Left ventricular noncompaction (LVNC) is a myocardial disorder probably due to the arrest of normal embryogenesis of the left ventricle. It could be isolated or associated with other extracardiac and cardiac abnormalities, including coronary artery anomalies. Despite the continuous improvement of imaging resolution quality, this cardiomyopathy still remains frequently misdiagnosed, especially if associated with other heart diseases. We report a case of LVNC association with both malposition of the great arteries and a very original coronary artery pattern.

Transcatheter aortic valve implantation (TAVI) technique represents a real revolution in the field of interventional cardiology and medicine, in particular for the treatment of severe aortic valve stenosis in elderly patients or in patients when the periprocedural risk for the traditional surgical option is considered too high, as an alternative to the traditional aortic valve replacement. Although experience on the valves of the last generation is still limited in terms of time, the data currently available are definitely moving in the direction of a minimum hospital mortality (1%) as well as a drastic reduction in the incidence of complications when compared to the devices of the previous generation. Finally, the evolution of specified materials of the newest generation have greatly enhanced safety and efficacy of TAVI procedures in the last years. In order to ensure the selection of the most appropriate valve and the success of the procedure, the role of cardiac imaging (computed tomography scan evaluation and angiography) is crucial. These examinations require the use of contrast medium in patients suffering from renal dysfunction at the baseline. The need for fluoroscopy and angiography using contrast agents to aid positioning of the valve may lead to contrast-induced nephropathy (CIN) as one form or one etiology of acute kidney injury (AKI), which is associated with increased morbidity and mortality. The aim of our study is to investigate the accuracy of intravascular ultrasound (IVUS-a technique which does not need contrast) for the assessment of native valve measures in patients undergoing TAVI by comparing values obtained with IVUS to those ones previously obtained in the same patients with computed tomography (CT) scans.

Takotsubo cardiomyopathy (TTC) is a form of acute left ventricular dysfunction usually reversible and with favorable prognosis. Ventricular septal perforation (VSP) is a very rare life-threatening complication. Percutaneous closure of VSP, despite being challenging, is a possible alternative to surgical repair. We present the first case of an 84-year-old patient with a TTC-related VSP treated by percutaneous approach. The case highlights the need of reconsidering the worldwide accepted consideration of TTC as benignant and allows some speculations on the optimal management of VSP in terms of timing, patient selection and possible alternative interventions.

Takotsubo cardiomyopathy (TTC) is characterized by transient systolic ventricular dysfunction. It is supposed to be caused by a cathecolaminergic wave which leads to myocardial stunning through a massive action on beta2-adrenoreceptor. Moreover, beta2-receptor hyperactivity negatively influences endothelial function. It can be detected by brachial flow mediated dilation (b-FMD) which assesses endothelium regulated vasomotility. The study aim is to analyze the b-FMD variability during hospitalization in 50 patients admitted with TTC. In addition, we investigated a possible correlation between b-FMD at admission and both length of hospital stay (LOHS) and troponin I peak. We detected b-FMD by measuring the hypoxic induced vasoreactivity through assessing brachial artery dilation after 5 min of iatrogenic ischemia obtained by inflating a sphygmomanometer cuff. Artery diameter modifications were assessed by high-resolution ultrasound, and a dedicated software calculated accurately the percentage of dilation after ischemia by comparing it to the basal. These values were measured at admission and on discharge. The obtained values were compared for each patient to explore their variability during hospitalization. Moreover, the correlation between the b-FMD at admission and both the troponin I peak and the LOHS was investigated. There was a statistical significant difference between mean FMD measured at admission and at discharge (respectively 1.54 ± 0.34 and 8.92 ± 2.48%; p < 0.001). Moreover, we found a significant negative correlation between troponin I peak and FMD values at admission (r = - 0.7645; p < 0.001) and a significant inverse correlation between FMD at admission and LOHS (r = - 0.7543; p < 0.001). There is a significant improvement of b-FMD during hospitalization in patients admitted for Tako-Tsubo Cardiomyopathy. Moreover, for the first time, a direct correlation among b-FMD, troponin I peak and LOHS has been detected.

