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• W2897330414 abstract "Sickle cell disease (SCD) is an autosomal recessive disease caused by a single point mutation in the HBB gene, resulting in the substitution of glutamic acid by valine. Morbidity and mortality in SCD arises from recurrent acute vaso-occlusive painful crises (VOC), acute chest syndrome (ACS), cerebrovascular events, splenic and renal dysfunction. Additionally, 6–11% of the sickle cell population have pulmonary hypertension (PH) (Parent et al, 2011; Fonseca et al, 2012). Cardiac catheterisation (CC) is an important part of the evaluation of patients with SCD, and is performed to confirm PH, assess the haemodynamic effects of treatment, evaluate patients for a heart or lung transplantation, and for intracardiac biopsies (Callan & Clark, 2016). Procedure-related complications have been reported previously, but the report did not include patients with SCD (Hoeper et al, 2006). These complications consist of haematoma, pneumothorax, arrhythmias, hypotension or vagal reaction; rarer complications include pulmonary infarction or pulmonary arterial rupture from prolonged inflation of the balloon catheter in the wedge position. The event rates reported by Hoeper et al (2006) (adverse event rate, 1·1%; mortality rate, 0·05%) were lower than previously reported (1·7% and 4·2% respectively) (Fuster et al, 1984). Haemodynamic results of CC have been previously reported in SCD patients (Gladwin et al, 2004; Mehari et al, 2013). However, the post-procedure rates of SCD-related adverse events (SCD-AEs) have not been well described. We therefore performed a retrospective analysis of patients with SCD who underwent CC under National Heart, Lung, and Blood Institute institutional review board-approved protocols from 2005 to 2016. CC typically included left and right heart catheterisation under moderate sedation via transjugular, transfemoral and/or transradial access, with nitric oxide vasodilator provocation for those with mean pulmonary artery pressures >25 mm Hg. Routine pre-procedure hydration was not implemented. Patients were monitored in a telemetry inpatient unit post-CC. Red blood cell (RBC) transfusion within 1 month prior to CC, haemoglobin levels 1 week pre- and 1 week post-CC, use of medications (e.g. hydroxycarbamide, PH-specific or narcotics), length of hospital stay and clinical events surrounding CC (e.g. pain, VOC, development of acute respiratory symptoms from pulmonary vasculopathy or cardiomyopathy) were captured from electronic medical records (Tables 1 and SI). Seventy-six patients underwent 110 CC procedures (Table 1). No post-CC haematoma, pneumothorax, arrhythmia, hypotention, vagal reaction, pulmonary infarction, pulmonary arterial rupture or death were observed in the follow-up period. PH was diagnosed in a total of 19 patients (25%); in seven patients, PH was newly diagnosed through serial CC. These 19 patients received therapy with sildenafil (n = 15), bosentan (n = 1), sildenafil and bosentan (n = 2) or a combination of tadalafil, treprostinil and bosentan (n = 1). Responses to PH therapies have been reported previously (Machado et al, 2011; Weir et al, 2017). A total of 10 patients (13%) experienced 11 SCD-AEs (10%) within 2 weeks of CC. Twenty patients had two or more CC, four patients had one SCD-AE after one of the CC. Five of 19 patients with PH had SCD-AEs post-CC versus five of 57 patients without PH. These complications also could be broadly separated into those having only pain or those having pain associated with respiratory symptoms (Table 2). Among the five patients experiencing only pain, three received short-acting opioids and another two received both short- and long-acting opioids prior to CC. None of them received RBC transfusion or were diagnosed with PH. In contrast, among the five patients having pain associated with respiratory symptoms, two received transfusions peri-CC and four patients were initiated on sildenafil therapy post-CC. These findings suggested that the respiratory symptoms could be related to underlying PH, as previously reported (Rich et al, 1987). Seven patients (with seven procedures) had haemoglobin levels below 70 g/l pre-CC, and none had SCD-AE post-CC. Three received RBC transfusions at physician discretion: one pre-, one post- and one pre- and post-CC (data not shown). Another 35 patients had haemoglobin levels between 70 and 80 g/l. Two of them experienced SCD-AEs, and none received RBC transfusions (Table 2). The remaining patients had haemoglobin >80 g/l, and several patients experienced SCD-AEs post-CC. Although pre-procedure transfusion prior to CC did not appear to reduce SCD-AEs, most patients had haemoglobin levels of ≥70 g/l, indicating this cut-off reflected the lower limit of the haemoglobin range typically observed in patients with SCD. Next, we compared haemoglobin levels before and after CC in the 10 patients with post-CC exacerbations. Three patients had decreased haemoglobin levels, three had increased levels as a result of RBC transfusions, and the remainder had no change (Table 2). It was unclear if the change in haemoglobin levels contributed to the development of SCD-AEs. The role of transfusion in close proximity to CC in altering cardiopulmonary dynamics for the eventual PH diagnosis was also unclear. Although a large number of CC were performed, this study represented the experience of a single centre and uses a retrospective design to evaluate SCD-AEs, which limited the generalisability of these findings. In summary, CC-related complications that were directly attributable to the procedure itself were very low in patients with SCD but the rates of post-procedure SCD-AEs were 10%. The stress of CC could have triggered acute VOC or pain, especially in patients who were already taking narcotics. Likewise, patients with suspected PH or previous diagnosis of PH were more likely to develop respiratory symptoms following CC. Finally, it is reasonable to expect similar SCD-AEs in SCD patients undergoing invasive procedures of short duration like CC, such as central venous catheter placement, endoscopy, liver biopsy, arthroscopy or oocyte retrieval. To prepare SCD patients prior to an invasive procedure, it seems prudent to formulate individualized treatment, including titration of hydroxycarbamide, consideration for pre- or post-CC RBC transfusion to minimize symptoms of anaemia, optimisation of chronic pain management and careful assessment of respiratory or other symptoms. This work is supported by the intramural research program of NHLBI at NIH. We thank Tyler Fong for data entry and Drs. Courtney Fitzhugh, Swee Lay Thein, and Nargues Weir for their review of the manuscript. Collection of data and data analysis: RDM, TNT, JN, MH. Patient care: AC, RJL, TR, CPM, GJK, MH. Manuscript preparation: RDM, AS, SB, MH. Manuscript review and approval: all. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article." @default.
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• W2897330414 date "2018-10-23" @default.
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• W2897330414 title "Sickle related events following cardiac catheterisation: risk implication for other invasive procedures" @default.
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