Hassan Alnuaimat

Pulmonary vasodilator testing and use of calcium channel blockers in pulmonary arterial hypertension.

Pulmonary arterial hypertension (PAH) encompasses a number of diseases responsible for a specific set of hemodynamic findings during right heart catheterization. During initial workup, pulmonary vasodilator testing is performed. A positive acute pulmonary vasodilator test predicts better survival and response to calcium channel blocker (CCB) therapy. There is lack of consensus on the preferred agent for determining acute pulmonary vasoreactivity. The ACCP guidelines and the 4(th) World Symposium on Pulmonary Hypertension support the use of intravenous epoprostenol or nitric oxide (NO) as the preferred agents for pulmonary vasodilator testing. A decrease in the mean pulmonary artery pressure by at least 10 mmHg to reach an absolute value of 40 mmHg or less without a decrease in cardiac output is currently considered a positive pulmonary vasodilator test. A positive test by the current recommended criteria is observed in about 10-15% of patients with idiopathic PAH. Approximately half of these patients will experience long-term benefits with CCBs. A positive test may select patients with an earlier or less aggressive form of disease, which may carry a better prognosis. A positive vasodilator test is observed very infrequently in patients with pulmonary arterial hypertension other than idiopathic PAH or anorexigen associated PAH. This article reviews the literature regarding pulmonary vasodilator testing and use of CCB therapy in patients with PAH, while identifying the gaps in knowledge concerning this diagnostic procedure.

Embolization of Hydrophilic Catheter Coating to the Lungs Report of a Case Mimicking Granulomatous Vasculitis

Hydrophilic coatings are used on intravascular devices to facilitate ease of manipulation and to minimize complications such as thrombosis during a procedure and vasospasm after a procedure. We report a case of embolization of hydrophilic coating of a central venous catheter to the lung that resulted in cavitary lung nodules in a 34-year-old woman. The microscopic features of this unusual complication warrant emphasis so that pathologists will not overlook the embolic foreign material and make a faulty diagnosis of noniatrogenic granulomatous vasculitis.

Hypoxia-induced endothelial CX3CL1 triggers lung smooth muscle cell phenotypic switching and proliferative expansion

Distal arterioles with limited smooth muscles help maintain the high blood flow and low pressure in the lung circulation. Chronic hypoxia induces lung distal vessel muscularization. However, the molecular events that trigger alveolar hypoxia-induced peripheral endothelium modulation of vessel wall smooth muscle cell (SMC) proliferation and filling of nonmuscular areas are unclear. Here, we investigated the role of CX3CL1/CX3CR1 system in endothelial-SMC cross talk in response to hypoxia. Human lung microvascular endothelial cells responded to alveolar oxygen deficiency by overproduction of the chemokine CX3CL1. The CX3CL1 receptor CX3CR1 is expressed by SMCs that are adjacent to the distal endothelium. Hypoxic release of endothelial CX3CL1 induced SMC phenotypic switching from the contractile to the proliferative state. Inhibition of CX3CR1 prevented CX3CL1 stimulation of SMC proliferation and monolayer expansion. Furthermore, CX3CR1 deficiency attenuated spiral muscle expansion, distal vessel muscularization, and pressure elevation in response to hypoxia. Our findings indicate that the capillary endothelium relies on the CX3CL1-CX3CR1 axis to sense alveolar hypoxia and promote peripheral vessel muscularization. These results have clinical significance in the development of novel therapeutics that target mechanisms of distal arterial remodeling associated with pulmonary hypertension induced by oxygen deficiency that is present in people living at high altitudes and patients with obstructive lung diseases.

Titanium exposure and yellow nail syndrome

Yellow nail syndrome is a rare disease of unclear etiology. We describe a patient who develops yellow nail syndrome, with primary nail and sinus manifestations, shortly after amalgam dental implants. A study of the patients nail shedding showed elevated nail titanium levels. The patient had her dental implants removed and had complete resolution of her sinus symptoms with no change in her nail findings. Since the patients nail findings did not resolve we do not believe titanium exposure is a cause of her yellow nail syndrome but perhaps a possible relationship exists between titanium exposure and yellow nail syndrome that requires further studies.

Severity of influenza A(H1N1) illness and emergence of D225G variant, 2013-14 influenza season, Florida, USA.

Despite a regional decline in influenza A(H1N1)pdm09 virus infections during 2013–14, cases at a Florida hospital were more severe than those during 2009–10. Examined strains had a hemagglutinin polymorphism associated with enhanced binding to lower respiratory tract receptors. Genetic changes in this virus must be monitored to predict the effect of future pandemic viruses.

