Citations

SAGE-Journals-Accessible-Video-Player 10.1089/vid.2012.0043.M1 sj-vid-1-vid-10.1089_vid.2012.0043

Blood pressure (BP) is a key measure of cardiovascular function, and accurate measurement is important to ensure proper clinical evaluation, diagnosis, and treatment. We compared intra-arterial (direct) and cuff auscultation (manual) measurement techniques at rest and during 2 levels of submaximal constant-load exercise (9 min at 40% and 75% maximum watts). Sixty-four adults (aged 29.0 ± 0.7 years; 48% male; height, 173.7 ± 1.2 cm; mass, 73.0 ± 1.7 kg; body mass index, 24.1 ± 0.4 kg·m−2; body surface area, 1.87 ± 0.03 m2) participated in the study. At rest, low, and moderate intensity, direct measurement demonstrated higher systolic BP (SBP) and diastolic BP (DBP) (bias for SBP: 22, 31, and 27 mm Hg and for DBP: 5, 7, and 17 mm Hg; rest, low-, and moderate-intensity, respectively; p < 0.01). At rest, the correlation and agreement between the 2 methods was modest (SBP: r = 0.56, bias = +22.1 mm Hg; DBP: r = 0.53, bias = +4.9 mm Hg; p < 0.001). There was good correlation and agreement with SBP at low and moderate intensity; however, DBP demonstrated a weaker relationship (SBP: r = 0.74 and 0.74, bias = +30.2 and +26.8 mm Hg; DBP: r = 0.39 and 0.28, bias = +7.1 and +13.4 mm Hg; for low and moderate intensity, respectively; p < 0.001). Further, manual measurement demonstrated a greater slope from rest to moderate exercise for the relationship between pulse pressure (PP) and cardiac output (13.6 ± 0.4 vs 12.3 ± 0.4, p = 0.03). As exercise intensity increases, manual DBP tends to bias low compared with direct DBP, which, when combined with parallel increases in SBP, leads to no differences in PP between methods at moderate exercise. Because PP is used to calculate other cardiovascular parameters (mean arterial pressure, systemic vascular resistance), measurement technique and exercise intensity should be considered when using cardiovascular variables as outcome measures.

Background— A hub-and-spoke telestroke network is an effective way to extend quality acute stroke care to remote hospitals and to improve patient outcomes. This study assessed the cost-effectiveness of a telestroke network in the management of acute ischemic stroke from the perspectives of a network, a hub hospital, and a spoke hospital. Methods and Results— A model was developed to compare costs and effectiveness with and without a telestroke network over a 5-year time horizon. The model considered differences in rates of teleconsultations, intravenous thrombolysis, endovascular stroke therapies, and spoke-to-hub transfers. These inputs were estimated through the use of data from Georgia Health Sciences University and Mayo Clinic telestroke networks. A network model with 1 hub and 7 spokes predicted that 45 more patients would be treated with intravenous thrombolysis and 20 more with endovascular stroke therapies per year compared with no network, leading to an estimate of 6.11 more home discharges. Each year, a telestroke network was associated with $358 435 in cost savings; each spoke had $109 080 in cost savings, whereas the hub had positive costs of $405 121. However, cost sharing can be arranged so that each hospital could achieve an equal amount of cost savings ($44 804/y). Results were sensitive to the number of spokes, marginal treatment costs in spokes and rates of transfer, and endovascular stroke therapies. Conclusions— The results of this study suggest that a telestroke network may increase the number of patients discharged home and reduce the costs borne by the network hospitals. Hospitals should consider their available resources and the network features when deciding whether to join or set up a network.

