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Background: Reverse homodigital island flaps (RHIFs) are increasingly used to reconstruct traumatic fingertip injuries, but there is limited evidence on the efficacy of this technique. We performed a systematic review of the literature to establish the safety and functional outcomes of RHIF for traumatic fingertip injuries. Methods: Electronic searches were performed using 3 databases (PubMed, Ovid Medline, Cochrane CENTRAL) from their date of inception to April 2020. Relevant studies were required to report on complications and functional outcomes for patients undergoing RHIF for primary fingertip reconstruction. Data were extracted from included studies and analyzed. Results: Sixteen studies were included, which produced a total cohort of 459 patients with 495 fingertip injuries. The index and middle fingers were involved most frequently (34.6% and 34.1%, respectively), followed by the ring finger (22%), the little finger (6.7%), and the thumb (2.6%). The mean postoperative static and moving 2-point discrimination was 7.2 and 6.7 mm, respectively. The mean time to return to work was 8.4 weeks. The mean survivorship was 98.4%, with the pooled complication rate being 28%. The pooled complication rate of complete flap necrosis was 3.6%, of partial flap necrosis was 10.3%, of venous congestion was 14.6%, of pain or hypersensitivity was 11.5%, of wound infection was 7.2%, of flexion contractures was 6.3%, and of cold intolerance was 17.7%. Conclusions: Reverse homodigital island flaps can be performed safely with excellent outcomes. To minimize complications, care is taken during dissection and insetting, with extensive rehabilitation adhered to postoperatively. Prospective studies assessing outcomes of RHIF compared with other reconstruction techniques would be beneficial. [ABSTRACT FROM AUTHOR]

Open in new tab Download slide Open in new tab Download slide OBJECTIVES The age at which the Fontan operation is performed varies globally. Over the last decade, the median age of patients having the Fontan in Australia and New Zealand has been 4.6 years, including 6% of patients younger than 3 years. Long-term outcomes of an early Fontan operation are unclear and are described in this study. METHODS Patients from the Australian and New Zealand Fontan Registry were grouped by age at Fontan. A Fontan before 3 years (early Fontan) was compared to the combined second and third quartiles by age at surgery in the Registry (3.6–6.1 years; control). Outcomes included Fontan failure (death, transplant, New York Heart Association functional group III/IV heart failure, Fontan takedown or conversion, protein losing enteropathy and plastic bronchitis), arrhythmias, thromboembolism and reinterventions. RESULTS A total of 191 patients who had early Fontan operations were compared to 781 controls. Profound or progressive cyanosis was noted more frequently in the early than in the control group (63% vs 23%; P  <   0.001). The early group was followed up for a median 22.1 years. The incidence of long-term failure was similar between the 2 groups (early, 1.08 failures per 100 patient-years of follow-up vs control, 0.99; log-rank P  =   0.79). Adjusted for risk factors, early age at Fontan was not a risk factor for long-term failure [hazard ratio (HR) 1.16, 95% confidence interval (CI) 0.77–1.76; P  =   0.48], new-onset arrhythmia (HR 0.93, 95% CI 0.63–1.39; P  =   0.73), thromboembolism (HR 0.50, 95% CI 0.28–0.91; P  =   0.024) or reintervention (HR 1.08, 95% CI 0.80–1.45; P  =   0.62). CONCLUSIONS Having the Fontan operation at an early age was not a risk factor for short- or long-term adverse outcomes in our cohort. [ABSTRACT FROM AUTHOR]

Aim: To explore the relationship between baseline uric acid (UA) levels and long‐term cardiovascular events in adults with type 2 diabetes (T2D) and to determine whether the cardioprotective effects of fenofibrate are partly mediated through its UA‐lowering effects. Methods: Data from the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) trial were utilized, comprising 9795 adults with T2D randomly allocated to treatment with fenofibrate or matching placebo. Plasma UA was measured before and after a 6‐week, active fenofibrate run‐in phase in all participants. Cox proportional hazards models were used to explore the relationships between baseline UA, pre‐to‐post run‐in reductions in UA and long‐term cardiovascular outcomes. Results: Mean baseline plasma UA was 0.33 mmol/L (SD 0.08). Baseline UA was a significant predictor of long‐term cardiovascular events, with every 0.1 mmol/L higher UA conferring a 21% increase in event rate (HR 1.21, 95% CI 1.13‐1.29, P <.001). This remained significant after adjustment for treatment allocation, cardiovascular risk factors and renal function. The extent of UA reduction during fenofibrate run‐in was also a significant predictor of long‐term cardiovascular events, with every 0.1 mmol/L greater reduction conferring a 14% lower long‐term risk (HR 0.86, 95% CI 0.76‐0.97, P =.015). This effect was not modified by treatment allocation (Pinteraction =.77). Conclusions: UA is a strong independent predictor of long‐term cardiovascular risk in adults with T2D. Although greater reduction in UA on fenofibrate is predictive of lower cardiovascular risk, this does not appear to mediate the cardioprotective effects of fenofibrate. [ABSTRACT FROM AUTHOR]

