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15 results on '"Formato, L"'

1. Semeiotica Chirurgica

Author

Abundo, R., Annibali, S., Bandieri, A., Barbato, L., Cei, S., Consolo, U., Di Lauro, A., Duvina, M., Festa, V. M., Formato, L., Fornaini, C., Francone, S., Gabriele, M., Gasparro, R., Generali, L., Iezzi, G., La Monaca, G., Greco Lucchina, A., Greco Lucchina, G. P., Maglione, M., Manfredi, M., Meleti, M., Merigo, E., Mortellaro, C., Mozzati, M., Parente, B., Piattelli, G. P. E. R. F. E. T. T. I. A., Pradella, R. P. I. P. P. I. F., Prota, E., Rizzo, S., Baena, R. R. Y., Sammartino, G., Scarpelli, M. L., Tetè, S., Tonelli, P., Tortorici, S., Trosino, O., Vescovi, P., Viviani, C., V. L. Z. I. Z. Z. A. R. , I., LAINO, Gregorio, LAINO, Luigi, MENDITTI, Dardo, RULLO, Rosario, R. Rullo, V.M. Festa, Abundo, R., Annibali, S., Bandieri, A., Barbato, L., Cei, S., Consolo, U., Di Lauro, A., Duvina, M., Festa, V. M., Formato, L., Fornaini, C., Francone, S., Gabriele, M., Gasparro, R., Generali, L., Iezzi, G., Laino, Gregorio, Laino, Luigi, La Monaca, G., Greco Lucchina, A., Greco Lucchina, G. P., Maglione, M., Manfredi, M., Meleti, M., Menditti, Dardo, Merigo, E., Mortellaro, C., Mozzati, M., Parente, B., Piattelli, G. P. E. R. F. E. T. T. I. A., Pradella, R. P. I. P. P. I. F., Prota, E., Rizzo, S., Baena, R. R. Y., Rullo, Rosario, Sammartino, G., Scarpelli, M. L., Tetè, S., Tonelli, P., Tortorici, S., Trosino, O., Vescovi, P., Viviani, C., and V. L. Z. I. Z. Z. A. R., I.

Published
2015

2. In vivo coronary plaque histology in patients with stable and acute coronary syndromes: relationships with hyperlipidemic status and statin treatment

Author

Pucci, A, Sheiban, Imad, Formato, L, Celeste, A, Brscic, E, Moretti, C, DE BERNARDI, A, Alberti, A, Bergamasco, Laura Maria, Trevi, Giampaolo, and Fuster, V.

Subjects
Atherectomy, Coronary, Male, Antigens, Differentiation, Myelomonocytic, Hyperlipidemias, Coronary Artery Disease, Middle Aged, Coronary Vessels, Immunohistochemistry, Antigens, CD, Heptanoic Acids, Acute Disease, Atorvastatin, Humans, Female, Pyrroles, Angina, Unstable, Glycophorins, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Aged, Pravastatin
Abstract

Aim of the study was to investigate whether maintained moderate statin treatment influence atheroma, macrophage content, neoangiogenesis and/or haemorrhage in coronary plaques from patients with non-fatal coronary syndromes.A total of 48 patients underwent elective directional coronary atherectomy on "de novo" culprit lesions; 16 patients had non-treated hypercholesterolemia, 16 patients received maintained moderate statin treatment for hypercholesterolemia and 16 had no lipoprotein abnormalities. These three patients groups were matched for age and clinical diagnosis of stable angina (SA) or unstable angina/non-ST-elevation myocardial infarction (UA/NSTEMI). Atherectomy specimens were stained with antibodies against macrophages, endothelial cells and glycophorin A. Results of histology and immunohistochemistry were morphometrically analyzed by using computer-assisted image analysis.Atheroma and fibrous tissue, neoangiogenesis, macrophage and haemorrhage (i.e., glycophorin A) differed between the three groups (P0.05). Statin-treated group showed significantly decreased atheroma (P=0.016), fibrous tissue (P=0.42), macrophage content (P=0.012), neoangiogenesis (P=0.00048) and haemorrhage (P=0.0092) as compared with the non-treated hyperlipidemic group.The present findings show that maintained moderate statin treatment may contribute to plaque stabilization in non-fatal coronary syndromes by decreasing intraplaque neoangiogenesis and haemorrhage, lipid burden and macrophage content, and, on the other hand, by increasing plaque collagenization.

Published
2006

9. Role of the Cardiologist in Management of Subarachnoid Haemorrhage

Author

Gaita, F., Formato, L., Bianchi, F., Vivalda, L., Giustetto, C., and Richiardi, E.

