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Biomedical subjects

E Arbustini

Publications and source records attributed to E Arbustini.

At least 163 records · Page 9Linked to original sources
PubMed1983

Effects of the cold pressor test on the left ventricular function of patients with coronary artery disease.

We used the cold pressor test as provocative of myocardial ischemia in 23 subjects evaluated for chest pain on effort. Seven of them (group N) had normal coronary arteries, and 16 (group CAD) had critical stenoses along the main branches of the left coronary artery. In both groups exposure to cold induced increase in arterial pressure and double product. Left ventricular end-diastolic pressure increased +60% from baseline (P less than 0.001). Angiocardiographic parameters, unchanged in group N, showed an impairment of left ventricular function in group CAD. End-diastolic volume increased +11% (P less than 0.01), ejection fraction decreased -8% (P less than 0.0025), with a significant reduction in segmental wall motion in the area of the diseased artery (P less than 0.001). The mean Vcf was slightly and not significantly reduced, while early-systolic and end-diastolic stress and the constant of stiffness consistently increased in both groups. The appearance or extension of ventricular wall contraction abnormalities in group CAD, in the absence of demonstrable coronary spasm and in the presence of a remarkable increase in left ventricular end-diastolic pressure and stress, was interpreted as due to ischemia secondary to increased extravascular resistances to coronary flow. The cold pressor test is proposed as a useful tool for the diagnosis and evaluation of patients with ischemic heart disease.

Adult↗
PubMed1983

Glutaraldehyde-preserved porcine bioprosthesis. Factors affecting performance as determined by pathologic studies.

The causes of porcine valve failure were evaluated pathologically in 129 bioprostheses (BP) removed at surgery or necropsy. Fifty-one BP had been in place for less than two months (early explants); most of the complications of this group were observed in the mitral position: left ventricular outflow obstruction (43 percent), thrombosis (23.5 percent), myocardial dysruption (20 percent), cardiac rupture (10 percent), and perivalvular leak (3.5 percent). Among the 78 explants in place for more than two months (late explants), 66 had evidence of dysfunction. Calcification was the leading cause of failure (46 percent), followed by thrombosis (17 percent), endocarditis (12 percent), fibrous tissue overgrowth (10 percent), perivalvular leak (9 percent), and primary cusp tears (6 percent). Calcific degeneration is a hallmark of the phenomenon of biodegradation, and experimental animal models are encouraged since they may represent the clue to preventing calcification and therefore enhancing performance and durability of the porcine BP.

Adolescent↗
PubMed1983

Cardiac ultrastructure in primary restrictive cardiomyopathy.

A five-year clinical follow-up and the results of myocardial biopsies are described in a patient with primary restrictive cardiomyopathy. Histologic examination of a right ventricular endomyocardial biopsy taken early in the course of the illness was not contributory. Histologic examination of a left ventricular endomyocardial biopsy five years later showed hypertrophy and disarray of myocytes, thickening of the endocardium, and interstitial fibrosis. Connective tissue was compact and regularly oriented in the endocardium, but tangled and irregularly oriented in the interstitium. It is concluded that the irregular network of collagen fibrils and elastic fibers limits diastolic relaxation and prevents ventricular dilatation; that the coexisting hypertrophy results from an attempt to maintain normal pump function; and that the myocyte disarray is a consequence of abnormal mechanical forces generated under conditions of severe fibrosis.

Biopsy↗
PubMed1982

Cusp disruption by massive lipid infiltration. A rare cause of porcine valve dysfunction.

A 68-year-old man underwent reoperation because of severe incompetence of a mitral valve xenograft, 96 months following implantation. Gross examination of the device showed yellow spots on the cusps, suggesting lipid infiltration, and a torn commissure. Plasmatic cholesterol and lipiprotein levels were normal. X-ray examination of the explants showed no calcific deposits. Histologic and electron microscopic studies disclosed massive accumulation of lipid clefts and droplets, predominantly at the level of the tear; focal loss and detachment of the endothelial lining and scanty porcine fibroblasts and collagen bundles with preserved periodicity were also noted. Primary disruption of porcine valvular bioprostheses without significant calcifications or collagen breakdown is uncommon. In the present case, lipid accumulation was the main determinant of tissue failure.

Aged↗
PubMed1981

[Interatrial defect functionally cancelled by a left atrial myxoma within the framework of embolizing mitral stenosis and insufficiency].

