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To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.forsciint.2009.10.025 Byline: Vittorio Fineschi (a), Manolis Michalodimitrakis (b), Stefano D'Errico (a), Margherita Neri (a), Cristoforo Pomara (a), Irene Riezzo (a), Emanuela Turillazzi (a) Keywords: Stress-induced cardiomyopathy; Catecholamine systems; Contraction band necrosis; Sudden death Abstract: Emotional, physiological and physical stress is associated with increased rates of cerebrovascular events and sudden deaths. The pathophysiology of stress-induced cardiomyopathy is not well understood. Proposed mechanisms for catecholamine-mediated stunning in stress cardiomyopathy include epicardial vasospasm, microvascular dysfunction, hyperdynamic contractility with midventricular or outflow tract obstruction, and direct effects of catecholamines on cardiomyocytes. Studies show evidence of significant heritable influences on individual responses to adrenergic stimulation. Data from such studies may be of help for a more accurate comprehension of clinical and morphological alterations of the heart. Irrespective of the cause, patients with the classic stress-induced cardiomyopathy morphology deserve special attention because this extensive distribution of wall motion abnormalities has implications for potential associated complications. Cardiac response may be significantly coupled to genetic differences at candidate loci that encode components of catecholamine biosynthesis, storage, and metabolic pathway. Given the role of the sympathetic nervous system in responses to acute stress, it is reasonable to explore whether genetically determined alterations in catecholamine system functions contribute to acute and chronic cardiovascular disorders such as stress-induced cardiomyopathy. Author Affiliation: (a) Department of Forensic Pathology, University of Foggia, Ospedale Colonnello D'Avanzo, Viale degli Aviatori 1, 71100 Foggia, Italy (b) Department of Forensic Sciences, University of Crete, School of Medicine, 71110 Heraklion, Greece Article History: Received 25 April 2009; Revised 25 September 2009; Accepted 20 October 2009

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.forsciint.2009.01.006 Byline: Vittorio Fineschi, Emanuela Turillazzi, Margherita Neri, Cristoforo Pomara, Irene Riezzo Keywords: Deep venous thrombosis; Pulmonary embolism; Thrombus; Histological age; Immunohistochemistry; Confocal laser scanning microscopy Abstract: The histological age determination of venous thromboses in fatal pulmonary embolism cases is an important task of forensic medicine and requires thorough knowledge of the general and specific pathology of pulmonary thromboembolism (PTE). The aim of our investigation was to carry out a chronological evaluation of the deep venous thrombosis (DVT) phenomenon, to assess the chronological transformation of the thrombus and to determine the causal relationship with PTE as cause of death. The clinical data and the autopsy records of the 2843 autopsies performed over the period 1 November 1998 to 31 December 2007 were retrospectively evaluated, and 140 cases in which PTE was pointed out as cause of death were selected. The dissection of the deep veins of the legs has been performed systematically to search for the starting point of venous embolism. 4.5% of pulmonary embolisms originated in the in iliac veins, 20.7% in the femoral veins, and 74.8% in the deep crural veins. In the venous sites of thrombosis, the histological assessment has been performed in conjunction with the surrounding vascular wall of uncut blood vessel with at least three to six different transverse incisions. Histological assessment of the embolus samples was also performed in conjunction with the venous sites of thrombosis. In our selected 140 cases of PTE, the DVT was classified as phase 1 in 48 cases (34.29%), as phase 2 in 70 cases (50%), and 22 cases (15.71%) were evaluated as older than 2 months (phase 3). The observed transformation of the thrombus by organization is suitable for a forensically utilizable age determination. However, only three chronological stages can be distinguished with any degree of certainty using immunohistochemistry and CLSM. Author Affiliation: Department of Forensic Pathology, University of Foggia, Ospedale Colonnello D'Avanzo, Via degli Aviatori 1, 71100 Foggia, Italy Article History: Received 7 June 2008; Revised 22 November 2008; Accepted 3 January 2009