Abstract

Patients with aneurysmal subarachnoid haemorrhage (SAH) frequently have cardiovascular complications that include: blood pressure fluctuations, cardiac arrhythmias and ECG changes.ECG abnormalities, haemodynamic instability and pulmonary oedema, frequently associated with this pathologic condition, contribute to the morbidity and mortality of subarachnoid haemorrhage (SAH). Actually ECG changes occur in 50% to 100% of the patients during the acute stage of SAH, with the most common abnormalities involving the ST segment, T wave and QT interval. In most cases, these abnormalities are clinically inconsequential and are attributed to neurally mediated electrophysiological effects. Some SAH patients, however, show evidence of structural cardiac damage. ECG abnormalities which are indistinguishable from those due to acute myocardial infarction (ST segment elevation or depression) have occasionally been reported in SAH. These patients exhibited findings (which are completely reversible) similar to an acute myocardial infarction on ECG examination, as well as elevated cardiac enzymes and findings of left ventricular wall motion abnormalities, mostly anterior wall akynesis, causing the reduction of left ventricular ejection fraction. Occurrence of pulmonary oedema has been described in ten to 25% of SAH patients. Pulmonary oedema may be neurogenic or cardiogenic in origin and both are a consequence of increased adrenergic tone. There is evidence that the most important consequence of cardiovascular effects secondary to subarachnoid haemorrhage is increased susceptibility to sudden death. The increased adrenergic tone, due to high catecholamine levels and sympathetic cranial nerves stimulation can explain the origin of tachyarrhythmias. The mechanism proposed to explain the origin of bradyarrhythmias is an increased vagal tone.

Published
2002
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11. PPARγ in coronary atherosclerosis: in vivo expression pattern and correlations with hyperlipidemic status and statin treatment.

Author

Pucci A, Formato L, Muscio M, Brscic E, Pizzimenti S, Ferroni F, Ribezzo M, Toaldo C, Pettazzoni P, Ciamporcero E, Barrera G, Rinaldi M, Bergamasco L, Sheiban I, and Spinnler MT

Subjects
Adult, Aged, Arteries metabolism, Coronary Artery Disease drug therapy, Female, Humans, Hyperlipidemias drug therapy, Immunohistochemistry methods, Inflammation, Macrophages metabolism, Male, Middle Aged, Plaque, Atherosclerotic drug therapy, Plaque, Atherosclerotic metabolism, U937 Cells, Coronary Artery Disease metabolism, Hydroxymethylglutaryl-CoA Reductase Inhibitors pharmacology, Hyperlipidemias metabolism, PPAR gamma metabolism
Abstract

Objective: Peroxisome proliferator-activated receptor-γ (PPARγ) is involved in regulation of macrophage inflammation and in atherosclerosis. Herein we investigate the influence of statin treatment on PPARγ expression in coronary artery disease., Method: PPARγ expression was investigated in coronary atherosclerotic atherectomies (N=48) and arteries (N=12) from patients with stable or unstable coronary syndromes or undergoing cardiac transplantation for end-stage ischemic cardiomyopathy, respectively, by immunohistochemistry. Plaque components and tissue factor immunoreactivity were also investigated. Atherectomies were obtained from de novo culprit lesions of hypercholesterolemic (16 statin-treated and 16 untreated) and normolipidemic (N=16) patients. Furthermore, PPARγ expression was evaluated in patients peripheral blood monocytes and in monocytic U937 cells after atorvastatin incubation, by Western blot analysis., Result: PPARγ expression was higher in coronary plaques and peripheral blood monocytes of statin-treated patients, and it significantly increased in monocytes after 24h atorvastatin incubation (p<0.05). Intra-plaque macrophage content, atheroma, neoangiogenesis and hemorrhage, and circulating CRP levels were lower in statin-treated than untreated hypercholesterolemic patients and comparable with normolipidemic subjects. PPARγ immunoreactivity was localized to neointima and media, its distribution pattern being different from that of tissue factor., Conclusion: PPARγ expression was enhanced in statin-treated patients with different distribution and behavior as compared to atheroma, macrophage content, tissue factor immunoreactivity and serum CRP. In vitro studies showed increased PPARγ expression in monocytes after atorvastatin incubation. These findings provide further evidence as to the protective role of statins in coronary artery disease and their influence on PPARγ expression in coronary plaques and on the inflammatory status of patients., (Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.)

Published
2011
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12. In vivo coronary plaque histology in patients with stable and acute coronary syndromes: relationships with hyperlipidemic status and statin treatment.

