Clinical Medicine Insights-Circulatory Respiratory and Pulmonary Medicine最新文献

We hypothesized that the slope of relation ventilation to carbon dioxide output (V'E/V'CO2-slope) could be predictive already during the very first days after submassive pulmonary embolism (PE) to right ventricular systolic pressure (RV_sys by echocardiography) after 6 months. We evaluated 21 hemodynamically stable patients at admittance, at days 3, 7, 90, and 180 by cardiopulmonary exercise testing and echocardiography. V'E/V'CO2-slope (48.4 ± 10.8) decreased within the first week (43.0 ± 9.8 at day 7) and normalized until follow-up at 6 months (35.0 ± 11.3; P < 10^-4), p(a-ET)CO₂ remained abnormal between days 1 and 3 (5.0 ± 3.9 to 6.7 ± 5.3 mmHg). RV_sys declined from 41.7 ± 14.3 to 26.3±13.1 mmHg (P < 10^-4) at 6 months. V'E/V'CO2-slope (r²= 0.27; P < .02) and RV_sys (r² = 0.28; P = .03) at day 7 correlated with RV_sys at 6 months. p_(a-ET)CO₂, p_(a-ET)O₂, V'D/V'T were not related to RV_sys after 6 months. RV_sys 6 months after acute PE is positively correlated with the V'E/V'CO2-slope at day 7.

Cardiac hemodynamic assessment during cardiopulmonary exercise testing (CPET) is proposed to play an important role in the clinical evaluation of individuals with cystic fibrosis (CF). Cardiac catheterization is not practical for routine clinical CPET. Use of oxygen pulse (O₂pulse) as a noninvasive estimate of stroke volume (SV) has not been validated in CF. This study tested the hypothesis that peak exercise O₂pulse is a valid estimate of SV in CF. Measurements of SV via the acetylene rebreathe technique were acquired at baseline and peak exercise in 17 mild-to-moderate severity adult CF and 25 age-matched healthy adults. We calculated $O_{2}pulse=\stackrel{.}{V}{O}_{2}HR$ . Baseline relationships between SV and O₂pulse were significant in CF (r = .80) and controls (r = .40), persisting to peak exercise in CF (r = .63) and controls (r = .73). The standard error of estimate for O₂pulse-predicted SV with respect to measured SV was similar at baseline (14.1 vs 20.1 mL) and peak exercise (18.2 vs 13.9 mL) for CF and controls, respectively. These data suggest that peak exercise O₂pulse is a valid estimate of SV in CF. The ability to noninvasively estimate SV via O₂pulse during routine clinical CPET can be used to improve test interpretation and advance our understanding of the impact cardiac dysfunction has on exercise intolerance in CF.

Inhaled corticosteroids are widely used in the treatment of chronic obstructive pulmonary disease (COPD). However, their use has been questioned for appropriate dose and a possible increased risk of pneumonia. Here, we reviewed patients with COPD who had received fluticasone-salmeterol combination treatment using data from a linked electronic medical record database. A total of 180 patients received salmeterol with 250 µg fluticasone propionate twice daily and 78 received salmeterol and 100 µg fluticasone propionate twice daily. In both groups, there was no difference in the improved forced expiratory volume in 1 second and COPD assessment test score and the proportion of patients with exacerbations. Although the incidence of common toxicity was approximately equal, that of pneumonia was much higher in the 250 µg group (8.9% vs 1.3%, P=.01). The beneficial effects of inhaled corticosteroids might be obtained at lower doses.

Background: Pulmonary hypertension (PH) is an underdiagnosed cause for chest pain in patients without significant coronary artery disease (CAD). Studies showed that enlarged pulmonary arterial (PA) and right ventricular chamber sizes correlate with the severity of PH. Therefore, we studied the association between chest pain, right ventricular dimensions (RVDs), and PA size on coronary coronary tomographic angiography (CCTA).

Methods: The CCTA of 87 patients presenting with chest pain without evidence of obstructive CAD was examined. The PA diameter (PAD), right atrial dimension (RAD), and RVD were measured. A comparative control cohort included 31 patients who presented without cardiopulmonary complaints and underwent thoracic CT. The risk for obstructive sleep apnea (OSA) was assessed using STOP-BANG questionnaires.

Results: Patients with chest pain without obstructive CAD showed markedly dilated right atrial and ventricular chambers compared with standard parameters (right atrium: 48 ± 6.4 mm; right ventricle long axis: 61 ± 9.5 mm). When comparing chest pain vs non-chest pain group, respectively, the mean PAD measured 25.92 ± 0.43 mm vs 22.89 ± 0.38 mm (P < .001), RAD2 measured 40.1423 ± 0.7108 mm vs 34.8800 ± 1.0245 mm (P = .0048), and RVD2 measured 31.7729 ± 0.7299 mm vs 27.6379 ± 1.6178 mm (P = .034). Chest pain was associated with higher PAD (odds ratio [OR]: 11.11, P < .05) after adjusting for age, sex, body mass index, history of hypertension, hyperlipidemia, congestive heart failure, chronic obstructive pulmonary disease, OSA, and smoking. The chest pain group had a mean STOP-BANG score of 3.9 ± 1.8 in all patients, and 3.62 ± 0.20 in patients without known history of OSA, representing an elevated risk index for the disease.