The case is presented by a 54 year-old woman, studied because of a clinical diagnosis of mitral valve disease, in which echocardiographic and angiocardiographic examination afforded the diagnosis of left atrial tumor. The surgical finding was of a large myxoma implanted on the atrial septum and prolapsing into the mitral opening and engaging with a branch into an atrial septal defect of the cavalis superior type. Some considerations are made on the times of possible origin and growth of the tumor; the complete absence of the increased pulmonary flow in the presence of a large interatrial communication suggested an early beginning of the tumor that, obstructing the defect, might have hindered the hemodynamic derangement.

Diagnosis, Differential↗
PubMedDate not supplied

Nonbiodegradable expanded polytetrafluoroethylene-covered stent implantation in porcine peripheral arteries: histologic evaluation of vascular wall response compared with uncoated stents.

PURPOSE: To test the vascular wall response to an expanded polytetrafluoroethylene-covered stent, compared with conventional stenting, up to 6 months after deployment in the vascular district of a swine model. METHODS: Fourteen minipigs underwent implantation of expanded polytetrafluoroethylene-covered stents (CS) and bare stents (BS) in five peripheral arteries. Animals were killed at different time points (from 1 to 180 days). Histopathologic assessment by morphologic and morphometric analysis and by scanning electron microscopy (SEM) were used to assess the incorporation characteristics and re-endothelialization extent of the two types of stents. RESULTS: A total of 70 stents (14 CS and 14 BS in the renal arteries; 28 CS in the iliac arteries, and 14 CS in the aorta) were implanted. Microscopic examination confirmed the absence of occlusive thrombi in both the CS and BS groups. Microthrombi were observed in 10 of 13 CS (77% of cases) and in four of four BS (100% of cases, p < 0.05). Inflammation was mild in 69% of segments in which a CS was implanted and in 74% of segments in which a BS was implanted (p = NS), while a severe inflammatory reaction was observed in 6% of CS segments and in 8% of BS segments (p = NS). No differences were detected at the long-term analysis between neointimal thickness in CS compared with BS segments (0.46 +/- 0.18 mm vs 0.42 +/- 0.26 mm at 90 days and 0.36 +/- 0.08 mm vs 0.35 +/- 0.04 mm at 180 days; p = NS, respectively). At SEM analysis, re-endothelization was evident 15 days after the implant in both CS and BS starting from the stent edges. CONCLUSION: CS implantation did not elicit a more severe thrombotic deposition compared with that of BS. A similar inflammatory reaction of the arterial wall was present in the two stent groups 3 and 6 months following the implant. In addition, CS implantation did not stimulate excessive neointimal formation when compared with BS.

Animals↗
PubMedDate not supplied

Incidence of graft rejection in small bowel transplanted pigs after immunosuppression withdrawal.

As intestinal grafts require heavy immunosuppression, there are no reports of immunosuppression withdrawal after clinical small bowel transplantation. In this large-animal study, we investigated the occurrence of graft rejection in intestinal-transplanted pigs after withdrawal. Large-White unrelated piglets were transplanted and divided in three groups: group 1 (n = 5), intestinal transplantation (ITx) with no immunosuppression; group 2 (n = 7), Itx and 60 days of treatment with tacrolimus and mycophenolate mofetil; group 3 (n = 5), Itx and donor bone marrow infusion (DBMi) and 60 days of treatment with tacrolimus and mycophenolate mofetil. Follow-up time after withdrawal was 120 days. Group 1 pigs died of graft acute cellular rejection (ACR) after a median of 11 days. In group 2, two pigs died of ACR-related infection and another two of ACR within 90 days. The remaining three animals (43%) were sacrificed at day 180, and their grafts showed no signs of ACR. In group 3, two pigs died of ACR-related infection and one of graft versus host disease within 80 days; at day 180 the two surviving animals showed signs of chronic rejection in the allograft. This study demonstrates that total withdrawal after ITx is followed by sudden and lethal ACR (or ACR-related infection) in more than 50% of the recipients. When a tolerance-inducing strategy as DBMi is applied, lethal graft versus host disease may also occur. In group 3, the intestinal allograft, to which the recipients were partially tolerant, developed chronic rejection that was probably associated with a decline with time of donor-leukocytes chimerism, as recently demonstrated in rats.

Acute Disease↗
PubMedDate not supplied

Functional, structural, and genetic mitochondrial abnormalities in myocardial diseases.

