PubMed Health⌕ Search

Biomedical subjects

Rossana Bussani

Publications and source records attributed to Rossana Bussani.

At least 19 recordsLinked to original sources
PubMed2006

Acute myocardial infarction and heart failure: role of apoptosis.

Apoptosis is a key pathologic feature in acute myocardial infarction and heart failure. Experimental animal studies have shown beneficial effects of inhibiting apoptosis. Understanding the mechanisms involved in the apoptotic cascade may be useful in better understanding of heart failure and its management. Not only in vivo detection of apoptosis may prove clinically useful in the diagnosis and risk stratification of patients with ischemic heart disease, but anti-apoptotic treatments (specific and non-specific) may be effective in the prevention and treatment of post-infarction remodelling and heart failure.

Animals↗
PubMed2006

Primary pulmonary Hodgkin's disease and tuberculosis in an 11-year-old boy: case report and review of the literature.

Tuberculosis (TB) has been described in association with different malignancies including Hodgkin's disease. However, the association with primary pulmonary Hodgkin's disease (PPHD) is hardly reported in literature and in teenage is quite exceptional. We report a case of an 11 years old boy in whom the diagnosis of tuberculosis preceded and delayed the diagnosis of PPHL.

Child↗
PubMed2005

Detection of focal renal perfusion defects in rabbits after sulphur hexafluoride-filled microbubble injection at low transmission power ultrasound insonation.

The aim of this study was to assess the feasibility of contrast-enhanced ultrasound (US) at low transmission power insonation for diagnosis of focal renal perfusion defects (RPDs) in rabbits. In seven adult New Zealand White rabbits focal RPDs were induced by polyvinyl alcohol embolizing particles (150-250 microm in diameter) injected into the abdominal aorta. Three other rabbits that were not subjected to embolization were considered as controls. Both kidneys were insonated at baseline and after injection of sulphur hexafluoride-filled microbubbles at low transmission power (mechanical index 0.09-0.12). One sonologist assessed on-site RPD dimensions and conspicuity (visual score 0-4). Digital cine-clips were also reviewed off-site by two other independent readers, blinded, who assigned a confidence level (grades 1-5) for the RPD diagnosis. At on-site analysis RPDs appeared as focal areas of absent or diminished enhancement with a median visual conspicuity score=4. At off-site analysis RPDs >6 mm in diameter were identified at contrast-enhanced US, and the confidence in RPD diagnosis improved significantly (P<0.05) after microbubble injection (area under receiver operating characteristic curve 0.615 vs 0.972 by reader 1; 0.720 vs 0.953 by reader 2). Contrast-enhanced US at low transmission power insonation effectively identified RPDs with diameters >6 mm in rabbits.

Animals↗
PubMed2005

Infarct-related artery occlusion, tissue markers of ischaemia, and increased apoptosis in the peri-infarct viable myocardium.

AIMS: Unfavourable cardiac remodelling often complicates acute myocardial infarction (AMI) as a result of increased cardiomyocyte apoptosis. It is currently unclear whether ongoing or recurrent ischaemia is an independent determinant for increased apoptosis in peri-infarct viable myocardium. METHODS AND RESULTS: In order to assess the link between infarct-related artery (IRA) occlusion, ischaemia, and apoptosis, 30 subjects dying 7-120 days after AMI (16 with IRA occlusion and 14 with patent IRA) and five control subjects were selected at autopsy. Cardiomyocytes were defined as apoptotic if co-expressing TUNEL and activated caspase-3. Expression of both hypoxia-inducible factor-1 and cyclo-oxygenase-2 was assessed in the peri-infarct myocardium and considered as tissue markers of ischaemia. Evidence of ischaemia was significantly more frequent in cases with IRA occlusion (53%) than in cases with patent IRA (15%) or control hearts (0%, P=0.026). The finding of IRA occlusion and markers of ischaemia identified cases with higher apoptotic rates (ARs) in the peri-infarct viable myocardium [12.2% (8.2-14.0), P<0.001 vs. others], whereas IRA occlusion without ischaemia was associated with lower AR, not significantly different from patent IRA [3.0% (1.0-7.9) vs. 2.2% (1.0-5.8), respectively, P=0.42] CONCLUSION: Ischaemia in the peri-infarct viable myocardium is present in over 50% of subjects dying late after AMI with IRA occlusion, and it is associated with increased apoptosis. Relief of ischaemia after AMI may prove of benefit in preventing apoptosis and its consequences.

