Importância da Presença de Lesões Adicionais Complexas no Contexto de Angioplastia Primária no Enfarte Agudo do Miocárdio no Prognóstico a Médio-Prazo

Introdução: Existe alguma controvérsia respeitante ao tipo de revascularização a efectuar no contexto de angioplastia (PCI) primária no enfarte agudo do miocárdio (EAM). A presença de lesões coronárias adicionais, particularmente complexas, poderá ter impacto no prognóstico. Objectivos: Avaliar o prognóstico a médio-prazo (1 ano) face à presença de lesões adicionais complexas após PCI primária. População e Métodos: Estudaram-se retrospectivamente 138 doentes consecutivos admitidos na nossa Unidade por EAM com elevação do segmento ST e submetidos a PCI primária. Os doentes foram seguidos por um período de 1 ano e divididos em 2 grupos: sem lesões adicionais complexas (n=69, 61 ± 14 anos, 62% sexo masculino) e com lesões adicionais complexas (n=69, 65 ± 13 anos, 73% sexo masculino, p=NS). Avaliaram-se as características demográficas, factores de risco para doença coronária, história prévia cardíaca, e presença de sinais de insuficiência cardíaca na admissão. Foram também avaliadas características angiográficas, medicação efectuada e resultado da PCI. Avaliou-se o impacto das variáveis na ocorrência combinada de morte/re-enfarte/revascularização miocárdica ao primeiro ano. Resultados: A taxa de sucesso angiográfico foi de 96,4%. O grupo com idade igual ou superior a 75 anos representa 24% da população e 4,3% apresentaram-se em classe Killip IV. A localização anterior foi ligeiramente superior no grupo sem lesões adicionais complexas (60% vs. 44%, p=0,06), a inferior no grupo com lesões adicionais complexas (26% vs. 42%, p=0,07). A doença de 1 vaso foi mais prevalente no grupo sem lesões adicionais complexas como esperado (86% vs. 11%, p<0,001). A utilização de stent foi mais frequente no grupo sem lesões adicionais complexas (96% vs. 86%, p=0,08). Não houve diferenças nas restantes variáveis. A taxa de morte/re-enfarte/revascularização foi superior no grupo com lesões adicionais complexas (13% vs. 32%, p=0,014). Até aos 13 dias de seguimento, ocorreram 67% dos eventos. Na análise univariada, os factores predizentes de eventos foram a classe Killip 2, fluxo TIMI < 3 no vaso relacionado com enfarte após PCI, a não utilização de antagonistas da glicoproteína IIb/IIIa, bloqueadores beta e estatinas, doença multivaso e presença de lesões adicionais complexas (Log-rank, p=0,003). Na análise multivariável, os factores predizentes independentes de prognóstico a 1 ano foram a classe Killip 2 (Odds ratio 0,28%; IC 95% 0,08-0,93, p=0,037) e a presença de lesões adicionais complexas (OR 0,32; IC 95% 0,12-0,84, p=0,020). Conclusões: A presença de lesões adicionais complexas após PCI primária tem um pior prognóstico ao primeiro ano, sugerindo a necessidade de intervenção para a sua estabilização, particularmente nos primeiros 30 dias após enfarte.

Anéis de Ferrara: - 4 Anos Depois

Os anéis intraestromais, nomeadamente o anel de Ferrara, constitui uma importante opção terapêutica das doenças ectásicas da córnea, de origem não inflamatória como o Queratocone. Os autores analisaram os primeiros 30 casos operados no Serviço de Oftalmologia do CHLC relativamente à eficácia, estabilidade e segurança deste procedimento ao longo dos 4 anos. Verificaram estabilidade refractiva, diminuição queratométrica e do equivalente esférico e boa tolerância ao material implantado. Os autores concluem que esta opção terapêutica para o queratocone é segura, reversível, com resultados estáveis que permitem adiar ou evitar a queratoplastia.

Slipped Capital Femoral Epiphysis. A Report of 4 Cases Occurring in One Family

We describe slipped capital femoral epiphysis in 4 members of a black, obese family, who were all first-degree relatives. The aetiology of slipped capital femoral epiphysis is unknown, although it is thought to be multifactorial. Genetic predisposition and environmental factors have been associated with the condition. A familial incidence with at least two cases in the same family has been reported. In epidemiological studies, this incidence ranges from 3% to 35%. Our cases were investigated in an attempt to find a possible aetiological genetic factor. A genetic predisposition with an autosomal dominant pattern of transmission is suggested, although environmental variables must be considered as provocative factors.

Chronic Allograft Dysfunction - Is There a Treatment?

