Impact of postoperative nadir hemoglobin and blood transfusion on outcomes after operations for atherosclerotic vascular disease

ObjectiveControversy surrounds the topic of transfusion policy after noncardiac operations. This study assessed the combined impact of postoperative nadir hemoglobin (nHb) levels and blood transfusion on adverse events after open surgical intervention in patients who undergo operative intervention for atherosclerotic vascular disease.MethodsConsecutive patients who underwent peripheral arterial disease (PAD)-related operations were balanced on baseline characteristics by inverse weighting on propensity score calculated as their probability to have nHb greater than 10 gm/dL on the basis of operation type, demographics, and comorbidities, including the revised cardiac risk index. A multivariate generalized estimating equation analysis was performed to investigate associations between nHb, transfusion, and a composite outcome of perioperative death and myocardial infarction. Logistic and Cox proportional hazards regressions were used to assess the impact of nHb and transfusion on respiratory and wound complications; and a composite end point (CE) of death, myocardial infarction during a 2-year follow-up. Level of statistical significance was set at alpha of 0.0125 to adjust for the increased probability of type I error attributable to multiple comparisons.ResultsThe analysis cohort included 880 patients (1074 operations). After adjusting for nHb level, the number of units transfused was not associated with the perioperative occurrence of the CE (odds ratio [OR], 1.13; P = .025). Adjusted for the number of units transfused, nHb had no impact on the perioperative CE (OR, 0.62; P = .22). An interaction term between transfusion and nHb level remained nonsignificant (P = .312), indicating that the impact of blood transfusion was the same regardless of the nHb level. Perioperative respiratory complications were more likely in patients receiving transfusions (OR, 1.22; P = .009), and perioperative wound infections were less common in patients with nHb >10 gm/dL (OR, 0.65; P = .01). During an average follow-up of 24 months, transfused patients were more likely to develop the CE (hazard ratio [HR], 1.15, P = .009), whereas nHb level did not impact the long-term adverse event rate (HR, 0.78; P = .373). The above associations persisted even after adjusting the Cox regression model for the occurrence of perioperative cardiac events.ConclusionsAlthough nHb less than 10 gm/dL is not associated with death or ACS after PAD-related operations, maintaining nHb greater than 10 gm/dL appears to decrease the risk of wound infection. Blood transfusion is associated with increased risk of perioperative respiratory complications. Until a randomized trial settles this issue definitively, a restrictive transfusion strategy is justified in patients undergoing operations for atherosclerotic vascular disease

Impact of cumulative intravascular contrast exposure on renal function in patients with occlusive and aneurysmal vascular disease

ObjectivePatients with occlusive or aneurysmal vascular disease are repeatedly exposed to intravascular (IV) contrast for diagnostic or therapeutic purposes. We sought to determine the long-term impact of cumulative iodinated IV contrast exposure (CIVCE) on renal function; the latter was defined by means of National Kidney Foundation (NKF) criteria.MethodsWe performed a longitudinal study of consecutive patients without renal insufficiency at baseline (NFK stage I or II) who underwent interventions for arterial occlusive or aneurysmal disease. We collected detailed data on any IV iodinated contrast exposure (including diagnostic or therapeutic angiography, cardiac catheterization, IV pyelography, computed tomography with IV contrast, computed tomographic angiography); medication exposure throughout the observation period; comorbidities; and demographics. The primary end point was the development of renal failure (RF) (defined as NFK stage 4 or 5). Analysis was performed with the use of a shared frailty model with clustering at the patient level.ResultsPatients (n = 1274) had a mean follow-up of 5.8 (range, 2.2-14) years. In the multivariate model with RF as the dependent variable and after adjusting for the statistically significant covariates of baseline renal function (hazard ratio [HR], 0.95; P < .001), diabetes (HR, 1.8; P = .007), use of an angiotensin-converting enzyme inhibitor (HR, 0.63; P = .03), use of antiplatelets (HR, 0.5; P = .01), cumulative number of open vascular operations performed (HR, 1.2; P = .001), and congestive heart failure (HR, 3.2; P < .001), CIVCE remained an independent predictor for RF development (HR, 1.1; P < .001). In the multivariate survival analysis model and after adjusting for the statistically significant covariates of perioperative myocardial infarction (HR, 3.9; P < .001), age at entry in the cohort (HR, 1.05; P = .035), total number of open operations (HR, 1.51; P < .001), and serum albumin (HR, 0.47; P < .001), CIVCE was an independent predictor of death (HR, 1.07; P < .001).ConclusionsCumulative IV contrast exposure is an independent predictor of RF and death in patients with occlusive and aneurysmal vascular disease