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.forsciint.2006.12.002 Byline: Emanuela Turillazzi, Sabina Di Donato, Margherita Neri, Irene Riezzo, Vittorio Fineschi Keywords: Acute interstitial pneumonitis; Hamman-Rich syndrome; Adult respiratory distress syndrome; Diffuse alveolar damage; Immunohistochemistry; Anti-surfactant apoprotein (PE-10); Cytokines Abstract: Acute interstitial pneumonitis (AIP), also known as Hamman-Rich syndrome, is a distinct type of idiopathic interstitial pneumonia affecting patients of both genders without pre-existing lung diseases. We describe the case of a fulminant form of AIP and discuss the pathophysiological mechanisms of AIP with reference to the histological pattern. A 15-year-previously-healthy male boy presented to the Hospital with a 6-day history of malaise, fever and cough. The clinical prodromes were followed by the acute onset of increasing shortness of breath rapidly progressing in acute respiratory failure. Chest X-ray demonstrated bilateral diffuse airspace opacification; the high resolution CT confirmed the presence of bilateral, symmetric diffuse ground-glass attenuation. The patient was admitted to the intensive care unit, but died after few hours. An autopsy was performed within 24h. The histological examination of lung specimens showed a pattern of diffuse alveolar damage. immunohistochemical, microbiological and toxicological tests were also carried out. The clinical presentation, the histological findings and the exclusion of infective, traumatic, toxic and metabolic causes of acute respiratory distress syndrome (ARDS) allowed us to conclude that the boy was affected by AIP. In conclusion, AIP is a diagnosis of exclusion. It has a mortality rate ranging about 50%, despite mechanical ventilation. In fatal cases of AIP diagnosis can be based on clinical presentation, radiological, histological and microbiological findings and can be further confirmed by immunohistochemical analysis. Author Affiliation: Department of Forensic Pathology, University of Foggia, Ospedali Riuniti, Via L. Pinto, 1, 71100 Foggia, Italy Article History: Received 27 March 2006; Revised 20 November 2006; Accepted 5 December 2006

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.forsciint.2009.12.012 Byline: Emanuela Turillazzi (a), Fabrizio Monaci (b), Margherita Neri (a), Cristoforo Pomara (a), Irene Riezzo (a), Davide Baroni (b), Vittorio Fineschi (a) Keywords: Explosive-related death; Explosive residues; Confocal laser scanning microscope; Inductively coupled plasma atomic emission spectrometer Abstract: In most deaths caused by explosive, the victim's body becomes a depot for fragments of explosive materials, so contributing to the collection of trace evidence which may provide clues about the specific type of device used with explosion. Improvised explosive devices are used which contain 'homemade' explosives rather than high explosives because of the relative ease with which such components can be procured. Many methods such as chromatography-mass spectrometry, scanning electron microscopy, stereomicroscopy, capillary electrophoresis are available for use in the identification of explosive residues on objects and bomb fragments. Identification and reconstruction of the distribution of explosive residues on the decedent's body may give additional hints in assessing the position of the victim in relation to the device. Traditionally these residues are retrieved by swabbing the body and clothing during the early phase, at autopsy. Gas chromatography-mass spectrometry and other analytical methods may be used to analyze the material swabbed from the victim body. The histological examination of explosive residues on skin samples collected during the autopsy may reveal significant details. The information about type, quantity and particularly about anatomical distribution of explosive residues obtained utilizing confocal laser scanning microscope (CLSM) together with inductively coupled plasma atomic emission spectrometer (ICP-AES), may provide very significant evidence in the clarification and reconstruction of the explosive-related events. Author Affiliation: (a) Department of Forensic Pathology, University of Foggia, Ospedale Colonnello D'Avanzo, Viale degli Aviatori 1, 71100 Foggia, Italy (b) Department of Environmental Sciences 'G. Sarfatti', University of Siena, Via P.A. Mattioli, Siena, Italy Article History: Received 27 July 2009; Accepted 6 December 2009

