Ischemic mitral regurgitation: Pathophysiology, diagnosis and surgical treatment

none5noIschemic mitral valve regurgitation often complicates acute myocardial infarction and also represents a negative prognostic factor for long-term survival in patients undergoing surgical myocardial revascularization. While severe mitral regurgitation should always be corrected during a coronary artery bypass operation, the decision making is more difficult in patients with a mild-to-moderate degree of regurgitation. Recent studies and experimental protocols have elucidated the pathophysiological mechanisms leading to mitral regurgitation with great interest in annular modifications and subvalvular alterations. These data suggest that new and integrated surgical approaches that address annuloplasty ring sizing, ring type selection and tethering phenomenon (i.e., chordal cutting, 'edge-to-edge' technique and left-ventricular plasty techniques) are required for a safer and durable valve repair. Transthoracic and transesophageal echocardiography are useful in determining the etiology and the degree of mitral regurgitation, to assess mitral deformation and to measure indexes of global and regional left-ventricular remodeling. Stress echocardiography may unmask higher degrees of mitral regurgitation. More data are needed in order to confirm the promising and interesting preliminary experimental findings of magnetic resonance imaging in diagnosis and clinical evaluation of ischemic mitral regurgitation. © 2006 Future Drugs Ltd.nonePaparella D.; Malvindi P.G.; Romito R.; Fiore G.; Schinosa L. de L.T.Paparella, D.; Malvindi, P. G.; Romito, R.; Fiore, G.; Schinosa, L. de L. T

Different gene expression in human heart tissue and progenitor cells from control and diabetic subjects: relevance to the pathogenesis of human diabetic cardiomyopathy

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