Transcatheter implantation of the MONARC coronary sinus device for mitral regurgitation: 1-year results from the EVOLUTION phase I study (Clinical Evaluation of the Edwards Lifesciences Percutaneous Mitral Annuloplasty System for the Treatment of Mitral Regurgitation).

Objectives: This study sought to assess the safety and efficacy of transcatheter valve annuloplasty in patients with mitral regurgitation (MR).

Background: Mitral regurgitation is associated with a worsened prognosis in patients with dilated cardiomyopathy. Surgical mitral annuloplasty reduces the septal-lateral dimension of the mitral annulus resulting in improved leaflet coaptation with a reduction in regurgitation.

GDF5 and BMP2 inhibit apoptosis via activation of BMPR2 and subsequent stabilization of XIAP.

GDF5 and BMP2, members of the TGF-beta superfamily of growth factors, are known to regulate apoptosis in different cell types either positively or negatively. We wanted to investigate the effects of GDF5 and BMP2 on vascular smooth muscle cells and mouse embryonic fibroblasts and disclose the mechanism by which GDF5 and BMP2 might exert anti-apoptotic effects. The effect of GDF5 and BMP2 on proliferation and/or programmed cells death was assessed in isolated human vascular smooth muscle cells and mouse embryonic fibroblasts.

Significance of close surveillance of patients with peripheral arterial disease.

Background: Peripheral arterial disease (PAD) indicates generalized atherosclerosis but is still underdiagnosed and undertreated.

Methods: Data were collected from patients with PAD from the Department of Cardiology and Angiology, University of Heidelberg, Germany. The prevalence of cardiovascular risk factors and medication were documented.

Abdominal aortic aneurysm repair in cardiac high risk patients--medication, surgery or stent?

With increasing age of the general population, a higher awareness of the disease, better screening methods and the option of less invasive therapeutical strategies, the incidence of abdominal aortic aneurysms (AAA) is rising steadily. Since AAA is a disease of the elderly patient with generalized atherosclerosis, there is a high coincidence with other vascular morbidities. Especially the presence of coronary artery disease and concomitant left ventricular dysfunction proves many of those patients to be cardiac high risk patients with respect to an operative approach.

Myocardial preconditioning and remote renal preconditioning--identifying a protective factor using proteomic methods?

It is still unknown whether remote ischemic preconditioning is mediated by a humoral or a neurogenic mechanism from the preconditioning to the preconditioned tissue. The purpose of the following study was to identify a possible humoral trigger of ischemic myocardial preconditioning and remote renal preconditioning. Open chest rats were subjected to a coronary artery occlusion period of 45 min followed by 2 h of reperfusion (Control animals; n = 6).

ACE inhibitors and statins acutely improve endothelial dysfunction of human coronary arterioles.

Long-term treatment with angiotensin-converting enzyme (ACE) inhibitors as well as angiotensin II type 1 (AT(1)) receptor antagonists and statins reduces cardiovascular mortality in patients with coronary artery disease as well as chronic heart failure. Little is known about the acute effects of these compounds on vascular reactivity of coronary resistance vessels. Coronary arterioles were obtained from patients undergoing coronary bypass operation (atherosclerosis group) or valve replacement (control group).

Sepiapterin reduces postischemic injury in the rat heart.

A reduced availability of tetrahydrobiopterin (BH4), an essential cofactor for NO-synthesis, is causally involved in the development of endothelial dysfunction associated with ischemia/reperfusion. We, therefore, investigated the effect of sepiapterin, a substrate for BH4 synthesis, on postischemic injury in myocardial infarction and myocardial stunning. In rats, myocardial stunning was induced by repetitive ischemia (5 x 10-min ligature of the left coronary artery, 5 x 20-min reperfusion) and myocardial infarction by 50-min ligature and 60-min reperfusion.