BACKGROUND: The major causes of renal transplant loss are death and chronic allograft dysfunction (CAD). The aims of this study were to determine the incidence of CAD in our population and the relation between allograft survival and immunosuppressive regimens. METHODS: We studied retrospectively 473 patients who received deceased donor kidney transplants with at least 1 allograft biopsy between January 1990 and May 2007. Clinical data included age, gender, biopsy data, and immunosuppression before and after kidney biopsy. Mean age was 45.4 +/- 12.7 years including 65% males with a mean follow-up of 6.7 +/- 4.5 years. CAD was observed in 177 of 473 biopsies: 48 patients showed interstitial fibrosis (IF); 101 chronic rejection (CR); 16 transplant glomerulopathy (TG); and 12, CR and TG. Mean follow-up since the discovery of the histologic feature was 60.5 +/- 50.5 months for IF; 38.3 +/- 40.8 for CR, and 18.2 +/- 19.2 for TG. RESULTS: CAD, which was more common in younger patients (P = .03), correlated upon univariate and multivariate analysis with CKD stage 5d development (P < .001). Deposition of C4d in peritubular capillaries was more frequent among CAD patients (P = .004), an association with particular relevance to recipients with CR (P = .02) and TG (P < .001). When we analyzed CAD subpopulation, we observed a positive correlation between allograft survival and immunosuppression modification after biopsy. Substitution of sirolimus (40/177) was shown in univariate, multivariate and Cox regression analyses to be a renal protector (P < .002). Allograft survival was also correlated with initial mycophenolate mofetil versus azathioprine, (62/177) immunosuppression (P < .001). CONCLUSION: CAD, a frequent histologic feature, may benefit from sirolimus conversion.

Impact of Donor and Recipient Cytokine Genotypes on Renal Allograft Outcome

Allelic differences in gene promoter or codifying regions have been described to affect regulation of gene expression, consequently increasing or decreasing cytokine production and signal transduction responses to a given stimulus. This observation has been reported for interleukin (IL)-10 (-1082 A/G; -819/-592 CT/CA), transforming growth factor (TGF)-beta (codon 10 C/T, codon 25 G/C), tumor necrosis factor (TNF)-alpha (-308 G/A), TNF-beta (+252 A/G), interferon (IFN)-gamma (+874 T/A), IL-6 (-174 G/C), and IL-4R alpha (+1902 G/A). To evaluate the influence of these cytokine genotypes on the development of acute or chronic rejection, we correlated the genotypes of both kidney graft recipients and cadaver donors with the clinical outcome. Kidney recipients had 5 years follow-up, at least 2 HLA-DRB compatibilities, and a maximum of 25% anti-HLA pretransplantation sensitization. The clinical outcomes were grouped as follows: stable functioning graft (NR, n = 35); acute rejection episodes (AR, n = 31); and chronic rejection (CR, n = 31). The cytokine genotype polymorphisms were defined using PCR-SSP typing. A statistical analysis showed a significant prevalence of recipient IL-10 -819/-592 genotype among CR individuals; whereas among donors, the TGF-beta codon 10 CT genotype was significantly associated with the AR cohort and the IL-6 -174 CC genotype with CR. Other albeit not significant observations included a strong predisposition of recipient TGF-beta codon 10 CT genotype with CR, and TNF-beta 252 AA with AR. A low frequency of TNF-alpha -308 AA genotype also was observed among recipients and donors who showed poor allograft outcomes.

Restrição do Crescimento Fetal - Casuística de 4 Anos

Overview and aims: Fetal growth restriction (FGR) affects 15% of pregnancies and is associated with both increased perinatal and neonatal morbidity and mortality and long-term effects in adult life. Our aim was to describe cases and outcomes of FGR from a tertiary perinatal care centre and identify the predictors of neonatal morbidity and mortality. Study design: retrospective cohort. Population: pregnancies with early or late FGR caused by placental factors followed from 2006 to 2009 in a tertiary perinatal care centre. Methods: we collected data from clinical records on demographics, clinical history and fetal ultrasound parameters. Perinatal and neonatal outcomes were stratiied according to gestational age (above or below 28 weeks) and we used bivariate analysis to identify any associations with clinical and imaging indings. Results: we included 246 pregnancies; hypertension was the most prevalent maternal risk factor (16%). There were 15 cases of early FGR, 11 of which had cesarean delivery due to deterioration of fetal Doppler parameters. Outcomes in this group included one fetal and three neonatal deaths. Of 231 cases of late FGR, 64% were delivered early given a non-reassuring fetal status i.e. due to changes in Doppler evaluation or altered Manning biophysical proile. There were four cases of perinatal death in this group, three of which delivered at 28 weeks. Neonatal morbidity was associated with lower gestational age, lower birthweight and progressive placental dysfunction (p<0.01). Conclusion: there was an association between neonatal morbidity and gestational age, birthweight and Doppler deterioration, particularly for deliveries below 28 weeks. The assessment of vascular changes through Doppler analysis allows anticipation of fetal deterioration and is a helpful tool in deciding the optimum timing of delivery.