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.forsciint.2009.01.021 Byline: Stefano D'Errico, Cristoforo Pomara, Irene Riezzo, Margherita Neri, Emanuela Turillazzi, Vittorio Fineschi Keywords: Pheochromocytoma; Cardiac failure; Sudden death; Epinephrine dosage; Heart morphology Abstract: A rare case of cardiac failure due to hypertensive crisis in pheochromocytoma in a 25-year-old young man is presented. In the Emergency Department the patient complained of persisting headache and vomiting; he was distressed but fully alert, his heart rate was 110b/min and blood pressure 180/80mmHg. Few hours after admission, the clinical course suddenly got worse with signs and symptoms of fatal cardiac shock (dyspnoea, cyanosis, pulmonary oedema, hypocontractility of left ventricle). Autopsy revealed a large tumour of the left adrenal gland. Histological examination confirmed macroscopic suspicion of pheochromocytoma. Catecholamine serum levels were analysed by high pressure liquid chromatography (HPLC) with electrochemical detection. The urine contained 35[mu]g/24h norepinephrine and 184[mu]g/24h epinephrine (normal range [less than or equal to]64 and [less than or equal to]36[mu]g/24h respectively). These laboratory findings impressively demonstrate that the tumour was active, secreting high levels of epinephrine. Cardiac failure due to an acute catecholamine-related hypertensive crisis was established as the cause of death. Author Affiliation: Department of Forensic Pathology, University of Foggia, Ospedale Colonnello D'Avanzo, Viale degli Aviatori, no. 1, 71100 Foggia, Italy Article History: Received 22 September 2008; Revised 19 January 2009; Accepted 29 January 2009

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.forsciint.2008.09.020 Byline: Irene Riezzo (a), Francesco Ventura (b), Stefano D'Errico (a), Margherita Neri (a), Emanuela Turillazzi (a), Vittorio Fineschi (a) Keywords: Cardiac sarcoidosis; Clinical diagnosis; Ventricular tachycardia; Post-mortem diagnosis; Extensive myocardial fibrosis Abstract: We present an uncommon case of sudden cardiac death in a 34-year-old white woman. She was found lifeless at home by her parents. Three months before death she was recovered at the Emergency Room for chest pain, palpitation and loss of consciousness. Subsequent cardiological evaluation with ECG showed sinusal rhythm, QRS deviation to the left, QS aspect, asymmetric and rounded T waves and slight length of QT. During hospitalization she presented some episodes of supraventricular paroxysmal tachycardia and non-sustained ventricular tachycardia. No echocardiography alterations were found. An anti-arrhythmic treatment was prescribed. Autopsy revealed some fibrotic scarring in the myocardium of left ventricle. The histological examination of the heart revealed diffuse and extensive fibrosis with non-caseating sarcoid granulomas. The lungs, kidneys and lymph node also showed the same non-caseating granulomas. The diagnosis of sarcoidosis with massive and extensive cardiac involvement was established as cause of death. Author Affiliation: (a) Department of Forensic Pathology, University of Foggia - Ospedale Colonnello D'Avanzo, Via degli Aviatori 1, 71100 Foggia, Italy (b) Department of Forensic Pathology, University of Genoa, Italy Article History: Received 22 March 2008; Revised 5 July 2008; Accepted 23 September 2008

* Context.--Androgenic anabolic steroids (AAS) used for improving physical performance have been considered responsible for acute myocardial infarction and sudden cardiac death. Objective.--To establish the relationship between AAS and cardiac death. Design.--Case report. Patients.--Two young, healthy, male bodybuilders using AAS. Main Outcome Measures.--Pathologic cardiac findings associated with AAS ingestion. Results.--The autopsy revealed normal coronary arteries. In one case, we documented a typical infarct with a histologic age of 2 weeks. A segmentation of myocardial cells at the intercalated disc level was observed in the noninfarcted region. This segmentation was the only anomaly detected in the second case. No other pathologic findings in the heart or other organs were found. Urine in both subjects contained the metabolites of nortestosterone and stanozolol. Comment.--A myocardial infarct without vascular lesions is rare. To our knowledge, its association with AAS use, bodybuilding, or both lacks any evidence of a cause-effect relationship. The histologic findings in our 2 cases and in the few others reported in medical literature are nonspecific and do not prove the cardiac toxicity of AAS. A better understanding of AAS action on the neurogenic control of the cardiac function in relation to regional myocardial contraction and vascular regulation is required. (Arch Pathol Lab Med. 2001;125:253-255), A Pathologic Study Androgenic anabolic steroids (AAS) are used worldwide to help athletes gain muscle mass and strength. They are beneficial in athletic competition and are particularly beneficial for power [...]