Thoracic endovascular repair versus open surgical repair — which is the more cost-effective intervention for descending thoracic aortic pathologies?

Objective: Endovascular treatment is increasingly used to treat complicated aortic pathology. The aim of the study was to assess if compared with operative repair, thoracic endovascular repair of aorta (TEVAR) was associated with a cost benefit in management of diseases affecting the descending thoracic aorta. We also compared early and mid-term outcomes between the two groups. Methods: Clinical characteristics, outcomes and hospitalisation costs of 84 consecutive patients undergoing intervention for conditions affecting the descending thoracic aorta were reviewed retrospectively. Hospitalisation costs were calculated from National Health Service (NHS) reference costs for staff time, consumables, transfusion and length of stay. Results: Apart from a higher frequency of acute type B dissection (16/45 vs 5/39, p = 0.047) in the TEVAR group, the baseline characteristics were similar. TEVAR was associated with significant reductions in morbidity (renal dysfunction 11 (31%) vs 5 (10%) p = 0.025; in-hospital death 7 (20%) vs 3 (6%), p = 0.03; median intensive therapy unit (ITU) stay 6 (3–11) vs 1 (1–4), p < 0.0001). TEVAR was associated with significantly increased procedural costs (£2468 (€2961) vs £9581 (€11495) p ≤ 0.0001). This was chiefly attributable to the cost of endovascular stents. There was no significant difference in overall hospitalisation costs. TEVAR was associated with significantly lower freedom from death or re-operation (log rank p = 0.048). Conclusions: TEVAR is associated with reduced morbidity and mortality in the short term. However, no cost benefit was seen with TEVAR even in the short term. In the long term, due to increased risk of re-interventions TEVAR may actually prove to be a more expensive therapeutic option.     

Bleeding incidence and risk factors among cancer patients treated with anticoagulation

Compared to age-matched controls, cancer patients have increased risk of bleeding when treated with anticoagulation. However, there are little data regarding bleeding as it relates to anticoagulant choice and other risk factors. We evaluated the six-month incidence of bleeding among patients treated with anticoagulation who had bleeding risk factors. Data were obtained from Explorys (IBM Watson, Inc.), which pools data from multiple US healthcare organizations. Cohorts of patients were created to compare bleeding events between cancer and non-cancer patients treated with anticoagulation within six months of starting anticoagulation. Potential bleeding risk factors such as cancer type, metastatic disease, obesity, chronic kidney disease stage III or higher, and platelet count were evaluated. We compared ratios of numbers of patients in specific cohorts using chi-squared tests with continuity correction. The cohort comprised 3 283 140 cancer patients, of whom 435 140 (13.3%) received anticoagulation within six months of their cancer diagnosis. Bleeding incidence was higher in cancer vs non-cancer patients across all anticoagulants studied: warfarin 20.2% vs 12.6%, rivaroxaban 16.7% vs 12.1%, LMWH 13.2% vs 9.7%, and apixaban 14.5% vs 9.3%, P < .001 for all comparisons. Among all anticoagulants except warfarin, we found increased bleeding incidence in cancer patients with metastatic disease, gastrointestinal primary, CKD ≥ stage III, and platelets <100,000 × 10⁹/L. Bleeding incidence was higher in cancer patients regardless of the anticoagulant used. Patients with gastrointestinal malignancies had a higher incidence of bleeding compared to other tumors across all anticoagulants. Other factors associated with increased risk of bleeding included metastatic disease, chronic kidney disease, and thrombocytopenia.     

Recent developments on coronary microvasculopathy after heart transplantation: a new target in the therapy of cardiac allograft vasculopathy

Heart transplantation (HTx) is the treatment of choice for patients with refractory end-stage heart diseases. Although the procedure is considered effective in extending and improving quality of life, the onset of cardiac allograft vasculopathy (CAV) continues to limit the long-term success of HTx. Emerging data indicate that the endothelium plays a significant role in the onset, progression and complication of this multifactorial disease, with both immunologic and nonimmunologic risk factors contributing to its development. Improving our understanding of the integral role of the coronary microcirculation in CAV is of crucial clinical interest since it could provide further insights into the related pathophysiological mechanisms and possible new strategies for CAV prevention and therapy. Assessment of coronary microvasculopathy has been shown to be of predictive value after HTx. Predominant allograft microvascular dysfunction is detectable in 15-20% of patients after HTx. Very recently, stenotic microvasculopathy (detected in biopsy samples) has been characterized as a prognostic factor for long-term survival after HTx. The ability to detect and distinguish changes in epicardial and microvascular function may aid in identifying modifiable factors that lead to CAV. Improved immunosuppressive drugs, including mycophenolate mofetil and proliferation signal inhibitors, as well as statins (in part via immunomodulation), may have a beneficial effect on coronary microcirculation after HTx, although there is still a need to confirm the impact of vasodilators in improving the prognosis of HTx patients. We review the role of coronary microvasculopathy in HTx, its prevention and new potential pharmacological interventions.     

Cardiomyopathy in patients with POMT1-related congenital and limb-girdle muscular dystrophy

Protein-o-mannosyl transferase 1 (POMT1) is a glycosyltransferase involved in α-dystroglycan (α-DG) glycosylation. Clinical phenotype in POMT1-mutated patients ranges from congenital muscular dystrophy (CMD) with structural brain abnormalities, to limb-girdle muscular dystrophy (LGMD) with microcephaly and mental retardation, to mild LGMD. No cardiac involvement has until now been reported in POMT1-mutated patients. We report three patients who harbored compound heterozygous POMT1 mutations and showed left ventricular (LV) dilation and/or decrease in myocardial contractile force: two had a LGMD phenotype with a normal or close-to-normal cognitive profile and one had CMD with mental retardation and normal brain MRI. Reduced or absent α-DG immunolabeling in muscle biopsies were identified in all three patients. Bioinformatic tools were used to study the potential effect of POMT1-detected mutations. All the detected POMT1 mutations were predicted in silico to interfere with protein folding and/or glycosyltransferase function. The report on the patients described here has widened the clinical spectrum associated with POMT1 mutations to include cardiomyopathy. The functional impact of known and novel POMT1 mutations was predicted with a bioinformatics approach, and results were compared with previous in vitro studies of protein-o-mannosylase function.