Conclusions: In patients presenting with chest pain without obstructive CAD on CCTA, there is a strong association between the presence of chest pain and enlarged PAD. They also represent a high-risk group for OSA.

We describe the first isolation of Mycobacterium hassiacum, a rapid-growing, partial acid-resistant mycobacterium, in a respiratory specimen from a patient with exacerbated chronic obstructive pulmonary disease. To provide therapeutic recommendation for future cases, antibiotic susceptibility testing of 3 clinical isolates was performed by broth microdilution. All strains tested showed susceptibility to clarithromycin, imipenem, ciprofloxacin, and doxycycline. The role of M hassiacum as a respiratory pathogen remains unclear and needs to be evaluated by future reports.

We developed a simplified automated algorithm to interpret noninvasive gas exchange in healthy subjects and patients with heart failure (HF, n = 12), pulmonary arterial hypertension (PAH, n = 11), chronic obstructive lung disease (OLD, n = 16), and restrictive lung disease (RLD, n = 12). They underwent spirometry and thereafter an incremental 3-minute step test where heart rate and SpO₂ respiratory gas exchange were obtained. A custom-developed algorithm for each disease pathology was used to interpret outcomes. Each algorithm for HF, PAH, OLD, and RLD was capable of differentiating disease groups (P < .05) as well as healthy cohorts (n = 19, P < .05). In addition, this algorithm identified referral pathology and coexisting disease. Our primary finding was that the ranking algorithm worked well to identify the primary referral pathology; however, coexisting disease in many of these pathologies in some cases equally contributed to the cardiorespiratory abnormalities. Automated algorithms will help guide decision making and simplify a traditionally complex and often time-consuming process.

Background: In 2015, New York City experienced the worst outbreak of Legionnaires' disease in the history of the city. We compare patients seen during the 2015 outbreak with sporadic cases of Legionella during the past 5 years.

Methods: We conducted a retrospective chart review of 90 patients with Legionnaires' disease, including sporadic cases of Legionella infection admitted from 2010 to 2015 (n = 55) and cases admitted during the 2015 outbreak (n = 35).

Results: We saw no significant differences between the 2 groups regarding demographics, smoking habits, alcohol intake, underlying medical disease, or residence type. Univariate and multivariate analyses showed that patients with sporadic case of Legionella had a longer stay in the hospital and intensive care unit as well as an increased stay in mechanical ventilation. Short-term mortality, discharge disposition, and most clinical parameters did not differ significantly between the 2 groups.

Conclusions: We found no specific clinicoradiological characteristics that could differentiate sporadic from epidemic cases of Legionella. Early recognition and high suspicion for Legionnaires' disease are critical to provide appropriate treatment. Cluster of cases should increase suspicion for an outbreak.

Chronic obstructive pulmonary disease (COPD) is one of the major causes of chronic morbidity and mortality worldwide. The development of markers of COPD onset is hampered by the lack of accessibility to the primary target tissue, and there is a need to consider other sample sources as surrogates for biomarker research. Airborne toxicants pass through the nasal epithelium before reaching the lower airways, and the similarity with bronchial histology makes it an attractive surrogate for lower airways. In this work, we describe the transcriptomics findings from the nasal epithelia of subjects enrolled in a clinical study focusing on the identification of COPD biomarkers. Transcriptomic data were analyzed using the biological network approach that enabled us to pinpoint the biological processes affected in the upper respiratory tract in response to smoking and mild-to-moderate COPD. Our results indicated that nasal and lower airway immune responses were considerably different in COPD subjects and caution should be exercised when using upper airway samples as a surrogate for the lower airway. Nevertheless, the network approach described here could present a sensitive means of identifying smokers at risk of developing COPD.

Nodular lung disease is a rare pulmonary manifestation of sarcoidosis and resembles metastatic neoplasm disease. Nodular sarcoidosis is rare, varying from 1.6% to 4% of patients with sarcoidosis. Radiographic nodules measure from 1 to 5 cm in diameter that typically consist of coalescent granulomas. There is limited data on this form of sarcoidosis and its presentation can mimic primary or metastatic pulmonary neoplasms. Nodular sarcoidosis has a favorable prognosis, and resolution can be seen with oral corticosteroids. Herein, we present such a case of nodular pulmonary sarcoidosis with a lung nodule measured up to 6 cm.

A 32-year-old man presented with a 10-day history of fever, chills, nausea, vomiting, myalgia, nonproductive cough, and worsening dyspnea after freshwater swimming in the Caribbean 1 week prior to presentation. Shortly after arrival at the hospital, the patient developed severe respiratory distress with massive hemoptysis. Based on serologic workup, he was diagnosed with leptospirosis pulmonary hemorrhage syndrome leading to diffuse alveolar hemorrhage, severe hypoxemic respiratory failure, and multiorgan failure. He received appropriate antibiotic coverage along with hemodynamic support with norepinephrine and vasopressin, mechanical ventilation, and renal replacement therapy in an intensive care unit. Introduction of extracorporeal membrane oxygenation was initiated to provide lung-protective ventilation supporting the recovery of his pulmonary function. Aminocaproic acid was used to stop and prevent further alveolar hemorrhage. He fully recovered thereafter; however, it is uncertain whether it was the use of aminocaproic acid that led to the resolution of his disease.