Author

Pucci A, Sheiban I, Formato L, Celeste A, Brscic E, Moretti C, De Bernardi A, Alberti A, Bergamasco L, Trevi G, and Fuster V

Subjects
Acute Disease, Aged, Angina, Unstable pathology, Antigens, CD metabolism, Antigens, Differentiation, Myelomonocytic metabolism, Atherectomy, Coronary, Atorvastatin, Coronary Artery Disease pathology, Coronary Vessels metabolism, Female, Glycophorins metabolism, Heptanoic Acids therapeutic use, Humans, Hyperlipidemias pathology, Immunohistochemistry, Male, Middle Aged, Pyrroles therapeutic use, Angina, Unstable drug therapy, Coronary Artery Disease drug therapy, Coronary Vessels pathology, Hydroxymethylglutaryl-CoA Reductase Inhibitors therapeutic use, Hyperlipidemias drug therapy, Pravastatin therapeutic use
Abstract

Objectives: Aim of the study was to investigate whether maintained moderate statin treatment influence atheroma, macrophage content, neoangiogenesis and/or haemorrhage in coronary plaques from patients with non-fatal coronary syndromes., Methods: A total of 48 patients underwent elective directional coronary atherectomy on "de novo" culprit lesions; 16 patients had non-treated hypercholesterolemia, 16 patients received maintained moderate statin treatment for hypercholesterolemia and 16 had no lipoprotein abnormalities. These three patients groups were matched for age and clinical diagnosis of stable angina (SA) or unstable angina/non-ST-elevation myocardial infarction (UA/NSTEMI). Atherectomy specimens were stained with antibodies against macrophages, endothelial cells and glycophorin A. Results of histology and immunohistochemistry were morphometrically analyzed by using computer-assisted image analysis., Results: Atheroma and fibrous tissue, neoangiogenesis, macrophage and haemorrhage (i.e., glycophorin A) differed between the three groups (P<0.05). Statin-treated group showed significantly decreased atheroma (P=0.016), fibrous tissue (P=0.42), macrophage content (P=0.012), neoangiogenesis (P=0.00048) and haemorrhage (P=0.0092) as compared with the non-treated hyperlipidemic group., Conclusions: The present findings show that maintained moderate statin treatment may contribute to plaque stabilization in non-fatal coronary syndromes by decreasing intraplaque neoangiogenesis and haemorrhage, lipid burden and macrophage content, and, on the other hand, by increasing plaque collagenization.

Published
2007
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13. The molecular mechanisms of angiogenesis: a new approach to cardiovascular diseases.

Author

Brizzi MF, Formato L, and Bonamini R

Subjects
Collateral Circulation physiology, Coronary Artery Disease physiopathology, Endothelial Growth Factors physiology, Endothelium, Vascular physiology, Fibroblast Growth Factors physiology, Growth Substances physiology, Humans, Lymphokines physiology, Receptors, Growth Factor physiology, Vascular Endothelial Growth Factor A, Vascular Endothelial Growth Factors, Cardiovascular Diseases physiopathology, Neovascularization, Physiologic physiology
Abstract

Although the role of new blood vessel formation in cancer and its development have been well documented, the strategy to manipulate angiogenesis in order to restore blood flow in the ischemic myocardium, a novel form of therapy currently undergoing clinical trials, has received less attention. Recent advances in our understanding of the stimuli and of the control mechanisms regulating the development of new blood vessels in coronary heart disease have led to an improved picture of the compensatory healing process that accompanies myocardial ischemia and infarction. However, we have to remind that, together with life- and tissue-saving effects, the angiogenetic process might alter the natural course of the consequences and organ manifestation of arterial diseases as in the atherosclerotic plaque. The purpose of this review is to provide an overview on the molecular mechanisms involved in the angiogenetic process. Angiogenesis during ontogenesis, neoangiogenesis (adult new vessel formation), arteriogenesis and the related regulators will be analyzed. Moreover, the role of neoangiogenesis in plaque development and instability will be discussed. Due to the introductory nature of this review and the large number of studies on neovascularization in ischemic limbs this topic has been omitted.

Published
2001

14. [Consumption coagulopathy associated with a case of an abdominal aortic aneurysm].

Author

Solli P, Benincasa A, Azzarone M, Tecchio T, Berardi G, Spaggiari L, Formato L, and Salcuni PF

Subjects
Aged, Aortic Aneurysm, Abdominal diagnosis, Aortic Aneurysm, Abdominal surgery, Combined Modality Therapy, Disseminated Intravascular Coagulation diagnosis, Disseminated Intravascular Coagulation therapy, Humans, Male, Postoperative Care, Aortic Aneurysm, Abdominal complications, Disseminated Intravascular Coagulation etiology
Abstract

Consumption coagulopathy with clinical symptoms reveals aortic arterial aneurysms in less than 5% of cases. The authors report a case of abdominal aortic aneurysm: surgical repair is able to remove the hemostasis abnormalities for a long time. Implications of the consumption coagulopathy are analyzed: diagnosis, preoperative correction of the coagulopathy, surgical technique.

Published
1997

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