Biomedical subjects

Roberta Maestri

Publications and source records attributed to Roberta Maestri.

7 recordsLinked to original sources

PubMed2006

Functional effects of nitric oxide-releasing aspirin on vein conduits of diabetic patients undergoing CABG.

BACKGROUND: Type 2 diabetes mellitus (DM) is known to negatively affect biological properties of venous vasculature, and, particularly, to reduce endothelium-derived nitric oxide release. This condition might influence venous graft function following coronary artery bypass surgery (CABG). The aim of this study was to evaluate the functional effects of a NO-releasing aspirin (NORA) on vein grafts (VG) of diabetics and control patients undergoing elective CABG. METHODS: In 40 consecutive ischemic heart disease patients, the effects of NORA were tested on segments of saphenous vein conduits harvested during elective CABG. Twenty patients had type-2 DM (mean age 69+/-2), whereas 20 patients had no DM (NDM) and represented the control group (mean age 67+/-4). Functional responses were tested by exposing VGs to NORA and to standard vasoactive agents in an organ-bath preparation. Histological features of VGs were also assessed by light and electronic microscopy. RESULTS: Significant impairment of endothelial-dependent vasodilation (acetylcholine induced) was documented in VGs of DM subjects. NORA induced a significant and comparable vascular relaxation in all venous segments of NDM and DM patients (56+/-12% of maximal relaxation vs 61+/-11% in the control group, respectively). Histology showed variable extent of vascular layer and cellular abnormalities in VGs of diabetics (intimal hyperplasia, calcific deposition, endothelial cell degeneration) likely responsible of the endothelial functional impairment, whereas control group VG showed preserved structures. CONCLUSIONS: This preliminary study confirms the impairment of endothelium-dependent vasodilative property of VGs in DM patients. It also indicates that NORA effectively induces vasodilation of VGs which was effective also in DM patients thereby representing a promising therapy for diabetics undergoing CABG with the use of VGs, although further studies are mandatory to conclusively assess the safety and benefits of this pharmacological agent.

Acetylcholine↗

PubMed2005

Myocyte changes and their left atrial distribution in patients with chronic atrial fibrillation related to mitral valve disease.

It has been found that the pulmonary veins and adjacent left atrial posterior wall (LAPW) are deeply involved in both the initiation and maintenance of atrial fibrillation (AF), and the identification of these high-risk sites has aroused great interest in investigating their histopathologic substrate. We used light and conventional electron microscopy to evaluate the differential myocyte and interstitial changes in LAPW and left atrial appendage (LAA) samples from 28 patients with chronic AF undergoing mitral valve surgery and from 12 autoptic controls. There were always more myocytes with loss of sarcomeres in the LAPW than in the LAA (19.9% +/- 7.7% versus 8.2% +/- 5.0%; P < .0001), and the LAPW showed more marked immunohistochemical evidence of dedifferentiation, characterized by the reexpression of smooth muscle actin. In pathological left atria, myocyte diameter in the LAPW and LAA was comparable (19.0 +/- 1.5 versus 18.5 +/- 2.0 microm; not significant) but larger than in the controls (11.9 +/- 0.8 and 12.1 +/- 1.3 microm, respectively; P < .0001). A terminal deoxynucleotidyltransferase assay did not reveal any myocyte apoptosis. The LAPW also showed more interstitial fibrosis than the LAA (7.49% +/- 3.34% versus 2.80% +/- 1.35%; P < .0001). Ultrastructural examination confirmed the presence of myocyte myocytolysis in the perinuclear area and showed changes in mitochondrial shape. In conclusion, the LAPW in patients with chronic AF related to mitral valve disease seems to be a particular anatomical site in which major myocyte and interstitial changes are concentrated, whereas the LAA is more protected. This remodeling may increase the heterogeneity of LAPW electrical conduction, thus confirming this location as an elective target for the ablation treatment of AF.

Adult↗

PubMed2004

Regional left atrial interstitial remodeling in patients with chronic atrial fibrillation undergoing mitral-valve surgery.

Ablation of the left atrial free wall around the pulmonary vein ostia (LAFW) may be effective in the treatment of chronic atrial fibrillation associated with mitral disease (CAF-MVD). Using light and conventional electron microscopy analyses, we wanted to evaluate, in CAF-MVD, the interstitial remodeling in the LAFW as well as in a more remote region, such as the left atrial appendage (LAA). LAFW and LAA samples were obtained from 33 CAF-MVD patients during combined mitral surgery and radiofrequency ablation and from 16 autoptic controls. Interstitial fibrosis (IF) and perivascular fibrosis (PF), capillary densities and the maximal oxygen diffusion distance were morphometrically determined. In CAF-MVD patients, the LAFW, compared with the LAA, showed a higher percentage of IF (7.16+/-3.23% versus 2.51+/-1.40%, respectively), a lower myocardial capillary density per mm(2) (830+/-106 versus 989+/-173) and an increased oxygen maximal diffusion distance (19.70+/-1.27 microm versus 18.13+/-1.58 microm). All these values were also significantly different than controls. No differences were found in evaluating PF. At variance with the LAA, in CAF-MVD patients, the LAFW around the pulmonary vein ostia is a region characterized by a marked interstitial remodeling such that it may be morphologically indicated as an appropriate target for ablation treatment aimed at sinus rhythm restoration.

