The available evidence shows that Helicobacter pylori serology or endoscopic population screening is cost-effective, while endoscopic surveillance of premalignant gastric lesions presents conflicting results. Better implementation of published guidelines and accomplishment of systematic detailed reviews are needed.
Risk-sharing agreements between pharmaceutical companies and payers stand out as a recent practice, the use of which has been increasing in the case of innovative medicines, particularly in the field of oncology, which aims to ensure better budgetary control and a lower risk of spending on medicinal products without full evidence of clinical benefit.In this article, the authors discuss the types of existing agreements, as well as those used in Portugal, their advantages, disadvantages and future challenges of implementation, as well as their potential role in access to therapeutic innovation, namely medicines for cancer treatment. For this purpose, a nonsystematic review of indexed and nonconventional literature was carried out.There is a tendency for the risk-sharing agreements established between payers and pharmaceutical companies to include a component of monitoring the use of medicines and outcomes measurement, involving real life data collection. Portugal is no exception and, although most agreements are still financial in nature, there is already a strong desire for other agreements, in particular clinical outcomes based.It is concluded that there is not yet a gold standard methodology in relation to the type of agreements to be practiced. Moreover, its opportunity cost, including the cost of implementation, remains to be scrutinised. However, regardless of the type of agreement, the advantages of adopting these agreements are well known, inevitably related with challenges of implementation. The need for an infrastructure to support information sharing is undisputed and urgent.The future of therapeutic innovation and increased pressure on health budgets will require alternative, more flexible models, personalized reimbursement models that allow alignment of medicines prices with the value they deliver in treating the several diseases.
In our population of acute HF patients, admission relaxin serum levels were associated with clinical and echocardiographic markers of pulmonary hypertension, RV dysfunction, and overload, suggesting a role for circulating relaxin as a biomarker in this setting.
After acute myocardial infarction (AMI), diastolic dysfunction is frequent and an important determinant of adverse outcome. However, few interventions have proven to be effective in improving diastolic function. We aimed to determine the effect of exercise training on diastolic and systolic function after AMI.One month after AMI, 188 patients were prospectively randomized (1:1) to an 8-week supervised program of endurance and resistance exercise training (n = 86; 55.9 ± 10.8 years) versus standard of care (n = 89; 55.4 ± 10.3 years). All patients were submitted to detailed echocardiography and cardiopulmonary exercise test, at baseline and immediately after the study. Diastolic function was evaluated by the determination of tissue-Doppler derived early diastolic velocities (E′ velocity at the septal and lateral sides of mitral annulus) and by the E/E′ (ratio between the E wave velocity from mitral inflow and the E’ velocity) as recommended in the consensus document for diastolic function assessment.At the end of the study, there was no significant change in E′ septal velocity or E/E′ septal ratio in the exercise group. We observed a small, although nonsignificant, improvement in E′ lateral (mean change 0.1 ± 2.0 cm/s; P = .40) and E/E′ lateral ratio (mean change of −0.3 ± 2.5; P = .24), while patients in the control group had a nonsignificant reduction in E′ lateral (mean change −0.4 ± 1.9 cm/s; P = .09) and an increase in E/E′ lateral ratio (mean change + 0.3 ± 3.3; P = .34). No relevant changes occurred in other diastolic parameters. The exercise-training program also did not improve systolic function (either tissue Doppler systolic velocities or ejection fraction).Exercise capacity improved only in the exercise-training group, with an increase of 1.6 mL/kg/min in pVO2 (P = .001) and of 1.9 mL/kg/min in VO2 at anaerobic threshold (P < .001).After AMI, an 8-week endurance plus resistance exercise-training program did not significantly improve diastolic or systolic function, although it was associated with an improvement in exercise capacity parameters.
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