BackgroundExercise training safely and efficiently improves symptoms in patients with heart failure due to left ventricular dysfunction. However, studies in congenital heart disease with systemic right ventricle are scarce and results are controversial. In a randomised controlled study we investigated the effect of aerobic exercise training on exercise capacity and systemic right ventricular function in adults with d-transposition of the great arteries after atrial redirection surgery (28.2±3.0years after Mustard procedure).Methods48 patients (31 male, age 29.3±3.4years) were randomly allocated to 24weeks of structured exercise training or usual care. Primary endpoint was the change in maximum oxygen uptake (peak VO2). Secondary endpoints were systemic right ventricular diameters determined by cardiac magnetic resonance imaging (CMR). Data were analysed per intention to treat analysis.ResultsAt baseline peak VO2 was 25.5±4.7ml/kg/min in control and 24.0±5ml/kg/min in the training group (p=0.3). Training significantly improved exercise capacity (treatment effect for peak VO2 3.8ml/kg/min, 95% CI: 1.8 to 5.7; p=0.001), work load (p=0.002), maximum exercise time (p=0.002), and NYHA class (p=0.046). Systemic ventricular function and volumes determined by CMR remained unchanged. None of the patients developed signs of cardiac decompensation or arrhythmias while on exercise training.ConclusionsAerobic exercise training did not detrimentally affect systemic right ventricular function, but significantly improved exercise capacity and heart failure symptoms. Aerobic exercise training can be recommended for patients following atrial redirection surgery to improve exercise capacity and to lessen or prevent heart failure symptoms. (Clinical Trial Registration: ClinicalTrials.gov #NCT00837603)

AIMS Restenosis after PCI and/or stent implantation is still one of the challenging problems in the field of interventional cardiology. Different approaches to prevent and to treat restenosis include the use of drug-eluting stents, which have shown to reduce restenosis. Another approach is the treatment with drug-coated balloons. This approach has been proven for different indications, e.g., in-stent restenosis and treatment of peripheral artery disease. METHODS AND RESULTS Patients from the PEPCAD III multicentre randomised trial in two study centres (Homburg and Hannover, Germany) were asked to participate in this intravascular ultrasound (IVUS) study at nine-month follow-up. At baseline (nine months before), patients were randomly assigned to receive either a paclitaxel-coated balloon (drug-coated balloon [DCB]) plus a premounted bare metal stent (DCB/BMS) or a sirolimus-eluting stent (drug-eluting stent [DES]) to treat de novo lesions. IVUS at follow-up was performed in order to analyse the restenosis for potential understanding of the mechanism leading to restenosis. IVUS data is available for 55 patients; 26 patients were treated with Cypher(®) DES (Cordis, Miami Lakes, FL, USA) and 29 patients with DCB/BMS. A focal malapposition of the stent was seen in six patients; four after DES and two after DCB/BMS. Stent expansion, calculated as symmetric expansion index, was equal for both groups (0.89 and 0.90). Mean stent area was also equal for both groups (6.25 ± 1.7 vs. 5.65 ± 1.5 mm(2), p=n.s.). The neointimal hyperplasia (calculated as stent area minus lumen area) was significantly different between both groups (0.69 ± 0.49 [DES] vs. 1.08 ± 0.53 mm(2) [DCB/BMS], p<0.01). This resulted in a significantly higher in-stent restenosis in the DCB/BMS group (19.7 vs. 11 %, p<0.01). There is no evidence of geographical mismatch. CONCLUSIONS First IVUS insights for the DCB/BMS showed a comparable, low incidence of malapposition for the combination of drug-coated balloon and premounted bare metal stent compared to the DES, and stent expansion was good and comparable to DES. However, at nine-month follow-up, the combination of drug-coated balloon and premounted bare metal stent showed higher in-stent restenosis compared to sirolimus DES. Geographical mismatch can be excluded as a reason for this result.