Integrative Effect of Carvedilol and Aerobic Exercise Training Therapies on Improving Cardiac Contractility and Remodeling in Heart Failure Mice

The use of b-blockers is mandatory for counteracting heart failure (HF)-induced chronic sympathetic hyperactivity, cardiac dysfunction and remodeling. Importantly, aerobic exercise training, an efficient nonpharmacological therapy to HF, also counteracts sympathetic hyperactivity in HF and improves exercise tolerance and cardiac contractility; the latter associated with changes in cardiac Ca2+ handling. This study was undertaken to test whether combined b-blocker and aerobic exercise training would integrate the beneficial effects of isolated therapies on cardiac structure, contractility and cardiomyocyte Ca2+ handling in a genetic model of sympathetic hyperactivity-induced HF (alpha(2A)/alpha 2C(-)adrenergic receptor knockout mice, KO). We used a cohort of 5-7 mo male wild-type (WT) and congenic mice (KO) with C57Bl6/J genetic background randomly assigned into 5 groups: control (WT), saline-treated KO (KOS), exercise trained KO (KOT), carvedilol-treated KO (KOC) and, combined carvedilol-treated and exercise-trained KO (KOCT). Isolated and combined therapies reduced mortality compared with KOS mice. Both KOT and KOCT groups had increased exercise tolerance, while groups receiving carvedilol had increased left ventricular fractional shortening and reduced cardiac collagen volume fraction compared with KOS group. Cellular data confirmed that cardiomyocytes from KOS mice displayed abnormal Ca2+ handling. KOT group had increased intracellular peak of Ca2+ transient and reduced diastolic Ca2+ decay compared with KOS group, while KOC had increased Ca2+ decay compared with KOS group. Notably, combined therapies re-established cardiomyocyte Ca2+ transient paralleled by increased SERCA2 expression and SERCA2: PLN ratio toward WT levels. Aerobic exercise trained increased the phosphorylation of PLN at Ser16 and Thr17 residues in both KOT and KOCT groups, but carvedilol treatment reduced lipid peroxidation in KOC and KOCT groups compared with KOS group. the present findings provide evidence that the combination of carvedilol and aerobic exercise training therapies lead to a better integrative outcome than carvedilol or exercise training used in isolation.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Fundação de Amparo à Pesquisa do Estado de Minas Gerais (FAPEMIG)Conselho Nacional de Pesquisa e DesenvolvimentoConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Univ São Paulo, Sch Phys Educ & Sport, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Biosci, Santos, BrazilDept Circulat & Med Imaging, Trondheim, NorwayKG Jebsen Ctr Exercise Med, Trondheim, NorwayUniv Fed Minas Gerais, Dept Physiol & Biophys, Belo Horizonte, MG, BrazilUniv São Paulo, Heart Inst InCor, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Biosci, Santos, BrazilFAPESP: FAPESP:2010/50048-1FAPESP: 06/56123-0CNPq: 302201/2011-4Web of Scienc

Transient Neuronal Populations Are Required to Guide Callosal Axons: A Role for Semaphorin 3C

Neurons, glia, and callosal axons operate as a “ménage à trois” in the development of the corpus callosum

Jaw claudication in the era of carotid stenting

Jaw claudication could result from external carotid artery (ECA) occlusive disease. Carotid artery stenting (CAS) has been shown to worsen the disease in the ECA. This could potentially worsen the symptoms in patients with pre-existing jaw claudication undergoing CAS. Meanwhile, ECA endarterectomy is routinely done during internal carotid artery endarterectomy (CEA). This has been shown to alleviate jaw claudication symptoms. We report a case of a high-risk patient for CEA who presented with symptomatic carotid disease as well as bilateral jaw claudication. Both symptoms resolved after CEA. We also present the case of another patient treated for recurrent high-grade carotid disease with CAS resulting in acute ECA occlusion and jaw claudication. High-risk patients with symptomatic carotid disease and jaw claudication should be considered for CEA and not only CAS