Leptin is known to exert cardiodepressive effects and to induce left ventricular (LV) remodelling. Nevertheless, the autocrine and/or paracrine activities of this adipokine in the context of post-infarct dysfunction and remodelling have not yet been elucidated. Therefore, we have investigated the evolution of myocardial leptin expression following myocardial infarction (MI) and evaluated the consequences of specific cardiac leptin inhibition on subsequent LV dysfunction. Anaesthetized rats were subjected to temporary coronary occlusion. An antisense oligodesoxynucleotide (AS ODN) directed against leptin mRNA was injected intramyocardially along the border of the infarct 5 days after surgery. Cardiac morphometry and function were monitored by echocardiography over 11 weeks following MI. Production of myocardial leptin and pro-inflammatory cytokines interleukin (IL)-1β and IL-6 were assessed by ELISA. Our results show that (1) cardiac leptin level peaks 7 days after reperfused MI; (2) intramyocardial injection of leptin-AS ODN reduces early IL-1β and IL-6 overexpression and markedly protects contractile function. In conclusion, our findings demonstrate that cardiac leptin expression after MI could contribute to the evolution towards heart failure through autocrine and/or paracrine actions. The detrimental effect of leptin could be mediated by pro-inflammatory cytokines such as IL-1β and IL-6. Our data could constitute the basis of new therapeutic approaches aimed to improve post-MI outcome.

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Prognoses for melanoma patients are currently based on statistically confirmed parameters, above all the Breslow thickness and number of lymph node and/or distant metastases. However, metastases can develop even with "thin" melanomas (< 0.7 mm), while survival has been recorded in patients with tumours classified as "thick" (> 4 mm). This review of the literature examines the most recent advances in prognostic markers for melanoma (serological, immunohistochemical, histological, genetic and surgical). These markers offer interesting possibilities in terms of diagnostic certainty, identification of early growth phases and estimation of the tumour's potential for progression and metastasis. It is reasonable to assume that their combined use can provide useful information for formulating prognoses that are not only statistically valid but also individualized.

The coronary-arteriographic and pathologic findings in a case of Prinzmetal's angina are reported. Right coronary arteriograms performed in the absence of pain showed only minor stenotic changes, whereas those performed during an anginal attack revealed a spastic occlusion involving almost the entire vessel. Anatomic examination revealed obstructive lesions of the right coronary artery, more pronounced at the site where spasm had started, due to concentric atherosclerotic thickening of the inner wall, whereas the elastic fibers and the muscular ring of the tunica media were preserved. These findings suggest (1) the need for great caution before assuming on purely angiographic bases that spasm may affect a normal coronary artery and (2) the possibility that spasm occurs in a markedly diseased and stenotic segment of a coronary artery as long as the contractile tissue of the tunica media is preserved.