Introduction: Atrial fibrillation (AF) is a major cause of stroke and premature death. Current AHA/ESC guidelines define subtypes of AF but these are not incorporated into risk scores of the complications of AF. Aims: To compare all cause mortality, ischaemic stroke and systemic thromboembolism in patients categorised by AF type (paroxysmal, persistent and permanent). Methods: Electronic searches were performed using Medline, PubMed, EMBASE, Cochrane Central Register of Controlled Trials, and the Cochrane Database of Systematic Reviews up until November 15, 2017. Results: Eleven studies with a total of 81030 patients were included for analyses, comprising 26753 paroxysmal, 18098 persistent and 36179 permanent AF patients. There were no baseline differences in gender and hypertension but diabetes, heart failure, previous stroke and CHADS score were different between subtypes and highest in permanent AF. The risk of ischemic stroke was higher in permanent compared with paroxysmal or persistent AF (permanent vs. paroxysmal: RR = 1.34, 95% CI: 1.12-1.59, p = 0.001; permanent vs. persistent: RR = 1.44, 95% CI: 1.22-1.69, p < 0.001; Fig. 1). A similar result was seen for systemic embolism. All-cause mortality was significantly higher in permanent compared with paroxysmal AF (RR = 1.62, 95% CI: 1.37-1.9, p < 0.001), and trended higher for permanent compared with persistent AF (RR = 1.51, 95% CI: 0.94-2.44, p = 0.09). Conclusion: Permanent AF, compared with paroxysmal and persistent AF, is associated with increased risk of ischemic stroke, systemic embolism and mortality. Our findings have implications for incorporation of AF duration and subtype into stroke risk assessment, as well as the development of therapies to halt and reverse progression of AF. Figure 1. Rate of ischaemic strokes comparing A) permanent vs. persistent AF; B) permanent vs. paroxysmal AF. AF = atrial fibrillation. [ABSTRACT FROM AUTHOR]

Introduction: Pulmonary hypertension complicating left heart disease (PH-LHD) is the most common cause of PH. Off-label use of pulmonary arterial hypertension (PAH) medications for PH-LHD is prevalent, despite a lack of clinical data supporting their use. Hypothesis: We hypothesized that PAH agents, when used for PH-LHD, would not produce any improvements in clinical outcomes. Methods: A systematic review and meta-analysis was performed. Comprehensive search of all available literature to date identified ten randomized, placebo controlled trials comprising 439 treated (Phosphodiesterase 5 inhibitors: n=206; guanylate cyclase stimulators: n=132; endothelin receptor antagonists: n=101) and 338 placebo patients. Random effects model was employed to assess outcomes in the treatment compared to the placebo control arm. Results: The risks of all-cause mortality, cardiovascular mortality and worsening heart failure were numerically higher in the treated compared to the control group, although not statistically (all-cause mortality: Risk Ratio (RR) = 1.97, 95% CI: 0.64-6.05, p = 0.24; cardiovascular mortality: RR = 2.01, 95% CI: 0.39-10.34, p = 0.4; worsening heart failure: RR = 1.23, 95% CI: 0.68-2.25, p = 0.49). Conversely, right heart hemodynamics improved numerically in the treated group, also without being significant (mean pulmonary artery pressure: Mean Weighted Difference (MWD) = -5.13 mmHg, 95% CI: -13.2-2.9, p = 0.21; systolic pulmonary artery pressure: MWD = -4.14 mmHg, 95% CI: -16.6-8.37, p = 0.52; pulmonary vascular resistance: MWD = -0.87 WU, 95% CI: -1.75-0.1, p = 0.053. Conclusions: This meta-analysis demonstrated that there is no current evidence to support the widespread use of PAH therapy in PH-LHD. On the basis of a numerically increased risk of clinical harm, these agents should not be prescribed in this situation, unless further evidence of benefit arises in the future. [ABSTRACT FROM AUTHOR]