Objectives The aim of this study was to investigate whether nebivolol has added effects on left ventricular (LV) dysfunction and remodeling early after myocardial infarction (MI) beyond its beta(1)-receptor-blocking properties.Background Nebivolol is a third-generation selective beta(1)-adrenoreceptor antagonist that stimulates endothelial cell nitric oxide (NO) production and prevents vascular reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activation. Both endothelial NO synthase-derived NO production and NADPH oxidase activation are critical modulators of LV dysfunction early after MI.Methods Mice with extensive anterior MI (n = 90) were randomized to treatment with nebivolol (10 mg/kg/day), metoprolol-succinate (20 mg/kg/day), or placebo for 30 days starting on day 1 after surgery.Results Infarct size was similar among the groups. Both beta(1)-adrenergic receptor antagonists caused a similar decrease in heart rate. Nebivolol therapy improved endothelium-dependent vasorelaxation and increased early endothelial progenitor cells 4 weeks after MI compared with metoprolol and placebo. Nebivolol, but not metoprolol, inhibited cardiac NADPH oxidase activation after MI, as detected by electron spin resonance spectroscopy analysis. Importantly, nebivolol, but not metoprolol, improved LV dysfunction 4 weeks after MI (LV ejection fraction: nebivolol vs. metoprolol vs. placebo: 32 +/- 4% vs. 17 +/- 6% vs. 19 +/- 4%; nebivolol vs. metoprolol: p < 0.05) and was associated with improved survival 4 weeks post-MI compared with placebo. Nebivolol had a significantly more pronounced inhibitory effect on cardiomyocyte hypertrophy after MI compared with metoprolol.Conclusions Nebivolol improves LV dysfunction and survival early after MI likely beyond the effects provided by conventional beta(1)-receptor blockade. Nebivolol induced effects on NO-mediated endothelial function, early endothelial progenitor cells and inhibition of myocardial NADPH oxidase likely contribute to these beneficial effects of nebivolol early after MI. (J Am Coll Cardiol 2011;57:601-11) (C) 2011 by the American College of Cardiology Foundation

Patients with patent foramen ovale (PFO) and cryptogenic stroke are at risk of recurrence. Therapeutic regimens range from no treatment to anticoagulation treatment to surgical or interventional closure. However, long-term follow-up is only available for up to 4 years.

The introduction of optical coherence tomography has provided a new method for evaluating the vascular response to drug-eluting stents (DESs). We used optical coherence tomography to compare neointimal coverage and stent malapposition among DESs in patients with ST-segment elevation myocardial infarction. Optical coherence tomography was performed at 9 months after implantation of 3 types of DESs at the culprit lesions in 46 patients with ST-segment elevation myocardial infarction (16 sirolimus-eluting stents [SESs, Cypher Select], 11 paclitaxel-eluting stents [PESs, Taxus Liberte], and 19 zotarolimus-eluting stents [ZESs, Endeavor Sprint]). The neointimal thickness and apposition at each strut at each 1-mm interval and the presence of thrombi in each stent were evaluated. A total of 11,512 stent struts were analyzed. SESs had the thinnest neointimal thickness (SES 62 ± 43 μm vs PES 244 ± 142 μm vs ZES 271 ± 128 μm, p <0.001). The incidence of uncovered struts and malapposed struts were significantly greater in SESs and PESs than in ZESs (SES vs PES vs ZES, 16.2 ± 17.8% vs 4.7 ± 7.4% vs 0.6 ± 1.5%, respectively, p = 0.001; and 4.0 ± 8.2% vs 2.1 ± 4.5% vs 0 ± 0%, respectively, p = 0.001). Thrombus was also detected more often in SESs and PESs than in ZESs (SES, 6 [38%] vs PES, 3 [27%] vs ZES, 1 [5%], p = 0.02). In conclusion, the rate of stent strut coverage and malapposition were significantly different among the DES types in ST-segment elevation myocardial infarction. In particular, most stent struts in ZESs were covered with neointima and well-apposed. These findings imply that the type of DES might affect the vascular response in thrombotic lesions of ST-segment elevation myocardial infarction.

