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Several clinical forms of mucormycosis are recognized. The tendency of mucoraceous zygomycetes to invade the blood vessels often produces a disseminated infection. A case of a disseminated mucormycosis complicated by a haemophagocytic syndrome (HS) in a 32-year-old Caucasian male is reported in this article. Few cases of infection-associated HS (IAHS), involving infections caused by fungi, have been reported. In all the recorded cases, the fungal infection coexists with malignant lymphoma, immunodeficiency and a long-term steroid therapy for renal transplant or Crohn's disease. This is the second described case of the HS due to mucormycosis.

Background: T-lymphocyte activation within atherosclerotic plaque, and widespread to the myocardium, has been shown in patients with acute coronary syndromes. Objective: To investigate the presence of T-lymphocyte infiltrate at different stages of acute coronary syndromes by studying patients with sudden coronary death, acute myocardial infarction (AMI) and healed infarction, in comparison with patients with myocarditis and patients with non-ischaemic heart failure. Methods: 72 cases were studied at autopsy: 12 dying of sudden coronary death (group 1), 12 dying 4 months after AMI (group 3), 12 with active lymphocytic myocarditis (group 4), 12 with hypertensive heart disease (group 5), and 12 control subjects (group 6). Light microscopy was performed to measure the number of activated T-lymphocytes (CD3+/DR+) in the myocardium and coronary artery wall, and intercellular adhesion molecule-1 (ICAM-1) expression in the myocardium. Results: Activated T-lymphocyte infiltrates and ICAM-1 myocardial expression in both remote and peri-infarction regions and activated T-lymphocytes within the epicardial coronary artery wall of both the infarct- and non-infarct-related arteries were found in groups 1, 2 and 3, whereas myocardial, but not coronary, infiltrates were found in groups 4 (p

Aim: We examined evidence on infective and non-infective endocarditis obtained from a database of 50,403 clinical autopsies performed at an Italian general hospital between January 1983 and December 2006. Materials and Methods: Out of 814 endocarditis cases, 409 were of infective endocarditis (IE) and 405 non-infective (NIE). The median age at the time of death was 78 years for those with IE and 83 for those with NIE. Data were collected on gender, clinical history, comorbidities, kind of affected valve (non-prosthetic/mechanical/biological), pathological features of endocarditis, endocarditis complications and microbiological agents. Results: The diagnosis of IE was frequently missed and these conditions were often complicated by cardiovascular events. IE was more common among patients with prior valve infection or cardiovascular surgery, while malignancies were frequent comorbidities of NIE. Conclusion: In general, we found several data that differ from those generally present in the scientific literature, and this could be explained by the fact that data on IE and NIE are generally obtained from surgical and clinical databases, while we analysed only autoptic cases.

Acutemyocarditisisanin flammatorydisorderoftheheartmuscleinwhichtheseverityofinjurydependsbothonthenatureoftheoffendingagent(i.e.virus)andontheensuinginflammatoryresponse.Thede fini-tion excludes, however, the response to ischemic or toxic injury. Theheart, however, like other organs, may provide a stereotyped responsetoinjury.Followingischemicinjury,theformationoftheinfl ammasomein the heart promotes heart failure [1].Theinflammasome is a macro-molecular structure activated during injury that amplifies the responseby processing Interleukin-1β (IL-1β) and IL-18, and promotion of celldeath [2]. Viral infections may lead to either death of the virus and thecell (pyroptosis), or survival of both cell and virus with persistence ofthe infection through inhibition of the inflammasome (evasion) [3].Therearenoreportsoftheinflammasomeinacutemyocarditis.Wehy-pothesize that the viral infection or the ensuing cellular destructionleads to the formation of the inflammasome, providing an opportunityto explore inflammasome-related markers for diagnostic or prognosticpurposes. Furthermore at present day, there are no specific treatmentsfor acute myocarditis, and thus inhibitors of the inflammasome couldrepresent a new therapeutic approach.We studied samples obtainedthrough endomyocardialbiopsy in11patients with acute lymphocytic myocarditis (b4 weeks of symptomsonset) in Trieste, Italy. The diagnosis was based upon pathology exam-ination and clinical scenario (Table 1). As a comparison group westudied autopsy samples of 11 patients with acute myocarditis diag-nosed post mortem, and 5 control subjects who had died withoutacute myocarditis or other acute cardiac conditions.Weemployedimmunofluorescencestainingtodetectin flammasomeaggregatesusingantibodiesraisedagainstthescaffoldprotein,ApoptosisSpeck-like protein containing a caspase-1 recruiting domain (ASC), and/or the effector protein, caspase-1, as previously described [1].Tocharac-terizethetypeofcell,weusedadoublestainingtechniquewithantibod-ies against cardiac actin to identify cardiomyocytes, S100A4 to identifyfibroblasts, andCD31 forendothelialcells. To overcomefor the auto fluo-rescence of sarcomeric proteins, we used a solution of 1% Sudan black in70% ethanol for 5 min. Images of samples were acquired with an IX70microscope and cellSens Dimension di gital imaging software (Olympus,Central Valley, PA) using a 40× objective (400× magnification). Filtersets for each separate fluorescence-conjugated antibody were layeredtorenderacompositeimage.Theinflammasome “specks” were countedby cell type (cardiomyocyte, leukocytes, fibroblasts and endothelialcells) per high power field of view (40×). Data are presented as medianand interquartile range and non-parametric Mann–Whitney test wasused.Intracellularaggregates of ASC and/ or caspase-1 indicative of the for-mation of the inflammasome were seen in leukocytes, cardiomyocytes,fibroblasts and endothelial cells in heart biopsy samples of all 11 cases(100%), and in heart samples of 10 of 11 post-mortem cases (91%), andin none of the controls (0%, P b 0.002)(Fig. 1). ASC aggregates co-localized with caspase-1 aggregates in virtually all cases. The numberof inflammasomes was variable across cases ranging between 3 and 14specks in biopsies, and between 0 and 45 specks per field in autopsies,without statistically significant differences (data not shown). Some

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. © 2004 Published by Elsevier Ireland Ltd.

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. © The European Society of Cardiology 2005. All rights reserved.