Actins↗
PubMed2005

Myocardial regeneration by activation of multipotent cardiac stem cells in ischemic heart failure.

In this study, we tested whether the human heart possesses a cardiac stem cell (CSC) pool that promotes regeneration after infarction. For this purpose, CSC growth and senescence were measured in 20 hearts with acute infarcts, 20 hearts with end-stage postinfarction cardiomyopathy, and 12 control hearts. CSC number increased markedly in acute and, to a lesser extent, in chronic infarcts. CSC growth correlated with the increase in telomerase-competent dividing CSCs from 1.5% in controls to 28% in acute infarcts and 14% in chronic infarcts. The CSC mitotic index increased 29-fold in acute and 14-fold in chronic infarcts. CSCs committed to the myocyte, smooth muscle, and endothelial cell lineages increased approximately 85-fold in acute infarcts and approximately 25-fold in chronic infarcts. However, p16(INK4a)-p53-positive senescent CSCs also increased and were 10%, 18%, and 40% in controls, acute infarcts, and chronic infarcts, respectively. Old CSCs had short telomeres and apoptosis involved 0.3%, 3.8%, and 9.6% of CSCs in controls, acute infarcts, and chronic infarcts, respectively. These variables reduced the number of functionally competent CSCs from approximately 26,000/cm3 of viable myocardium in acute to approximately 7,000/cm3 in chronic infarcts, respectively. In seven acute infarcts, foci of spontaneous myocardial regeneration that did not involve cell fusion were identified. In conclusion, the human heart possesses a CSC compartment, and CSC activation occurs in response to ischemic injury. The loss of functionally competent CSCs in chronic ischemic cardiomyopathy may underlie the progressive functional deterioration and the onset of terminal failure.

Apoptosis↗
PubMed2005

Implications of the serine protease HtrA1 in amyloid precursor protein processing.

The defining features of the widely conserved HtrA (high temperature requirement) family of serine proteases are the combination of a catalytic protease domain with one or more C-terminal PDZ domains and reversible zymogen activation. Even though HtrAs have previously been implicated in protein quality control and various diseases, including cancer, arthritis, and neuromuscular disorder, the biology of the human family members is not well understood. Our data suggest that HtrA1 is directly involved in the beta-amyloid pathway as it degrades various fragments of amyloid precursor protein while an HtrA1 inhibitor causes accumulation of Abeta in astrocyte cell culture supernatants. Furthermore, HtrA1 colocalizes with beta-amyloid deposits in human brain samples. Potential implications in Alzheimer's disease are discussed.

Aged↗
PubMed2005

Hypoxia inducible factor-1 expression mediates myocardial response to ischemia late after acute myocardial infarction.

We report hypoxia-inducible factor-1 (HIF-1) expression in myocardium of patients with recent acute myocardial infarction (AMI), supporting the hypothesis of HIF-1 as a possible mediator of response to ischemia. A potential diagnostic role of determining tissue expression of HIF-1 as a marker of ischemia, and potential therapeutic implications by trying to modulate HIF-1 activity in order to promote beneficial effects of HIF-1 related genes (e.g. expression of vascular endothelial growth factor (VEGF)) may derive.

Aged↗
PubMed2005

Radiologic-pathologic correlations of intratumoral tissue components in the most common solid and cystic renal tumors. Pictorial review.