Die schwere symptomatische Aortenklappenstenose ist eine zunehmende Erkrankung der alternden Bevölkerung, die mit einer deutlichen Morbidität und Mortalität verbunden ist. Bei vielen älteren Patienten wird aufgrund eines erhöhten Risikos nicht die Indikation zur Operation gestellt. Für diese Hochrisikopatienten ist die kathetergestützte Implantation der Aortenklappe eine viel versprechende Alternative. Vor einer weiteren Anwendung bei anderen Patientengruppen sind die Ergebnisse randomisierter Studien abzuwarten. Die Mitralklappenrekonstruktion mit Hilfe des MitraClips®-Systems ist eine von vielen innovativen kathetergestützten Ansätzen zur Therapie einer schweren primären (degenerativen) und sekundären (funktionellen) Mitralklappeninsuffizienz bei Patienten mit erhöhtem Risiko für eine konventionelle Operation. Der kathetergestützte Ersatz der Pulmonalklappe (PK) ist eine neue Behandlungsmethode für junge und ältere Patienten mit angeborenem Herzfehler. Nach primärer Versorgung in der frühen Kindheit benötigen einige Patienten wiederholte Operationen im Bereich der PK. Diese Eingriffe sind mit einer zunehmenden Mortalität und Morbidität verbunden. Durch die Anwendung des interventionellen Ersatzes der PK kann die Anzahl an Folgeoperationen und das perioperative Risiko dieser Patienten verringert werden.

Methods and Results: One-hundred and fourteen patients with PFO (60 men; age: 47 +/- 13 years) and >= 1 thromboembolic event were included. Other causes for embolism were excluded. PFO-closure was successful in all patients. All patients were treated with aspirin (100 mg/day) and clopidogrel (75 mg/day) for 6 months. TEE was repeated at a mean of 10.3 months. Mean clinical follow-up period was 18 +/- 9 months. After a mean of 10 months, no patient had either a significant residual shunt nor a suspected thrombus formation on the occluder. During follow-up, 5 patients suffered from neurological events (1 stroke, 2 TIAs, 2 epileptic seizures), though complete closure of the PFO was documented by TEE. One patient suffered from bleeding complications (upper GI-bleeding).Conclusion: Percutaneous closure of PFO in symptomatic patients by Amplatzer (R) occluder represents an effective therapy with a low incidence of peri-interventional complications and recurrent thromboembolism. Thrombus formations on the occluder system were not detected in this cohort. (J Interven Cardiol 2011;24:85-91).

Background: Symptomatic severe aortic stenosis is associated with increased mortality and morbidity. Early identification of these patients by echocardiography is crucial. We conducted this study to evaluate a handheld ultrasound device (HCU) in patients with suspected severe aortic stenosis (AS) in comparison to a standard echocardiography device (SE). Methods: A HCU (Vivid I; GE Healthcare) and a SE device (Philips iE 33) were used to evaluate 50 consecutive patients with suspected severe AS. Two consecutive echocardiographic studies were performed by two experienced and blinded examiners using HCU and SE device. AS was graded by mean transaortic pressure, aortic valve area (AVA), and indexed AVA (AVA adjusted for body surface area). Results: Mean difference for mean transaortic gradient, AVA and indexed AVA for the SE and HCU device were 1.28 mmHg (−0.70 to 3.26 mmHg), −0.02 cm2 (−0.06 to 0.01 cm2), and −0.01 cm2/m2 (−0.03 to 0.01 cm2/m2), respectively. Discrepancies between both devices were not associated with misinterpretation of the degree of AS. Conclusion: Our study demonstrates that HCU can be used to evaluate patients with suspected AS. (ECHOCARDIOGRAPHY 2010;27:481‐486)