Introduction: Our previous work revealed that uridine and UDP were associated with 4 separate coronary artery disease (CAD) loci in >1000 subjects in the Framingham Heart Study. Using cryopreserved human myocardial tissue, we now extend our investigations of the uridine, and other pathways, in human ischemic heart disease (IHD). Aims: 1. Determine if previously implicated IHD pathway perturbations in human plasma were also dysregulated in human IHD myocardial tissue; 2. Comprehensively examine the functional genomic pathway perturbations in human IHD myocardium. Methods: 193 metabolites and 5,400 proteins were measured by LC-MS in myocardial tissue from cryopreserved hearts of 14 patients with ischaemic heart disease and 10 healthy donor hearts. Mann-Whitney tests were used to compare the protein and metabolite data in IHD versus controls, and permutation-based FDR. Results: Uridine metabolites uridine (P=7E-6) and uridine metabolite 2-deoxycitidine (P=4.6E-5), and protein uridine 5-monophosphate synthase (P=3.7E-2) were significantly elevated, and proteins pseudouridine 5-phosphatase (P=1.3E-2), and UDP-N-acetlyglucosamine-peptide N-acetlyglucosaminyltansferase (P=2E-3) were significantly decreased in IHD myocardium compared to control. Plasma methionine was previously associated with two CAD loci: WDR12 (P=3.5E-2), and COL4A1/COL4A2 (P=1.5E-2). In IHD myocardium, methionine metabolites taurine (P=1.2E-3) and cysteamine (P=2.7E-4) were significantly elevated, whereas methionine (P=5E-4) was significantly reduced. Purines allantoin and guanosine monophosphate (GMP) were previously associated with two CAD loci: allantoin with PPAP2B (P=1.2E-2); GMP with CDKN2B (P=1.95E-2). Purines allantoin (P=1E-6), ADP (P=1.3E-2), xanthosine (P=3.1E-2) and xanthenuric acid (P=2E-4) were significantly elevated in ischaemic myocardium, whereas cAMP was reduced (P=4.8E-2). Conclusions: Integration of genomic, proteomic, and metabolomic data in a large community-based cohort and in human IHD myocardium implicates the uridine, methionine, and purine pathways. These highly novel findings may offer new therapeutic strategies in IHD, which we will investigate mechanistically in model systems. [ABSTRACT FROM AUTHOR]

Introduction: Patients undergoing TKA or THA have traditionally been managed post-operatively as inpatients. However, with current surgical techniques and pain management, there is evidence that outpatient joint arthroplasty can be safely performed in selected patient. This systematic review and meta-analysis aimed to compare the post-operative complication rates of outpatient and inpatient TJA with subgroup analysis of TKA and THA., Methods: Electronic searches were performed using five databases from their date of inception to October 2018. Relevant studies were identified, with data extracted and meta-analyzed from the studies., Results: From seven included studies, 176,179 patients were inpatient TJA and 1613 were outpatient TJA. The outpatient and inpatient TJA cohorts had similar mean age and BMI, with a greater proportion of females in the inpatient group. For TJA we found no significant difference in total complications (P = 0.06), major complications (P = 0.59), readmissions (P = 0.60), DVT (P = 0.94), UTI (P = 0.50), pneumonia (P = 0.42) and wound complications (P = 0.50) between the outpatient and inpatient groups. However, there were fewer transfusions (P = 0.05) but increased reoperations (P = 0.02) in the outpatient TJA group. Subgroup analysis of TKA (P = 0.25) and THA (P = 0.39) also found no significant differences in total complications between the outpatient and inpatient groups., Conclusion: Outpatient TJA had comparable total complication rates to inpatient TJA. Along with that outpatient TJA can significantly reduce costs to healthcare systems but careful pre-operative patient selection is required to optimize outcomes. More quality randomized controlled trials with longer follow-up periods are needed to add to this body of evidence., (© 2019 Professor P K Surendran Memorial Education Foundation. Published by Elsevier B.V. All rights reserved.)