Malignant pericardial effusions: A retrospective look at etiology and prognosis in a tertiary oncological center.

PURPOSE: Cancer and the associated treatments are important causes of pericardial effusion. However, the natural history of malignant pericardial effusion is largely unknown, especially in the context of newer cancer treatments. We investigated the causes of pericardial effusions in a tertiary oncology center, with particular focus on the prognosis of malignant effusions in the era of contemporary oncological therapies. METHOD: We obtained data from electronic medical records. Survival analyses were performed utilizing the Kaplan-Meier method. We performed Cox regression to explore the potential clinical factors associated with survival. RESULTS: Forty-four patients had pericardial effusion treated with pericardiocentesis during the study period. The mean age was 62-years, and 55% were female. Sixty-eight percent of these patients also had cancer, with approximately half (47%) receiving prior chemotherapy, and a quarter (27%) having had chest radiotherapy. Seventy percent of the patients with active cancer had malignant cells on cytology of pericardial fluid. The median survival of the cohort was 227 days, with malignant effusions having a median survival of 62-days compared to nonmalignant effusions with 1408 days (Logrank statistic 7.4, p-value .007). Malignant cytology was significantly associated with mortality on univariable analysis (HR 2.5, 95% CI 1.2-5.3). Complication rates were low, with no deaths as a direct complication of pericardiocentesis. CONCLUSION: Malignancy is the most common cause of pericardial effusion in this tertiary medical and oncological center. Abnormal cytology with malignant cells has a poor median survival, despite advances in oncological treatment over the last decade. Pericardiocentesis is a safe procedure for these patients.

Myocardial perfusion imaging failed to improve patient risk classification compared with the revised cardiac risk index for early cardiac complications after major non-cardiac surgery.

BACKGROUND: Myocardial perfusion imaging (MPI) is frequently used for cardiac risk assessment before major non-cardiac surgery, but its ability to improve patient risk classification beyond simple clinical assessment is unknown. AIM: To explore the prognostic utility of MPI above a simple clinical risk calculator, the revised cardiac risk index (RCRI). METHODS: A retrospective cohort study of at-risk patients who underwent MPI before major non-cardiac surgery in a tertiary hospital was conducted. Major adverse cardiac events (MACE) was defined as any myocardial infarction, acute pulmonary oedema, ventricular arrhythmia or cardiac death within 30 days of surgery. We analysed the predictive value of MPI for MACE using multivariable logistic regression and categorical net reclassification index. RESULTS: MACE occurred in 47 (7.4%) cases from 635 surgical procedures in 629 patients. MPI-identified medium or large-sized reversible perfusion defects (P = 0.02; odds ratio 2.9; 95% confidence interval 1.1-7.1) and RCRI score two or more (P = 0.03; odds ratio 2.3; 95% confidence interval 1.1-4.8) were significantly associated with MACE after adjusting for age, coronary revascularisation, surgical priority, need for general anaesthesia, left ventricular ejection fraction (LVEF) and fixed perfusion defects. MPI risk factors (LVEF, reversible perfusion and fixed perfusion defects) did not improve risk classification above baseline risk factors (age, RCRI and surgical priority). CONCLUSION: MPI risk factors are weak predictors for early cardiac complications after major non-cardiac surgery and failed to improve patient risk classification beyond essential assessment using age, RCRI and surgical priority. Clinicians should consider alternative risk assessment strategies because of MPI's poor prognostic utility and its associated time and financial costs.

Influence of insulin on follicular development and the intrafollicular insulin-like growth factor I (IGF-I) system in sows after weaning.

Twenty-four crossbred primiparous sows were used to investigate the influence of insulin administration after weaning on the intrafollicular insulin-like growth factor i (IGF-I) system. Sows received 0.4 i.u. insulin kg-1 bodyweight or an equivalent volume of saline for 3 days (n = 5 insulin; n = 4 saline) or 5 days (n = 5 insulin; n = 6 saline) after weaning or served as untreated controls on day 1 (n = 4). The number and diameters of ovarian follicles were recorded, and fluid was aspirated from the 20 largest follicles for determination of oestradiol and IGF-I by radioimmunoassay and of insulin-like growth factor-binding proteins (IGFBPs) by western ligand blotting. The walls of the follicles were collected for mRNA analysis by RNase protection assay or granulosa cells were collected for estimation of apoptosis by flow cytometry. Insulin treatment resulted in smaller diameters of all follicles (P < 0.05) and tended (P < 0.07) to increase the number of follicles available on day 5 compared with saline-treated animals (19.8 versus 17.8). The concentration of oestradiol in follicular fluid from large (7-10 mm) follicles on days 3 and 5 was reduced (treatment by size class interaction; P < 0.05) by insulin treatment. Insulin also reduced intrafollicular concentrations of IGF-I at days 3 and 5 after weaning (treatment by day interaction; P < 0.02) while the amounts of IGFBP-3 and IGFBPs of molecular mass 30 and 22 kDa decreased from day 3 to day 5 in saline-treated animals only (treatment by day interaction; P < 0.05). Gene expression for IGF-I increased in saline-treated animals but decreased fourfold in insulin-treated sows from day 3 to day 5 (treatment by day interaction; P < 0.002). Gene expression for IGFBP-d decreased (P < 0.04) from day 3 to day 5, while expression of IGFBP-2 was unaffected by treatment or day. Overall, insulin influenced the IGF-I system in a manner consistent with slowing follicular growth and possibly allowed more follicles to become available for ovulation.