This paper describes the correlation between US-CT images and pathologic findings in the most common solid and cystic renal tumors, to better differentiate malignant and benign renal masses. Several intratumoral tissue components present correlation with US-CT images. Macroscopic components, corresponding to necrotic, hemorrhagic and cystic changes, are identified by visual analysis of the gross specimen, while microscopic components are identified by histopathologic analysis. Microscopic components are classified as cellular [(1) high cellularity with poor extracellular stroma, +/-high nucleus-cytoplasm ratio+/-high uniformity in tumoral cells dimensions; (2) low cellularity with large extracellular stroma+/-low nucleus-cytoplasm ratio+/-low uniformity in tumoral cells dimensions], stromal [(1) fibrotic; (2) fibrovascular; (3) fibromyxoid], vascular related to neoangiogenesis, necrotic [(1) coagulative; (2) colliquative; (3) hemorrhagic], calcific, and adipose.

Cysts↗
PubMed2004

Widespread myocardial inflammation and infarct-related artery patency.

BACKGROUND: Diffuse coronary vascular inflammation is associated with acute coronary syndromes. However, it is unknown whether inflammation also occurs within the myocardium. Therefore, this study was aimed at assessing the presence of activated cells in unaffected remote myocardium of patients with acute myocardial infarction (AMI), in comparison to the peri-infarct region from the same cases, and in comparison to myocardial specimens from control hearts. METHODS AND RESULTS: Sixteen patients dying 1 to 12 weeks after AMI and 16 control subjects were selected at autopsy. Myocardial specimens were taken at remote unaffected viable regions and at peri-infarct regions in cases with AMI. Confocal microscopy was performed to measure the number of activated cells (DR+), T-lymphocytes (CD3+), and activated T-lymphocytes (CD3+/DR+). Activated cells and activated T-lymphocytes were found in remote unaffected regions in 11 of 16 cases (69%), in peri-infarct zone in all cases (100%), and in none of the control hearts (0%, P<0.001 versus others). A greater myocardial inflammatory burden in remote regions but not in peri-infarct regions was associated with persistent infarct-related artery occlusion (P<0.05). CONCLUSIONS: This study for the first time shows the presence of activated T-lymphocytes in remote unaffected myocardial regions in approximately two thirds of patients with recent AMI. Because these cells are associated with persistent infarct-related artery occlusion, our data may suggest that an antigenic stimulus present also in the myocardium triggers an immune response that may be critical to precipitate artery occlusion.

Aged↗
PubMed2004

Increased apoptosis in remote non-infarcted myocardium in multivessel coronary disease.

BACKGROUND: Multivessel coronary disease after myocardial infarction is a major risk factor for unfavorable cardiac remodeling and death due to pump failure, but underlying pathophysiologic mechanisms are still uncompletely established. Post-infarction myocardial apoptosis has been recently implicated as a cause of ongoing cell loss leading to cardiac failure. Our aim was to assess the role of post-infarction myocardial apoptosis and pro-apoptotic factor expression in the non-infarcted remote myocardium of subjects with multivessel coronary disease. METHODS: Twenty-one males dying after recent myocardial infarction with permanent occlusion of the infarct-related artery were selected at autopsy. Apoptosis was assessed at viable myocardial regions remote from infarction by co-staining for in situ end-labeling of DNA fragmentation and cleaved caspase-3. Expression of pro-apoptotic factor bax and hypoxia-induced factor-1alpha was evaluated by immunohistochemistry. RESULTS: Subjects with multivessel disease (N=11) showed a significantly two-fold higher myocardial apoptosis in comparison to subjects with single vessel disease (N=10) (0.9% vs. 0.5%, p=0.013). Similarly, myocardial bax expression was increased in patients with multivessel disease (3.0% vs. 1.4%, p=0.029). Stratification for the number of diseased coronary vessels confirmed the association between extent of coronary disease and apoptotic rates (p=0.022). Even in subjects dying over 30 days after infarction multivessel disease remained predictive of enhanced myocardiocyte apoptosis at remote regions (p=0.033). CONCLUSIONS: Post-infarction myocardial apoptosis and bax expression in remote left ventricular regions are significantly increased in male patients with multivessel coronary disease in comparison to those with isolated infarct-related artery occlusion. These findings suggest that apoptotic cell loss in the viable non-infarcted myocardium, possibly due ongoing ischemia, may play a relevant role in the unfavorable clinical course typical of multivessel disease after myocardial infarction.