Objectives: To evaluate the relation of echocardiographic parameters of diastolic function, exercise capacity (expressed as peakVO2) and NT-proBNP in patients with transposition of the great arteries (TGA) and Mustard procedure. Methods: Diastolic function was determined by measuring tricuspid flow velocities (Ea/Aa ratio), isovolumic relaxation time (IVRT), and deceleration time (DT). E/Ea ratios were calculated. For assessment of systolic function, CMR was applied. Results: E/A (r = 0.07, p = 0.66), E/Ea medial (r = 0.03, p = 0.84), E/Ea lateral (r = –0.01, p = 0.92), IVRT (r = –0.13, p = 0.44), and DT (r = –0.05, p = 0.76) were not correlated with peakVO2. NT-proBNP showed a significant correlation with IVRT (r = 0.44, p = 0.004) and Ea/Aa medial (r = –0.34, p = 0.025). No correlation was found between RV systolic function and peakVO2 (r = 0.07, p = 0.63). Conclusions: Exercise capacity in patients with TGA and Mustard procedure is not related to echocardiographic parameters of diastolic function. NT-proBNP is associated with selected echocardiographic parameters of diastolic function.

Background— In patients with myocardial infarction, high serum levels of interleukin-6 cytokines predict a poor outcome. The common receptor of interleukin-6 cytokines, glycoprotein-130 (gp130), signals via janus kinase/signal transducer and activator of transcription (STAT), cytoplasmic protein tyrosine phosphatase/extracellular signal-regulated kinase, and phosphoinositide-3-kinase/Akt pathways, and the regulation of these pathways depends at least in part on the gp130 tyrosine-757 residue. By analyzing cardiomyocyte-specific gp130 Y757F mutant mice, we investigated the effect of disturbed gp130 signaling after myocardial infarction. Methods and Results— The cardiomyocyte-restricted α-myosin heavy chain-Cre-recombinase-loxP system was used to generate mice with gp130 Y757F mutant cardiomyocytes ( αMHC-Cre tg/− ;gp130 fl/Y757F [Y 757 F]); all other cells carried at least 1 functional gp130 gene, ensuring normal gp130 signaling. Y 757 F mice displayed normal cardiac function and morphology at 3 months of age comparable to their nonmutant littermates. In response to myocardial infarction, Y 757 F mice displayed higher mortality associated with increased left ventricular rupture rate, sustained cardiac inflammation, and heart failure. These adverse effects were associated with prolonged and enhanced STAT3 activation and increased expression of interleukin-6 and of the complement-activating mannose-binding lectin C. Pharmacological inhibition of the complement system by cobra venom factor attenuated inflammation, prevented left ventricular rupture, and improved cardiac function in Y 757 F mice. Stronger effects were observed with a genetic reduction of STAT3 (STAT3 flox/+ ) restricted to cardiomyocytes in Y 757 F mice, which prevented extensive upregulation of interleukin-6, complement activation, and sustained inflammation and lowered left ventricular rupture rate, heart failure, and mortality in subacute myocardial infarction. Conclusion— Impaired downregulation of gp130-mediated STAT3 activation in subacute infarction promotes cardiac inflammation, adverse remodeling, and heart failure, suggesting a potential causative role of high interleukin-6 serum levels after myocardial infarction.

