Evaluation of atrial function after surgical ablation of atrial fibrillation: a Speckle tracking study.

AIM: AIM of our study was to assess atrial function in patients who underwent atrial fibrillation (AF) surgical ablation by a novel echocardiographic technique (speckle tracking). METHODS: From February 2006 to April 2008, in 11 consecutive pts with paroxysmal or persistent AF (6 males, mean age 69.6±9.7 years) undergoing cardiac surgery, concomitant AF surgical ablation was performed with bipolar radiofrequency clamp (Cobra_Bipolar® system). These pts, all in stable sinus rhythm (SR), were echoed after a mean follow-up of 14.6±9.3 months from surgery. Speckle tracking was used to estimate global LA strain, peak strain and the standard deviation of the time-to-peak (% of R-R' interval) of the deformation of 6 segments identified along the septum, the roof and the lateral wall of LA in a 4-chamber view. RESULTS: These patients showed a mild LA enlargement (mean volume 43.4±11.6 mL/sqm). In 5 of them (45.4%) no A waves were detected on MPWD and pulmonary venous flow, but speckle tracking showed preserved atrial function with a mean global strain of 5.5 ± 3.3 %, a mean peak strain of 10.4 ± 5.7 % and a TP-SD of 15.1±8.7 ms. CONCLUSION: Our study seems to show that surgical AF ablation has a lower impact on atrial function in comparison with data from literature about percutaneous catheter ablation. This is probably related to an higher sensitivity of this type of echocardiography evaluation, but this finding must be confirmed by other trials.

Twelve-year follow up with the Sorin Pericarbon bioprosthesis in the mitral position.

BACKGROUND AND AIMS OF THE STUDY: The aim of this study was to evaluate the long-term follow up of the Pericarbon pericardial bioprosthesis implanted in the mitral position. METHODS: Between January 1985 and January 1991, 78 patients (26 males, 52 females; mean age 56.9 +/- 7.8 years) underwent isolated mitral valve replacement with a Pericarbon valve. All bioprostheses were size 29 mm and implanted by the same surgeon. RESULTS: Total follow up was 663.2 pt-years and it was 97% complete. Early mortality was 1.3% (1/78); two minor cerebral embolisms were observed as early complications. At 12 years the overall survival rate was 85.0 +/- and valve-related survival 93.1 +/- 3.0%; freedom from embolic events was 83.0 +/- 4.5% and from endocarditis 98.7 +/- 1.3%. Freedom from primary tissue failure was 56.8 +/- 6.6%; it was 86.3 +/- 7.5% in patients aged > 60 years and 36.8 +/- 8.2% in younger patients. There were 27 reoperations, 26 for primary tissue failure, one for endocarditis. Comparison between basal and follow up echocardiographic studies showed a significant stenotic deterioration of the bioprosthesis and a negligible incidence of regurgitation. Morphological findings of explanted bioprostheses were characterized by stenotic and diffuse microcalcification, but no tissue tear was observed. CONCLUSIONS: These results confirm that the Pericarbon bioprosthesis is structurally safe and free from the fatigue problems which afflicted the first and second generation of pericardial valves. As with other tissue valves, the rate of calcification is age-dependent, suggesting preferential use of the Pericarbon prosthesis in elderly people.

Levosimendan induces NO production through p38 MAPK, ERK and Akt in porcine coronary endothelial cells: role for mitochondrial K(ATP) channel.

BACKGROUND AND PURPOSE: Levosimendan acts as a vasodilator through the opening of ATP-sensitive K(+) channels (K(ATP)) channels. Moreover, the coronary vasodilatation caused by levosimendan in anaesthetized pigs has recently been found to be abolished by the nitric oxide synthase (NOS) inhibitor N(omega)-nitro-L-arginine methyl ester, indicating that nitric oxide (NO) has a role in the vascular effects of levosimendan. However, the intracellular pathway leading to NO production caused by levosimendan has not yet been investigated. Thus, the purpose of the present study was to examine the effects of levosimendan on NO production and to evaluate the intracellular signalling pathway involved. EXPERIMENTAL APPROACH: In porcine coronary endothelial cells (CEC), the release of NO in response to levosimendan was examined in the presence and absence of N(omega)-nitro-L-arginine methyl ester, an adenylyl cyclase inhibitor, K(ATP) channel agonists and antagonists, and inhibitors of intracellular protein kinases. In addition, the role of Akt, ERK, p38 and eNOS was investigated through Western blot analysis. KEY RESULTS: Levosimendan caused a concentration-dependent and K(+)-related increase of NO production. This effect was amplified by the mitochondrial K(ATP) channel agonist, but not by the selective plasma membrane K(ATP) channel agonist. The response of CEC to levosimendan was prevented by the K(ATP) channel blockers, the adenylyl cyclase inhibitor and the Akt, ERK, p38 inhibitors. Western blot analysis showed that phosphorylation of the above kinases lead to eNOS activation. CONCLUSIONS AND IMPLICATIONS: In CEC levosimendan induced eNOS-dependent NO production through Akt, ERK and p38. This intracellular pathway is associated with the opening of mitochondrial K(ATP) channels and involves cAMP.

Hemodynamic effect of intracoronary administration of levosimendan in the anesthetized pig.

In this study the hemodynamic effects of intracoronary injection of levosimendan in anesthetized pigs and the mechanisms involved were examined. In 12 anesthetized pigs instrumented for measurement of heart rate (HR), aortic blood pressure (ABP), central venous pressure (CVP), left ventricular end-diastolic blood pressure, left ventricular contractility and relaxation, and mean coronary blood flow (CBF), levosimendan has been injected into the left anterior descending coronary artery at doses corresponding to the ones commonly used in clinics as bolus administration but adapted to the measured CBF. In a further 9 pigs levosimendan has been administered after the blockade of alpha and beta adrenoceptors, muscarinic receptors, and coronary nitric oxide synthase (NOS) to investigate the action mechanism of the drug. The intracoronary bolus administration of doses of levosimendan corresponding to 12 and 24 microg/kg in 10 minutes exerted, respectively, CBF increases of 26.3% and 41.3% of the control values in the absence of changes in the other hemodynamic variables. The blockade of the autonomic nervous system did not prevent the coronary vasodilation, which was, however, abolished by the NOS inhibition. The intracoronary administration of levosimendan exerts positive effects on myocardial blood supply without changes in ABP, HR, CVP, or in myocardial kinetics. The coronary effects of levosimendan are related to NO production.