Chest
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In the past, thoracic and cardiac imaging were two distinct specialties of radiology. The technical evolution, however, has changed their boundaries with an important impact on CT imaging practices and has opened the new era of "cardiothoracic" imaging, due to the strong anatomic, mechanical, physiologic, physiopathologic, and therapeutic cardiopulmonary correlations. ⋯ The advent of ECG gating and state-of-art CT scanner faster rotation speed, high spatial and temporal resolution, high-pitch mode, shorter acquisition time, and dedicated cardiac reconstruction algorithms has opened new possibilities for chest imaging, integrating cardiac morphologic and even functional information within a diagnostic chest CT scan. The aim of this review is to briefly show and summarize the concept of integrated cardiothoracic imaging, which redefines the boundaries of chest CT imaging, opening the door to a new radiologic specialty.
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Pulmonary arterial hypertension (PAH) is a disorder in which mechanical obstruction of the pulmonary vascular bed is largely responsible for the rise in mean pulmonary arterial pressure, resulting in a progressive functional decline despite current available therapeutic options. The fundamental pathogenetic mechanisms underlying this disorder include pulmonary vasoconstriction, in situ thrombosis, medial hypertrophy, and intimal proliferation, leading to occlusion of the small to mid-sized pulmonary arterioles and the formation of plexiform lesions. Several predisposing or promoting mechanisms that contribute to excessive pulmonary vascular remodeling in PAH have emerged, such as altered crosstalk between cells within the vascular wall, sustained inflammation and dysimmunity, inhibition of cell death, and excessive activation of signaling pathways, in addition to the impact of systemic hormones, local growth factors, cytokines, transcription factors, and germline mutations. ⋯ However, over the past decade, a better understanding of new key regulators of this irreversible pulmonary vascular remodeling has been obtained. This review examines the state-of-the-art potential new targets for innovative research in PAH, focusing on (1) the crosstalk between cells within the pulmonary vascular wall, with particular attention to the role played by dysfunctional endothelial cells; (2) aberrant inflammatory and immune responses; (3) the abnormal extracellular matrix function; and (4) altered BMPRII/KCNK3 signaling systems. A better understanding of novel pathways and therapeutic targets will help in the designing of new and more effective approaches for PAH treatment.
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Observational Study
Is a raised bicarbonate, without hypercapnia, part of the physiological spectrum of obesity-related hypoventilation?
Obesity hypoventilation syndrome (OHS) conventionally includes awake hypercapnia, but an isolated raised bicarbonate, even in the absence of awake hypercapnia, may represent evidence of "early" OHS. We investigated whether such individuals exhibit certain features characteristic of established OHS. ⋯ These data suggest that obese individuals with a raised BE, despite normocapnia while awake, should probably be regarded as having early obesity-related hypoventilation. This has important implications for clinical management as well as randomized controlled treatment trials, as they may represent a group with a more reversible disease process.
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Despite guideline recommendations, patients suspected of having COPD often are treated empirically instead of undergoing spirometry to confirm airflow obstruction (AFO). Accurate diagnosis and treatment are essential to provide high-quality, value-oriented care. We sought to identify predictors associated with AFO among patients with and treated for COPD prior to performance of confirmatory spirometry. ⋯ Comorbidities associated with somatic complaints of dyspnea were associated with a lower risk of having airflow limitations, suggesting that empirical diagnosis and treatment of COPD may lead to inappropriate treatment of individuals who do not have AFO.
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Polymorphisms in the MUC5B promoter, TOLLIP, and nine additional genetic loci have been associated with idiopathic pulmonary fibrosis (IPF) within non-Hispanic white populations. It is unknown whether these variants account for risk of IPF in other racial/ethnic populations. We conducted a candidate single nucleotide polymorphism (SNP) association study in cohorts of Mexican and Korean patients with IPF. ⋯ The strongest identified genetic risk factor for IPF among the non-Hispanic white population, the MUC5B promoter polymorphism, is also a strong risk factor in a Mexican population, but is very rare in a Korean population. The majority of genetic variants that account for risk of IPF in groups other than non-Hispanic whites are unknown. Hispanic and Asian populations should be studied separately to identify genetic risk loci for IPF.