Our results challenge the dogma that the adult heart is a postmitotic organ and indicate that the regeneration of myocytes may be a critical component of the increase in muscle mass of the myocardium.

Tumours metastatic to the heart (cardiac metastases) are among the least known and highly debated issues in oncology, and few systematic studies are devoted to this topic. Although primary cardiac tumours are extremely uncommon (various postmortem studies report rates between 0.001% and 0.28%), secondary tumours are not, and at least in theory, the heart can be metastasised by any malignant neoplasm able to spread to distant sites. In general, cardiac metastases are considered to be rare; however, when sought for, the incidence seems to be not as low as expected, ranging from 2.3% and 18.3%. Although no malignant tumours are known that diffuse preferentially to the heart, some do involve the heart more often than others--for example, melanoma and mediastinal primary tumours. This paper attempts to review the pathophysiology of cardiac metastatic disease, epidemiology and clinical presentation of cardiac metastases, and pathological characterisation of the lesions.

LV involvement was found in 76% of hearts with ARVC, was age dependent and was associated with clinical arrhythmic events, more severe cardiomegaly, inflammatory infiltrates and heart failure. ARVC can no longer be regarded as an isolated disease of the right ventricle.

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 telomerasecompetent 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 Ϸ85-fold in acute infarcts and Ϸ25-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 Ϸ26,000͞cm 3 of viable myocardium in acute to Ϸ7,000͞cm 3 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.cardiac progenitor cells ͉ human heart ͉ myocardial infarction M yocardial regeneration occurs in humans after ischemic injury (1, 2), and myocyte proliferation appears to be restricted to the viable myocardium adjacent to and remote from the infarct (2). The identification of cardiac stem cells (CSCs) in the adult heart (3-7) suggests that replicating myocytes may constitute a subpopulation of rapidly growing amplifying cells originated from more primitive cells. CSCs are distributed throughout the heart, raising the possibility that those located within the infarct or in its proximity could divide and differentiate reconstituting dead myocardium. If this hypothesis were the case, strategies may be developed to enhance myocardial growth promoting partial restoration of the infarct. This response would reduce infarct size, improve function, and decrease mortality. Myocardial regeneration within the infarct could have escaped earlier observations because the heart was not viewed as a self-renewing organ, and myocyte replacement was considered to be regulated by a subset of cells capable of a few rounds of doubling, located by necessity in the spared portion of the ventricle (2). Alternatively, the lack of myocardial regeneration might reflect CSC death within the infarct and͞or the inability of CSCs to migrate and reach the necrotic area. Thus far, no evidence has been presented that CSCs can reconstitute i...