Impact of inter-hospital transfer on success of angioembolization for lower gastrointestinal bleeding.

BACKGROUND: Angioembolization is a useful therapeutic tool for lower gastrointestinal bleeding (LGIB) however is only available at centres with specialist interventional radiology departments. Delay in angioembolization of greater than 120-150 minutes is associated with higher rates of non-therapeutic angioembolization. METHODS: This retrospective review analysed the impact of interhospital transfer on timing and success of angioembolization in adults with LGIB. RESULTS: Of the 121 patients who underwent CTMA at a peripheral hospital for LGIB, only 20.7% had positive CTMA (n = 25). Of the 24 patients who were transferred for the purpose of angioembolization, only five ultimately had successful embolisation (20.1%). Patients who had unsuccessful angioembolization had a significantly longer mean time from arrival at the tertiary hospital to angioembolization compared to patients who had successful angioembolization (mean 375 versus 175 min, P = 0.001). There was no association of patient haemodynamics, use of anticoagulant or antiplatelet therapy, and transfusion requirement with success of angioembolization. CONCLUSION: Interhospital transfer is associated with delay in angioembolization. Delay after arrival at the receiving hospital is associated with unsuccessful angioembolization.

Severe heart failure and early mortality in a double-mutation mouse model of familial hypertrophic cardiomyopathy.

BACKGROUND: Familial hypertrophic cardiomyopathy (FHC) is characterized by genetic and clinical heterogeneity. Five percent of FHC families have 2 FHC-causing mutations, which results in earlier disease onset, increased cardiac dysfunction, and a higher incidence of sudden death events. These observations suggest a relationship between the number of gene mutations and phenotype severity in FHC. METHODS AND RESULTS: We sought to develop, characterize, and investigate the pathogenic mechanisms in a double-mutant murine model of FHC. This model (designated TnI-203/MHC-403) was generated by crossbreeding mice with the Gly203Ser cardiac troponin I (TnI-203) and Arg403Gln alpha-myosin heavy chain (MHC-403) FHC-causing mutations. The mortality rate in TnI-203/MHC-403 mice was 100% by age 21 days. At age 14 days, TnI-203/MHC-403 mice developed a significantly increased ratio of heart weight to body weight, marked interstitial myocardial fibrosis, and increased expression of atrial natriuretic factor and brain natriuretic peptide compared with nontransgenic, TnI-203, and MHC-403 littermates. By age 16 to 18 days, TnI-203/MHC-403 mice rapidly developed a severe dilated cardiomyopathy and heart failure, with inducibility of ventricular arrhythmias, which led to death by 21 days. Downregulation of mRNA levels of key regulators of Ca(2+) homeostasis in TnI-203/MHC-403 mice was observed. Increased levels of phosphorylated STAT3 were observed in TnI-203/MHC-403 mice and corresponded with the onset of disease, which suggests a possible cardioprotective response. CONCLUSIONS: TnI-203/MHC-403 double-mutant mice develop a severe cardiac phenotype characterized by heart failure and early death. The presence of 2 disease-causing mutations may predispose individuals to a greater risk of developing severe heart failure than human FHC caused by a single gene mutation.