We assessed whether a single intracoronary infusion of autologous bone marrow cells (BMCs) can have a sustained impact on left ventricular ejection fraction (LVEF) in patients after ST-elevation myocardial infarction (STEMI). In the BOne marrOw transfer to enhance ST-elevation infarct regeneration (BOOST) trial, 60 patients with STEMI and successful percutaneous coronary intervention were randomized to a control and a cell therapy group. As previously reported, BMC transfer led to an improvement of LVEF by 6.0% at 6 months (P = 0.003) and 2.8% at 18 months (P = 0.27).Left ventricular ejection fraction and clinical status were re-assessed in all surviving patients after 61 +/- 11 months. Major adverse cardiac events occurred with similar frequency in both groups. When compared with baseline, LVEF assessed by magnetic resonance imaging at 61 months decreased by 3.3 +/- 9.5% in the control group and by 2.5 +/- 11.9% in the BMC group (P = 0.30). Patients with an infarct transmurality > median appeared to benefit from BMC transfer throughout the 61-month study period (P = 0.040).A single intracoronary application of BMCs does not promote a sustained improvement of LVEF in STEMI patients with relatively preserved systolic function. It is conceivable that a subgroup of patients with more transmural infarcts may derive a sustained benefit from BMC therapy. However, this needs to be tested prospectively in a randomized trial.

We have recently observed that intracoronary autologous bone marrow cell (BMC)-transfer improves parameters of diastolic function in patients after acute myocardial infarction at 6 and 18 months. There is no clinical study addressing the long-term effect of BMC transfer on diastolic function. Therefore, we conducted a 5-year follow-up of the BOOST trial to evaluate a sustained benefit on echocardiographic parameters on diastolic function.After successful primary percutaneous coronary intervention (PCI) for acute ST-elevation MI, patients were randomized to a control (n = 28) or BMC transfer group (n = 28). Echocardiography was performed at 4.5 +/- 1.5 days after PCI, at 6, 18, and 60 months. Diastolic function was determined by measuring transmitral flow velocities (E/A ratio), diastolic myocardial velocities (E(a)/A(a) ratio), isovolumic relaxation time (IVRT), and deceleration time (DT). All analyses were performed in a blinded fashion. There was an overall treatment effect of BMC transfer on E/A (0.25 +/- 0.10; 95% CI 0.05-0.44; P = 0.01). E/A ratio was significantly lower at 6 (Control 0.90 +/- 0.07; BMC 1.23 +/- 0.14; P = 0.03) and 18 months (Control 0.87 +/- 0.04; BMC 1.13 +/- 0.09; P = 0.01) in the control group, whereas E/A ratio was not different at 60 months between both groups (Control 0.90 +/- 0.06; BMC 1.05 +/- 0.07; P = 0.12). We found no overall effect of BMC transfer on E(a)/A(a) ratio (0.21 +/- 0.14; 95% CI -0.03 to 0.46; P = 0.09), DT (-12 +/- 11 ms; 95% CI -21 to 28; P = 0.75), IVRT -6 +/- 7 ms; 95% CI -9 to 19; P = 0.43), and E/E(a) ratio (0.58 +/- 0.88; 95% CI -1.18 to 2.34; P = 0.51).Intracoronary autologous BMC transfer provides an overall treatment effect on echocardiographic parameters of diastolic function in patients after AMI. However, this effect is basically related to an early improvement of parameters of diastolic function without a sustained effect on long-term follow-up.

Die Mitralklappeninsuffizienz (MI) ist die zweithäufigste Klappenerkrankung in Europa. Grundsätzlich ist zwischen einer primären und sekundären bzw. funktionellen MI zu unterscheiden. Bei einer primären MI liegt die Ursache in einem morphologischen Defekt der Mitralklappe, der zur Volumenbelastung, linksventrikulären Dilatation und schließlich zur Einschränkung der linksventrikulären systolischen Funktion führt. Bei Patienten mit primärer MI ist eine frühzeitige operative Korrektur in Form einer Mitralklappenrekonstruktion oder eines Mitralklappenersatzes Therapie der Wahl.

As the first reliable prosthetic heart valve to be introduced, the Starr-Edwards ball valve prosthesis has gained worldwide clinical acceptance. Although very few instances have been described of valve durability exceeding 30 years, the case is reported of a patient with a well-functioning Starr-Edwards ball valve prosthesis in the aortic position, 43 years after implantation.