Apoptosis↗
PubMed2004

Anticipating events of in-hospital cardiac arrest.

STUDY OBJECTIVES: To determine whether in-hospital cardiac arrests occurring in regular wards are preceded by some event(s), and the diagnostic and therapeutic measures adopted. METHODS: From 1 May 1999 to 31 December 2001, events occurring in the 6 h preceding cardiac arrest were reviewed by checking the medical and nurse records and interviewing the attending staff. Exclusion criteria were (a) location in the Coronary Care Unit, the Intensive Care Unit, the Emergency Department and the operating rooms; (b) the presence of rapidly fatal disease; (c) the lack of adequate documentation. RESULTS: Overall, 263 cardiac arrests occurred in the period under consideration. A total of 148 patients (61 women, 87 men, aged 74.3+/-1.2 years) fulfilled the entry criteria. Anticipating events were reported in 128 patients (86.4%). These included alterations in consciousness, cardiac arrhythmias, dyspnoea and chest pain. The restoration of cardiac rhythm was obtained in 23 patients (15.5%). Eight (5.4%) survived without major neurological sequelae. Survivors were significantly younger than non-survivors (survivors 44.3+/-6.8 years; non-survivors 76.7+/-2.1 years; P<0.005). In a substantial number of cases, ranging from 23 to 81%, according to the anticipating event, no diagnostic investigations were performed. CONCLUSION: Most in-hospital cardiac arrests are preceded by events that often go overlooked and whose correct interpretation could be associated with a reduced mortality rate.

Adult↗
PubMed2004

[How the natural history of dilated cardiomyopathy has changed. Review of the Registry of Myocardial Diseases of Trieste].

Dilated cardiomyopathy (DCM), a heart muscle disease characterized by ventricular dilation and dysfunction, is a leading cause of mortality and morbidity. In the present paper we will consider the main results of studies on the natural history of DCM in 581 consecutive patients prospectively enrolled and systematically followed in the Heart Muscle Disease Registry of Trieste in the last 25 years. In the last decades prognosis of DCM significantly improved over time, mainly as a consequence of optimized treatment with ACE-inhibitors and beta-blockers. However, a strong heterogeneity of prognosis was observed among patients both in familial and sporadic cases. Early diagnosis and treatment allowed to recognize two distinct subgroups, one with a rapidly progressive downhill course, high mortality and urgent indication to heart transplantation, another with a more favorable outcome. Long-term optimized treatment with ACE-inhibitors (in 90% of cases) and beta-blockers (in 87% of cases) was associated with a remarkable clinical improvement in 50% of patients and apparent "healing" in 16% of cases. A systematic and accurate echocardiographic follow-up showed in these cases a significant improvement of the left ventricular ejection fraction (LVEF) with "reverse remodeling", frequently associated with a decrease of severity of functional mitral regurgitation and regression of the restrictive filling pattern. The response to optimal treatment showed a strong relation to long-term outcome. The 8-year transplant-free survival, starting from the evaluation at 2 years, was 31% in patients with persistent NYHA class III-IV, 64% in NYHA class I-II and LVEF < or = 40%, 83% in NYHA class I-II and LVEF > 40% and 94% in patients with apparent "healing" (p < 0.0001). Long-term follow-up showed a significant clinical progression of the disease in 33% of cases, independently of the initial clinical response to treatment. Predictive factors of a favorable response to beta-blocker treatment associated with ACE-inhibitors were a history of mild hypertension, an early diagnosis and treatment and the presence of sinus tachycardia. The risk of sudden death was increased particularly in patients with long-term persistent or progressive left ventricular dilation and dysfunction. A rigorous pharmacological approach (optimization of beta-blockers, withdrawal or decrease of dosage of digitalis), and selective non-pharmacological strategy (automated implantable cardioverter-defibrillators for primary prevention in high-risk patients) are potentially effective to decrease the incidence of sudden death during long-term follow-up. In conclusion, the Heart Muscle Disease Registry of Trieste gave us in the last 25 years new insights into the natural history of DCM, underlying the importance of a rigorous and systematic approach both at clinical presentation and during long-term follow-up on optimized medical treatment.

