11±3 ml/k/min, p 120 mg%, respectively (p=0.015), 95% vs. 75% in the patents with RAP 8 mHg (p=0.002), 93% vs. 73% in those with peak exercise SBP > and 37, respectively (p=0.001). The 2and 3-years survival rates were, respectively, of only 59% and 47% in the patients with a RAP > 8 mHg and a peak exSBP 8 mHg and a VE/VCO2slope > 37. In conclusion, simple hemodynamic parameters, which may be assessed also noninvasively, and the ventilatory response to ex may identify subgroups of patients with chronic HF at high risk of subsequent events despite long-term BB therapy.

Background: Apoptosis is a key feature in postinfarction remodelling leading to progressive myocyte loss. Both proapoptotic and antiapoptotic factors contribute to the delicate balance between death and survival. The survivin pathway has emerged as essential in the control of apoptosis, although its role in heart disease is unknown. Aim: To evaluate survivin expression after acute myocardial infarction (AMI). Methods: Survivin expression was assessed immunohistochemically in the peri-infarct and remote viable myocardium in 17 consecutive patients who died 1–30 weeks after AMI and in four control hearts. Results: Survivin was expressed by myocytes in the peri-infarct area in eight patients and in the remote region in 13 patients. The rate of survivin expression after AMI was significantly higher in the remote versus peri-infarct regions and compared with control hearts. Its expression was inversely associated with the presence of dilated cardiopathy and of apoptosis, independently from the gross pathology infarct size. Conclusions: Survivin myocardial expression after AMI may be associated with the survival of at risk myocardium and may be indicative of more favourable remodelling after AMI. These findings identify a potential new target for the treatment of postinfarction remodelling.

While demonstration of cells with DNA synthesis is common in postinfarction models, the true significance of these cells is questionable. As we find that these markers are closely linked to apoptosis and unfavorable cardiac remodeling, they are likely to represent either early or late events in the mitotic failure leading to cell death. Because the differentiation of dying myocardiocytes in oncotic, apoptotic and mitotic deaths is mostly academical, these markers should be considered unfavorable prognostic markers for cell loss, unless true demonstration of effective cell replication is presented.

Background Infarct‐related artery (IRA) patency after acute myocardial infarction (AMI) is associated with a more favourable clinical course, in particular in patients with high‐risk features. As it has been recently reported that IRA patency is associated with a reduced postinfarction apoptotic rate (AR), the aim of our study was to assess whether IRA status late after AMI had a different impact on AR in high‐ vs. low‐risk patients.

Adrenal cortical carcinoma (ACC), a rare and highly malignant neoplasm of the cortical tract of the adrenal gland, is usually diagnosed at an advanced stage of development and often when metastatic spread already has begun. We report a very rare case of low-stage, non-metastasized ACC, the first clinical appearance of which was a large retroperitoneal hemorrhage caused by the rupture of the neoplastic mass. To the best of our knowledge, this is the third reported case of ACC rupture.

In recent years, the diagnosis and management of leptomeningeal carcinomatosis have gained increased attention as patients with neoplasms live longer and the condition becomes more common. Conclusive hallmarks of this disease have yet to be identified. We report and discuss a case of massive invasion of the cerebral leptomeninges by neoplastic cells from a malignant melanoma in a shoulder. Symptoms of cerebral dysfunction were the first indication of neoplasm. The onset of symptoms, magnetic resonance imaging, and patient death all occurred within a brief time span. To our knowledge, this is the first case of meningeal melanomatosis in a patient not treated with chemotherapeutic drugs in which the radiologic evidence is virtually synchronous with direct anatomic observation. Thus the images provided with this report may be of use in the radiographic diagnosis of cerebrospinal metastatic colonization.

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 (greater than or equal to10 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 greater than or equal to10 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. (C) 2003 by the American College of Cardiology Foundation.

BACKGROUND:Cardiac remodelling after acute myocardial infarction (AMI) is characterised by molecular and cellular mechanisms involving both left and right ventricles, and biventricular failure identifies patients with an extremely unfavourable prognosis.AIMS:To assess whether a link exists between increased myocardial apoptotic rates (AR) at sites of recent infarction and patterns of unfavourable cardiac remodelling, such as biventricular enlargement after left ventricular (LV) infarction.METHODS:Twelve patients with recent AMI involving the LV and not the right ventricle (RV) and with permanent infarct related artery occlusion were selected at necropsy. Gross pathological characteristics, such as LV and RV dilatation, and AR at site of infarction were assessed. Potential false positive results (DNA synthesis and RNA splicing) were excluded from the cell count.RESULTS:RV enlargement, defined as a tricuspidal ring greater than 120 mm, was found in five cases and was associated with LV dilatation. These patients showed significantly higher AR than the others. When the subjects were divided into three groups according to progressive cardiac remodelling (absence of cardiac dilatation, isolated LV dilatation, and biventricular enlargement), the last group had significantly higher ARs than the other two groups, showing that myocardiocyte apoptosis is increased in more unfavourable forms of cardiac remodelling.CONCLUSION:Patients with severely unfavourable cardiac remodelling, such as biventricular enlargement, have extremely high myocardiocyte apoptosis at necropsy, even late after LV myocardial infarction, supporting the role of myocardiocyte loss in determining post-infarction adverse remodelling.