Mitral regurgitation (MR) is the second most frequent valve disease in Europe. In addressing the current therapy for MR, it is useful to distinguish primary from secondary or functional MR. In primary MR, there is derangement of the mitral valve itself causing left ventricular volume overload and left ventricular dysfunction. By contrast, in secondary MR, the valve and its components are typically normal and MR is related to changes of annular size (dilatation) and papillary muscle displacement due to left ventricular damage caused by myocardial infarction or dilated cardiomyopathy.In primary MR, mitral valve repair or replacement is the first-line therapy. In secondary MR, the best management includes standard medical therapy for heart failure and cardiac resynchronization therapy in selected patients. Since there is no evidence from randomized studies that surgery improves mortality, this approach may only be considered in patients who remain symptomatic despite optimal medical therapy or in patients undergoing coronary revascularization.

BACKGROUND Prevalence of patent foramen ovale (PFO) is higher in patients with paradoxical embolism and associated with increased risk for recurrent thromboembolic events. By percutaneous closure of PFO, surgical closure or permanent oral anticoagulation can be avoided. So far, published series included different occluder systems and various indications and regimens of postprocedural anticoagulation. The aim of the present study was to evaluate the short- and long-term results after implantation of the Starflex occluder in patients with PFO using an intensified anticoagulation regimen. METHODS AND RESULTS 154 patients with PFO (94 men; age: 44 +/- 13 years) and >or=1 thromboembolic event were included. Other causes for embolism were excluded. PFO closure was successful in 147 patients (95.5%). All patients were treated with phenprocoumon (INR 2.5) and aspirin (100 mg/die) for 6 months. Transesophageal echocardiography (TEE) was repeated at 6 months. Mean clinical follow-up period was 26 +/- 18 months. After 6 months, five patients had a significant residual shunt, and five patients had suspected thrombus formation on the occluder. In three of these five patients, the occluder was surgically removed and foreign body reaction was noted. During follow-up, nine patients suffered from neurological events (two strokes, seven transient ischemic attacks [TIA]), though complete closure of the PFO was documented by TEE. Two patients died during follow-up; three patients had bleeding complications. CONCLUSION Percutaneous closure of PFO in symptomatic patients by Starflex occluder represents an effective therapy with a low incidence of periinterventional complications and recurrent thromboembolism. However, thrombus formation at the occluder system may occur in some patients despite an aggressive anticoagulation regimen.

Accumulating evidence suggests a critical role of increased reactive oxygen species production for left ventricular (LV) remodeling and dysfunction after myocardial infarction (MI). An increased myocardial activity of the NAD(P)H oxidase, a major oxidant enzyme system, has been observed in human heart failure; however, the role of the NAD(P)H oxidase for LV remodeling and dysfunction after MI remains to be determined. MI was induced in wild-type (WT) mice (n=46) and mice lacking the cytosolic NAD(P)H oxidase component p47 phox (p47 phox −/− mice) (n=32). Infarct size was similar among the groups. NAD(P)H oxidase activity was markedly increased in remote LV myocardium of WT mice after MI as compared with sham-operated mice (83±8 versus 16.7±3.5 nmol of O 2 − · μg −1 ·min −1 ; P <0.01) but not in p47 phox −/− mice after MI (13.5±3.6 versus 15.5±3.5 nmol of O 2 − · μg −1 ·min −1 ), as assessed by electron-spin resonance spectroscopy using the spin probe CP-H. Furthermore, increased myocardial xanthine oxidase activity was observed in WT, but not in p47 phox −/− mice after MI, suggesting NAD(P)H oxidase–dependent xanthine oxidase activation. Myocardial reactive oxygen species production was increased in WT mice, but not in p47 phox −/− mice, after MI. LV cavity dilatation and dysfunction 4 weeks after MI were markedly attenuated in p47 phox −/− mice as compared with WT mice, as assessed by echocardiography (LV end-diastolic diameter: 4.5±0.2 versus 6.3±0.3 mm, P <0.01; LV ejection fraction, 35.8±2.5 versus 22.6±4.4%, P <0.05). Furthermore, cardiomyocyte hypertrophy, apoptosis, and interstitial fibrosis were substantially reduced in p47 phox −/− mice as compared with WT mice. Importantly, the survival rate was markedly higher in p47 phox −/− mice as compared with WT mice after MI (72% versus 48%; P <0.05). These results suggest a pivotal role of NAD(P)H oxidase activation and its subunit p47 phox for LV remodeling/dysfunction and survival after MI. The NAD(P)H oxidase system represents therefore a potential novel therapeutic target to prevent cardiac failure after MI.

