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PURPOSE OF REVIEW: Along with population aging, the incidence of both heart failure (HF) and cancer is increasing. However, little is known about new-onset cancer in HF patients. This review aims at showing recent discoveries concerning this subset of patients. RECENT FINDINGS: Not only cancer and HF share similar risk factors but also HF itself can stimulate cancer development. Some cytokines produced by the failing heart induce mild inflammation promoting carcinogenesis, as it has been recently suggested by an experimental model of HF in mice. The incidence of new-onset cancer is higher in HF patients compared to the general population, and it significantly worsens their prognosis. Moreover, the management of HF patients developing new-onset cancer is challenging, especially due to the limited therapeutic options for patients affected by both cancer and HF and the higher risk of cardiotoxicity from anticancer drugs.
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Insuficiência Cardíaca/epidemiologia , Neoplasias/epidemiologia , Antineoplásicos/efeitos adversos , Cardiotoxicidade , Humanos , Incidência , Fatores de RiscoRESUMO
Although there have been many improvements in prognosis for patients with cancer, anticancer therapies are burdened by the risk of cardiovascular toxicity. Heart failure is one of the most dramatic clinical expressions of cardiotoxicity, and it may occur acutely or appear years after treatment. This article reviews the main mechanisms and clinical presentations of left ventricular dysfunction induced by some old and new cardiotoxic drugs in cancer patients, referring to the most recent advances in the field. The authors describe the mechanisms of cardiotoxicity induced by anthracyclines, which can lead to cardiovascular problems in up to 48% of patients who take them. The authors also describe mechanisms of cardiotoxicity induced by biological drugs that produce left ventricular dysfunction through secondary mechanisms. They outline the recent advances in immunotherapies, which have revolutionised anticancer therapies.
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Anthracyclines are widely used in anticancer protocols, but can induce cardiotoxicity by mechanisms that mainly involve oxidative damage and mitochondrial dysfunction. Radiotherapy (RT) can also impair cardiac function by promoting myocardial fibrosis, microvascular damage, and decreased density of myocardial capillaries. Hence, we aim at investigating prospectively whether RT impacts heart function in lymphoma patients who had been already treated with anthracyclines. Twenty-nine consecutive patients with Hodgkin or non-Hodgkin lymphomas underwent echocardiography at baseline (before antineoplastic treatments), and then every 2 months, until 6 months after treatment completion. Echo evaluation included standard two-dimensional and speckle tracking. Twenty-two patients treated with anthracycline-based regimens were eligible. Out of the 22 patients, 8 received chemotherapy (CT) only (subgroup 1), while 14 underwent RT after CT [subgroup 2 (S2)]. At the end of CT, ejection fraction was significantly reduced in the whole population. At 6 months after completion of therapies, E/E' increased and global longitudinal strain was compromised in S2, suggesting additional damage induced by RT after CT. On the basis of the data from our small prospective study, we can hypothesize that in lymphoma patients, anthracyclines can worsen cardiac function, and RT may have an additional unfavorable myocardial impact.
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Antraciclinas/efeitos adversos , Antraciclinas/uso terapêutico , Antineoplásicos/efeitos adversos , Antineoplásicos/uso terapêutico , Linfoma/tratamento farmacológico , Linfoma/radioterapia , Adulto , Idoso , Idoso de 80 Anos ou mais , Antibióticos Antineoplásicos/efeitos adversos , Antibióticos Antineoplásicos/uso terapêutico , Doxorrubicina/efeitos adversos , Doxorrubicina/uso terapêutico , Ecocardiografia , Feminino , Cardiopatias/diagnóstico , Cardiopatias/etiologia , Humanos , Masculino , Pessoa de Meia-Idade , Estudos Prospectivos , Adulto JovemRESUMO
A quantum probability model is introduced and used to explain human probability judgment errors including the conjunction and disjunction fallacies, averaging effects, unpacking effects, and order effects on inference. On the one hand, quantum theory is similar to other categorization and memory models of cognition in that it relies on vector spaces defined by features and similarities between vectors to determine probability judgments. On the other hand, quantum probability theory is a generalization of Bayesian probability theory because it is based on a set of (von Neumann) axioms that relax some of the classic (Kolmogorov) axioms. The quantum model is compared and contrasted with other competing explanations for these judgment errors, including the anchoring and adjustment model for probability judgments. In the quantum model, a new fundamental concept in cognition is advanced--the compatibility versus incompatibility of questions and the effect this can have on the sequential order of judgments. We conclude that quantum information-processing principles provide a viable and promising new way to understand human judgment and reasoning.
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Julgamento , Modelos Psicológicos , Probabilidade , Cognição , Humanos , Matemática , Modelos Estatísticos , Teoria QuânticaRESUMO
OBJECTIVE: To evaluate the role of a dedicated neurosonographer in prenatal diagnosis of isolated complete agenesis of the corpus callosum (iCACC) and to asses the postnatal outcome of these infants. METHODS: Prospective study between January 2004 to December 2004 at Fetal Maternal Medical Centre 'Artemisia', Rome, Italy. A detailed ultrasound scan was performed in fetuses affected by iCACC by a dedicated fetal neurosonographer (CG). In all cases, magnetic resonance imaging (MRI) within 5 weeks and 13-15 months after birth was performed. A comparison was made between prenatal findings following the ultrasound scan and postnatal MRI. In these cases, a follow-up of 4-years was performed with a neurological evaluation. RESULTS: Among 23 cases of ACC diagnosed at our centre in the study period, CACC was diagnosed in 17 fetuses. Two were then excluded due to associated malformations, one was lost at follow-up and one patient opted to terminate her pregnancy. Newborn MRI confirmed the ultrasonographic diagnosis of iCACC in all 13 cases. A regular development was present in 92.3% of prenatally diagnosed iCACC. CONCLUSION: A dedicated neurosonographer could diagnose the iCACC with the same accuracy as MRI and in up to 90% of cases the newborn will have a regular development.
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Síndrome Acrocalosal/diagnóstico por imagem , Ultrassonografia Pré-Natal , Síndrome Acrocalosal/genética , Adulto , Feminino , Idade Gestacional , Humanos , Recém-Nascido , Cariotipagem , Imageamento por Ressonância Magnética , Gravidez , Estudos ProspectivosRESUMO
BACKGROUND: Mother-to-child transmission of hepatitis C virus (HCV) has been reported in around 5% of cases, and is much more likely to occur in case of coinfection with HIV. However, other cofactors influencing the vertical transmission are still debated. AIM: To assess the serum concentration of endogenous interferon (IFN) during pregnancy, and its eventual role on the vertical transmission of HCV. METHODS: Forty-seven HCV-infected pregnant women, and 3 control groups: (1) 75 HCV-negative pregnant women; (2) 29 HCV-positive nonpregnant women; (3) 29 HCV-negative nonpregnant women entered into the study. Endogenous IFN was assayed by enzyme-linked immunosorbent assay. The following parameters were also analyzed: viral load, HIV infection, risk factors for acquiring HCV, parity, gestational age, mode and course of delivery. RESULTS: Vertical transmission of HCV was observed in 2 cases (4.3%). Plasma levels of IFN were significantly higher in HCV-positive pregnant women compared with either HCV-positive and HCV-negative nonpregnant women. The 2 mothers who transmitted the infection had IFN levels within the same range as the women who did not transmit the infection. CONCLUSIONS: In HCV-positive pregnant women, there is an increased production of endogenous IFN-alpha. Further studies are warranted for clarifying the mechanisms of this cytokine in the prevention of HCV transmission.