Myocardial homing factors are upregulated in ICM when compared with DCM hearts. Reduced homing of stem cells might therefore explain the increased number of CD34(+) cells in DCM patients. These findings may open a new insight into the pathology and the treatment of idiopathic DCM.

Background— Excessive formation of reactive oxygen species contributes to tissue injury and functional deterioration after myocardial ischemia/reperfusion. Especially, mitochondrial reactive oxygen species are capable of opening the mitochondrial permeability transition pore, a harmful event in cardiac ischemia/reperfusion. Thioredoxins are key players in the cardiac defense against oxidative stress. Mutations in the mitochondrial thioredoxin reductase (thioredoxin reductase-2, Txnrd2) gene have been recently identified to cause dilated cardiomyopathy in patients. Here, we investigated whether mitochondrial thioredoxin reductase is protective against myocardial ischemia/reperfusion injury. Methods and Results— In mice, α-MHC-restricted Cre-mediated Txnrd2 deficiency, induced by tamoxifen ( Txnrd2-/-ic ), aggravated systolic dysfunction and cardiomyocyte cell death after ischemia (90 minutes) and reperfusion (24 hours). Txnrd2-/-ic was accompanied by a loss of mitochondrial integrity and function, which was resolved on pretreatment with the reactive oxygen species scavenger N-acetylcysteine and the mitochondrial permeability transition pore blocker cyclosporin A. Likewise, Txnrd2 deletion in embryonic endothelial precursor cells and embryonic stem cell-derived cardiomyocytes, as well as introduction of Txnrd2-shRNA into adult HL-1 cardiomyocytes, increased cell death on hypoxia and reoxygenation, unless N-acetylcysteine was coadministered. Conclusions— We report that Txnrd2 exerts a crucial function during postischemic reperfusion via thiol regeneration. The efficacy of cyclosporin A in cardiac Txnrd2 deficiency may indicate a role for Txnrd2 in reducing mitochondrial reactive oxygen species, thereby preventing opening of the mitochondrial permeability transition pore.

Recordings made by this patient-operated ECG device allow to detect arrhythmias and other ECG changes with high accuracy compared with a standard ECG. It may help to improve accurate diagnosis of transient ECG changes such as paroxysmal AF in palpitations or other unexplained cardiac symptoms.

Purpose of this survey was to estimate the value of MRI for the assessment of the anatomical and functional features of sinus venosus atrial septal defect (SVD). This prospective study included 13 surgically proven cases of SVD out of 81 subjects submitted to MRI due to inconclusive transthoracic echocardiography (TTE) or suspicion of high intracardiac and/or extracardiac shunt volumes based on echocardiographic findings. MRI examination included cine SSFP sequences, contrast-enhanced 3D gradient-echo (GE) sequences for MR angiography (MRA) and phase-contrast flow-measurements. MRI revealed nine patients with a superior and four with an inferior SVD. Anomalous pulmonary venous drainage (APVD) was observed only in subjects with a superior SVD, and it was right-sided in all cases. All MRI and MRA results for the SVD patients were confirmed intraoperatively. The Correlation coefficient between MR flow measurements and cardiac catheterisation was 0.94 (P<0.0001). According to MRI the rest of the subjects (n=68) presented a secundum ASD, whereas in 18% an APVD coexisted. The latter MR outcomes concurred with the cardiac catheterisation (n=56) and operative (n=12) results. MRI provides a reliable, non-invasive method for evaluation of SVDs, APVDs and shunt quantification.

Background and Objectives: Mitral stenosis with extensive mitral annular calcification (MAC) remains surgically challenging in respect to clinical outcome. Prolonged surgery time with imminent ventricular rupture and systolic anterior motion can be considered as a complex of causal factors. The aim of our alternative hybrid approach was to reduce the risk of annual rupture and paravalvular leaks and to avoid obstruction of the outflow tract. A review of the current literature was also carried out. Materials and Methods: Six female patients (mean age 76 ± 9 years) with severe mitral valve stenosis and severely calcified annulus underwent an open implantation of an Edwards Sapien 3 prosthesis on cardiopulmonary bypass. Our hybrid approach involved resection of the anterior mitral leaflet, placement of anchor sutures and the deployment of a balloon expanded prosthesis under visual control. Concomitant procedures were carried out in three patients. Results: The mean duration of cross-clamping was 95 ± 31 min and cardiopulmonary bypass was 137 ± 60 min. The perioperative TEE showed in three patients an inconspicuous, heart valve-typical gradient on all implanted prostheses and a clinically irrelevant paravalvular leakage occurred in the anterior annulus. In the left ventricular outflow tract, mild to moderately elevated gradients were recorded. No adverse cerebrovascular events and pacemaker implantations were observed. All but one patient survived to discharge. Survival at one year was 83.3%. Conclusions: This “off label” implantation of the Edwards Sapien 3 prosthesis may be considered as a suitable bail-out approach for patients at high-risk for mitral valve surgery or deemed inoperable due to extensive MAC.