Arrhythmias, Cardiac↗
PubMed2004

[The natural history of dilated cardiomyopathy: a review of the Heart Muscle Disease Registry of Trieste].

Dilated cardiomyopathy (DCM), a heart muscle disease characterized by ventricular dilation and dysfunction, is a leading cause of mortality and morbidity. In the present paper we will consider the main results of studies on the natural history of DCM in 581 consecutive patients prospectively enrolled and systematically followed in the Heart Muscle Disease Registry of Trieste in the last 25 years. In the last decades prognosis of DCM significantly improved over time, mainly as a consequence of optimized treatment with ACE-inhibitors and beta-blockers. However, a strong heterogeneity of prognosis was observed among patients both in familial and sporadic cases. Early diagnosis and treatment allowed to recognize two distinct subgroups, one with a rapidly progressive downhill course, high mortality and urgent indication to heart transplantation, another with a more favorable outcome. Long-term optimized treatment with ACE-inhibitors (in 90% of cases) and beta-blockers (in 87% of cases) was associated with a remarkable clinical improvement in 50% of patients and apparent "healing" in 16% of cases. A systematic and accurate echocardiographic follow-up showed in these cases a significant improvement of the left ventricular ejection fraction (LVEF) with "reverse remodeling", frequently associated with a decrease of severity of functional mitral regurgitation and regression of the restrictive filling pattern. The response to optimal treatment showed a strong relation to long-term outcome. The 8-year transplant-free survival, starting from the evaluation at 2 years, was 31% in patients with persistent NYHA class III-IV, 64% in NYHA class I-II and LVEF < or = 40%, 83% in NYHA class I-II and LVEF > 40% and 94% in patients with apparent "healing" (p < 0.0001). Long-term follow-up showed a significant clinical progression of the disease in 33% of cases, independently of the initial clinical response to treatment. Predictive factors of a favorable response to beta-blocker treatment associated with ACE-inhibitors were a history of mild hypertension, an early diagnosis and treatment and the presence of sinus tachycardia. The risk of sudden death was increased particularly in patients with long-term persistent or progressive left ventricular dilation and dysfunction. A rigorous pharmacological approach (optimization of beta-blockers, withdrawal or decrease of dosage of digitalis), and selective non-pharmacological strategy (automated implantable cardioverter-defibrillators for primary prevention in high-risk patients) are potentially effective to decrease the incidence of sudden death during long-term follow-up. In conclusion, the Heart Muscle Disease Registry of Trieste gave us in the last 25 years new insights into the natural history of DCM, underlying the importance of a rigorous and systematic approach both at clinical presentation and during long-term follow-up on optimized medical treatment.

Adult↗
PubMed2004

Fatal myocarditis: morphologic and clinical features.

BACKGROUND: Autopsy studies report a frequency of myocarditis ranging from 0.11 to 5.5% in the general population, reaching almost 50% in selected groups. Myocarditis is often undiagnosed and the incidence of fatal course myocarditis has never been evaluated. The aim of our study was to assess the frequency of fatal course myocarditis in a consecutive series of autopsies and to describe the clinical, histological and morphologic features of the disease. METHODS: From January 1, 1995 to January 31, 1996, 2560 autopsies were performed, and 143 cases of active myocarditis were diagnosed (5.6%). RESULTS: In 39 cases (1.5%; 12 males; 4/39 aged < or = 35 years) active myocarditis was identified as the final cause of death. Only in 1 case was myocarditis suspected ante-mortem. The histological pattern was lymphocytic in 64% of cases. A mixed inflammatory infiltration was found in 33% and a granulomatous infiltration in 3%. In 49% of cases myocarditis was localized in both ventricles and the interventricular septum. The clinical presentation of myocarditis was heart failure in 18/39 patients (46%), cardiac arrest in 4/39 patients (10%) and syncope and chest pain in 1/39 patient (3%). The mean creatine phosphokinase levels were 890 +/- 2742 IU/I (assessed in 11/39 patients, 28%) but they were increased only in 7/39 (18%). ECG (performed in 29/39 patients, 74%) showed sinus rhythm in 16/39 patients (55%, > 100 b/min in 41%), atrioventricular or interventricular conduction defects in 10/39 patients (34%) and a pathological Q wave in 4/39 patients (14%). At echocardiography (performed in 7/39 patients, 18%), right and/or left ventricular dysfunction was found to be present in 5 cases (71%) and a pericardial effusion in 4 cases (57%). CONCLUSIONS: Myocarditis is underdiagnosed ante-mortem. A high index of clinical suspicion is mandatory for prompt diagnosis and treatment of this fatal disease seen also in the young.