Background— Giant cell myocarditis (GCM) typically causes fulminant heart failure, arrhythmias, or heart block, necessitating aggressive immunosuppression, ventricular assist device insertion, or cardiac transplantation. We describe a novel variant of GCM, primarily involving the atria, that displays distinctive clinical features and follows a more benign course than ventricular GCM. Methods and Results— We identified 6 patients (median age 67.5 years, 4 male) with atrial GCM in our pathology consultation practices from 2010 to 2012. Clinical history, imaging, and pathology materials were reviewed. Clinically, 4 patients had atrial fibrillation, 1 had acute heart failure, and 1 had incidental disease at autopsy. Among the 5 living patients, echocardiography revealed severe atrial dilatation (5 cases), mitral/tricuspid regurgitation (5), atrial mural thrombus (3), atrial wall thickening (2), and atrial hypokinesis (2). Ventricular function was preserved in all 5. Histological review of surgically resected atria showed giant cell and lymphocytic infiltrates, lymphocytic myocarditis-like foci, cardiomyocyte necrosis, and cardiomyocyte hypertrophy in all cases. Other features included interstitial fibrosis (5), poorly-formed granulomas (4), eosinophils (4), neutrophils (1), and vasculitis (1). Treatment consisted of steroids and cyclosporine (1), pacemaker placement for sick sinus syndrome (1), and supportive care (3). All 5 living patients returned to baseline exercise tolerance after 6 to 16 weeks of follow-up. Conclusions— Atrial GCM represents a distinct clinicopathologic entity with a more favorable prognosis than classic ventricular GCM. This disorder should be included in the differential diagnosis of atrial dilatation, particularly when associated with atrial wall thickening. The utility of immunomodulatory therapy for this condition remains unknown.

Background and objective Survival of patients with pancreatic adenocarcinoma is limited and few prognostic factors are known. We conducted a two-stage genome-wide association study (GWAS) to identify germline variants associated with survival in patients with pancreatic adenocarcinoma. Methods We analysed overall survival in relation to single nucleotide polymorphisms (SNPs) among 1005 patients from two large GWAS datasets, PanScan I and ChinaPC. Cox proportional hazards regression was used in an additive genetic model with adjustment for age, sex, clinical stage and the top four principal components of population stratification. The first stage included 642 cases of European ancestry (PanScan), from which the top SNPs (p≤10 −5 ) were advanced to a joint analysis with 363 additional patients from China (ChinaPC). Results In the first stage of cases of European descent, the top-ranked loci were at chromosomes 11p15.4, 18p11.21 and 1p36.13, tagged by rs12362504 (p=1.63×10 −7 ), rs981621 (p=1.65×10 −7 ) and rs16861827 (p=3.75×10 −7 ), respectively. 131 SNPs with p≤10 −5 were advanced to a joint analysis with cases from the ChinaPC study. In the joint analysis, the top-ranked SNP was rs10500715 (minor allele frequency, 0.37; p=1.72×10 −7 ) on chromosome 11p15.4, which is intronic to the SET binding factor 2 (SBF2) gene. The HR (95% CI) for death was 0.74 (0.66 to 0.84) in PanScan I, 0.79 (0.65 to 0.97) in ChinaPC and 0.76 (0.68 to 0.84) in the joint analysis. Conclusions Germline genetic variation in the SBF2 locus was associated with overall survival in patients with pancreatic adenocarcinoma of European and Asian ancestry. This association should be investigated in additional large patient cohorts.

Snoring is a common phenomenon and results from vibration of the soft tissue structures in the upper airway. Snoring may occur alone or as a sign of upper airway resistance syndrome (UARS) or obstructive sleep apnea syndrome (OSA). Snoring carries social consequences and has been linked to increased risk for cardiovascular disease, although this relationship may be confounded by undiagnosed OSA. UARS is characterized by daytime dysfunction and repetitive respiratory effort-related arousals, episodes of increasingly intense breathing efforts that terminate with an arousal from sleep before a hypopnea (episode of partial airflow reduction) or apnea (episode of complete airflow reduction) occur. There is controversy whether UARS is a distinct clinical entity or part of the OSA spectrum. Long-term cardiovascular consequences of UARS are unclear. Risk factors for snoring and UARS are similar and include obesity, nasal congestion, ingestion of pharyngeal relaxing substances before bed such as alcohol, hypnotics, and skeletal muscle relaxants, and abnormalities of the bony and soft tissue structures of the head and neck. Treatment options for snoring and UARS overlap and include risk factor modifications, oral appliances to advance the mandible during sleep, continuous positive airway pressure, and upper airway surgeries.