The The aim of our study is to investigate the molecular mechanisms of diabetic cardiomyopathy through the identification of remarkable genes for the myocardial function that are expressed differently between diabetic and normal subjects. Moreover, we intend to characterize both in human myocardial tissue and in the related cardiac progenitor cells the pattern of gene expression and the levels of expression and protein activation of molecular effectors involved in the regulation of the myocardial function and differentiation to clarify whether in specific human pathological conditions (type 2 diabetes mellitus, cardiac failure, coronary artery disease) specific alterations of the aforementioned factors could take place. Thirty-five patients scheduled for coronary artery bypass grafting (CABG) or for aortic or mitral valve replacement were recruited into the study. There were 13 men and 22 women with a mean age of 64.8 +/- 13.4 years. A list of anamnestic, anthropometric, clinical, and instrumental data required for an optimal phenotypical characterization of the patients is reported. The small cardiac biopsy specimens were placed in the nourishing buffer, in a sterile tube provided the day of the procedure, to maintain the stability of the sample for several hours at room temperature. The cells were isolated by a dedicated protocol and then cultured in vitro. The sample was processed for total RNA extraction and levels of gene expression and protein activation of molecular effectors involved in the regulation of function and differentiation of human myocardium was analyzed. In particular, cardiac genes that modulate the oxidative stress response or the stress induced by pro-inflammatory cytokines (p66Shc, SOCS-1, SOCS-3) were analyzed. From a small sample of myocardium cardiac stem cells and cardiomyoblasts were also isolated and characterized. These cells showed a considerable proliferative capacity due to the fact that they demonstrate stability up to the eleventh passage. Analysis of gene expression in a subgroup of subjects showed the trend of a decrease in levels of expression of cardiac-specific transcription genes and oxidative stress-related proteins in tissues of diabetic patients compared with controls subjects. This trend is not confirmed in isolated cells. As for the coronary artery disease, diabetic cardiomyopathy could be associated with a reduction of the cardiac stem and progenitor cells pool. The expansion of the cardiac resident cells pool could be associated with a preservation of cardiac performance, suggesting that a preserved stamina compartment can counteract the impact of diabetes on the myocardium.

To report the use of endografts to manage multiple aneurysms due to Cogan syndrome (CS). A 38-year-old woman with descending thoracic aorta and right common carotid artery aneurysms due to CS was treated with endovascular grafts. After 4 years, angio computed tomography scan demonstrated complete exclusion of the aneurysms with no signs of endoleak, whereas echo color Doppler showed patency of the carotid graft, no signs of restenosis, no progression of the disease in the landing zones, and complete aneurysm exclusion. Endovascular repair seems to have favorable long-term outcomes and should be considered a viable alternative to surgery in unfit for open surgery patients, even if they are young, and when the aneurysm size and location would pose a higher risk of perioperative and postoperative complications after an open surgical procedure.

Increased apoptosis of cardiac progenitor cells (CPCs) has been proposed as a mechanism of myocardial damage and dysfunction. Glucagon-like peptide-1 (GLP-1) has been shown to improve heart recovery and function after ischemia and to promote cell survival. The protective effects of GLP-1 on oxidative stress-induced apoptosis were investigated in human CPCs isolated from human heart biopsies. Mesenchymal-type cells were isolated from human heart biopsies, exhibited the marker profile of CPCs, differentiated toward the myocardiocyte, adipocyte, chondrocyte, and osteocyte lineages under appropriate culture conditions, and expressed functional GLP-1 receptors. CPCs were incubated with GLP-1 with or without hydrogen peroxide (H(2)O(2)). Phospho- and total proteins were detected by immunoblotting and immunofluorescence analysis. Gene expression was evaluated by quantitative RT-PCR. The role of the canonical GLP-1 receptor was assessed by using the receptor antagonist exendin(9-39) and receptor-specific silencer small interfering RNAs. Cell apoptosis was quantified by an ELISA assay and by flow cytometry-detected Annexin V. Exposure of CPCs to H(2)O(2) induced a 2-fold increase in cell apoptosis, mediated by activation of the c-Jun N-terminal protein kinase (JNK) pathway. Preincubation of CPCs with GLP-1 avoided H(2)O(2)-triggered JNK phosphorylation and nuclear localization, and protected CPCs from apoptosis. The GLP-1 effects were markedly reduced by coincubation with the receptor antagonist exendin(9-39), small interfering RNA-mediated silencing of the GLP-1 receptor, and pretreatment with the protein kinase A inhibitor H89. In conclusion, activation of GLP-1 receptors prevents oxidative stress-mediated apoptosis in human CPCs by interfering with JNK activation and may represent an important mechanism for the cardioprotective effects of GLP-1.

Background Coronary artery disease (CAD) commonly coexists with degenerative aortic stenosis. The impact of CAD in patients undergoing transcatheter aortic valve implantation (TAVI) raises concerns due to the lack of comprehensive and consistent data on this topic. We sought to evaluate the impact of CAD on clinical outcomes in patients undergoing TAVI. Methods Consecutive patients(N = 663) who underwent TAVI with the 18-French CoreValve ReValving System (CRS) (Medtronic Inc, MN USA) from June 2007 through December 2009 at 14 institutions across Italy were included in this prospective web-based registry. Four patients were excluded from the analysis due to failure to successfully release the prosthesis inside the native aortic valve. Previous percutaneous or surgical myocardial revascularizations were used to identify the existence of concomitant CAD (N = 251; 38%). The primary endpoint was the incidence of Major Adverse Cerebrovascular and Cardiac Events (MACCE) and all-cause death in CAD and no-CAD groups. Results Patients with CAD were no more likely to develop MACCE within 12-months of the procedure than those who did not (CAD group vs no-CAD group, 15.7% vs 18.3%; adjusted hazard ratio [HR] 0.76; 95% confidence interval [CI] 0.42 to 1.36; p = 0.353). The 12-month mortality was 14.5% and 15.9% in CAD group and no-CAD group, respectively (adjusted HR 0.74; 95% CI 0.40 to 1.36; p = 0.331). Conclusions Coexisting CAD does not impact procedural outcomes and mid-term incidence of MACCE and survival in elderly patients undergoing TAVI with CRS prosthesis.