Adolescent↗
PubMed2003

In vitro percutaneous absorption of cobalt.

OBJECTIVES: To evaluate skin absorption of cobalt powder in an in vitro system. Experiments with volunteers show that cobalt powder can permeate through the skin, but there are no data with regard to the mechanism or the amount of permeation. METHODS: Skin permeation was calculated by the Franz diffusion cell method with human skin. A physiological solution was used as receiving phase and the cobalt powder was dispersed in synthetic sweat. The amount of metal passing through the skin was analysed by electro-thermal atomic absorption spectrometry (ETAAS). Parallel polarographic analysis (differential pulse polarography-DPP) allowed evaluation of cobalt present as ions (Co(2+)) in donor and receiving phases. Measurements of cobalt skin content were also performed. RESULTS: Evaluation of metal in the receiving phase allowed us to demonstrate the permeation of cobalt through the skin. Steady-state flow of percutaneous cobalt permeation was calculated as 0.0123+/-0.0054 microg cm(-2) h(-1), with a lag time of 1.55+/-0.71 h. CONCLUSIONS: The experiments show that cobalt powder can pass through the skin when applied as a dispersion in synthetic sweat, oxidising metallic cobalt into ions, which permeate the skin. These experiments show for the first time how cobalt can permeate the skin.

Cobalt↗
PubMed2003

Increased myocardial apoptosis in patients with unfavorable left ventricular remodeling and early symptomatic post-infarction heart failure.

OBJECTIVES: The purpose of this study was to evaluate a potential correlation between apoptotic rate (AR), post-infarction left ventricular (LV) remodeling, and clinical characteristics in subjects who died late (>or=10 days) after an acute myocardial infarction (AMI) with evidence of persistent occlusion of the infarct-related artery at autopsy. BACKGROUND: Apoptosis contributes to myocardiocyte loss in cardiac disease and may have a pathophysiologic role in post-infarction LV remodeling. METHODS: The AR was calculated at the site of infarction and in remote unaffected LV regions, using co-localization of in situ end labeling for deoxyribonucleic acid fragmentation and immunohistochemistry for caspase-3, in 14 subjects who died within two months after AMI. Correlation between AR and clinical characteristics such as age, site of AMI, transmural extension, multivessel coronary disease, and signs and/or symptoms of heart failure (HF), at the time of initial hospitalization for AMI or subsequently before death, was assessed using non-parametric statistical tests. Parameters of LV remodeling including diameters, free wall thickness, diameter-to-wall-thickness ratio, and mass were measured at gross examination at autopsy. Values are expressed as median (interquartile range). RESULTS: Among clinical variables, early symptomatic post-infarction HF (9 cases, 64%) was associated with nearly fourfold increased AR at the site of infarction (26.2% [24.5% to 28.8%] vs. 6.4% [1.9% to 13.3%], p = 0.001). Moreover, AR both at the site of infarction and in unaffected regions was significantly correlated with parameters of progressive LV remodeling (p < 0.05). CONCLUSIONS: Our data show that in patients dying >or=10 days after AMI, myocardial apoptosis is strongly associated with and may be a major determinant of unfavorable LV remodeling and early symptomatic post-infarction HF.

Aged↗