Increased β-adrenergic inotropy in ventricular myocardium from Trpm4-/- mice.

Rationale: The Trpm4 gene has recently been associated with several disorders, including cardiac conduction diseases and Brugada syndrome. Transient receptor potential member 4 (TRPM4) proteins constitute Ca2+ -activated, but Ca2+ -impermeable, nonselective cation channels and are expressed both in atrial and in ventricular cardiomyocytes. The physiological function of TRPM4 in the heart remains, however, incompletely understood.

NO-dependent endothelial dysfunction in type II diabetes is aggravated by dyslipidemia and hypertension, but can be restored by angiotensin-converting enzyme inhibition and weight loss.

Aims: Insulin resistance, dyslipidemia and hypertension are independent mediators of endothelial dysfunction. It is incompletely defined whether dyslipidemia and hypertension in addition to diabetes mellitus type II (DMII), as seen in the metabolic syndrome (MS), worsen diabetes-induced endothelial dysfunction. Furthermore, it is unclear whether treatment influences endothelial dysfunction similarly in MS and DMII.

ACE-inhibition, but not weight reduction restores cardiomyocyte response to β-adrenergic stimulation in the metabolic syndrome.

Background: Diabetic cardiomyopathy is characterized by systolic and early diastolic ventricular dysfunction. In the metabolic syndrome (MS), ventricular stiffness is additionally increased in a later stage. It is unknown whether this is related to intrinsic cardiomyocyte dysfunction, extrinsic factors influencing cardiomyocyte contractility and/or cardiac function, or a combination of both.

Angiotensin-converting enzyme inhibition and food restriction restore delayed preconditioning in diabetic mice.

Background: Classical and delayed preconditioning are powerful endogenous protection mechanisms against ischemia-reperfusion damage. However, it is still uncertain whether delayed preconditioning can effectively salvage myocardium in patients with co-morbidities, such as diabetes and the metabolic syndrome. We investigated delayed preconditioning in mice models of type II diabetes and the metabolic syndrome and investigated interventions to optimize the preconditioning potential.

Angiotensin-converting enzyme inhibition and food restriction in diabetic mice do not correct the increased sensitivity for ischemia-reperfusion injury.

Background: The number of patients with diabetes or the metabolic syndrome reaches epidemic proportions. On top of their diabetic cardiomyopathy, these patients experience frequent and severe cardiac ischemia-reperfusion (IR) insults, which further aggravate their degree of heart failure. Food restriction and angiotensin-converting enzyme inhibition (ACE-I) are standard therapies in these patients but the effects on cardiac IR injury have never been investigated.

Surgical angioplasty and unroofing technique for intramural coronary anomaly.

A malign intramural course of the left main coronary artery is a rare anatomical anomaly. Surgical repair is mandatory since the condition is associated with myocardial ischemic syndromes and sudden death. Unroofing the intramural part and reconstructing a neo-ostium is challenging if the neo-ostium is immediately adjacent to the intercoronary commissure as there is a risk of narrowing the newly created ostium.

Effect of sutureless implantation of the Perceval S aortic valve bioprosthesis on intraoperative and early postoperative outcomes.

Objective: Prolonged aortic crossclamping can increase mortality and morbidity after aortic valve replacement in elderly and high-risk patients. Sutureless implantation of the prosthesis has the potential to shorten aortic crossclamp time.

Methods: The Perceval S valve (Sorin Biomedica Cardio Srl, Sallugia, Italy), a sutureless implantable aortic bioprosthesis, was used in 32 patients (median age, 78 years; median logistic euroSCORE, 9.

Increased catecholamine secretion contributes to hypertension in TRPM4-deficient mice.

Hypertension is an underlying risk factor for cardiovascular disease. Despite this, its pathogenesis remains unknown in most cases. Recently, the transient receptor potential (TRP) channel family was associated with the development of several cardiovascular diseases linked to hypertension.

Long-term blinded placebo-controlled study of SNT-MC17/idebenone in the dystrophin deficient mdx mouse: cardiac protection and improved exercise performance.

Aims: Duchenne muscular dystrophy (DMD) is a severe and still incurable disease, with heart failure as a leading cause of death. The identification of a disease-modifying therapy may require early-initiated and long-term administration, but such type of therapeutic trial is not evident in humans. We have performed such a trial of SNT-MC17/idebenone in the mdx mouse model of DMD, based on the drug's potential to improve mitochondrial respiratory chain function and reduce oxidative stress.

Pericardial synovial sarcoma: 14-year survival with multimodality therapy.

We report a case of recurrent primary synovial sarcoma of the pericardium. Reverse transcriptase-polymerase chain reaction analysis for t(X,18) demonstrated the presence of the chimeric transcript SYT/SSX. Because of the rarity of this entity, optimal therapy is unknown.