Myocardial tissue is highly dependent on energy supplied by normal mitochondrial function. Therefore defects of energy production or utilization affect the heart in both syndromic and isolated disorders. Knowledge of the peculiar structural, functional, and genetic characteristics of mitochondria provides the basis for identification and classification of mitochondrial defects as well as for establishment of a diagnostic workup useful for related cardiac disorders. This review is therefore dedicated to the characteristics of normal mitochondria and the pathologic alterations of these organelles in various cardiovascular diseases.

Cardiomyopathies↗
PubMedDate not supplied

Phenotype commitment in vascular smooth muscle cells derived from coronary atherosclerotic plaques: differential gene expression of endothelial nitric oxide synthase.

Unstable angina and myocardial infarction are the clinical manifestations of the abrupt thrombotic occlusion of an epicardial coronary artery as a result of spontaneous atherosclerotic plaque rupture or fissuring, and the exposure of highly thrombogenic material to blood. It has been demonstrated that the proliferation of vascular smooth muscle cells (VSMCs) and impaired bioavailabilty of nitric oxide (NO) are among the most important mechanisms involved in the progression of atherosclerosis. It has also been suggested that a NO imbalance in coronary arteries may be involved in myocardial ischemia as a result of vasomotor dysfunction triggering plaque rupture and the thrombotic response. We used 5' nuclease assays (TaqMan PCRs) to study gene expression in coronary plaques collected by means of therapeutic directional coronary atherectomy from 15 patients with stable angina (SA) and 15 with acute coronary syndromes (ACS) without ST elevation. Total RNA was extracted from the 30 plaques and the cDNA was amplified in order to determine endothelial nitric oxide synthase (eNOS) gene expression. Analysis of the results showed that the expression of eNOS was significantly higher (p<0.001) in the plaques from the ACS patients. Furthermore, isolated VSMCs from ACS and SA plaques confirmed the above pattern even after 25 plating passages. In situ RT-PCR was also carried out to co-localize the eNOS messengers and the VSMC phenotype. The eNOS gene was more expressed in ACS plaques and VSMCs cultured from them, thus indicating that: a) the expression of the most important differentiation markers is retained under in vitro conditions; and b) NO may play a pivotal role in coronary artery disease. Our findings suggest a new cell system model for studying the pathophysiology of unstable angina and myocardial infarction.

Angina Pectoris↗
PubMedDate not supplied

Multicolor fluorescence technique to detect apoptotic cells in advanced coronary atherosclerotic plaques.

Apoptosis occurring in atherosclerotic lesions has been suggested to be involved in the evolution and the structural stability of the plaques. It is still a matter of debate whether apoptosis mainly involves vascular smooth muscle cells (vSMCs) in the fibrous tissue or inflammatory (namely foam) cells, thus preferentially affecting the cell-poor lipid core of the atherosclerotic plaques. The aim of the present investigation was to detect the presence of apoptotic cells and to estimate their percentage in a series of atherosclerotic plaques obtained either by autopsy or during surgical atherectomy. Apoptotic cells were identified on paraffin-embedded sections on the basis of cell nuclear morphology after DNA staining and/or by cytochemical reactions (TUNEL assay, immunodetection of the proteolytic poly (ADP-ribose) polymerase-1 [PARP-1] fragment); biochemical procedures (identifying DNA fragmentation or PARP-1 proteolysis) were also used. Indirect immunofluorescence techniques were performed to label specific antigens for either vSMCs or macrophages (i.e., the cells which are most likely prone to apoptosis in atherosclerotic lesions): the proper selection of fluorochrome labeling allowed the simultaneous detection of the cell phenotype and the apoptotic characteristics, by multicolor fluorescence techniques. Apoptotic cells proved to be less than 5% of the whole cell population, in atherosclerotic plaque sections: this is, in fact, a too low cell fraction to be detected by widely used biochemical methods, such as agarose gel electrophoresis of low-molecular-weight DNA or Western-blot analysis of PARP-1 degradation. Most apoptotic cells were of macrophage origin, and clustered in the tunica media, near or within the lipid-rich core; only a few TUNEL-positive cells were labeled for antigens specific for vSMCs. These results confirm that, among the cell populations in atherosclerotic plaques, macrophage foam-cells are preferentially involved in apoptosis. Their death may decrease the cell number in the lipid core and generate a possibly defective apoptotic clearance: the resulting release of matrix-degrading enzymes could contribute to weakening the fibrous cap and promote the plaque rupture with the risk of acute ischemic events, while increasing the thrombogenic pultaceous pool of the plaque core.

Apoptosis↗