Publications

J CARDIOVASC MAGN RESON (2017) 19: 75. DOI: 10.1186/S12968-017-0389-8: In the original publication of this article [1] the "Competing interests" section was incorrect. The original publication stated the following competing interests.

BACKGROUND

Dermatomyositis, an inflammatory myopathy with cutaneous involvement, is associated with malignancy and often manifests paraneoplastically. While co-occurrence with small cell carcinoma is well attested, primary lung adenocarcinoma, which may present as focal ground-glass opacification on computed tomography of the thorax, is less frequently coincident.

CASE PRESENTATION

We report the case of a 72-year-old female patient with dermatomyositis - treated with a combination of prednisone, methotrexate, and intravenous immunoglobulin - and an indolent, subsolid, non-hypermetabolic pulmonary lesion, which was determined to be invasive primary lung adenocarcinoma. Supporting a paraneoplastic basis, immunosuppressive therapy was discontinued following tumor excision without relapse of signs or symptoms of dermatomyositis.

CONCLUSIONS

While dermatomyositis prodromal to lung adenocarcinoma is not without precedent, association with an indolent, subsolid lesion has, to the best of our knowledge, not been reported. The case described herein illustrates the importance of maintaining a high index of suspicion for malignancy in the setting of dermatomyositis.

OBJECTIVES

This study sought to evaluate the influence of race/ethnicity on the relationship between body mass index (BMI) and mortality in heart failure with preserved ejection fraction (HFpEF) and HF with reduced EF (HFrEF) patients.

BACKGROUND

Prior studies demonstrated an "obesity paradox" among overweight and obese patients, where they have a better HF prognosis than normal weight patients. Less is known about the relationship between BMI and mortality among diverse patients with HF, particularly given disparities in obesity and HF prevalence.

METHODS

The authors used Get With The Guidelines-Heart Failure data to assess the relationship between BMI and in-hospital mortality by using logistic regression modeling. The authors assessed 30-day and 1-year rates of all-cause mortality following discharge by using Cox regression modeling.

RESULTS

A total of 39,647 patients with HF were included (32,434 [81.8%] white subjects; 3,809 [9.6%] black subjects; 1,928 [4.9%] Hispanic subjects; 544 [1.4%] Asian subjects; and 932 [2.3%] other subjects); 59.7% of subjects had HFpEF, and 30.7% were obese. More black and Hispanic patients had Class I or higher obesity (BMI ≥30 kg/m) than whites, Asians, or other racial/ethnic groups (p < 0.0001). Among subjects with HFpEF, higher BMI was associated with lower 30-day mortality, up to 30 kg/m with a small risk increase above 30 kg/m (BMI: 30 vs. 18.5 kg/m), hazard ratio (HR) of 0.63 (95% confidence interval [CI]: 0.54 to 0.73). A modest relationship was observed in HFrEF subjects (BMI: 30 vs. 18.5 kg/m; HR: 0.73; 95% CI: 0.60 to 0.89), with no risk increase above 30 kg/m. There were no significant interactions between BMI and race or ethnicity related to 30-day mortality (p > 0.05).

CONCLUSIONS

This work is one of the first suggesting the obesity paradox for 30-day mortality exists at all BMI levels in HFrEF but not in patients with HFpEF. Higher BMI was associated with lower 30-day mortality across racial/ethnic groups in a manner inconsistent with the J-shaped relationship noted for coronary artery disease. The differential slope of obesity and mortality among HFpEF and patients with HFrEF potentially suggests differing mechanistic factors, requiring further exploration.

BACKGROUND

Air pollution exposure is associated with acute exacerbation, disease progression, and mortality in patients with idiopathic pulmonary fibrosis (IPF). The objective of this study was to describe the impact of air pollution exposures on disease severity, as well as changes in lung function, in patients with IPF.

METHODS

Using home spirometers and symptom diaries, 25 patients with IPF prospectively recorded FVC weekly for up to 40 weeks. Residential addresses were geocoded to estimate weekly mean air pollution exposures for ground-level ozone (O), nitrogen dioxide (NO), and particulate matter < 2.5 or 10 μm in aerodynamic diameter (PM and PM, respectively). The dependence of weekly clinical measurements on preceding levels of each pollutant was assessed with the use of linear mixed models, yielding beta-coefficients with 95% CIs, using varying lag times.

RESULTS

Lower mean FVC % predicted was consistently associated with increased mean exposures to PM in the 2 to 5 weeks preceding clinical measurements (range, -0.46 to -0.39 [95% CI, -0.73 to -0.13]; P < .005). Lower mean FVC % predicted over the study period was inversely related to mean levels of NO (-0.45 [95% CI, -0.85 to -0.05]; P = .03), PM (-0.45 [95% CI, -0.84 to -0.07]; P = .02), and PM (-0.57 [95% CI, -0.92 to -0.21]; P = .003), averaged over the study. Weekly changes in FVC and changes over 40 weeks were independent of pollution exposures.

CONCLUSIONS

Higher air pollution exposures were associated with lower lung function, but not changes in lung function, in patients with IPF. Further studies are needed to characterize the mechanisms underlying this relationship.