Faculty Bibliography

OBJECTIVE: To determine the clinical significance of tachycardia in the postoperative period. PATIENTS AND METHODS: Individuals 18 years or older undergoing hip and knee arthroplasty were included in the study. Two data sets were collected from different time periods: development data set from January 1, 2011, through December 31, 2011, and validation data set from December 1, 2012, through September 1, 2014. We used the development data set to identify the optimal definition of tachycardia with the strongest association with the vascular composite outcome (pulmonary embolism and myocardial necrosis and infarction). The predictive value of this definition was assessed in the validation data set for each outcome of interest, pulmonary embolism, myocardial necrosis and infarction, and infection using multiple logistic regression to control for known risk factors. RESULTS: In 1755 patients in the development data set, a maximum heart rate (HR) greater than 110 beats/min was found to be the best cutoff as a correlate of the composite vascular outcome. Of the 4621 patients who underwent arthroplasty in the validation data set, 40 (0.9%) had pulmonary embolism. The maximum HR greater than 110 beats/min had an odds ratio (OR) of 9.39 (95% CI, 4.67-18.87; sensitivity, 72.5%; specificity, 78.0%; positive predictive value, 2.8%; negative predictive value, 99.7%) for pulmonary embolism. Ninety-seven patients (2.1%) had myocardial necrosis (elevated troponin). The maximum HR greater than 110 beats/min had an OR of 4.71 (95% CI, 3.06-7.24; sensitivity, 47.4%; specificity, 78.1%; positive predictive value, 4.4%; negative predictive value, 98.6%) for this outcome. Thirteen (.3%) patients had myocardial infarction according to our predetermined definition, and the maximum HR greater than 110 beats/min had an OR of 1.72 (95% CI, 0.47-6.27). CONCLUSION: Postoperative tachycardia within the first 4 days of surgery should not be dismissed as a postoperative variation in HR, but may precede clinically significant adverse outcomes.

Background/Purpose: Systemic lupus erythematosus (SLE) is a complex autoimmune disease characterized by heterogeneity of presentation, an undulating course, and elevated risk for premature cardiovascular disease. Platelets have been understudied as a relevant contributor. Yet, these cells, which contain transcripts and the necessary molecular machinery to conduct translation, are intercellular regulators of inflammation and immune activation and play a key role in atherothrombosis. Platelets express low affinity type 2 receptors (FcgammaRIIA) whose ligand is the Fc portion of IgG. A single amino acid substitution, H131R, in the extracellular ligand binding domain increases the affinity for IgG and may account for individual variation in platelet activation, specifically an increase of function. Accordingly, this study addressed the hypothesis that FcyRIIA genotype associates with preclinical atherosclerosis and platelet hyperreactivity. Methods: Genotyping at rs1801274 (allelic discrimination, HWE P=NS) was performed in 71 SLE patients and 30 healthy controls. In 49 of the SLE patients and 30 healthy controls, carotid ultrasound for plaque (>50% increase over background IMT in any arterial segment); levels of soluble E-selectin as a proxy of endothelial cell activation; and C3, C4 to reflect complement activation were assessed. In 22 SLE patients, monocyteplatelet (MPA) and leukocyte-platelet aggregates (LPA), and light transmission aggregometry (LTA) in response to submaximal concentrations of collagen and arachidonic acid were evaluated. Results: Overall genotyping for FcgammaRIIA revealed 43 SLE patients carrying at least one copy of the variant allele and 28 patients who were homozygous for the ancestral allele. For the 49 with IMT, carotid plaque was reported in 22. A significant enrichment of carotid plaque was identified in patients with a variant compared to those who were homozygous ancestral (58% vs 25%, p=0.039). In contrast, among 30 healthy controls, the presence of carotid plaque was not associated with the variant or ancestral genotype (15% vs 15%). Soluble Eselectin (mean + 2SD, shown as dichotomous being above normal controls) was significantly increased in those patients with the variant vs ancestral (64% vs 23%, p=0.013). Complement levels, a proxy of circulating immune complexes, were lower in patients with the variant vs ancestral (64% vs 40%). With regard to platelet reactivity, among 22 SLE subjects evaluated, there was a significant increase in MPA and LPA (above controls, mean + 2SD) in those carrying at least one variant compared to the ancestral group (86% vs 37%, p=0.02 and 46% vs 12%, p=0.05, respectively). Platelet aggregation was more robust for those patients with the variant vs ancestral in response to 160 uM arachidonic acid and 1 ug/mL collagen (47% vs 19% and 47% vs 14%, respectively). Conclusion: These data suggest a model in which an FcgammaRIIA polymorphism associates with preclinical atherosclerosis and confers increased platelet activity in the setting of SLE, a disease characterized by circulating immune complexes

BACKGROUND: In a prospective study, cardiac MRI (CMR) and intravascular ultrasound were performed in women with myocardial infarction (MI) and nonobstructive coronary artery disease (MINOCA). Forty participants underwent adenosine-stress CMR (sCMR). HYPOTHESIS: Abnormal perfusion may co-localize with ischemic late gadolinium enhancement (LGE) and T2-weighted signal hyperintensity (T2+), suggesting microvascular dysfunction contributed to MI. METHODS: Qualitative perfusion analysis was performed by 2 independent readers. Abnormal myocardial perfusion reserve index (MPRI) was defined as global average