The impact of frailty on outcomes after cardiac surgery: a systematic review.

OBJECTIVE: Current preoperative assessments for cardiac surgery, such as the European System for Cardiac Operative Risk Evaluation II and the Society of Thoracic Surgeons risk score, are limited in their ability to predict postoperative outcomes. This is thought to be due to the reliance on chronological age as a predictor of health. In geriatrics, frailty assessments have been developed as a tool in determining physiologic functioning capacity. Whether or not frailty predicts postoperative outcomes independent of existing cardiac preoperative risk scores remains unknown. METHODS: We performed a systematic review to determine the association of frailty with negative postoperative outcomes such as major adverse cardiac and cerebrovascular events (MACCE) in patients undergoing cardiac surgery. We searched PubMed, EMBASE, the Cochrane library, and Ageline from inception until July 2013 and screened 5913 abstracts for potential inclusion. Of these, 6 studies examined the relationship between objective frailty assessments and postoperative outcomes. Our included studies evaluated 4756 patients undergoing cardiac surgery. RESULTS: Frailty, defined using multiple criteria, had a strong positive relationship with the risk of MACCE (odds ratio, 4.89; 95% confidence interval, 1.64-14.60). Relationships were stronger in older patients undergoing transcatheter aortic valve replacement (TAVR) than younger patients undergoing coronary artery bypass grafting and valvular surgery (hazard ratio for frailty in TAVR, 3.31-4.89 vs hazard ratio for non-TAVR, 1.10-3.16). CONCLUSIONS: Patients deemed frail, determined using an objective assessment tool, have a higher likelihood of experiencing mortality, morbidity, functional decline, and MACCE following cardiac surgery, regardless of definition. Further study is needed to determine which components of frailty are most predictive of negative postoperative outcomes before integration in risk prediction scores.

What your patient reads: creating a value-added tool for physicians.

Through a number of media sources, today's consumers have unprecedented access to health information of varying reliability and authority. Empowered by this information, patients are more involved in their health care decisions and more willing to question physicians' advice. This poses a challenge for physicians who must now find time to read mass media health reports in addition to medical research. In order to help physicians with this task, librarians at the University of Manitoba Health Sciences Libraries created What Your Patient Reads - one-page summaries of health-related media reports supplemented with references to evidence-based medical literature.

Signaling of angiotensin II-induced vascular protein synthesis in conduit and resistance arteries in vivo.

BACKGROUND: From in vitro studies, it has become clear that several signaling cascades are involved in angiotensin II-induced cellular hypertrophy. The aim of the present study was to determine some of the signaling pathways mediating angiotensin II (Ang II)-induced protein synthesis in vivo in large and small arteries. METHODS: Newly synthesized proteins were labeled during 4 hours with tritiated leucine in conscious control animals, or animals infused for 24 hours with angiotensin II (400 ng/kg/min). Hemodynamic parameters were measure simultaneously. Pharmacological agents affecting signaling cascades were injected 5 hours before the end of Ang II infusion. RESULTS: Angiotensin II nearly doubled the protein synthesis rate in the aorta and small mesenteric arteries, without affecting arterial pressure. The AT1 receptor antagonist Irbesartan antagonized the actions of Ang II. The Ang II-induced protein synthesis was associated with increased extracellular signal-regulated kinases (ERK)1/2 phosphorylation in aortic, but not in mesenteric vessels. Systemic administration of PD98059, an inhibitor of the ERK-1/2 pathway, produced a significant reduction of protein synthesis rate in the aorta, and only a modest decrease in mesenteric arteries. Rapamycin, which influences protein synthesis by alternative signaling, had a significant effect in both vessel types. Rapamycin and PD98059 did not alter basal protein synthesis and had minimal effects on arterial pressure. CONCLUSION: ERK1/2 and rapamycin-sensitive pathways are involved in pressure-independent angiotensin II-induced vascular protein synthesis in vivo. However, their relative contribution may vary depending on the nature of the artery under investigation.

Vessel-specific stimulation of protein synthesis by nitric oxide synthase inhibition: role of extracellular signal-regulated kinases 1/2.

Although conduit arteries develop hypertrophy after chronic NO synthesis blockade, resistance arteries remodel without hypertrophy under the same conditions. Similar findings have been described in essential hypertension. We postulated that this regional difference may be related to a heterogeneous effect of endogenous NO on proliferation along the vascular tree. Newly synthesized proteins were radiolabeled in vivo with [(3)H]L-leucine in basal conditions and during NO synthase inhibition, with or without PD98059 (inhibitor of the extracellular signal-regulated kinases [ERK] 1/2). Blocking the generation of NO by 3 different L-arginine analogues increased protein synthesis by an average of 75% in the aorta, in association with enhanced ERK 1/2 phosphorylation. PD98059 significantly reduced L-arginine analogue-induced protein synthesis and ERK 1/2 phosphorylation, confirming the involvement of ERK 1/2 as an important signaling element. In small arteries, L-arginine analogues did not influence the extent of protein synthesis, although phosphorylation of ERK 1/2 was also enhanced. To determine the role of NO in a condition of enhanced protein synthesis, angiotensin II was infused for 24 hours. Angiotensin II augmented protein synthesis in mesenteric arteries and the aorta, and was additive to NO synthase blockade in the aorta. In conclusion, endogenous NO exerts a tonic inhibitory influence on aortic growth, with limited impact on small arteries in basal and hypertrophic conditions. This heterogeneous role of NO on vascular growth may explain the heterogeneity of vascular remodeling observed in essential hypertension, a condition associated with endothelial dysfunction.