Publications

Interventional cardiovascular medicine is in continuous evolution. Introduction of drug-eluting stents (DES) in clinical practice drastically improved the efficacy of percutaneous coronary intervention by reducing the risk of in-stent restenosis through the abluminal elution of an antiproliferative drug to suppress neointimal hyperplasia. Unfortunately, safety issues rose with first-generation DES due to incomplete luminal stent strut endothelialization and subsequent risk of late and very-late thrombosis. While 2nd-generation DES addressed some of the safety issues observed with 1st-generation DES, some limitations remain. Dual therapy stenting is an innovative technology developed with the rationale of combining a highly effective antiproliferative drug elution on the abluminal side and an endothelial progenitor cell capture system on the luminal side to accelerate stent strut endothelialization; thus potentially preventing the early and late complications of incomplete endothelial coverage while maintaining an antirestenotic effectiveness. Additionally, a DES platform associated with more predictable and faster endothelialization pattern may be an important therapeutic option in patients at high-risk for bleeding who cannot tolerate even short regimens of dual antiplatelet therapy. The present article reviews the most recent developments in dual therapy stenting from its rationale to the preclinical and clinical studies.

BACKGROUND

Women with a history of hypertensive disorders of pregnancy are at an increased risk of hypertension and cardiovascular disease in later life. Lactation has been associated with a reduced risk of maternal hypertension, both in the postpartum period and later life. However, little is known about whether lactation is also cardioprotective in women with hypertensive disorders of pregnancy such as preeclampsia or gestational hypertension.

OBJECTIVE

This study aimed to characterize the relationship between lactation and postpartum blood pressure among women with preeclampsia and gestational hypertension.

STUDY DESIGN

Data were obtained from women who participated in the Prenatal Exposures and Preeclampsia Prevention study (n = 379; 66% African American; 85% overweight or obese). Women enrolled during pregnancy and attended a postpartum visit (on average, 9.1 months after delivery) during which data on lactation duration and blood pressure were collected. The significance of the associations between postpartum blood pressure and lactation among women who remained normotensive during pregnancy, developed gestational hypertension, or developed preeclampsia were assessed with an analysis of variance. Linear regression models were used to adjust for maternal age, race, education, prepregnancy weight, and time since delivery.

RESULTS

Gestational hypertension affected 42 subjects (11%) and preeclampsia affected 33 (9%). Lactation was reported by 217 (57%) with 78 (21%) reporting ≥ 6 months of lactation. Women who lactated were somewhat older, more educated, and had higher socioeconomic status. Among women who had gestational hypertension, lactation was associated with lower systolic blood pressure (P = .02) and diastolic blood pressure (P = .02). This association persisted after adjustment for age, race, education, prepregnancy weight, and time since delivery. However, for women who had preeclampsia and women who remained normotensive during pregnancy, lactation was not associated with postpartum blood pressure in either bivariate or multivariate analyses.

CONCLUSION

This study found that lactation is associated with lower postpartum blood pressure among overweight women who develop gestational hypertension but not among women who develop preeclampsia. Future studies are needed to explore the association of lactation and blood pressure in later life for women with hypertensive disorders of pregnancy.

BACKGROUND

Observational studies have reported an association between type 2 diabetes and osteoarthritis (OA) development and progression. However no systematic review of the literature exists assessing whether this association is consistently true. We aimed to systematically review the association between type 2 diabetes and the presence, development, and progression of OA.

METHODS

We searched MEDLINE, SCOPUS, EMBASE, the Web of Science, and Grey Literature (through August 2014) for prospective cohort, cross-sectional, and case-control studies with confidence intervals (CI) that reported an association between type 2 diabetes and impaired glucose tolerance (IGT) and the development or presence of OA of any joint.

RESULTS

Ten studies and fourteen ratios were included in the analysis. The pooled population size in our meta-regression was 16,742 patients. Type 2 diabetes was significantly associated with the development or presence of OA (OR; 1·21, 95% CI: 1·02-1·41). In the subset of 7 studies that did control for weight or BMI there was an increased odds of OA associated with type 2 diabetes was (OR: 1·25, 95% CI: 1·05-1·46) from a smaller pool of patients (n=7156).

CONCLUSIONS

Type 2 diabetes is associated with the development and presence of radiographic and symptomatic OA even when controlling for body mass index and weight.

In its report Global Health 2035, the Commission on Investing in Health proposed that health investments can reduce mortality in nearly all low- and middle-income countries to very low levels, thereby averting 10 million deaths per year from 2035 onward. Many of these gains could be achieved through scale-up of existing technologies and health services. A key instrument to close this gap is policy and implementation research (PIR) that aims to produce generalizable evidence on what works to implement successful interventions at scale. Rigorously designed PIR promotes global learning and local accountability. Much greater national and global investments in PIR capacity will be required to enable the scaling of effective approaches and to prevent the recycling of failed ideas. Sample questions for the PIR research agenda include how to close the gap in the delivery of essential services to the poor, which population interventions for non-communicable diseases are most applicable in different contexts, and how to engage non-state actors in equitable provision of health services in the context of universal health coverage.

CONTEXT

Serum creatinine has been reported to increase in patients receiving Vemurafenib, yet neither the prevalence nor the mechanism of this adverse event are known.

OBJECTIVE

We aimed to evaluate the frequency and the mechanisms of increases in plasma creatinine level in patients receiving Vemurafenib for advanced melanoma.

METHODS

We performed a retrospective monocentric study including consecutive patients treated with Vemurafenib for an advanced melanoma. We collected clinical and biological data concerning renal function before introduction of Vemurafenib and in the course of monthly follow-up visits from March 2013 to December 2014. Cystatin C-derived glomerular filtration rate was evaluated before and after Vemurafenib initiation, as increase in serum cystatin C is specific to a decrease in the glomerular filtration rate. We also performed thorough renal explorations in 3 patients, with measurement of tubular secretion of creatinine before and after Vemurafenib initiation and a renal biopsy in 2 patients.

RESULTS

70 patients were included: 97% of them displayed an immediate, and thereafter stable, increase in creatinine (+22.8%) after Vemurafenib initiation. In 44/52 patients in whom Vemurafenib was discontinued, creatinine levels returned to baseline. Serum cystatin C increased, although proportionally less than serum creatinine, showing that creatinine increase under vemurafenib was indeed partly due to a renal function impairment. In addition, renal explorations demonstrated that Vemurafenib induced an inhibition of creatinine tubular secretion.

CONCLUSION

Thus, Vemurafenib induces a dual mechanism of increase in plasma creatinine with both an inhibition of creatinine tubular secretion and slight renal function impairment. However, this side effect is mostly reversible when Vemurafenib is discontinued, and should not lead physicians to discontinue the treatment if it is effective.