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Abstract. Lundin P, Jensen J, Eriksson SV (Department of Medicine, Danderyd Hospital, Danderyd, Sweden, and Department of Medicine, Huddinge Hospital, Stockholm, Sweden). Reproducibility of on-line vectorcardiography measurements in patients with and without acute ischaemic heart disease. J Intern Med 1997; 242: 117-24.Objectives. The aim of the present study was to determine inter and intraobserver variations of measurements with on-line vectorcardiography (VCG). Design. The VCG registrations were evaluated by two independent observers. One observer also evaluated the VCG registrations on two separate occasions. Monitored VCG variables were: ST vector magnitude (ST-VM), ST vector lead X (ST-X), ST change vector magnitude (STC-VM) and QRS vector difference (QRS-VD). Subjects: On-line VCG was performed for 24 hours in 60 patients (10 with low probability of ischaemic heart disease, 25 with unstable angina pectoris and 25 with acute myocardial infarction). Results. A close correlation between the two observers and small coefficients of variation were found regarding the ST-VM initial value (r ϭ 0.99, 4.7), the ST-X maximum depression (r ϭ 0.99, 3.2) and the QRS-VD end value (r ϭ 0.98, 5.6). A less close correlation and higher coefficients of variation were found regarding the number of QRS-VD episodes (r ϭ 0.94, 41.5), ST-VM episodes (r ϭ 0.89, 37.8) and STC-VM episodes (r ϭ 0.87, 35.1). Correlation coefficients and coefficients of variations for VCG measurements performed on two separate occasions by one observer ranged from 0.97 to 0.99 and from 18.1 to 1.8 respectively. Three (12%) of 25 patients with acute myocardial infarction did not meet the VCG infarction criterion (QRS-VD Ն 15 Vs) by both observers. In addition, five (20%) of the 25 patients with unstable angina pectoris met the VCG infarction criterion by both observers. Conclusion. The inter and intraobserver variation for VCG interpretations was low, but the number of QRS-VD, ST-VM and STC-VM episodes varied between the two observers. This finding suggests that additional training may improve the results. Caution is also recommended in using VCG to rule out or establish the diagnosis of acute myocardial infarction.

31By applying whole exome sequencing and deep targeted sequencing on bladder 32 tumors, it was recently shown that tumors developed years apart in the same patients 33 share multiple mutations and hence are clonally related 1-3 . Furthermore, apparently 34 normal urothelium has been documented to contain mutations with low allele 35 frequencies (~3%) that are typically observed at high frequencies in tumors (clonal 36 mutations) 1-3 . Multiple studies have investigated genomic alterations in normal 37 appearing bladder tissue from cystectomy specimens, however using technologies 38 that do not allow detection of low-frequency mutations. The genomic alterations 39 observed in these studies include copy number alterations of chromosome 5, 9, 13, 40 16, and 17 as well as mutations or loss of RB1 and TP53 4-9 . These findings 41 corroborates the suggestions of the presence of field cancerization in the bladder. 42 Similar results have been reported in other tissue types, where studies have revealed 43 the presence of mutations in well-characterized cancer driver genes in apparently 44 healthy tissue and pre-cancer lesions 10-13 . 45 46 Bladder cancer (BC) is multifocal in almost half of the cases with primary tumour and 47 101 102 Analysis of field cancerization. Patients 1 and 2 presented with multifocal disease, 103 whereas patients 3 and 4 had unifocal disease. In patients 1 and 2, 39% (25/64) of the 104 mutations were N-Mutations, and 34% (22/64) were S-Mutations. Mutations called in 105 patients 3 and 4 were mainly T-Mutations, with only 5% (7/143) being N-Mutations and 106 13% (19/143) S-Mutations -indicating that uni-and multifocal patients may show 107 different levels of field cancerization. Mutations in known BC driver genes were 108 detected in both N-, S-and T-Mutation groups, most of them being among T-109 Mutations. However, in patient 1, two N-mutations were observed in bladder cancer 110 driver genes. Damaging mutations were present in all N-, S-and T-Mutation groups. 111 We detected the introduction of premature stop codons, mainly in the T-Mutation 112 group. However, for patient 1 premature stop codons were solely observed within the 113 N-and S-Mutations. Mutation allele frequencies (AFs) varied for the different 114 mutations detected but were generally low for N-Mutations and high for T-Mutations. 115 See Figure 1b and Table 1 for details. 116 117 131 132 Allele frequencies (median (min-max)) N-Mutations 0.042 (0.029-0.091) 0.067 (0.035-0.15) 0.070 (0.049-0.091) 0.059 (0.049-0.091) T-Mutations 0.23 (0.049-0.31) 0.13 (0.031-0.40) 0.17 (0.039-0.50) 0.16 (0.032-0.67) S-Mutations (Normal pool) 0.022 (0.0074-0.14) 0.033 (0.0064-0.063) 0.10 (0.014-0.13) 0.025 (0.0065-0.13) S-Mutations (Tumor pool) 0.20 (0.067-0.44) 0.077 (0.016-0.56) 0.13 (0.057-0.19) 0.15 (0.020-0.61)