Adult↗

PubMed2004

Eosinophilic myocarditis in a patient with idiopathic hypereosinophilic syndrome: insights into mechanisms of myocardial cell death.

Idiopathic hypereosinophilic syndrome (HES) consists of a prolonged state of eosinophilia of unknown origin with organ involvement. We describe the case of a patient who developed fatal eosinophilic myocarditis. A 23-year-old woman with an 8-month history of eosinophilia presented with symptoms of myocarditis. Histological evaluation of an endomyocardial biopsy specimen revealed marked endomyocardial eosinophilic infiltration with eosinophil-rich granulomas and areas of myocyte necrosis. A terminal deoxynucleotidil transferase assay revealed apoptosis in several cardiomyocytes and vascular cells, mainly in the myocardial areas with higher eosinophil density. Evaluation of an endomyocardial biopsy specimen obtained after steroid therapy demonstrated that the eosinophils had disappeared, but there was marked myocardiosclerosis and scattered apoptotic cells. The patient slowly developed heart failure and died of sudden arrhythmic death. HES can cause severe myocarditis with extensive myocyte loss, probably due to both necrosis and apoptosis. Myocardial fibrosis may occur despite treatment, and patients may be at risk for fatal arrhythmias.

Adrenal Cortex Hormones↗

PubMed2004

Apoptotic/mytogenic pathways during human heart development.

OBJECTIVE: The aim of our study was to assess myocytes apoptosis/mitosis and associated intracellular signalling pathways during heart development. SETTING AND PATIENTS: Eight human fetal hearts (at different gestation ages) and seven human adult hearts were chosen as controls (five normal and two pathological) and studied from both a histological and a molecular point of view. RESULTS: Our results are as follows: (i) all Shc isoforms are expressed and activated in the human fetal heart; (ii) a progressive fading of Shc and ERK expression are evident during gestation; (iii) JNK is present but it is not activated in the human fetal heart; (iv) CD95 is present in the first week of gestation and fades progressively; (v) apoptotic/proliferative processes are present in the early gestation phase and fades progressively; (vi) in the human heart, Shc isoform with medium weight is 55 kD and not 52 kD and it is upregulated in adult myocardial ischaemia. CONCLUSIONS: Myocyte underwent apoptosis/mitosis during gestation. Shc isoforms, together with ERK maintain the homeostasis of the heart.

Adaptor Proteins, Signal Transducing↗

PubMed2003

Cardiac hypertrophy and microvascular deficit in kinin B2 receptor knockout mice.

Experimental and clinical evidence suggests kinin involvement in adaptive myocardial growth. Kinins are growth-inhibitory to cardiomyocytes. Knockout of kinin B2 receptor (B2R) signaling causes dilated and failing cardiomyopathy in 129/J mice, and a 9-bp deletion polymorphism of human B2R is associated with reduced receptor expression and exaggerated left ventricular growth response to physical stress. We reasoned that genetic background and aging may significantly influence the impact of B2R mutation on cardiac phenotype. The theory was challenged in C57BL/6 mice, a strain that naturally differs from the 129/J strain, carrying 1 instead of 2 renin genes. C57BL/6 B2R knockouts (B2R-KO) showed higher blood pressure and heart rate levels (P<0.05) compared with wild-type controls (WT) at all ages examined. At 12 months, left ventricular contractility and diastolic function were mildly altered (P<0.05) and histological and morphological analyses revealed ventricular hypertrophy and cardiomyocyte enlargement in B2R-KO (P<0.01). Reparative fibrosis was enhanced by 208% and capillary density reduced by 38% (P<0.01). Functional and structural alterations induced by B2R deletion in C57BL/6 mice were less severe than those reported previously in the 129/J strain. We conclude that interaction of B2R signaling with other genetic determinants influences aging-related changes in myocardial structure and function. These findings may help us understand the role of kinins in the development of cardiac failure.

Animals↗

PubMedDate not supplied

The ventricular epicardial fat is related to the myocardial mass in normal, ischemic and hypertrophic hearts.

BACKGROUND: The purpose of the present study was to evaluate the extent of the ventricular epicardial fat and its relationship with the underlying myocardium, neither of which is still completely understood. METHODS: A total of 117 autoptic human hearts was subdivided into four groups: normals (N), ischemics (I), hypertrophics (H) and hypertrophic-ischemics (HI). In each heart, the ventricular myocardial and epicardial fat weights were measured. On the basis of these data, the epicardial fat percentage within the ventricles was calculated. RESULTS: The left, right and total ventricular fat weights were greater in H and HI than in N and I (P<.05, P<.05, P<.01, respectively). No differences were detected in the epicardial fat weights in comparing H versus HI and N versus I. Moreover, the fat percentage in each ventricle did not vary between the four groups. However, if compared with the right ventricle, the left ventricle showed an epicardial fat percentage consistently lower (P<.0001). In nonhypertrophied hearts (N and I), the body mass index and the total epicardial fat weight were correlated (P<.05), whereas in hypertrophied hearts (H and HI), they were not. CONCLUSIONS: A constant fat-muscle ratio exists in each ventricle, which is not influenced by ischemia or hypertrophy. Accordingly, during the hypertrophic process, the ventricular fat and the underlying myocardium show a parallel and correlated increase in their masses.

Adipose Tissue↗