Pulmonary arterial hypertension and acute respiratory distress syndrome in a patient with adult-onset stills disease:

Adult-onset Still’s disease (AOSD) is an inflammatory disorder characterized by recurrent fevers, arthralgia, leukocytosis, and a salmon-colored rash. Diagnosis is made based on the Yamaguchi criteria. Various cardiac and pulmonary manifestations have been described in association with AOSD, including acute respiratory distress syndrome (ARDS) and pulmonary arterial hypertension (PAH). We describe the first case of both PAH and ARDS in a patient with AOSD who, despite aggressive therapy, declined rapidly and ultimately died. There was concern for pulmonary veno-occlusive disease given the rate of her decompensation, but this was found not to be the case on autopsy. Treatment of AOSD with cardiopulmonary involvement requires rapid identification of AOSD followed by aggressive immunosuppression.

An observational study of inhaled-treprostinil respiratory-related safety in patients with pulmonary arterial hypertension

Inhaled treprostinil (Tyvaso) has been shown to be a safe and effective addition to pulmonary arterial hypertension (PAH) oral therapies; however, the respiratory-related safety profile of inhaled treprostinil required further elucidation in the setting of routine clinical care. The objectives of this study were to characterize respiratory-related adverse events (AEs) associated with current or recent treatment with inhaled treprostinil and to compare the incidence of respiratory-related AEs in PAH patients treated with inhaled treprostinil with that in patients treated with other Food and Drug Administration (FDA)–approved PAH therapies. This was a long-term, prospective, observational study. All respiratory-related AEs were recorded during the study. The number of PAH patients enrolled was 1,333, 666 treated with inhaled treprostinil and 667 controls (treated with an FDA-approved PAH therapy other than inhaled treprostinil), for a total of 958 and 1,094 patient-years of exposure, respectively. In the inhaled-treprostinil group, 1,281 respiratory-related AEs were reported in 403 patients (61%), and in the control group, 1,295 respiratory-related AEs were reported in 388 patients (58%). Cough, throat irritation, nasal discomfort, and hemoptysis were the most common respiratory-related AEs (occurring in ≥2% of patients in either treatment group) that demonstrated a higher number of events per patient-year of exposure in the inhaled-treprostinil group than in the control group (risk ratio [95% confidence interval]: 1.487 [1.172–1.887], 3.777 [2.050–6.956], 2.039 [1.072–3.879], and 1.957 [1.024–3.741], respectively). Overall, inhaled treprostinil was well tolerated by PAH patients in routine clinical care, with respiratory-related AEs consistent with the known safety profile (trial registration: clinicaltrials.gov identifier: NCT01266265).

A Review of Targeted Pulmonary Arterial Hypertension-Specific Pharmacotherapy

Significant advances in the understanding of the pathophysiology of pulmonary arterial hypertension over the past two decades have led to the development of targeted therapies and improved patient outcomes. Currently, a broad armamentarium of pulmonary arterial hypertension-specific drugs exists to assist in the treatment of this complex disease state. In this manuscript, we provide a comprehensive review of the current Food and Drug Administration (FDA)-approved pulmonary arterial hypertension-specific therapies, and their supporting evidence for adults, targeting the nitric oxide, soluble guanylate cyclase, endothelin, and prostacyclin pathways.

Erratum for Drusano et al., “Dilution Factor of Quantitative Bacterial Cultures Obtained by Bronchoalveolar Lavage in Patients with Ventilator-Associated Bacterial Pneumonia”

George L. Drusano,a Michael L. Corrado,b Gino Girardi,c Evelyn J. Ellis-Grosse,d Richard G. Wunderink,e Helen Donnelly,e Kenneth V. Leeper,f Mona Brown,f Tasnova Malek,f Robert Duncan Hite,g Michelle Ferrari,g Danijela Djureinovic,g Marin H. Kollef,h Lisa Mayfield,h Ann Doyle,h Jean Chastre,i Alain Combes,i Thomas J. Walsh,j Krisztina Dorizas,j Hassan Alnuaimat,k Brooks Edward Morgan,k Jordi Rello,l Cristopher A. Mazo,l Ronald N. Jones,m Robert K. Flamm,m Leah Woosley,m Paul G. Ambrose,n Sujata Bhavnani,n Christopher M. Rubino,n Catharine C. Bulik,n Arnold Louie,a Michael Vicchiarelli,a Colleen Bermana

Sepsis outcomes in the correctional system: more potential disparity

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