BACKGROUND:Mice with a knockout (KO) of muscle LIM protein (MLP) exhibit many morphologic and clinical features of human cardiomyopathy. In humans, MLP-expression is downregulated both in ischemic and dilative cardiomyopathy. In this study, we investigated the effects of MLP on the electrophysiologic phenotype in vivo and on outward potassium currents. METHODS AND RESULTS:MLP-deficient (MLPKO) and wild-type (MLPWT) mice were subjected to long-term electrocardiogram (ECG) recording and in vivo electrophysiologic study. The whole-cell, patch-clamp technique was applied to measure voltage dependent outward K+ currents in isolated cardiomyocytes. Long-term ECG revealed a significant prolongation of RR mean (108 +/- 9 versus 99 +/- 5 ms), P (16 +/- 3 versus 14 +/- 1 ms), QRS (17 +/- 3 versus 13 +/- 1 ms), QT (68 +/- 8 versus 46 +/- 7 ms), QTc (66 +/- 6 versus 46 +/- 7 ms), JT (51 +/- 7 versus 34 +/- 7 ms), and JTc (49 +/- 5 versus 33 +/- 7 ms) in MLPKO versus MLPWT mice (P < .05). During EP study, QT (80 +/- 8 versus 58 +/- 7 ms), QTc (61 +/- 6 versus 45 +/- 5 ms), JT (62 +/- 9 versus 43 +/- 6 ms), and JTc (47 +/- 5 versus 34 +/- 5 ms) were also significantly prolonged in MLPKO mice (P < .05). Nonsustained VT was inducible in 9/16 MLPKO versus 2/15 MLPWT mice (P < .05). Analysis of outward K+ currents in revealed a significantly reduced density of the slowly inactivating outward K+ current IK, slow in MLPKO mice (11 +/- 5 pA/pF versus 18 +/- 7 pA/pF; P < .05). CONCLUSION:Mice with KO of MLP exhibit significant prolongation of atrial and ventricular conduction and an increased ventricular vulnerability. A reduction in repolarizing outward K+ currents may be responsible for these alterations.

A 48-year-old woman was admitted to our hospital for evaluation of chronic heart failure (NYHA III). Her past medical history showed a chronic anemia due to a myelodysplastic syndrome (MDS), requiring 136 transfusions of erythrocytes for the last 10 years. Six months ago she additionally developed diabetes mellitus, hypothyroidism, breast cancer and renal impairment.

We are presenting a case of floating left and right atrial formations on an atrial septal defect occluder system (23mm StarFLEX)-Occluder) initially supposed to be thrombotic appositions in a 57-year-old man. The closure was performed on the background of left hemispheric stroke and atrial septal aneurysm (ASA) with patent foramen ovale (PFO). The suspect structures were detected in the 6-month follow-up by transesophageal echocardiography (TEE). The patient underwent a successful surgical explantation of the closure device and closure of the patent foramen ovale (PFO) using a pericardial patch. The pathological evaluation of the biatrial device associated appositions revealed hytrophic heart muscle tissue with perifocal scarring and purulent abscess-forming, granulating and foam-cell including inflammatory foreign body reaction instead of the expected thrombus formation.