waves during cardiac catheterization both prior to and 15 min after BMV than group B patients (all p values < 0.05). In group A, nitroglycerin administration was associated with a decrease in LV end-diastolic pressure (p = 0.049), LA pressure (p < 0.001), and peak V wave (p < 0.001) that was still persistent 30 min after its administration, reaching values similar to those observed in group B early after BMV. At multivariate analysis, the only independent predictors of LV dysfunction early after BMV were found to be LV early- (p = 0.015) and end-diastolic (p = 0.023) pressures at baseline and the Wilkins' score (p = 0.004). CONCLUSIONS: After successful BMV a transient lack of LV adaptation to the increased LV preload resulting in a persistently elevated LA pressure is predicted by higher baseline LV diastolic filling pressures and higher Wilkins' scores. It is promptly and steadily reversed by nitroglycerin administration through a transient LV unloading, thus allowing a correct hemodynamic evaluation of the immediate results of the procedure

Prokineticin system modulation as a new target to counteract the amyloid beta toxicity induced by glutamatergic alterations in an in vitro model of Alzheimer's disease

The accumulation of β-amyloid (Aβ) is one of the hallmarks of Alzheimer disease (AD). Beyond the inflammatory reactions promoted by Aβ, it has been demonstrated that the prokineticin (PK) system, composed of the chemokine prokineticin 2 (PK2) and its receptors, is involved in Aβ toxicity. In this study we have analyzed how the Aβ chronic treatment affects the glutamatergic transmission on neurons from primary cortical cultures, clearly demonstrating the PK system involvement on its action mechanism. In fact, we have observed a significant increase of the ionic current through the AMPA receptors in primary cortical neurons and an up-regulation of the PK system in cultures chronically treated with Aβ. All effects were nullified by the prokineticin antagonist PC-1. Moreover, we have herein firstly demonstrated that the incubation of primary cortical culture with Bv8, the amphibian homologue of PK2, was able to increase in neurons the AMPA currents at specific doses and exposure times, measured both as evoked and as spontaneous currents. This effect was not due to a modification of the AMPA receptor subunit expression. In contrast, the up-modulation of AMPA currents were blocked by PC-1 and were mediated by the activation of the intracellular protein kinase C (PKC) transduction pathways because Gö6983, the PKC inhibitor added in the medium, nullified the effect. Finally, cellular death induced by kainate was also reduced following treatment with PC1. In conclusion, our results show that the prokineticin system may be a key mediator in the Aβ-induced neuronal damage, suggesting PK antagonists as new therapeutic compounds to ameliorate the AD progression