Abstract BACKGROUND: Implantable cardioverter-defibrillators (ICDs) have a role in preventing cardiac arrest in patients at risk for life-threatening ventricular arrhythmias. PURPOSE: To compare ICD therapy with conventional care for the primary prevention of death of various causes in adults with ischemic or nonischemic cardiomyopathy. DATA SOURCES: MEDLINE, Cochrane Central Register of Controlled Trials, Google Scholar, and EMBASE databases, as well as several Web sites, from 1 April 1976 through 31 March 2017. STUDY SELECTION: Randomized controlled trials, published in any language, comparing ICD therapy with conventional care and reporting mortality outcomes (all-cause, sudden, any cardiac, or noncardiac) in the primary prevention setting. DATA EXTRACTION: 2 independent investigators extracted study data and assessed risk of bias. DATA SYNTHESIS: Included were 11 trials involving 8716 patients: 4 (1781 patients) addressed nonischemic cardiomyopathy, 6 (4414 patients) ischemic cardiomyopathy, and 1 (2521 patients) both types of cardiomyopathy. Mean follow-up was 3.2 years. An overall reduction in all-cause mortality, from 28.26% with conventional care to 21.37% with ICD therapy (hazard ratio [HR], 0.81 [95% CI, 0.70 to 0.94]; P = 0.043), was found. The magnitude of reduction was similar in the cohorts with nonischemic (HR, 0.81 [CI, 0.72 to 0.91]) and ischemic (HR, 0.82 [CI, 0.63 to 1.06]) disease, although the latter estimate did not reach statistical significance. The rate of sudden death fell from 12.15% with conventional care to 4.39% with ICD therapy (HR, 0.41 [CI, 0.30 to 0.56]), with a similar magnitude of reduction in patients with ischemic (HR, 0.39 [CI, 0.23 to 0.68]) and those with nonischemic disease (HR, 0.44 [CI, 0.17 to 1.12]). Noncardiac and any cardiac deaths did not differ significantly by treatment. LIMITATION: Heterogeneous timing of ICD placement; heterogeneous pharmacologic and resynchronization co-interventions; trials conducted in different eras; adverse events and complications not reviewed. CONCLUSION: Overall, primary prevention with ICD therapy versus conventional care reduced the incidence of sudden and all-cause death. PRIMARY FUNDING SOURCE: None.

Mitral regurgitation (MR) is the most prevalent valvular heart disease (VHD) and represents an important cause of heart failure. Medical therapy has a limited role in improving symptoms and does not hinder the progression of valvular disease. Surgery is the treatment of choice for severe symptomatic MR; valve repair is currently the preferred surgical approach because it reduces peri-operative mortality and ensures a good medium- to long-term survival outcome. Nevertheless, a non-negligible proportion of patients with indications for surgical correction are considered to be at prohibitive perioperative risk, mainly because of old age and multiple comorbidities. The introduction of percutaneous interventions to clinical practice has changed the natural history of this population. Percutaneous edge-to-edge transcatheter mitral valve repair (Mitraclip®, Abbott Vascular, Menlo Park, CA) is a state-of-the-art therapy for approaching MR in patients with a high surgical risk. Despite having been only recently introduced, this transvenous transfemoral percutaneous intervention has already been performed in more than 40,000 subjects worldwide, with reassuring post-operative results in terms of safety, feasibility, mortality and morbidity. Since Mitraclip® is considered to be minimally invasive, it is currently indicated in "frail" patients with severe comorbidities. We provide a critical review of the literature to clarify current indications, procedural details, patient selection criteria, and future perspectives for this innovative technique.

Cryptogenic stroke is the final diagnosis in almost 40% of ischemic acute cerebrovascular events. There is currently no definitive clinical evidence that percutaneous closure of patent foramen ovale (PFO) can prevent the recurrence of stroke or transient ischemic attack (TIA). Identification of the causes of neurologic ischemic syndromes is essential for any strategy intended to prevent the catastrophic consequences of cerebral infarction. Since the initial reports of an unexpectedly high prevalence of PFO in younger patients with cryptogenic stroke in 1988, there has been growing interest and experience in diagnosing and treating these patients, both medically and/or with percutaneous closure, in particular for the potential to eliminate paradoxical embolism via PFO, which is a likely mechanism for stroke in these patients. Selection of the appropriate occluder device is of paramount importance for the success of the procedure. While devices like the Amplatzer™ PFO Occluder (St. Jude Medical), which, based on the extended follow-up of the RESPECT Trial, was approved by the U.S. Food and Drug Administration last year for recurrent stroke prevention, have become generally accepted as being better than medical therapy for patients needing treatment, concerns remain regarding device- and procedure-related complications. NobleStitch™ EL is a novel device that offers a simple non-prosthetic implant method of PFO closure without the inherent risks seen with septal occluders: no risk of device embolization, device thrombosis or late erosion, and probably no risk of arrhythmia. Futhermore, there is no material that would hinder future access to the left atrium and no requirement for anti-coagulation.